The complex relationship between the built

There’s something in my head (but it’s not me).

The complex relationship between the built environment and schizophrenia - from aetiology to recovery.

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Papers and exegesis submitted for the degree

Doctorate of Philosophy

Sydney University, June 2012

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Jan Golembiewski, BFA, BArchS, MArch

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DECLARATION

This work is original and wholly the work of the candidate, Jan Golembiewski, including all the enclosed papers, except where duly cited.

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Supervisor Dr. Peter G. Armstrong (FADP, U. Syd).

Other expert guidance and associate supervision also received from:

Dr. Rena Archer (FADP, U. Syd.), Dr. Michael Robertson (Medical Ethics and the Law, Psychiatry, U. Syd.), Dr. Arne Dietrich (Neuroscience American University of Beirut), Dr. Branka Spehar (Psychology, UNSW) and Dr. Richard White (Psychiatry, U. Syd.), Dr. Martes Alison.

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SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

CONTENTS

CONTENTS ............................................................................................................................................. 3 ABSTRACT ............................................................................................................................................. 8 ACKNOWLEDGEMENTS ................................................................................................................... 10 THANKS ................................................................................................................................................................. 13 FOREWORD: READING A RHYZOMIC THESIS. .......................................................................... 16 INTRODUCTION: THE EXECUTIVE SUMMARY ......................................................................... 21 PURPOSE STATEMENT .................................................................................................................... 25 POTENTIAL SIGNIFICANCE ............................................................................................................ 26 INCIDENCE RATES ................................................................................................................................................ 29 SOCIO-‐ECONOMIC COSTS .................................................................................................................................... 33 RESEARCH QUESTIONS ................................................................................................................... 34 QUESTION 1: SPECIALIST PSYCHIATRIC FACILITIES TO HELP PEOPLE WITH SCHIZOPHRENIA .............. 35 QUESTION 2: WHAT IS SCHIZOPHRENIA? ....................................................................................................... 41 QUESTION 3: THE ROLE OF THE BUILT ENVIRONMENT IN THE AETIOLOGY AND SYMPTOMS OF SCHIZOPHRENIA ................................................................................................................................................... 44

HOW THIS RESEARCH MAY HELP ................................................................................................ 47 METHODOLOGY ................................................................................................................................. 50

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THESIS INCLUDING PUBLICATION: LIMITATIONS AND ADVANTAGES ........................... 56 PAPERS, PRESENTATIONS AND INCOMPLETE ARTICLES NOT INCLUDED .................... 59 QUESTION ONE: HOW CAN SPECIALIST PSYCHIATRIC FACILITIES IMPROVE THE WAY THEY HELP PEOPLE WITH SCHIZOPHRENIA? ......................................................................... 61 START MAKING SENSE: APPLYING A SALUTOGENIC MODEL TO ARCHITECTURAL DESIGN FOR PSYCHIATRIC CARE. ............................................................................................................................................. 62

SO YOU’RE GOING TO DESIGN A MENTAL HEALTH FACILITY? HOW TO MAKE IT FUTURE-‐PROOF. ....... 97 MENTAL ILLNESS AND THE URBAN ENVIRONMENT .......................................................... 125 DETERMINISM AND DESIRE: SOME NEUROLOGICAL PROCESSES IN PERCEIVING THE DESIGN OBJECT. .............................................................................................................................................................................. 126 A TAXONOMY OF THE NEURO-‐CORRELATES OF PERCEPTION, ACTION AND DESIRE. ............................. 129 Affordances; the heart of perception and the automation of action. ................................... 130 Behaviour-‐settings: the context of affordances and the automation of inhibition. ........ 132 Creativity and awareness: the deliberate extension of affordances and behaviour-‐ settings. ............................................................................................................................................................ 135 WHAT DRIVES ENGAGEMENT? THE FACTORS OF SALIENCY. ..................................................................... 138 USING THEORY IN PRAXIS: DETERMINISM .................................................................................................... 149 CONCLUSIONS ..................................................................................................................................................... 156 GENERAL HOSPITAL DESIGN ...................................................................................................... 158 THE NEUROLOGICAL BASIS OF SALUTOGENIC HEALTHCARE DESIGN. ...................................................... 159 A BROADER APPLICATION OF THE SALUTOGENIC METHODOLOGY IN MENTAL HEALTH SERVICES ......................................................................................................................... 182

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MOVING FROM THEORY TO PRAXIS ON THE FLY: INTRODUCING A SALUTOGENIC METHOD TO EXPEDITE MENTAL HEALTH CARE PROVISION IN DISASTER SITUATIONS. ................................................................. 183

2. QUESTION TWO: WHAT IS SCHIZOPHRENIA? .............................................................. 199 SCHIZOPHRENIA AND PERCEPTUAL EXPERIENCE ............................................................. 200 THE RIDDLE OF PSYCHOTIC PERCEPTION RESOLVED: THE INTEGRATED FINDINGS OF AN IN-‐DEPTH ANALYSIS OF CURRENT HYPOTHESES FOR SCHIZOPHRENIA. ..................................................................... 204

Healthy salience ........................................................................................................................................... 210 The neural architecture of healthy attention ................................................................................. 238 The emergence of symptoms .................................................................................................................. 257 Summary: Solving the aberrant salience riddle ............................................................................. 284 Appendix I: The psychotic spectra continuum ................................................................................ 286 Appendix II: Refuting noise theories .................................................................................................... 289 Appendix III: Notes on data sources for table 3. ............................................................................ 293 3. QUESTION THREE: WHAT IS THE ROLE OF THE BUILT ENVIRONMENT IN THE AETIOLOGY AND SYMPTOMS OF SCHIZOPHRENIA? ........................................................... 295 LOST IN SPACE: THE ROLE OF THE ARCHITECTURAL MILIEU IN THE AETIOLOGY AND TREATMENT OF SCHIZOPHRENIA. ................................................................................................................................................ 296

EMOTIONAL AFFORDANCES ............................................................................................................................. 307 Physical affordances ................................................................................................................................... 309 Identification affordances ........................................................................................................................ 310 Narrative affordances ............................................................................................................................... 312 Addressing bottom-‐up attention deficits ........................................................................................... 323 Aesthetic and natural engagement: .................................................................................................... 325

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Environmental generosity ....................................................................................................................... 327 Dealing with top-‐down superfluity ...................................................................................................... 329 ARE DIVERSE FACTORS PROXIES FOR ARCHITECTURAL INFLUENCES? A CASE FOR ARCHITECTURE IN THE AETIOLOGY OF SCHIZOPHRENIA. ............................................................................................................. 336

AUTOMATIC AND OPPORTUNISTIC PSYCHOTIC BEHAVIOURS ...................................... 356 COMMON PSYCHOTIC SYMPTOMS CAN BE EXPLAINED BY THE THEORY OF ECOLOGICAL PERCEPTION. .............................................................................................................................................................................. 358 Ecological perception ................................................................................................................................ 361 PSYCHIATRIC VIOLENCE .............................................................................................................. 372 INTRODUCING THE CONCEPT OF REFLEXIVE AND AUTOMATIC VIOLENCE: A FUNCTION OF ABERRANT PERCEPTUAL INHIBITION. ................................................................................................................................ 373

Automatic perception and reflexive action ...................................................................................... 379 Deficits of perceptual inhibition ............................................................................................................ 382 Automatic triggers and delusional rationalizations: .................................................................. 386 PSYCHIATRIC SUICIDE .................................................................................................................. 396 FURTHER RESEARCH .................................................................................................................... 398 GLOSSARY OF TERMS ........................................................................................................................................ 401 AUTHOR AND KEYWORD INDEX ............................................................................................... 425 BIBLIOGRAPHY ............................................................................................................................... 433

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Callan Park, in Rozelle, Sydney is typical of the buildings designed by John Soan for Tomas Storey Kirkbride, a Quaker in the mid nineteenth Century who advocated the moral treatment of the insane. This thesis is not a historical account. The intentions of Kirkbride can be read into my own approach. I see the environment as no less active than the social environment or even psychotropic medications. Like Kirkbride, I believe that architects, clinicians and researchers have a moral responsibility to the patients who our efforts will serve. (Source: Simon Fieldhouse) 7


ABSTRACT

This thesis explores schizophrenia and the dynamics it has with the built environment. In doing this, three research questions are addressed. The answers are all delivered in article format – most of which have been published.

Question one: ‘what can architects do with the design of specialist psychiatric facilities to help people with schizophrenia?’ required a greater depth of the understanding of schizophrenia than is available in print. My need to know not only what schizophrenia is (the psychogenesis), but what it does to perception (the phenomenology) drove a second research question; ‘What is schizophrenia?’ The answer to this question is a cogent integrative meta-hypothesis, spanning and integrating datasets and ideas from areas of science that are rarely connected.

Findings in this research led to speculation on the possible role of the built environment beyond the treatment of the syndrome - possibly even as an aetiological factor. As such, the thesis finishes with the question three: What is the role of the built environment in the aetiology and symptoms of schizophrenia?

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Pithy answers to the questions are:

Q.1) Designing with a view to fostering a sense of coherence promises that design decisions will firstly ‘do no harm’. Further, by building opportunities for patients to explore the sensibilities of meaning, comprehensibility and by providing for manageability, facilities themselves may assist with recovery.

Q.2) Schizophrenia appears to be a syndrome where bottom-up perception diminishes and top-down perception becomes over stimulated and over focused. This combination gives rise to eight syndromes. These syndromes can explain all the symptoms of schizophrenia.

Q.3) The role of the built environment in schizophrenia is found to be at least as significant as any other major known epidemiological factors. But the many functions of the built environment are complex, leaving several possibilities worthy of future exploration.

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ACKNOWLEDGEMENTS

I must dedicate this thesis to my father, Olek (Alex) Golski because a thesis must explore a gap and his death forced me to learn about impossible gaps and have the courage to span them.

My father knew gaps like few others. As a young boy he was cast into one of the most fabled gaps of history: one of Hitler’s concentration camps. The gap I have chosen to explore is also fabled and for many of the same reasons. Like the holocaust, schizophrenia is better described as an abyss than a gap. And like the holocaust, schizophrenia has claimed untold numbers of lives to a madness that few of us have the courage to attempt to understand.

It is not just a poetic metaphor – it’s a central premise of this thesis that the edge of a cliff demands a leap. I discovered this precipice in 2006 while designing a new mental health facility for the New South Wales Health Department and I was unsatisfied with the regulatory guidelines that drove the project and still drives similar projects. Like many other architects faced with similar jobs, I intuitively felt that there is a relationship between mental illness and the built environment. But it was a commercial necessity to ignore that relationship because knowledge is time consuming and difficult to come by. 10


Little did I know then that it’s not psychiatrists or psychologists but architects that do almost all the research that ever goes into the design of better psychiatric facilities, and if we have a problem with the guidelines, it’s ours (as a profession) to fix. I did my best then, but no sooner had the project come to a close, and I returned to university and to address that gap.

The research component of my Master’s degree was far from sufficient. To return to my metaphor, the research I did for the Master’s was really just scouting around the edge. My leap occurred only when I arrived at Sydney University at the beginning of 2009, to commence this PhD.

I have a lot of people to thank for this privilege. Nobody could have been more kind and supportive than Dr. Bem Le Hunte, my wife. Without her constant support, her training and her pressure to complete this project in good time (‘have you finished yet?’ became a daily chant, well before the thesis was even due), I would have never made this leap, much less found my way to the other side.

I also have to thank my supervisor, Dr. Peter Armstrong. In a supervision meeting, very early on, Peter and I were discussing the scope of this project and the time it may take in achieving my goal. Peter leaned back and said, “It’s an awfully big gap isn’t it?” Once I admitted that neither he, nor I knew the half of it, he added. “Well, if I’ve ever met a man who can pull a rabbit out of a hat, it’s you.” I don’t know, Peter, if this thesis is a rabbit exactly. To me it resembles a jumbo-jet, but whatever – you deserve thanks for 11


the continual support you have given me and for helping me through the trials I’ve had on the way. I’ve always suspected that you kept me on a loose rein because you (like me) intuitively felt that there is another horizon, and that the world could be a better place if I find it. Only recently, schizophrenia claimed your sister’s life. I know it’s presumptuous but I felt, throughout the entire period, that it was her experience that you reflected on when reading and hearing about my discoveries. I hope, that in some way, this thesis helps you better understand your sister’s trial – her gap – the great unexplained algebra of the schizophrenia diagnosis.

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Thanks

My mother, Kathy Golski, for feeding and helping me when I’ve been pressed for time.

My supervisors – Dr. Peter Garth Armstrong, my principle supervisor from the outset. There are many times when I may have looked well out of my depth. Thanks for bearing with me and taking this journey to the end.

Dr. Branka Spehar, Dr. Arne Dietrich and Dr. Michael Robertson. All of you had deep insight into the mechanisms of the human mind and were able to steer me out of the deep end. Thanks for your time and patience.

Dr Rena Czaplinska Archer, Thank you for finding me a place in the faculty. With a project as peculiar as mine, it was difficult to find someone willing to say “I’ll do it,” and you were my hero at the moment when that counted.

Dr. Richard (Dick) White and Dr. Anthony Harris. Thanks for taking the time to read through my work and be of assistance, even for the short periods you were available.

Tuesday (Martes Alison) for being a sounding board particularly as I gathered hypotheses and data on the psychogenesis of schizophrenia.

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To my friends and colleagues at the Schizophrenia Research Institute, the Schizophrenia International Research Society, The International Academy for Design and Health and the countless other researchers elsewhere who provided the stepping-stones I needed to cross this gap.

My kids, for all the time I should have been doing stuff with them – and especially Taliesin who, when I’ve been stuck was always great at explaining basic scientific principles that evaded my memory.

The university staff; Joanna, Penny, Kim, Suzanne, Jennifer and others who beaver away in secret, sorting out all the paperwork that proliferates at the university. The librarians: Tom, Rosemary, Bill, Tina and others for teaching me Endnote, finding obscure documents deep in storage and for locating books in faraway places. Bruce for the hundreds of times he’s helped me out when I’ve lost my keys, and to Leslie, Ben, Julius and Ken for all their technical assistance.

To other students and academics, both at Sydney and other universities, who have kept me on track and inspired. Some deserve a special mention – those who have reviewed my work (often doubly blinded) and who have always given valuable feedback.

I also want to acknowledge my starting point as I reach for my terminal degree. As a boy, Peter Muller took it upon himself to be my mentor and to teach me the basic principles of architecture. I was only in my mid teens when he taught me how to cut 14


sections and draw plans. This work is much more theoretical than those practical origins, but in everything I write, I hope that its applicability to praxis is always present.

To all of you, a big and heartfelt thanks.

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FOREWORD: READING A RHYZOMIC THESIS.

This thesis was written to be useful. It was to have broad and practical application but this came at the expense of the tight and cogent narrative structures that PhD theses traditionally aspire to. The thesis is largely composed of separate articles, each with its own practical focus.

I wanted a PhD degree, but a tome gathering dust in the Fisher Library like a medieval manuscript was not my objective. I always wanted to do my PhD by publication and viva voce as my colleagues have done in Cambridge and Berkeley, but that’s not currently allowed at University of Sydney. I fancifully considered writing an article on the background for my study, another on my literature review, an article about my methodology and another on my findings, but this goal is not particularly practical, nor is it very likely to succeed. Every article needs its own literature search, methodology and findings – otherwise they have little value and won’t get published, and even if they did, their usefulness would be questionable. What good is a literature review that covers a gap as broad as mine? Instead the thesis became a collection of mini-theses. And there’s the possibility that it’ll be read that way – as a fractured document that says many things rather than honing in on the archetypal single gap and approaching it with new empirical studies the way a thesis normatively is expected to. 16


The perception that the thesis might be fractured is also driven by a second reason – it set out to cover a cavernous knowledge gap. Thus some articles were conceived as scaffolding for others: (Golembiewski, in review-d) provides support for other articles such as (2013), for example. Sure this logic is linear, but a reader can equally trace other linear tracks through the thesis to come to other conclusions. (2010b) Provides a scaffolding and a methodology for (2012e), but more complex still, the basis of (2010b) is analysed on a neurological level in (in review-d) and (2012e) provides a foundation for (2010b). As jumbled as it all sounds, each of these threads is coherent. But this thesis can be read any number of other ways – and should be, depending on what a reader wishes to take from it.

Instead of tracing a singular narrative from the front to the back, the logic of my thesis is more like an academic book than a fairy-tale. It’s intended to be read in parts, entered and exited at any point, by people who are interested in the subject matter and want to find out more but not in material that is of peripheral interest, indeed it’s intended to be read principally as separate articles. Thus the thesis structure is in a fundamental way quite rhizomic, as Deleuse and Guittari proposed that academic writing should be.

But the Deleusian model doesn’t apply in full. I’m not a post-modernist and the thesis can also be taken as a whole. In its completeness it is more than the sum of its parts. The thesis is thus also arbourescent, and its structure is ultimately very simple – although still non-linear. Each of the three research questions make a section, and these are sandwiched between the front and back matter of the exegesis: 17


Part 1: Background, Aims, Methodology etc.

Part 2: Question One: How can architects improve specialist psychiatric facilities for people with schizophrenia?

Part 3: Question Two: What is Schizophrenia?

Part 4: Question Three: What is the Role of the Built Environment in the Aetiology and Symptoms of Schizophrenia?

Part 5: Further Research, Index and bibliography.

In a single-minded reading, the thesis is an exploration of the influence of the architectural environment on schizophrenia. And ultimately, the findings are singular also: Schizophrenia is conceived as a diagnosis given to the bizarre behavioural symptoms that follow an imbalance within the perceptual system. But it’s really a coincidence that my aims and findings actually link up well. At the top level, the thesis looks broadly at the phenomenology of schizophrenia, because when perception is awry, phenomenal experience suffers. The behavioural peculiarities of schizophrenia sufferers are not disingenuous but are genuine reactions to a very odd take on the world. This is particularly important in the architectural context because the built environment is usually all that is left once the social environment is depleted (as is always the case in

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any valid diagnosis of schizophrenia by American Psychiatric Association, 1994, p. 285 criteria.)

This is a very important reading of the thesis, and it would be lovely if academics and practitioners would take note and change their perspectives because of it. But I’m sceptical about whether academics and practitioners ever consult theses, much less change their opinions because of what they read therein. Even published books are a little old fashioned, and it’s my belief that people are more likely to read journals – so in the interests of effective dissemination, my chosen mode is the academic article.

Realistically, how the thesis is to be read depends on what (and how much) a reader needs to know and why. If you are a health architect, you’ll find it really useful to know how patients tick, and what kinds of interventions may be useful for given situations. You may also want to know the implications for healthy people. For you, question 1 will be recommended reading. In this case the papers in the later sections of the thesis provide only empirical support, which you’d only bother with if you were sceptical. If you were a clinical psychologist wanting to understand patient symptoms, question 2 would be your target. If you wanted to understand patient behaviour, question 3 might also be useful. An epidemiologist would start with question 3 and might go no further.

The result is, that the reading of the thesis is a very personal experience. The writing was too. The process consumed me for several years, and there can be no denying my passion for the subject and my findings. This is reflected in my writing style. Criticise it 19


as you may, it’s a fallacy that the academic can be truly extricated from their work. So I don’t hesitate to insert my personal viewpoint into my articles nor this exegesis. Where there is no first-person voice, you can assume that reviewers have been through and whitewashed the content to create the false veneer of impassive neutrality.

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INTRODUCTION: THE EXECUTIVE SUMMARY

If asked, what is the single most important contribution this thesis makes to knowledge, I would like to assert that ‘the Riddle…’ (from page 204) is the only comprehensive hypothesis for schizophrenia. It’s an outlandish claim, considering that the subject has been scrutinised for a century or so by thousands of researchers the world over - the keyword ‘schizophrenia’ turns up in over 6000 citations per year in a Medline search (see p. 206).

I never anticipated pulling such a body of data together. In fact, I never even realised that I was even trying to do so. It’s just that I naïvely thought that there must be someone who already had, and I thought I was trying to locate something that had surely been cognised before – some pearl of wisdom, while I write up what I find.

I knew that schizophrenia hadn’t been understood to the level where the effect of the environment meant, and I saw that as my job: a relatively appropriate step to take as a PhD project. But another Medline review of nearly 2000 articles carrying the keywords “schizophrenia AND hypothes*” revealed that at best, authors would focus on just one side of the syndrome (either the negative signs or just the positive symptoms) and ignore the other, yet in the schizophrenia diagnosis both sides of the syndrome are 21


ubiquitous, even if they are not directly observed by a clinician (American Psychiatric Association, 1994, p. 277). More often, authors hone in on a single gene or neuron and offer no cogent explanation why save saying that ‘it was implicated in schizophrenia.’ (Eg. Welch et al., 2011) Notable exceptions such as Gray, Feldon, Rawlins, Hemsley (1991), Fletcher and Frith (2009) and Kapur (2003) were inevitably also profoundly skewed, but at least all of these made some attempt to pull themselves from the mire of partially digested data and explain schizophrenia more holistically. It is like this small number of authors apparently spent enough time staring at the broader field of data (like some great random dot autostereogram) to discern some really relevant patterns, but still they missed the big picture. Like the autostereogram, the data on schizophrenia is apparently plagued by random data with produces definable patterns but no clear picture. It’s only after staring at it and going wall-eyed (that is seeing everything in inversed perspective) that a holistic 3D image becomes suddenly evident.

In three years of reading the most notable hypotheses and literally thousands of other findings, I suddenly saw that every one of the thousands of articles I read, as well as every diagnostic criteria and other symptom actually does make sense – and not only in a scattered way, but with a singular cogence. It was a bit like seeing the big image in the aforementioned autostereogram. Methodologically, it was like the payoff of a grounded theory approach, but not situated among people, but ideas and data. Like in a Hollywood movie, it happened not during my studying hours, but during a vivid dream.

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The exploration was intended to provide for better questions about the relevance of the built environment in schizophrenia, not to be the heart of the thesis, but there it was. If ever I needed to advance new knowledge, here was my opportunity. I had discovered something quite unexpected. As an architect I should have ignored it – the aetiology and psychopathology of schizophrenia was none of my business. But do you ignore the diamonds you find in a gold mine, just because you’re a gold-miner? I very nearly jumped boat and abandoned the hunt for ‘gold’ and made this question alone my PhD topic, but I was restricted by formal constraints. I was in the Faculty of Architecture, Design and Planning and my supervisor was an architect with no more than a flirting interest in schizophrenia. So I had to plough on and pursue the question of the built environment.

Even so, the model for schizophrenia that I present is quite literally the heart of the thesis, making up the whole of section 2 (from p. 204). It serves as a wonderful foundation – allowing my assertions about the environment to be translational rather than being based on original empirical studies. The theory I developed was that schizophrenia is fundamentally an illness of the perceptual system and that all perceptual stimulation must either make the condition more severe or incrementally better.

Fortunately this finding was very relevant to the built environment because the built environment is a ubiquitous a source of perceptual stimuli, and one that profoundly affects phenomenal experience. 23


In this context, the built environment (on all scales) reflects a concentration of many potentially active percepts, with each individual building offering a range perceptual opportunities – some of which are good, others harmful. Effectively this makes the built environment aetiologically culpable as a likely transmission pathway – in itself innocent an innocent agent, except as it carries dangerous psycho-agonists: like water for cholera.

The two other sections effectively emerged from the second: the first (question 1, from page 62) is how tailored environments should be shaped to mitigate the effects of schizophrenia. These articles are not about aetiology, but are about treatment.

The articles in the third section are about the culpability of designed objects, architecture and the urban environment in the aetiology of schizophrenia and related mental illnesses. This section (from page 296) finds the stimulation provided by the built environment culpable twice over. Firstly, for a lack of consideration of how it stimulates the formation and maintenance of delusions and hallucinations. But perhaps more importantly there’s the other side – the failure of architecture to stimulate where it can and should.

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PURPOSE STATEMENT

It is my aim to discover what influence the architectural environment has on schizophrenia.

Ultimately I want this work will reveal new architectural innovations and affordances that will assist: a) in urban planning to avoid schizophrenia onset and b) to assist in the treatment and management of schizophrenia.

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POTENTIAL SIGNIFICANCE

Schizophrenia is a debilitating and deadly illness that can strike in any social context anywhere in the world – although epidemiology of schizophrenia is subject to enormous variation (Kirkbride, Fearon, et al., 2007). The normative opinion among researchers is that schizophrenia not uncommon but reliable figures on schizophrenia incidence show only that it is subject to extreme variation. The fact is that 0.2% of Australia’s population had a diagnosis of schizophrenia in 2001 (a simple calculation extrapolated from reported figures (Carr et al., 2002) and the Australian population at the same time (Australian Bureau of Statistics, 2011)). Thus even the incidence of schizophrenia is a subject worthy of in-depth research.

For an analysis of incidence, please see p.29: Incidence of schizophrenia Schizophrenics lose their ability to interact meaningfully with society. They lose their somatogenic perception, meaning the connection with the senses that inform them about pain, hunger, comfort and other essentials is lost or unusually poor. People with schizophrenia also lose their abilities to manage day-to-day tasks. (Osmond, 1966; Searles, 1960; S. Williams, 2002b). Finally, and most famously, the ability to perceive 26


the outside world is hampered by interference from delusions, internal projections and hallucinations (Fletcher & Frith, 2009).

For hypotheses explaining the symptoms, signs and other consequences of schizophrenia, please see the articles starting on p. 204, p.358 and p.373. Furthermore, schizophrenia should be considered a deadly illness. About 5 to 8.5% of schizophrenics die by suicide (Harris & Barraclough, 1997; Palmer, Pankratz, & Bostwick, 2005), and a similar number by accident or unspecified violence (Ösby, Correia, Brandt, Ekbom, & Sparén, 2000). An estimated 2% die from catatonic complications (Wyatt, Alexander, Egan, & Kirch, 1988) and many others die from comorbid illnesses that would be treatable in healthy people but are difficult to treat in schizophrenia

because

of

negativism,

poor

comprehension

and

compliance.

Comorbidities lower life expectancy by about 9 years (Dembling, Chen, & Vachon, 1999). Overall, diagnosed schizophrenics have a life expectancy that is much lower than the general population, with two thirds of excess mortality being from ‘natural causes’ including heart disease and poorly managed diabetes (Auquier, Lançon, Rouillon, & Lader, 2007).

I propose that much of the suicide and accidental and violent death of schizophrenic patients (as well as the occasional

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violent death of others) is automatic opportunism. Please see psychiatric suicide on p. 396. Medication, the main mode of treatment, is well recognised as being ineffective in about 30% of cases (H. M. Jones, 2004), and when it is effective, it only treats some symptoms (Golembiewski, in review-d) (Page 199-). Psychotropic medication is thus is better understood as symptom management than treatment. Medication is rarely a perfect fit for patients and it causes an incredible array of undesirable side effects, some of which are permanent (S. Williams, 2002a). Psychotherapy is normatively considered useless for schizophrenics (S. Williams, 2002a) although clinicians sporadically report good results with various forms of talk therapy (Searles, 1960, 1965), CBT (cognitive behavioural therapy), physical therapy (Vancampfort et al., 2012) and even placebo treatment even though the efficacy of psychotropic medications is apparently decreasing (D. H. Freedman, 2010).

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Although it has been suspected for a long time that modifications to the environment will improve the well-being of the schizophrenics (Foley & Lacy, 1967; Osmond, 1966), very little research has been done to discover what those changes could be. This area of research has more or less vanished with the growth of other areas of focus - most schizophrenia research currently focuses on genetics and pharmacology.

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Incidence rates

Schizophrenia can develop anywhere, in any population and demographic. Despite this, its incidence is far from even. The most commonly reported figure for the worldwide average incidence is 1% over the course of a lifetime, but the reality is that the figure seems to be far lower, although in some locations at some points in history the figures have crept up and even exceeded this figure. The 1% is a ‘strategic’ number, presumably intended to bring attention to this very important cause, in the tradition of Florence Nightingale, who manipulated statistics to dramatize causes of preventable deaths and bring attention to her new methods of healthcare (H. Woodbury, 2008). A meta-analysis of 1,458 rates taken from 33 countries suggests that the incidence spans a distribution curve running from 7.7 to 43.0 cases per 100 000 people (i.e., 0.0077% to 0.043%) (J. J. McGrath, Saha, et al., 2004).

But the heterogeneity of rates is far more extreme than normalization curves would have us believe because the incidence is subject to extreme fluctuation based diagnostic criteria and paradigms (even before on social and physical environment are considered). At the moment, the sober figure mentioned by McGrath et al is modified by the removal of pellagra, scurvy, syphilis and hyperthyroidism from the diagnosis by the identification of distinct pathologies and by the removal of bipolar disorder, various forms of developmental disorder, affective psychoses and geriatric dementias by reclassification (American Psychiatric Association, 1994; Berrios, Luque, & Villagrán, 29


2003; Boyle, 2002; Hoffer & Osmond, 1963). As many as 1% of the population were committed in psychiatric hospitals and estimates of uncommitted and undiagnosed cases were estimated to make up 3% of the entire population of the USA in 1957 (Campbell, 1958).

Although schizophrenia was thought to have a relatively even distribution in terms of population-wide levels at that time, this opinion was based on assumptions rather than methodological empiricism (Campbell, 1958) and even on much smaller scales, the variation of incidence was already known to be enormous (Faris & Dunham, 1939). Since then, incidence patterns must have changed radically. The removal of nosological conditions from the schizophrenia diagnosis had marked huge changes in distribution of incidence patterns. Until the mid twentieth century, pellagra was common in the USA for instance. Especially in rural areas of the southern states where the diet (being based on maize) had no natural vitamin A. It’s possible that the inner city prevalence of schizophrenia at the time was also a product of diet – as poor people were removed from natural sources of vitamin C, it is conceivable that incidence of scurvy rose, although by the time of Faris and Dunham’s study, the cause of scurvy was well known and should not have been reflected in the data they collected.

With increasingly narrow diagnostic criteria, the heterogeneous incidence patterns of schizophrenia have become more predictable. As mentioned earlier, incidence tends to increase with exposure to urban settings. Against this backdrop, there is only one known outlier to this rule: the incidence in Chandigarh, a modern city designed by Le 30


Corbusier, in the state of Punjab, (India) which has lower incidence than its surrounding rural areas (Varma et al., 1997; Wig et al., 1993). The reason for this, like anything about schizophrenia, is unknown and has not been formally hypothesised. Chandigarh is an interesting case however, because it is exception it’s the exceptions that explain bigger patterns.

The conditions for the design of Chandigarh are discussed in depth in my paper: Determinism and Desire: A neurological language for architectural design (Golembiewski, 2013) (starting on page 126). This paper does not focus on schizophrenia, but it does outline why Chandigarh may be an exceptional case. Other known exceptions are high incidence rates among rural populations (their relationship with the nearest cities has not yet been tested to my knowledge). These occur in the north west of Ireland, in rural Scandinavia (especially in the north), and in Istria, a peninsula jutting into the Adriatic, currently part of Croatia, on the Italian and Slovenian border.

The placement of Istria is traditionally in the warpath of just about every major European conflict. And being in close proximity to Italy, Slovenia, Austria, Germany, Hungary and Bosnia-Herzegovina, its population has never recovered from the wars of

31


the twentieth Century and most of its buildings are still in ruins. Rather than mark an anomaly, the conditions in Istria possibly marks a local statistical aberration.

32


Socio-economic costs

Schizophrenia represents a huge social and financial burden to society – but not evenly distributed over the whole of society. Rather the strain is patchy and uneven because of inconsistent models of care, and because the greatest burden is usually handled by the families of those who suffer (Beecham & Knapp, 2001). Incidence and recovery rates also vary from region to region. But as a whole, the cost to Australia in 2001 alone was estimated to be $1.85 billion (about 0.5% of the GDP). Over a third of this was borne by families, and another $661 million in direct costs to the healthcare system and finally the indirect costs at $772 million in lost income and increased morbidity etc. (Carr et al., 2002).

To estimate the potential financial impact on this figure by the research that was conducted for this thesis will be a futile process because we cannot guess at the impact that my work may have. This thesis affects three domains: urban planning (where outcomes are intended to reduce the epidemiology of schizophrenia), psychiatric facility design (where outcomes are intended to improve treatment) and in the general understanding of the syndrome (which promises more abstract, but high-level impacts). Just how much does it help to have someone understand the syndrome? Will that improve medical and social treatment? It is conceivable. Will this understanding also help hone the broad study of schizophrenia to more practical outcomes? Once again, it’s conceivable but immeasurable. 33


RESEARCH QUESTIONS

34


Question 1: Specialist psychiatric facilities to help people with schizophrenia

Originally “How can specialist psychiatric facilities be improved in the way they help people with schizophrenia?” was to be my one and only research question. An extraordinarily naïve one too – loaded with assumptions that somewhere someone may not only know what schizophrenia was, but also may know what may help.

The research question that asks about the design of specialist facilities is largely explored in pages 61-198. I started out by researching suitable models to understand how innovation in the built environment may improve the wellbeing and health outcomes of schizophrenic patients. I had previously worked on mental healthcare design and had been frustrated by the scarcity of tools for designers who are tackling the problems that come with designing a psychiatric facility – unless they are designing a dementia facility, in which case there’s a fair amount of quality information available (largely due to the efforts of John Zeisel, Ian Forbes and a few others) but Alzheimer’s and other old age dementias don’t share a lot with schizophrenia, certainly not on a neurological level. Where dementia is defined by the loss of memory, schizophrenia is better defined by losses of awareness of the ‘unexpected’ coupled with intense awareness of expected events (see the section on schizophrenia, page 204 onwards). 35


I approached my problem as an architect, with a concern for praxis. I wanted to create a tool that would be easy and fast to use and would generate better outcomes regardless of theoretical concerns about the relationship between schizophrenia and the built environment.

Other design researchers pointed the way. In the first decade of the 21st century, a number of authors started to write about a salutogenic approach to healthcare design (Bahrs et al., 2003; Dilani, 2008; Edvardson, Sandman, & Rasmussen, 2005; Eriksson & Lindsrom, 2008; Eva Langeland et al., 2005; Eva Langeland, Wahl, Kristoffersen, & Hanestad, 2007). These papers brought my attention to Aaron Antonovsky’s psychosocial model for understanding the parabolic continuum that spans the theoretical states of perfect health and death (Antonovsky, 1987, 1996). These researchers used the term ‘salutogenics.’ They also roughly sketched out the principles of salutogenesis and its benefits over other models of psycho-supportive design. But I turned the theory into a methodology, designed, as I needed it, for use in design praxis.

The method isn’t only applicable for architectural praxis, but for anyone who has to make decisions about other people’s well being on the fly. In 2009 I demonstrated this in a symposium held to look at rural emergency management (Golembiewski, 2009a), and in 2012 the conference paper was published in the Australian government bulletin:

36


Australian Journal of Emergency Management (Golembiewski, 2012b) (starts on page 148). There are any number of studies that demonstrate the relative strength of salutogenic theory, but how the theory works is relatively obscure. Antonovsky did explore this question, but he did so in the mid 1970’s to the mid 1980’s and what was acceptable then (in terms of psychological explanation) seems weak now. At any rate, I had to dive deeper than the theory of salutogenics. And in order to find substance to make my terms of reference deeper, I had to look at schizophrenia itself. How could I know how the environment affects schizophrenia (and vice versa) until I knew what schizophrenia actually was? As it happens, I was eventually led to make associations between the principles of salutogenic theory and the psychogenesis of schizophrenia (Golembiewski, in review-d) (Starts on page 204). This is a paper that returns to salutogenic theory to find neurological causes: ‘The neural basis for the salutogenic method of healthcare design.’ It is presented here from page 159.

In the outset, the possibility that salutogenic theory may present answers to what schizophrenia actually is was not on the horizon. Another serendipitous association came from the depths of architectural theory.

While studying undergraduate architecture, I came across the ecological theory of perception in Lang’s textbook on theoretical drivers for architecture (1987). It was one of my associate supervisors, Dr. Spehar who directed me back to it, suggesting it may 37


have relevance. This theory, whilst relatively well known among perceptual psychologists, is virtually unknown among clinical psychologists, yet it did seem relevant. Already some fringe areas of medicine were picking up on the theory to explain the ‘mirror neuron’ phenomena that was being observed in interpersonal communications. The ecological theory of perception essentially proposes that perception is direct and directly stimulates action and such a model could explain a lot that cognitive models of perception can’t. It seemed plausible that schizophrenia – when conceived as a dysfunction of perception, may be partly a dysfunction of ecological perception. I have explored this possibility in several papers, most notably ‘The Riddle of Psychotic Perception Resolved,’ (reprinted here from p.204), ‘Common Psychiatric Symptoms…’ (reprinted on p.358), and ‘Lost in Space…’ (Reprinted from p.296.)

Because of these lines of enquiry, and because of my dissatisfaction with the dismal lack of understanding of the phenomenology of schizophrenia, the question “what is schizophrenia” became my second, but most important research question.

My work on the nature of schizophrenia is where my deepest research has taken place, and where my breakthroughs have been most profound. I thus consider my work on schizophrenia itself to be the heart of my thesis. I would have been happy to let my findings about the nature of schizophrenia be the topic and substance of this thesis.

I attribute any success I have had in neuro-psychological enquiry to my architectural, rather than scientific training. Architects must address wicked problems on a regular 38


basis, and they learn to be comfortable with the unknown and unresolved. Furthermore, there are reasons why many scientists would not be able to approach the subject of schizophrenia as I have. Scientists have a commonality in their training and language, they have common normative values and frequently researchers emerge from under a focused umbrella of enquiry that is dominated by their supervisors. None of these factors affected me. In effect I was freed by my independence and lack of awareness of the dogmas that are so prevalent in the scientific method.

For the articles I have published or am publishing in this space please see ‘Common symptoms…’ (Golembiewski, 2012a, in review-b) page 358, for presentations see (Golembiewski, 2009b; Jan Golembiewski, 2010a; Jan Golembiewski, 2010), for peer reviewed online discussions see (March, Kirkbride, Veling, & Golembiewski, 2009; Volavka et al., 2011) – (Presentations and on-line discussions have not been reprinted here, except as they are cited in more significant works.) I have yet to see whether my principle work on this subject shall be published, but it is enclosed here (Golembiewski, in review-d) starting on page 204. It was the demand from healthcare architects planners and facility managers have made it impossible to put questions about psychiatric design off until I finished my PhD – in 39


effect it was industry that has kept me focused on my original question. It was little things that kept me to my original question – the need for designers to know more, the questions raised by my colleagues in the Faculty of Architecture Design and Planning, and the opportunities I was given such as a paper on how my neurological findings may be applied generally and deterministically to any design project, from object design, to buildings to urban scale design.

The paper was produced and presented. It is now in press: Determinism and Desire… (Golembiewski, 2013) (Starts on page 126). I was then asked to present a paper to a symposium on mental healthcare design (Golembiewski, 2011b). This opened a floodgate, and the pressure for me to produce more and more of this material is evident, several more offers of plenary addresses at conferences have accelerated the interest in this material. I started to get approached by the health departments around Australia and by several prominent architecture firms who work in this space; HASSELL Healthcare, Bates Smart, BVN, Woods Bagot and MAAP (UK). I have been asked to guest edit an edition of Facilities on the subject and also to write a piece for the Australian Journal of Psychiatry.

In short, I had little choice but to return to the space I had started out in: health design.

40


Question 2: What is schizophrenia?

The great algebra of what schizophrenia is and what may cause it has dominated the three years of my PhD research. Originally it was because the depth of answers I needed (about the relationship between schizophrenia and the environment) could only emerge from a very deep understanding of the phenomenology of schizophrenia itself. I could, perhaps have spent time with a sizable number of schizophrenia patients and conducted an ethnographic methodology, but this approach never felt right, and besides, I never had a means to access to a significant numbers of patients in diverse environmental contexts. Professor Perkins (in review) relates his experience doing just that. The findings that he and his students and colleagues discovered are very reasonable and offer great depth to his field of enquiry (landscape design for psychotic patients). The principles Perkins et al. devised are intimately related to the salutogenic methodology I published and present in this thesis, but the issue of the life-world of schizophrenic patients is one that Perkins et al. wisely skirted around. Indeed, his work makes no great distinction between the phenomenology of schizophrenia and the phenomenology of other mental illnesses.

In any case, I did not choose an ethnographic methodology but a speculative enquiry through literature. It was not going to be sufficient to rely on other’s hypotheses, simply because the vast bulk of them just didn’t ring true. And besides, many were useless for understanding how schizophrenia interacts with the built environment and vice-versa. 41


Schizophrenia is not an illness as such, but a diagnosis based on loose but cohesive sets of symptoms. There are significant diagnostic differences between some of the published diagnostic system (such as the DSM-IV and the ICD-9), and on a finer level there is a range of different sets of symptoms apparent even within a single diagnosis. It is hardly surprising, then, that the established knowledge base about schizophrenia is subject to a few contradictions and huge open-ended questions.

At a minimum I had expected to find that research and practice might be unified by a common theory – or at least a common hypothesis. But what I found was that every one of tens of thousands of researchers and clinicians harbour their own heuristic ideas. Of these, few reach far beyond the very limited scope of their own very limited areas of enquiry. Because the definition of schizophrenia is so nebulous, theoreticians take permission to break the illness into component parts and address the bits, while dismissing the holistic presentation of the illness. The pet interests of the theorists only exacerbate the problem; the very ephemerality of the question means that answers appear to be skewed to match or prove a-priori agendas. Examples include beliefs that human consciousness is a delusion (Taylor, 2010), or that heeled shoes have a knock-on effect that causes mental illness (Flensmark, 2004), or that thin people are have a territorial nature (Kellett, 1973). If I had tailored practical solutions to such limited hypotheses, it is unlikely that they would be of much use. An analogy that we can all understand it that the schizophrenia researchers of the world are apparently attempting to draw a 1:1 scale map of the world of schizophrenia, but are ignoring the mountains, lakes and forests as they concentrate on the contours of bits of gravel. 42


So I persevered, placing a great deal of interest in the hypotheses that focused on what I figured may ‘bridge’ the individual mind and the world we all live in. This meant I prioritised hypotheses that focused on perception such as (Fletcher & Frith, 2009; Gray, Feldon, Rawlins, Hemsley, & Smith, 1991; Kapur, 2003). As useful as they were, these hypotheses held a consistently naïve model of perception. Certainly the models of perception they employed were never as sophisticated as the ecological theory of perception, developed by James J Gibson (1979). The discoveries I have made, with the question “what is schizophrenia” at least partly involves matching schizophrenic phenomenology to the ecological theory of perception.

My working hypothesis for schizophrenia is my second question and is largely contained within a single article. See the section running from p.199-294.

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Question 3: The role of the built environment in the aetiology and symptoms of schizophrenia

Contrary to the views of many researchers, to me it seems obvious that the aetiology of schizophrenia cannot be meaningfully separated from the symptoms. There is a twofold reason for this: firstly because schizophrenia is a diagnosis and not a nosological condition. The diagnosis is based on symptoms, absences of normal behaviour it is thus a behavioural expression. And whenever pathogens or other nosological conditions are discovered that cause these symptoms (or similar ones), they are automatically exempted and re-classified, because the diagnosis of schizophrenia is specifically invalidated when and if nosological disorders are identified (American Psychiatric Association,

1994).

In

the

past

many

other

causes

of

schizophrenic-like

symptomatologies have thus been excluded. They include pellagra, scurvy, syphilis, hyperthyroidism, autism and drug abuse (American Psychiatric Association, 1994; Boyle, 2002; Hoffer, 1970; Hoffer & Osmond, 1963).

The other reason that the aetiology and symptomatology of schizophrenia cannot be disentangled is that genetic and environmental factors that come into play do so because they create a predisposition for schizophrenia and a context into which schizophrenia is expressed: the environmental and genetic factors thus moderate and mediate the symptoms through moderating and mediating experience. This is reflected in behaviour

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and thus also in diagnosis. Like genetics, the environment cannot be considered as directly causal, but it does inextricably contribute to the diagnostic symptomatology.

As an illustration of this point, a patient of Dr. H. Searles remarks (while trying to express what it means to experience schizophrenia) “how would you like to have square eyes?” at this point Searles realised that the patient was being quite literal. The experience of having ‘square eyes’ demonstrated a lack of differentiation with the external physical environment. The square eyes the patient complained of were the windows of Searles’ office (Searles, 1960, p. 51).

The very inability to disentangle schizophrenia from the environment is very interesting from the perspective of an architect because this viewpoint involves the built environment in the very aetiology and psychogenesis of schizophrenia and can be spotted in cross-sectional epidemiological studies.

One of the most interesting findings about schizophrenia is that it is predominantly an urban syndrome. The incidence of schizophrenia grows with exposure to urban centres (Kelly et al., 2010). This was first observed nearly a century ago (Faris & Dunham, 1939). But there are few hypotheses that lend themselves to understand this phenomenon. Some say that cities are places of greater social anxiety (Selten & CantorGraae, 2005, 2007), places of social ghettoization and stigma (Kirkbride, Fearon, et al., 2007; Kirkbride et al., 2006; Kirkbride, Morgan, et al., 2007; March et al., 2009), places where noise and air pollution are rife (Halpern, 1995), others have suggested that one of 45


the symptoms of schizophrenia is urban drift, and that people end up in the cities in search of cheaper accommodation (Evans, 2003; D. Freeman, 1994; Lapouse, Monk, & Terris, 1956), some arguments have been rejected by cross-sectional studies (the noise and air pollution proposals for example) but for most, the jury is still out (March et al., 2008).

I was part the debate about this question in an online conversation (peer reviewed and edited) on Schizophrenia Research Forum. (March et al., 2009) My third question is: “what role does the built environment itself play in the aetiology and epidemiology?” The strong relationship between the built environment and schizophrenia means that this question remains valid, even if the popular hypotheses (that don’t point to the physical environment as an aetiological factor) are found to be true. Minimally, the built environment makes up the context within which schizophrenia is experienced.

Importantly to me, a designer, the question has a suffix: what does the correlation between schizophrenia and place mean for us, the designers of the built environment – whether we design psychiatric units, cities, or the buildings that they are built from?

These questions are tackled in the section of the thesis that runs from page 295 to page 397.

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HOW THIS RESEARCH MAY HELP

It is the central premise of this thesis that the relationship between psychotic conditions and the built environment is inextricable.

The reason is an argument in logic: Both schizophrenia and bipolar-1 are diagnoses based on behaviour. As mentioned earlier, the moment a nosological disorder is identified, which presents similarly to schizophrenia (or bipolar), it is withdrawn from the diagnosis by a general exclusion of other identifiable disorders (American Psychiatric Association, 1994). This effectively means that these psychoses cannot be considered as illnesses. These conditions can be no more than behavioural manifestations – that is distinctive sets of florid symptoms and deficit signs. As psychotic illness is defined by behaviour, the built environment is the ubiquitous context for that behaviour.

Behaviour reflects experience:

1. Somatogenic experience, which is opaque to observers.

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2. The internal experience of a common context (the phenomenology of the outside world), this may be noticeable by others.

Behaviour is the outward expression of experience (called symptoms when the behaviour is especially unusual), and behaviour occurs within a common context. All behaviour reflects the context in which it is expressed, both by interaction and also by expectations of appropriateness. By interaction I mean that there is a big difference in sitting on the floor of a Japanese room with tatami mats and sitting in the muck of a pigsty. An example of contextual expectations is in the rowdiness, which is expected in a schoolyard, but not in church. All behaviour is, at least in equal part, environmental.

But logic aside, epidemiological studies consistently find the 'urban milieu' to account for about 30% of all incidence, even once all other known factors are accounted for (Kelly et al., 2010; Krabbendam & van Os, 2005).

If this evidence is insufficient, then the Camberwell walk study can be called in; a study of 17 paranoid psychiatric patients undertook a PANSS test before and after a 10minute walk through the busy Camberwell High Street of London. The test showed that paranoia and other psychotic scales were increased after this short 'dose' of urban life (Ellett, Freeman, & Garety, 2008). Even without going into my PhD research into why this may be so, the evidence is amply triangulated. The environment is an inextricable factor in psychosis and we, as the designers and planners of the environment are culpable. 48


Just as a building has to have foundations on the earth, psychosis is an expression of the mind as it meets experience. And for most of us, most of the time, that experience is of the built environment.

Now that we know how implicated the environment is in psychotic conditions, it is time to look back at the environments we prescribe for psychotic patients. Could they be better? How would I feel if I were 'on the edge' and in this space? Are there any provisions to improve a patient's sense of coherence? (See the research question on p.35 and how it is addressed starting on p. 62)

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METHODOLOGY

My methodology has been unorthodox. What started as naïvely pursuing very diverse research questions – over a period became my guiding methodology. Over the last three years, I have discovered that one line of questioning gives perspective to the other. Typically scientific enquiry is approached in very small steps and with close guidance from a supervisor who is doing research in a closely related field. The resulting research findings will be published in a small collection of papers with the supervisors name on the right and the student as the first or second author. The process taken by a PhD student called Melissa Green typified this trajectory, right here at Sydney University. Her topic was specific, doable, and likely to produce publishable results: ‘Facial affect processing in delusion-prone and deluded individuals: a continuum approach to the study of delusion formation’ (Green, 2001). The research questions addressed little gaps and solidly filled them with new findings using established lab-based methodologies. If I had been in the psychology department (as Green was) my thesis question would not have been accepted, much less my far more expansive research questions. But in the faculty of Architecture, Planning and Design, my supervisor wasn’t to know that I had taken on a subject that is normatively taken to be impossible.

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But I’m not at all upset that I took this route because it yielded results. My approach meant that I had to come to understand schizophrenia using very broad-brush strokes, and then to refine the knowledge I acquired. This is the opposite of the normative approach, which is to learn first-up that the solution is not in sight and that a researcher has to focus on one little piece of the puzzle. Forget schizophrenia – look at delusions. The researcher then reads everything about delusions, but focus their own studies on a single piece of that puzzle. There’s no doubt – that method works, and it’s far less risky, but I more or less did the opposite.

Architects are practical people, yet people that are able and trained to address wicked problems (Kunz & Rittel, 1972) and find practical solutions. This is, in fact possibly the most useful talent architects possess and there is a whole research school in Stanford (The D School) to study ‘Design Thinking’ (R. Buchanan, 1992). Architects are trained to find the simple bits of information that are needed allow them to make lateral innovations that solve many problems. My approach to PhD research followed this practical approach, only I didn’t ask simple questions. At first I just wanted to know what schizophrenia was, so I could establish solid design guidelines for an incredibly vulnerable and marginalized population, so I started reading. As I went, I wrote one hypothesis after another. As and when they became coherent, I sent them off to be published. Inevitably, most were rejected, but rarely without some sound advice: look at this or that. Sometimes my associate supervisors gave similar advice: look at this or that. As they got more refined, my papers started being reviewed, and usually still knocked back. The reviewers’ advice was always well considered and to the point. But 51


none ever suggested that I should abandon my questions. So I continued. I resolved difficult issues, I integrated disparate seams of knowledge and my hypothesis for what schizophrenia is became more and more cogent.

But it seems that there aren’t many people who do approach schizophrenia research with such a design-thinking approach. Green’s PhD topic is normatively considered to be expansive and an ideal question to consider for three to six years. In the last few decades there have been very few comprehensive hypotheses for the illness – and all have somehow lacked the integrative holism that I sought. Out of all of them, Gray, Feldon, Rawlins, Hemsley, & Smith was in 1991 (Gray et al., 1991). It was by far, the hypothesis with the broadest reach, and it has also remained remarkably good over the last 20 years, but since it was published, another 75 000 or so related articles have come off the press (MacDonald & Schulz, 2007). In many ways, my own hypothesis (Golembiewski, in review-d) which starts on page 204, is very compatible, although it comes to the argument from a completely different route, and is naturally more up-to date on its sources. Gray et al. 1991 was an uncharacteristic leap, stretching far further than any hypothesis since. Subsequent broad stroke hypotheses include (Kapur, 2003), for instance. Despite it’s reputation for being an ‘extravagantly comprehensive synthesis’ (H. M. Jones, 2004), the author himself defends it as a hypothesis for no more than ‘psychosis within schizophrenia’ (Kapur, 2004). Far from the reach of Gray et al, this putatively explains but a handful of symptoms from the ‘complex constellation of schizophrenia’(American Psychiatric Association, 1994). A last opus magnum on schizophrenia was Fletcher and Frith’s 2009 Bayesian hypothesis (Fletcher 52


& Frith, 2009), that studiously avoided mention of Kapur 2003, yet didn’t reach far beyond it. But typically the authors marched knowledge forward incrementally; they very cleverly synthesized the growing consensus to the Bayesian understanding of Friston (2003).

My method was two pronged, and indeed, the rigor and substance I was able to bring to the theory of design from my scientific discoveries has been well received, and as I write, have been accepted into press or published in several international journals. My scholarship has also been awarded with many prizes and even a guest editorship in Facilities Journal.

In terms of formal methods, I’m not ashamed to say that all my research has been conducted with an integrative literature review methodology employing logical argumentation (Groat & Wang, 2002). Exactly the same method was used by (Gray et al., 1991) in their landmark thesis. The decision to take this approach was based on the advice of Dr. Peter Armstrong (my supervisor) and Professor Hemsley (in personal conversation, at the IoP in 2011). Despite this heritage, the method is sure to attract negative attention. Once again, there is a normative expectation (at least in the sciences) that PhD theses will generate new empirical data. Here there is another great benefit in being in architecture. Architecture is not a science, and so the requirement for new data can be dismissed without further thought. But even so, I feel compelled to refute this expectation. I did take (and methodologically analyse) a dataset, only it was not one of my making. 53


Although there is a cavernous gap of knowledge around the spatial and material needs for psychiatric patients, there is too much knowledge about schizophrenia, and these opposites are complimentary. In 2007 there were 4400+ articles and other publications of schizophrenia related issues published. That’s up from about 4200 in 2006 and 3700 in 2005. This steady upward climb has continued since at least 1987 (MacDonald & Schulz, 2007). The data isn’t up to date, but at the same rate of growth, estimates are that this year will see about 7000 – about 52 articles a week. If there ever was a data feed that is really comparable to drinking from a fire-hose, this is it.

It was from my emersion in this data that I noticed patterns and brought them to light. Methodologically this is very similar to a Grounded Theory method (Corbin & Strauss, 1990; Strauss & Corbin, 1990), except that instead of grounding myself in a social milieu, I grounded myself in published data. Where a Grounded Theorist typically takes noted on observed behaviour until saturation has been achieved, I took notes on data. Where a Grounded Theorist diligently ignores what people say they are doing (to observe the reality of their actions), I ignored what authors said their findings were, to focus on what they materially discovered.

Inevitably my methodology will not please everyone and for those who remain critical about it, it’s worth remembering what a methodology is for. It is a routine, an accepted road-map to approach a gap in knowledge. Methodologies are not only useful for pointing a researcher the right way, so they make their discoveries efficiently, they are particularly useful for justifying failures. If a PhD student were to finish their tenure 54


without discovering anything, they had better be able to explain what they did, that they could find so little. If their approach was systematic (such as taking half the rooms in a mental health unit, painting them in different colours and comparing the in and out PANNS scores over time), and still the study found nothing conclusive, then the researcher could safely write: ‘the colour of rooms appears to make no difference to the PANNS scores of patients over time.’ It is thus safe, and useful, even when an experiment fails to have a highly structured methodology.

I had intentions of undertaking such a methodological approach (I intended to do grounded research within a mental health unit, ethics permission allowing it), but I didn’t because I started making discoveries about the time I started applying for ethic permission. As I was aware that I would not need to justify a failure post-hoc because my findings looked like they would be ample, I knew that I wouldn’t need to undertake a massive design intervention or some similar new empirical study.

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THESIS INCLUDING PUBLICATION: LIMITATIONS AND ADVANTAGES

Among first-rank universities around the world, it is now de rigeuer that a PhD can be granted by publication and a viva voce. Unfortunately University of Sydney hasn’t made this step, and instead, a PhD may be given to a series of publications that are accompanied by an exegesis.

What an exegesis is, and what form this PhD including publication takes is all but clear. Professor Adrian Snodgrass once said, “all I want to see in an exegesis is one short sentence: ‘It’s all in the papers.’” On the other hand, some still feel there is value in the traditional tome.

There are advantages either way. The ‘by papers’ route exposes a candidate to the rigours of the international academy early. Internationally accepted experts review papers as they are produced and the candidate (me in this case) gets to work on their advice. At the same time the candidate builds a portfolio of publications and a reputation in their field before the PhD is even granted – these benefits serve the university too.

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The disadvantage of this approach, as I see it, is that when papers are collected into a tome (as mine have), they can sometimes be a bit repetitive: sometimes the same arguments are employed in two or more papers, and if one paper draws on another, they may recap on findings. Furthermore, the thesis is likely to lose its monolithic narrative structure. If you as a reader find these problems in the published works of this thesis, please forgive me. Rather than re-write the papers to fit the tome, I have kept them much as they were published, excepting only changing the language to The Queen’s English, whenever a work was written to be published in an American Journal.

Another thing I have noticed is that ideas do move on. Data emerges that is contradictory, logical fallacies are discovered in retrospect, etc. Knowledge is capricious, and an idea that has enough validity to be published need not be futureproof. Although publishing gives knowledge an aura of finality, it doesn’t stop it from being falsified. Indeed this has happened in my own papers. My finding that negativity motivates common psychotic symptoms (Golembiewski, 2012a) (reprinted here from page 358) is at least partly falsified by my work on the psychogenesis of schizophrenia, (Golembiewski, in review-d) (also reprinted here from page 204). The reasons are detailed on page 356, but in a traditional tome contradictions like these would probably not be acceptable. Once again, here I must present my papers much as they are being read by others, not with an apology (I shouldn’t need to apologise for publishing after all) but with a note to explain the odd U-turn or logical contradiction over a series of works. Believe me I am aware of these, and it is my intention that readers of this exegesis should be also. 57


Finally the exegesis with publications doesn’t follow a logical linear structure that one may expect from a thesis. Obviously since Nietzsche, Wittgenstein and with postmodernity, the days of the singular narrative are a bit passé anyway, but I do see the value in in-depth linear analysis, and for all those who are inclined to agree, the enclosed paper “The Riddle…” (from page 204), is nearly 20 000 words, plus another 5 000 if citations are included, you are welcome to take that as the thesis and ignore the rest!

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PAPERS, PRESENTATIONS AND INCOMPLETE ARTICLES NOT INCLUDED

A neurological language for determinism in design. Seminar presented at HASSEL, Melbourne (19 April, 2012). (Also presented at AAA seminar series)

Schizophrenia and Violence, Case Not Closed. Volavka, J., M. Large…Golembiewski, JA et al. Schizophrenia Research Forum. Edited Live Discussions. V. Wilcox (ed.), Schizophrenia Research Forum (2011).

The dopamine-mediation of perception hypothesis and the implications for schizophrenia. Australian and New Zealand Journal of Psychiatry (2010) 44, A51. (Paper presented at the ASC2010 Molecules to Mind Conference, Schizophrenia Research Institute, Sydney, September 2010)

Design for disability lecture for the Masters studio, Faculty of Architecture, Design and Planning, University of Sydney (2010)

Environment in Psychiatric Research Outstanding Challenges and Future Directions. Live Discussions. V. Wilcox (ed.), Schizophrenia Research Forum (2009). 59


Perception, attention, working memory and the dopamine salience hypothesis. Cognitive Neuropsychiatry. (Awaiting resubmission after review).

We are our architecture. Science and Non-duality Conference. San Rafael, California, Centre for Consciousness Studies, (University of Arizona) (2009). SND29-315 DVD 3/3. (Also presented at AAA seminar series)

There’s something in my head (but it’s not me): The complex relationship between the built environment and schizophrenia. Paper presented at the Research Visions Conference, University of Sydney.

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QUESTION

ONE:

HOW

CAN

SPECIALIST

PSYCHIATRIC FACILITIES IMPROVE THE WAY THEY HELP PEOPLE WITH SCHIZOPHRENIA?

The salutogenic methodology for the design of psychiatric facilities

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Start making sense: Applying a salutogenic model to architectural design for psychiatric care.

Published in: Facilities (2010), 28(3/4), 100-117. Doi: 10.1108/02632771011023096

Winner of the Emerald Literati Outstanding Paper Award 2010.

Abstract

Purpose This paper aims to look into the significance of architectural design in psychiatric care facilities. There is a strong correlation between perceptual dysfunction and psychiatric illness, and also between the patient and his environment. As such, even minor design choices can be of great consequence in a psychiatric facility. It is of critical importance, therefore, that a psychiatric milieu is sympathetic and does not exacerbate the psychosis.

Design/methodology/approach This paper analyses the architectural elements that may influence mental health, using an architectural extrapolation of Antonovsky’s salutogenic theory, which states that better health results from a state of mind which has a fortified sense of coherence.

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According to the theory, a sense of coherence is fostered by a patient’s ability to comprehend the environment (comprehensibility), to be effective in his actions (manageability) and to find meaning (meaningfulness).

Findings Salutogenic theory can be extrapolated in an architectural context to inform design choices when designing for a stress-sensitive client base.

Research limitations/implications – In the paper an architectural extrapolation of salutogenic theory is presented as a practical method for making design decisions (in praxis) when evidence is not available. As demonstrated, the results appear to reflect what evidence is available, but real evidence is always desirable over rationalist speculation. The method suggested here cannot prove the efficacy or appropriateness of design decisions and is not intended to do so.

Practical implications The design of mental health facilities has long been dominated by unsubstantiated policy and normative opinions that do not always serve the client population. This method establishes a practical theoretical model for generating architectural design guidelines for mental health facilities.

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Originality/value The paper will prove to be helpful in several ways. First, salutogenic theory is a useful framework for improving health outcomes, but in the past the theory has never been applied in a methodological way. Second, there have been few insights into how the architecture itself can improve the functionality of a mental health facility other than improve the secondary functions of hospital services.

Start making sense: Applying a salutogenic model to architectural design for psychiatric care.

There is growing evidence that the design of a healthcare facility will directly affect the health outcomes of patients (Ulrich, 2006). But designing a healthy psychiatric unit is a difficult task as the patients are prone to distorted perceptual systems that make them especially vulnerable to confusing building forms and layouts, or even to a lack of tactile, acoustic, temporal, olfactory or visual stimulus (E. T. Hall, 1975). This article analyses various aspects of design, ranging from apparently minor interior choices such as texture, decoration and finishes through to the enveloping architectural form. By doing this we should be able to see how design decisions may affect patients’ health outcomes. To establish these links, the analysis looks at the transactional nature of perception and applies a salutogenic framework to assess design choices (largely recommendations drawn from literature) for psychiatric health facilities. It is hoped that this methodology will be useful for making informed decisions in circumstances where 64


there is no empirical evidence available and when architectural decisions have to be made regardless.

There is a reasonable body of literature about the design of hospitals and related buildings, and even about mental healthcare facilities, but the material is severely limited when compared to the complexity of problems that an architectural team faces. Without specific studies into the specific questions that an architect has to face hundreds of times a day, how are architects and other team members to know that the choices he or she has made are the best for the subject group? There are no studies on the psychological benefits for basic design elements that are mandatory in mental health facilities. And it is the moral obligation of all facility planners’ to question any details that may not be in the best interests of the facilities reason d’être, which is to assist patients in recovery. How do architects know how a space with cushioned vinyl walls and floors will affect the wellbeing of patients inhabiting that space?

As it happens, the architect is often given little choice about the layout and finishes of standard rooms within a programme as standards and codes have already pre-empted any decision-making. “The Australian Health Facility Guidelines” (HCAMC & CHAA, 2007) for example, specifies the layout and finishes of most of the spaces within a mental healthcare unit.

Facility planning teams will also have to resolve occasional contradictory findings or opinions – many of these will not be impartial. One study that observes the benefits of 65


opening up nurses’ stations and other spaces in mental wards (Whitehead, Polsky, Crookshank, & Fik, 1984), is contradicted by another article calling for the same wards to be ‘locked down’ and made more secure (Osmond, 1958; Sine, 2008)1. It’s important that the lead architect is proactive and has perspective; architects have to pose a question to others on the design team; “Who are we designing for, why, and how will this decision help to do that job well?”2 A strong guiding theoretical hypothesis makes rational decision-making easier where there are no relevant empirical studies to provide support. For this reason salutogenics – a theory gaining interest in recent literature reviews for linking the environment to health outcomes (Dilani, 2008; Schweitzer, Gilpin, & Frampton, 2004) may prove to be useful for formulating robust principles for the design of psychiatric units.

1

Mr. David Sine, the author, is president of Safety Logic Systems, a company that may

well have vested interests in locking patients down. 2

Of course the diverse needs of clinical and non clinical staff, of facility directors, local

governments and other involved people are also very important, but great care must be taken that their needs do not come before those of the patients. (Osmond, 1958) These negotiations won’t be easy, as empowering the patients will to some degree mean wrestling control from staff some of who may well be part of the planning team. (Searles, 1960). 66


Figure 1: Dr Osmond writes that the seclusion room must not be merely pleasant, but the best room of any ward (Osmond 1958). The rooms he describes have hardly changed since 1958 and are better used for storing dangerous chemicals than treating distressed and vulnerable patients. This room was designed according all the recommendations of the 2007 Australasian Health Facilities Guidelines (ACAMC & CHAA 2007). 67


Spaces not dissimilar from this have been shown in repeated tests to cause hallucinations even among people with ‘normal’ perceptual abilities. Scatological, violent or apsophilic behaviour in such an environment is a defence against psychosis.

Salutogenics is a psychosocial study of what keeps people healthy, starting from the perspective that illness and health are different points on the same continuum. Where treatment may be required when one is ill, a supportive environment is always required to assist and maintain good health. The primary premise of salutogenic theory is that a ‘sense of coherence’ (SOC) is strongly linked to better resistance to illness. A strong SOC

is

supported

by

feelings

of

comprehensibility,

manageability

and

meaningfulness. Ultimately a SOC builds a dynamic feeling of confidence that one’s internal and external environments are predictable and that there is a high probability that things will work out as well as can reasonably be expected (Antonovsky, 1987; Bahrs et al., 2003).

68


Active forces

{ DEATH

Generalised Resistance Resources (GRR’s) Sense of coherence derived from: Meaning, comprehensibility and manageability and other treatment

Generalised resistance deficits (GRD’s) such as inabilities, illnesses and stresses

Deterioration

Better health State of well being

LIFE

The salutogenic effect

Figure 2: The concept that a state of health or well-being is a point on a continuum is central to salutogenic theory. Forces that support better health are called generalised resistance resources. They include treatment and a sense of coherence. Illnesses, inabilities and other generalized resistance deficits work the other way.

The idea that the environment has a direct effect on health through psychology is both intuitive and well supported in research. As Ulrich writes ‘the concept of stress provides a credible departure point for understanding why design should affect health outcomes…’ (Ulrich, 1997). Ulrich and others have created a model associating psychological stress to poor health outcomes; the maxim is that anything likely to increase stress levels is to be avoided in health design. The stress model is simple and in most instances it is appropriate for healthcare design and especially for mental health. 69


But the stress model is not comprehensive nor specific, and it does come under criticism by Antonovsky who points out that there are times when stress can have a salutogenic effect; that is when a person is subjected to stressors whilst receiving high levels of environmental support the result can be fortifying. Furthermore in the salutogenic model, stress is understood to be omnipresent and not just a feature or an absence of the environment (Antonovsky, 1987; Bahrs et al., 2003). Lawton and Nahemow support this viewpoint by observing that an environment that lacks challenges leads to atrophy, but then too much challenge can be damaging (Lawton & Nahemow, 1973). They add that patients have a reduced capacity to adapt when they are ill or infirm. Aside from this caveat, the salutogenic model seems an appropriate broad framework in which to locate the stress model because it supports the stress model with much needed substance – effectively filling the causation gap between action and effect.

Understanding the environment from a salutogenic perspective. From the perspective of architectural design, the salutogenic framework is compelling, as it understands the environment as a source of meaning, as a sphere of influence3 and for its readability4. From the point of view of mental health design, the salutogenic framework provides a direct link between architectural language and psychiatry.

3

Being able to influence the surrounding environment is the basis of manageability.

4

Readability is an architectural simile for comprehensibility. 70


What is interesting about salutogenics from the psychiatric point of view is that in this model the relationship between a patient and the environment is understood as being transactional, not fixed; the environment effectively changes according to the subject’s sensory and perceptual abilities and conditioning (E. T. Hall, 1990). Perception is a complex neurochemical process that is highly reactive to the surrounding environment and yet it is the only channel for receiving new information of any sort5. It has been postulated that a great deal of mental health problems occur because of imbalances and distortions in the perceptual system, causing hallucinations, instability, unpredictability and delusions. Thus, the act of perception itself can trigger psychotic events (E. T. Hall, 1975, 1990; Maeissner, Perry, Dorr, & Rowan (Ed.), 1965; Osmond, 1957, 1958, 1966; Searles, 1960; Weckowicz, 1957).

5

It is conceivable that old information (memory) is stored and retrieved through non-

perceptual means, but this is not the area of this study. 71

Object

b

Culture

Knowledge (epistemology)

(sight, smell etc.)

Memory

a

Sensation

Perceptual Ability


Experience

Object as experienced

Subject

The process of object cognition Figure 3: When Searles reported a woman who genuinely experienced people as trees he is not suggesting that people are trees or that people are like trees but that, for this woman, people are experienced as trees. This effect is because object comprehension is not a one-way process. Cognition is manufactured through the filters of memory, culture and a pre-existing epistemology. Thus we understand the environment through association with familiar concepts, languages, objects, forms, materials, textures, emotions and expectations. Under normal circumstances a is similar enough to b that problems don’t occur, but perceptual problems, lack of experience, knowledge gaps and cultural norms can undermine experience. (E. T. Hall, 1990; Searles, 1965)

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Comprehensibility – reading the environment. The importance of making sense of experience cannot be underestimated (Searles, 1960; M. Woodbury & Woodbury, 1969), and in the case of psychiatric patients, this may mean making sense of a living nightmare (M. Woodbury & Woodbury, 1969). It is therefore important that all decision makers in design teams for psychiatric wards understand that hallucinatory experience is very real to those who suffer from it and that the environment we create may either intensify or elevate such experiences. Hallucinations are stressful and often spiral into a vicious cycle of disorienting experience, which in turn is stressful (Searles, 1960; M. Woodbury & Woodbury, 1969). There may be cases when there is a well informed psychologist within the team who will take responsibility for relevant design decisions, but it cannot be assumed that those on the client side will always understand the sensitivity of this issue or the complexity of behavioural psychology (Philip, 1996).

If we accept that perception (whether visual, acoustic, haptic, temporal or olfactory) is synthetic, (there are arguments either way, but there is little doubt that sensory ‘data’ must at some point be translated onto neurochemicals and electrical impulses, implying at least some level of post-experiential synthesis (Ames & Princeton University Psychology Research Center, 1955; Collerton, Perry, & Ian, 2005; Grossberg, 2003a; Ullman, 1980)) then the relationship between comprehensibility and the environment that we draw experience from is personal. Not all people will gather the same information from the same experience (E. T. Hall, 1990; Searles, 1960). However, in normal circumstances, the ‘gap’ between a subjective experience and the reality of the 73


objective world is acceptable and is resolved without consideration. But with schizophrenics the disjuncture between the experiential reality and objective reality is confusing for the patient (Searles, 1965; Weckowicz, 1957). For this reason it is important that the environment is designed to reduce the possibility of perceptual distortion. Size perspective, for example, is a ‘natural’ effect whereby the apparent size of an object reduces as it retreats into the distance. The severity of a schizophrenic episode is illustrated by just how much the patient thinks an object has shrunk rather than moved backwards in space (Weckowicz, 1957). The distortion caused by size perspective can be limited by keeping spaces small and to comfortable proportions (Osmond, 1957).

There are a number of other perceptual functions that are also subject to distortion, misreading or loss. These functions include very basic skills such as the understanding of distance, relative dimensions, mass, spatial orientation, the passage of time etc. (E. T. Hall, 1990). Cognitive scientists have counted at least thirteen distinct ways that people comprehend the relative depth of space visually and several other ways when we include the various tactile, thermal and acoustic perceptual systems. Whilst I shall not discuss them in any depth here6 some provision can be embedded into the environment to assist patients in these tasks. Hall notes that where one sensory ability might fail,

6

A handy summary is found in the appendix of Hall (1990) and in more depth in James

Gibson’s original texts. 74


there are others that will provide support (Osmond, 1957). Textured surfaces assist with textural perspective7.

Horizontal courses in masonry or timber assist linear

perspective8. Various objects (outside; the presence of trees, landscape features; and inside; pieces of furniture, paintings, rugs, light fittings etc.) assist with size perspective9, the various perspectives of parallax10 and other perspectives11 (E. T. Hall, 1990; Osmond, 1957, 1958, 1966; Searles, 1960). As all these perspectives support the same cognitive function, that is the measuring and comprehension of space, the more provisions for these functions the better for reducing the likelihood of misreading and hallucination.

7

The density of texture appearing to increase as space recedes.

8

Parallel lines appear to converge to a vanishing point.

9

Relative size apparently decreasing with distance.

10

The angular difference as seen from one eye and the other; (binocular vision) and

motion parallax where distant objects appear to move slowly, but objects up close move quickly relative to the viewer.

11

Including blur perspective, aerial perspective, relative upward location in the visual

field, textural shifts when one object is placed before another, completeness of outline and changes in light and shade. 75


Figure 4: This hospital corridor in Argenteuil, France could be anywhere, not just because there are no windows to connect the interior to the exterior, but also because the corridor is typical of these spaces in hospitals around the world. These spaces are disorientating; it is difficult to tell the walls from the floor from the ceiling. Bare drab spaces provide no sense of meaning and they offer no opportunities to affect any change to the environment. From a salutogenic perspective it is hardly any wonder such spaces bring out the worst in mental health patients. Source: Julie Kertesz (release granted). 76


Comprehensibility isn’t only a matter of spatial cognition, however. Understanding what objects are and what they are for is also of great importance. But the purpose of a place or an object is not directly cognised. Object comprehension is manufactured through the filters of memory, culture and a pre-existing epistemology (E. T. Hall, 1990; Searles, 1965). Thus we understand the environment through association with familiar concepts, languages, objects, forms, materials, textures, emotions and expectations. For this reason it is important, as far as possible, to provide a familiar environment for psychotic patients to increase the likelihood of comprehension and to reinforce messages that aren’t likely to increase stress levels or paranoid delusions. For this reason Osmond, Elliot and Bayes Friba recommend that the typology of a psychiatric facility is not institutional; instead it should present as something both ubiquitous and desirable; a cosy and safe home (Elliot & Bayes Friba, 1972; Linebaugh, 2002; Osmond, 1957).

Searles points out that all mental illnesses affect perceptual cognition although schizophrenia does so most dramatically (Searles, 1960). It’s therefore imperative that the design team considers visual, acoustic, haptic, temporal and olfactory sensibilities in their designs, not just to avoid excessive sensory pollution (such as street sounds and kitchen smells,) but to avoid distortion generally. Echoes have been found to be disturbing to patients who hear voices anyway. Excessive or repetitive noise can also be disturbing, especially for patients with neurotic complications. A sense of real time to treat temporal distortion can be promoted by including elements that track time such as clocks, calendars, up-to-date magazines and judicious use of TV (Osmond, 1957). 77


Beyond perceptual distortion, facility designers need to be aware of environmental symbolism that might be amplified, de-contextualised or misunderstood by sufferers of a broad range of mental illnesses (Halpern, 1995). Though there haven’t been a great deal of studies into this effect in mental institutions12, problems have been found in how patients interpret the symbolism inherent in nurses’ uniforms, which have on occasion been found to bring back wartime memories and other paranoid delusions (Richardson, 1999). When designing a mental facility, aesthetic choices and forms need to be carefully critiqued. Is the design reminiscent of schools, prisons, courts, orphanages, religious institutions or hospitals?

12

Halpern’s observations were in the wider community. 78


Figure 5: This hospital in San Lorenzo, Italy shows an attempt to open this corridor to the outside and provides a clear sense of destination. As such it is a great improvement to the traditional hospital corridor. Care still has to be taken to ensure the space is readable. The red stripes, texture-less and colourless surfaces and cut ceilings don’t relate to any traditional forms and could prove very confusing to a pa79


tient suffering from spatial disorientation. Source: Gualtiero Bertoldi (release granted)

In order to maximise comprehensibility, ambiguity should be avoided (Osmond, 1957). Objects should look, sound and feel like whatever they are (except, of course for institutions, which should have charm and personality and should be the functional equivalent of a ‘home’ (Chrysikou, 2009; Osmond, 1957)). Thus a door should be ‘door-like’ and should have a comfortable thud when closed (Osmond, 1958). Needless to say, there are a range of other details that have not been tested and therefore where an understanding of salutogenics becomes useful in lieu of proper evidence. Questions about whether walls have to be solid and run perpendicular to the ground or whether they should have coved skirtings can be tested against salutogenic criteria; in this case, against likely impacts on comprehensibility. If details may pose a challenge to patients’ perceptual abilities then the team might consider other available options. The choice of sliding glazed doors for example. Because sliders are walls, doors and windows all at the same time this could pose a problem to patients with categorisation impairments (a symptom13 of schizophrenia (American Psychiatric Association 1994)). Other things that could come under scrutiny for comprehensibility might be the material palette. Can

13

Technically a symptom is positive and refers to an unusual phenomenon.

Categorisation impairment is the opposite; a sign. As it is negative - an absence of normal ability. 80


the team avoid the use of ambiguous materials? Could materials appearing to be something other than what they are such as veneer or printed timber patterns are confusing to some patients? Perhaps there are other advantages still for choosing real exposed timber, stone, natural carpet and quality pressed brick; being ubiquitous the world over, they will resonate with a wider range of cultural backgrounds. Natural materials are also replete with textures to assist with difficulties in perceptual cognition.

A design team that adopts salutogenics as a guiding theory might find the framework at odds with architectural fashion. In the interests of promoting comprehensibility, some architectural mannerisms might not be appropriate. Postmodern double readings, façadism, deconstructionalism and tectonic expressionism are all deliberately confusing, but do not necessarily need to be abandoned altogether. These are decisions the team will have to make. Dr. Sivadon found that the practice of gradually exposing schizophrenic patients to more and more complex social environments was an effective treatment (Baker, Llewelyn, & Sivadon, 1959; E. T. Hall, 1975). The medical specialists on the team may propose that something similar is done with the built environment.

Other fashions are much clearer in terms of intentions and can also be considered with care; Modernist chic tends to plainness and mechanical functionality, both of which have been identified as undesirable for schizophrenic patient populations (American Psychiatric Association, 1994). Woodard Smith recognises this and points out that advances in engineering have enabled plasticity of form, giving bad designers scope to 81


extend worst practice past the restrictions of traditional construction techniques. When it comes to form, mental institutions benefit from the strong structural grid and small spaces associated with traditional building methods (Woodard Smith, 1959).

Manageability; the importance of being able to make a difference. Architectural form itself can amplify or deny power. If one questions the validity of this major psychological effect, then consider the effect of Albert Speer’s Reich Chancellery, related in The Edifice Complex. Sudjic tells how it was the disempowering ‘architectural stage set’ of Nazi architecture in 1939 that caused Emil Hácha, Czechoslovakia’s president, to hand over his state to Germany without even engaging the ‘well equipped Czech army with modern artillery, technologically advanced aircraft and Skoda tanks’ that were waiting to defend Czechoslovakia’s border. From the broad architectural grammars of form and space through to minute details of door-handles, architecture can work with us or against us.

The second of the principles of salutogenics is manageability. The feeling that a person is in control of his or her environment and life circumstances is very fortifying. And, as illustrated by Sudjic, the feeling that you are totally out of control is absolutely disempowering. All patients are subject to loss of control in the hospital system, with those who forfeit control being seen by staff as ‘good patients’ and those who struggle to maintain control as being ‘bad’ (Sloan Devlin & Arneill, 2003). This is even more true for psychiatric patients than any other group; as patients are overtaken by mental illness, control (manageability) is one thing that is lost entirely, not just because of 82


pressure from the hospital staff or the disempowering nature of the hospital environment, but also because they lose trust in their own perceptions, memories, their own selves. With this loss goes all social support; patients frequently lose their old lives, their jobs, their sense-of-self and their perceptual abilities (Searles 1960). For this reason it is imperative that the shreds of control that patients still have left are supported and not withheld (Osmond, 1958). Interpersonal relationships

There are a host of things facility planners and architects can do to nurture a patient’s sense of control and ability to be effective. Right up on top of the list is keeping unit numbers small and making arrangements so that numbers are never bigger than those of the archetypal human community; the nuclear family. More than five or six patients should not have to come into contact if they don’t wish to (Osmond, 1966). The tendency of institutions to put people together in large dayrooms, dining rooms, living rooms and other spaces is well known for exacerbating psychotic symptoms, because the number of human interactions compounds with every extra person present. And at a time when the capacity to relate to one another is hampered anyway, this equates to a direct loss of control (Osmond, 1958). Consider that control in a social setting relies on an awareness of your ‘place’. In which case, two people will have one relationship. In other words, they only have to maintain an awareness of one another. Three people will have three dynamics. They maintain awareness of each other and of a single new dynamic, which is the relationship between the other two. Four people already have six dynamics to maintain an awareness of, and seven people have twenty. By the time there are fifty people, a setting plays host to one thousand two hundred and twenty five 83


relationships (Osmond, 1966). Any resulting confusion is further complicated by the delusions of the patients, which will make even a simple set of relations potentially deleterious14. Interpersonal relationships

14

It is normal for schizophrenic patients to attribute non-human qualities to themselves

or to other patients, objects or even to perceive themselves as being several disconnected entities. (Osmond, 1957) 84


2:1

5:10

3:3

6:15

4:6

7:20

Chart showing the compounding numbers of relationships among small groups. The first figure shows the number of participants (p), the second the number of relationships (r) in the dynamic (d).

Figure 6: Consider that control in a social setting relies on an awareness of your “place” among all the possible one – to – one relationships in the milieu: two people will have a single dynamic; that is they have to maintain an awareness of each other. Three people will have three dynamics. They are aware of one another and each is aware of a single new dynamic, which is the relationship between the other two. Four have 20. By the time there are 50 people, a setting plays host to 1225 one to one interpersonal relationships. 85


The problem of overcrowding leads to one of the classic issues that define mental health problems in the public imagination: the ‘madman in the cupboard.’ E. T. Hall (1975) relates this anecdote of Dr. Woodbury

“…In one of the violent ‘back’ wards, where most of the communication was spatial… the ‘currency’ of the ward was space. Woodbury observed that the organization of the ward was territorial rather than social. In terms of hierarchy of freedom of movement, the dominant patient could go anywhere. Below this patient were two patients, each of whom could move freely in his own half of the ward. Each of these dominated the territory of other patients who were restricted to increasingly smaller areas. At the bottom of the hierarchy was a patient who slept under a bench and was not permitted even to use the spit hole in the centre of the floor. His so-called ‘incontinence’ was a function of the fact that the toilet was not in his territory and therefore he was not permitted to use it.’ (M. A. Woodbury, 1958)

As control of the environment is lost, psychiatric patients frequently need to be retaught everything: how to wash, how to cook, clean, or use a toilet (Osmond, 1957). For this reason provisions for these basic tasks should be very simple. It should be very easy to maintain personal hygiene and for a patient to clean up if mistakes are made (Osmond, 1957). The relearning of these ordinary tasks is now generally considered as part of the therapeutic process and is both empowering and essential for life outside of an institution. For this reason one of the beneficial innovations over the last half-century 86


in psychiatric architecture is the reintroduction of ordinary facilities that are essential in the outside world, such as kitchens, laundries, baths, telephones15 etc. ADL (Activities of Daily Living) facilities (as they are called,) are now a part of the normal programme for a new institution and there are recommended guidelines for their design (Osmond, 1957). Unfortunately the ADL facilities are usually in locked rooms and don’t actually serve real-life functions; that is, they are only for structured lessons or diagnosis. Planning teams should consider placing the ADL kitchens centrally and having them open (even if the ovens etc. have to be locked to prevent accidents,) to replicate a domestic environment as recommended by Elliot and Bayes Friba (1972). In the same spirit there are many other tools that are present outside of institutions that people should be able to exercise their control over, lest patients’ abilities atrophy. Opening windows and adjustable heating and cooling are very obvious examples. Such features will assist in maintaining successful control of the environment and will have the additional benefit of deinstitutionalising the milieu (Osmond, 1957).

It has been observed that sports such as table tennis have a salutogenic effect for mental patients, (not just for the players, but for the greater patient populations) as the events assist in structuring and re-engaging human relationships, developing coordination and

15

ADL (Activities of Daily Living) services are usually used as teaching and diagnostic

facilities with the supervision of staff 87


perceptual abilities and tackling apathy and boredom, both of which lead to skills atrophy (1972).

There are other ways to humanise mental hospitals and make them more manageable and comprehensible. Unhomely corridors and unnecessarily enlarged spaces should be avoided as they exacerbate the worst aspects of schizophrenia (Osmond, 1957). Physical retreats must be provided (Elliot & Bayes Friba, 1972; Osmond, 1957, 1958, 1966); Furniture should be movable, but solid enough to feel secure (Osmond, 1957). Of course there are many other details that will also be useful but are more simply recognised with a basic understanding of salutogenic principles rather than being listed here.

Meaning: a reason for seeing. Meaning, it seems, is essential to the maintenance of life (Antonovsky, 1987; Frankl, 1963) and is therefore the most significant ingredient of a sense of coherence. And while meaning is found in the environment, it is illusive and difficult to provide for, as questions of meaning steer pretty quickly to philosophical and cultural/social debate rather than to the simple cause and effects so desirable in the physical sciences. Of all the sources of environmental meaning, there is little doubt that it is primarily found in the social environment – in love and communication, in family, friendship and in sexual relations. But the one thing that is common to all mental patients with no exceptions – is that they have experienced a rupture in interpersonal relationships resulting in alienation from the greater community and they are to a greater or lesser extent socially 88


isolated (Osmond 1957). Even so, good facilities for receiving social support must be considered to enable recovery The current practice of affording space meet up with family and old friends (HCAMC & CHAA, 2007) is very important and, in the interests of fostering meaning, might even be extended with the provision of extra facilities for friends and family to stay over. (Gutkowski, Ginath, & Guttmann, 1992; Osmond, 1966; Whitehead, Ellison, Kerpen, & Marshall, 1976; Whitehead et al., 1984; M. Woodbury & Woodbury, 1969)

A salutogenic perspective means that affordances for pets may be considered. They have been shown to radically improve mental well-being (Searles, 1960, 1965, 1986; Wells, 2007) and while affordances for cats and dogs may be too difficult, too dangerous and raise any number of health issues including the possibility of allergies, it must be remembered that relationships with pets are often of more significance to the mentally ill than relationships with other humans and are often important stepping stones for re-establishing human relationships and other milestones for recovery such as the development of self awareness and moral conscience (Searles 1960).

When interpersonal relationships have broken down the material environment can be of life saving significance (Searles 1960). Mental patients regularly place huge importance and feel very emotional about things and places, with schizophrenics frequently confusing their environments and themselves. Searles relates dozens of anecdotes about how the material environment waxes in importance as social relationships collapse. One patient spoke poignantly during therapy about having lost herself. During the 89


session it emerged that the ‘self’ she was referring to was the home she used to live in. Her identity was inextricably linked her childhood home and all it meant to her and it was when she left the house she started experiencing mental problems. Another case Searles reported was of critical melancholia; a man who preferred to spend his life in bed, not doing anything lest he should see someone caring for a garden. He was overwhelmed with grief about the loss of his closest companion: his own garden. The same man refused to leave therapy sessions. It turned out that Searles’ telephone reminded him of one that he had owned.

Whilst these fixations might sound trivial to people who don’t suffer from psychosis, it must be remembered that schizophrenic patients don’t speak figuratively. These experiences are very real, not poetic interpretations and they are symptomatic of a very deep and painful ontological crisis (Searles, 1960, 1962, 1965) A designer must be aware of how meaning and its inverse (meaninglessness) may be structured into the environment. The negative effects an ugly and dehumanising space can have on such a patient cannot be underestimated (Osmond, 1966). And neither can the reassurance that comes with a space that is highly refined and aesthetically considered. As De Botton (a popular philosopher) suggests, architecture really only comes into its own when we have to plumb life’s deepest questions; when we have to deal with pain, grief and confusion, and it is at these times that no pill can help (De Botton, 2006).

Ulrich has made some very important associations between accessibility of the natural environment and better health outcomes. Whilst it hasn’t been explicitly noted in his 90


papers, it is likely that the health benefits derived from access to a natural landscape occurs because meaning is so easily found in nature (Ulrich & Parsons, 1990).

It seems that meaning is fostered through environmental richness; through complexity, order and aesthetic considerations (Bachelard & Orion Press (Tr.), 1958, 1964 (Tr.)). The more afflicted the patient, the more significant it is that the spaces they use are truly beautiful. Obviously such a term raises all kinds of prickly issues, (like who is to be the final arbiter of taste,) but the point, (raised by Osmond,) is not so much about the aesthetic of the final solution, but that the ‘usual’ drabness of hospital architecture is avoided. The detailing of mental facilities should be more considered (aesthetically) than a ‘nice’ home because it is only when patients’ expectations are exceeded that they will feel a sense of ease (Osmond, 1958). Currently there is a long way to go; the surroundings in mental health wards hark back to their genealogy; as lockups, dungeons, and more recently as asylums (Osmond, 1966; Sine, 2008). These associations must be rejected entirely as there should be no sense of ‘punishment’ embodied in health architecture.

Bare, drab spaces directly affect perception (even of healthy individuals,) in a very dramatic way. A reduced environment causes hallucinations, delusions, confusion, the impairment of organised thinking, oppression and depression, even for healthy people (Hebb, Heath, & Stuart, 1954; Osmond, 1966; Searles, 1965; Solomon, Leiderman, Mendelson, & Wexler, 1957) and the inverse; a multi-sensory environment that is rich in complexity, has been linked to improvements in emotional, cognitive and immune 91


system functions (Schweitzer et al., 2004; Woodard Smith, 1959). To this end, Osmond suggests that spaces for psychiatric care should be exceptionally generous in the way they’re decorated and finished (Huntoon, 1959; Osmond, 1957, 1958), even going so far as recommending fresh cut flowers in the private spaces. Any fears about patients’ scatological and autoerotic behaviour (presumably the reason for vinyl surfaces in the first instance,) can be largely allayed. According to Osmond, a patient is only likely to resort to ‘apsophilic activities, touching the staff and painting the walls with faeces’ when left with no other more acceptable sensory gratification (Osmond, 1958).

Although nostalgia can be a symptom of schizophrenia, Searles (1960) describes how it can also be a very important transitional fixation in the process of re-engagement with the outside world. It is very important that patients aren’t separated from their preexisting lives, as this completes a disjuncture that is already a serious problem for mental health. Patients should be able to bring in photos and to stick them on their walls (Osmond, 1966; Searles, 1960). Ideally they will have some kind of music system in their rooms also, so they can listen to their favourite tunes (Osmond, 1958). Of course these things can give rise to melancholy, but they can also be restorative as they remind a patient that there is meaning in life; be it love, desire, friendship or something else more pertinent (Searles, 1960).

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Figure 7: CCTV Surveillance of seclusion rooms in Kansas City. It is hardly any wonder that patients indulge in apsophilic and scatological behaviour in such a sensory void, painting the walls with faeces and masturbating are the only available options for sensory gratification. Such acts are the last resort in preventing further mental deterioration. Research shows that people with no history of psychosis will 93


soon start to hallucinate in such an environment Source: Victor Van Hee (release granted).

Conclusion Under normal circumstances people have a great deal of ability to adapt to new surroundings – even in stressful situations – and such changes can actually support the overall robustness of wellbeing. However, when environmental factors start to erode a general sense of coherence – when meaning, control and comprehensibility are lost – resistance to disease weakens and perceptual difficulties are exacerbated, often creating a vicious circle of increased vulnerability and anxiety.

It is imperative, therefore, that health facility planning teams carefully scrutinise plans for anything that may not be in the patient’s interests. A basic understanding of what makes an environment supportive in order to assist and maintain good health will provide a useful framework for this critique. To this end, Salutogenic theory is a particularly useful tool as it is specific16 and easily applied to an architectural application.

Essentially the theory proposes that a ‘sense of coherence’ (SOC) is an integral part of the natural healing process and that a strong SOC is supported by feelings of

16

A hypothesis about the specific effects of each decision can be established with

relative ease. 94


comprehensibility, manageability and meaningfulness, all of which have architectural ramifications. Of course the use of a salutogenic framework does not mean that no further research is required and nor does it insure that all the choices the design team makes will be the very best decisions in the given circumstances, but in providing a basis for making purposeful decisions about any aspect of the design on the fly, it means that the architectural teams are empowered to design the very best facilities they can, given restricted time and budgets and a the general paucity of useful empirical evidence.

There are many things that can be done with the architecture of a facility that may alleviate mental symptoms, lessen the likelihood of future psychotic episodes, alleviate stress and assist with basic cognitive functions. These innovations can be broken into three categories in an architectural extrapolation of salutogenic theory:

Designing to foster a sense of coherence through:

1. Comprehensibility; making sure that perceptual cues are present to assist perceptual processes. These include attention to texture and materiality, controlling the size of spaces and the numbers of patients and expressing environmental features in a normal way. 2. Manageability: that is allowances for patients to exercise control of the environment, details such as opening windows and the provision of ADL and sporting facilities. 95


3. Meaningfulness: enriching the environment with complexity, order and aesthetic considerations as well as providing good spaces for visitors special personal belongings and possibly even for pets. All of these approaches come together to create an architecture that really serves the needs of mental health patients, fortifying their overall sense of coherence and mental wellbeing and improving recovery.

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So you’re going to design a mental health facility? How to make it future-proof.

Published in: World Health Design Scientific Review, (2012); Psychiatric Design: Using a salutogenic model for the development and management of mental health facilities. 5(2), 74-79.

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Abstract

The prevailing model of psychiatric design (the world over) does not fulfil its potential in supporting the healing process. In order to design for future usability, design teams must have a vision beyond current paradigms and understand the direction healthcare is going. More importantly still, models of care that will actually improve mental health outcomes instead of just managing patient behaviour must be considered.

To create this vision, a methodological salutogenic approach can be employed for the project development and management phases – from design of the buildings through to the design of the models of care. This approach advocates taking an interdisciplinary and collaborative approach to actively improve a sense of coherence for all users including patients and staff. This can be done at every decision point by choosing to foster manageability, comprehensibility and most importantly meaning.

How to plan for psychiatric recovery through more supportive design? The current paradigm of the design of psychiatric facilities has a long history. But many historical approaches to the treatment of mental illness were not supportive to healing process. Even today vestiges of the ancient traditions of imprisonment and punishment of psychiatric patients can still be found in the buildings that healthcare designers are presenting today – and these are for current models of care and for units that are expected to be in place for a generation at least. In many other healthcare typologies 98


there is a lot of value to be retained in existing models of care and paradigms of design. The same cannot be said for mental healthcare. To move into the future, we have to escape the past.

This paper does not take aim at the worst aspects of psychiatric care. It isn’t necessary to be explicit about the shortfalls of seclusion and other compromising methods that are maintained in current paradigms. To designers, facility managers and directors, magistrates, nursing staff, clinicians, politicians and local community groups – the problem areas of the psychiatric milieu are quite obvious and need no elaboration. Instead, this paper outlines a challenge and a methodology for achieving this appropriate goal – to design a mental health facility that is appropriate for the task and supportive of the healing process.

The challenge is paradigmatically new – but is familiar nonetheless. In several years of in-depth study of the psychiatric milieu, I have seldom met anyone who doesn’t already feel the challenge tapping away at their consciences. The challenge is to bring humanity, aesthetics, love and meaning back into the psychiatric milieu to address the cause of mental illness – not only to manage the symptoms.

This is the methodology that medicine has to adopt in order to become sustainable. Obscure, as it is now, the salutogenic method will become universal over the years to come if mental units are to be of service in the future.

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The future of healthcare The current escalation of healthcare costs is financially, socially and environmentally unsustainable. Even in places that are highly dependent on private health insurance, government subsidies to the healthcare industry are a major economic problem. The reason is because it is very expensive to treat an illness once it has become critical. The cost of keeping a person alive when they are suffering from the failure of a major organ is enormous.

Antonovsky visualized health as a continuum and the progress of disease as entropic (Antonovsky, 1987) pp. 71-72), meaning the fall from a state of health accelerates. The more entrenched illness becomes, the more energy is required to arrest that fall. For this reason 80% of a country’s health budgets are spent trying to prevent the inevitable – the hospitalisation and treatment costs that arise in the last year of life from preventable disease (Sylvan, 2012). And this cost is increasing.

With limited resources we must reverse the entropy of disease much earlier, while it is still affordable. In many cases, this can take place before disease ever occurs. Not only is early intervention much cheaper, but the benefits are not only economic but social and environmental also. Worldwide vaccination programmes and similar massive scale interventions have already tested this approach and found them to be spectacularly successful.

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A number of remarkable studies show how minor and apparently non-causal interventions can improve health outcomes and shorten hospital stays. There have been hundreds of such studies. These studies identify views of nature, passive plants, handwashing, single bedrooms, designed soundscapes, appropriate lighting and a number of other interventions (Ulrich, 2006). Even in mental health, small things like the décor of a unit reduce stays by 25% (Vaaler, Morken, & Linaker, 2005). But can such interventions occur earlier still? Before a patient ever gets sick by preventing the risk factors that are embodied in the built environment?

Antonovsky shows that they can – and it’s never too late, although the best time is before pathologies arise. The principles he proposes are called salutogenics.

Salutogenics The theory of salutogenics is critical of the current model of illness. An illness doesn’t occur with the development of a distinct pathology, but well before, with any slippage from an idealised state of health. In this model the state of health is a continuum, with an idealised state of perfect health and well-being at one end, and with illness at the other. The only point of definition is at the far end of illness, and it is death – the point of no return (see

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Active forces

{

Deterioration/Pathogenesis

DEATH

Generalised resistance deficits (GRD’s) There are no absolute GRD’s. GRD’s are any forces that erode the ability to cope. Typically these include under- or overloads.

Better health/Salutogenesis

State of well being

LIFE

Antonovsky’s salutogenic theory (1987)

Figure 8).

Active forces

{


Deterioration/Pathogenesis

DEATH

Generalised resistance deficits (GRD’s) There are no absolute GRD’s. GRD’s are any forces that erode the ability to cope. Typically these include under- or overloads.

Better health/Salutogenesis

State of well being

LIFE

Antonovsky’s salutogenic theory (1987)

Figure 8: The principles of Salutogenics as visualised by Antonovsky. Two sets of forces that affect the state of well-being compete, with generalised resistance resources (GRR’s) promoting health and generalised resistance deficits (GRD’s) exerting a deleterious influence. The GRD’s are entropic – without GRR’s, there is not homeostasis, 102


but decline into inevitable illness and death (Antonovsky, 1987; Frankl, 1963).

This continuum has competing forces working in either direction. The forces driving a person toward health are called generalised resistance resources (GRR’s) and those that drive toward illness and ultimately to death are generalised resistance deficits (GRD’s). Both GRR’s and GRD’s are the same thing – they are life events. But it is not what they are – it is how they are dealt with that is important to designers and facility staff. A stressor may push one person over the edge, and another may not notice the stressor at all – they may even treat it as a challenge.

The difference lies in what Antonovsky called the sense of coherence (SOC). “The confidence that, as in the past, things by and large, work out well” (Antonovsky, 1987), p. 133). Three engines power the SOC: Manageability, comprehensibility and meaning. The GRD’s on the other hand, reflect inabilities in dealing with situations, paralysis in the face of life’s continual challenges. These reflect deficits in comprehensibility, manageability and/or meaning.

A strong SOC provides motivation for action and an understanding of the situation at hand, but a weak SOC is paralysing. There is no impetus to act, nor knowledge of what’s at stake or what action to take in any case. Thus very similar circumstances have very different effects on different people. In Antonovsky’s time this was difficult to prove. Questionnaires like the ones used by Antonovsky could show no more than 103


correlations, because individual circumstances could never exactly be the same and variables in real life situations are impossible to control - even inside a lab. To get around this, some scientists created a virtual reality experiment where people were given a virtual experience of a trip on the London Underground (D. Freeman & Freeman, 2008). In this way, the expressions and behaviours of every passing stranger could be guaranteed to be identical, and strictly neutral. The virtual reality experiment showed that even healthy people interpreted the same circumstances very differently and behaved differently accordingly. Where one subject said things like “It was nice – much nicer than a real experience. I thought they (the virtual commuters) were pretty friendly,” another subject said, “there was something dodgy about that guy. Like he was about to do something – assault someone, plant a bomb, say something not nice to me, be aggressive (D. Freeman & Freeman, 2008) pp. 71-72). These reactions depend hugely on the SOC.

Evidence-based design, research-based design, or design guideline-based design? Very recent reviews of all the mental health units in New South Wales (Australia) and the Australian Health Facilities Guidelines (CHAA, 2009) found that the decisions embodied into existing units and even the guidelines themselves were based on little or no evidence at all. In many cases, the units and the guidelines contrasted starkly to existing evidence (Barach & Potter-Forbes; forthcoming). Fortunately (and possibly as a result) the Department of Health Infrastructure in New South Wales made a statement that the guidelines are “only guidelines” and that the reliance on them is being “rolled back” (Rust, 2012). This will improve the healthcare design, because it liberates design 104


teams to employ evidence-based design

17

(where it exists – for a brief review see

(Shepley, Pasha, & Huffcut, in review). But perhaps more importantly, it allows the teams to reach for non-targeted research to inform their decision-making in what is called research-based design. Approaches can be very methodical. An example is the salutogenic method for psychiatric healthcare design, which is currently the only, published evidence-informed design methodology specifically for psychiatric unit design (Jan Golembiewski, 2010b) (reprinted here from page 62).

The architect’s problem As every architect knows, a hundred decisions have to be made every day. Some of these will be critical – like in writing the functional program; but most of the decisions will be small; which cornice, which colours, textures, finishes and specs. As the virtual reality experiment above demonstrates, it isn’t only critical things that people with a low SOC will react to (everybody reacts to those!) How can we make even these tiny decisions in the best interests of the end-users?

The answer isn’t as difficult as it may seem. But before we go into the specifics of the salutogenic method, we must acknowledge that the patients who are going to use the facilities we design are likely to be there because in some ways, it’s too late to rely only

17

The term evidence-based design (EBD) is often regarded as a marketing tool and

certification programme – the term ‘research-based design’ does not have these connotations, nor are the research criterion so formulaic. 105


on salutogenics, because many of those patients are going to be suffering acutely before they even arrive.

Customisation Most mental disorders don’t have known pathologies, and for these there are no universally effective treatments. Psychotropics suppress some symptoms, cognitive behavioural therapy (CBT) and other therapies help patients to get themselves on their feet – but none offer a cure. This means that a lot is left for the environment to do and that’s a big responsibility. But it’s one we designers should embrace.

A very important starting point is to understand the treatment profile of the patients who are expected to use the facility. I recommend dedicated units for specific psychotic disorder spectra– these can be roughly classed into two:

Those who are depressed, with dementia and mood disorders; and those who are hyperaroused, with psychosis and mania.

Institutional resistance As a single cog in a big wheel, you’d be justified in fearing resistance to the introduction of new ideas – especially if they are the foundational ones that are seldom questioned. Institutional change is difficult to achieve because it carries the inertia of habit. But there’s reason to be positive that change will be received well. In the years I have studied the design of mental health facilities, the only people who are happy with 106


the current paradigm are those who sell anti-ligature hardware, vandal-proof windows and other products that are customised for the current paradigm (eg, Sine, 2008). The list of those who know that structural changes are needed include everybody from patients, clinicians, nurses, ancillary staff, family and even politicians.

To some extent the fear that a new paradigm may be mistaken is mitigated by the reality that mistakes are already well entrenched, and short of a reversal to total barbarism, with a bit of common sense we could hardly do worse.

Positivity from the start Negativity and positivity are both processed differently, and in different regions of the brain. This is possibly why early judgements are very slow to reverse, so first perceptions are pivotal on how a new unit will be accepted.

A positive initial

experience will mean that users will be forgiving of a few mistakes. A bad start, on the other hand, will mean that a unit may never be loved – despite having brilliant vision and innovations (Golembiewski, 2012a, 2012c) (Articles are included on pages 358and 159-.)

A positive first experience is essential for all new users of a new facility, whether they are clinical, non-clinical, patients or visitors.

Although negativity and positivity are processed differently in the brain, they both use the same neurotransmission system: the dopamine receptors in the mesolimbic 107


dopamine pathways. Here we run into one of the most difficult complications in predicting the experience of someone with mental illness. Dopamine dysfunction is central to the psychopathology of most mental illness – and the inhibition of dopamine transmission is the central task of all anti-psychotic medications (Ginovart & Kapur, 2010). Meanwhile anti-depressants and anti-Parkinsonian medications excite the same neurotransmitters (Dunnett & Bentivoglio, 2005; Pei et al., 2010).

Being one of the four central neurotransmission systems of the mammalian physiology, dopamine serves many functions. One of these, and possibly the most relevant in this context, is that the dopamine receptors moderate attention. This means that the subject of experience (engagement, attentional focus) is largely determined by a system that is dysfunctional in most mental illness (Golembiewski, in review-d) (p. 204- q.v.) The focus of mental health patients is frequently bizarre and unpredictable. Having said this, the diagnoses of mental illnesses are very useful for drawing generalisations, because the standardised diagnoses are largely based on symptoms that reflect the specifics of attentional dysfunction rather than by pathology.

The attentional biases of various mental disorders can be understood in simplified terms according to Table 1.

Superfluity Deficits

Top-down Hyper-arousal, mania, paranoid psychosis Depression Forgetfulness

Bottom-up Hyper-arousal Flat affect Poor self-awareness

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Table 1: The attentional biases of various mental illnesses can be understood in terms of attentional dysfunctions. Top-down attention is intent and habit driven, and bottom-up attention is stimulus driven.

Many mental illnesses are the combination of two dysfunctions. Paranoid schizophrenia, for instance, is likely the superfluity of top-down attention with a simultaneous deficit of bottom-up attention (Golembiewski, in review-d) (Page 204- q.v.)

Neutral perception As the virtual reality experiment of Freeman and Freeman (2008) above demonstrates, there’s no such thing as a neutral perception. This is a reflection of the fact that affective positivity and negativity are processed differently on a neurological level (also above). In practice, neutral is processed either as positive when it occurs in a positive context, or as negative when neutrality occurs in a negative context. With healthy people, all perception, including personal communication, carries a natural affective positive bias, meaning that the ambiguity of so-called ‘neutral’ perceptions is taken as positive by default. This bias is reversed in psychotic conditions (other psychiatric conditions have yet to be tested), meaning that an entrenched negative bias tends to dominate in psychiatric conditions (Golembiewski, 2012a) (See article on p. 358 q.v.) The result is that everyone and the environment must work hard to counter this bias. For psychiatric patients, ambiguity is much harder to resolve and is much more likely to be taken badly.

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Person to person communication is particularly important to analyse in the context of the polarisation of perception, because it touches the sorest points of paranoid thinking (Chadwick, 1992; Freeman & Freeman, 2008). Psychiatric patients are often bizarrely unaware of their surroundings unless they relate in some small way to the underlying narratives of their delusional scripts. At which point, they become highly attuned. If patients are paranoid (a very high proportion of schizophrenics, bipolar, substance related psychosis and dementia patients are), then ambiguous or negative communication will not go unnoticed, even if it is very subtle. It is easy to scoff at the idea that patients will pick up on any subtleties at all, when the circumstances of their existence deny the fact so completely. Schizophrenic patients are frequently oblivious to the fact that their shoes are on the wrong feet, and the fact that they sleep in between six lanes of traffic, so how could they pick up on nuances that most of us would miss?

Several studies demonstrate that schizophrenic patients are an order of magnitude more sensitive to expected stimuli than healthy controls, especially when those expectations relate to delusional ideas (Brennan & Hemsley, 1984; Dakin, Carlin, & Hemsley, 2005; Shergill, Bays, Frith, & Wolpert, 2003).

Negativity in communication is ubiquitous. Carrere and Gottman (1999); Gottman (1996); Gottman, McCoy, and Coan (1996) are able to identify ten common negative communication behaviours within three minutes of any conversation. It’s important that staff are trained to identify their own negative words and actions, lest negativity is present in communication with patients, because if they are, the architecture cannot 110


come to the rescue. The common negative communications are: contempt, disgust, defensiveness, belligerence, stonewalling, domineering, anger, whining, sadness and fear. There is ample evidence that communication failures frequently lead to the use of coercive measures such as sedation or seclusion (Hoekstra, Lendemeijer, & Jansen, 2004). One of the recommended ways to dispose of these facilities is to, “Try to gain trust: suit the action to the word and the word to the action (and…) try to get in touch with patients by talking to them and showing genuine interest… Don’t shy away from physical contact with patients.” (Hoekstra et al., 2004, p. 282) In other words, to train staff in appropriate and ultra-humane communication.

Design and treatment fit Many healthcare units are high reliability organisations where a small practitioner error can have sudden and catastrophic consequences. In these circumstances the fit between spatial design and the routines established in clinical praxis are critical to the functioning of the facility (Sanchez & Barach, 2012).

A major shift in models of care will be required before equivalent spaces in the mental healthcare milieu can be developed because these facilities are essentially domestic. The main treatment rooms in a mental health facility include bedrooms, courtyards, living rooms and rooms that can be used to retrain patients in the use of normal activities of daily life (ADL) including kitchens, bathrooms, and laundries. Other clinical spaces also serve normal human functions and thus are best if they are human in scale and layout: consultation and assessment rooms, rehabilitation gyms, and spaces for other person-to– 111


person treatments. The exact details of these seldom matter, aside from good acoustic privacy, appropriate lighting, and the inclusion of practitioner escape routes.

The spaces in existing units that are possibly the most design sensitive are seclusion and medication rooms. Both are useful only when models of care have failed.

Consultation or interactive collaboration? Consultation is an attempt to engage interest groups in the design process. How this works depends a lot on the all those involved, but it’s rare that consultation is a two-way conversation – unless those on the design side see the opportunity for a PR exercise. Certainly it’s rare that a genuine dialogue evolves that requires an on-going commitment from those that are consulted. Collaboration, on the other hand, requires that both problems and solutions be shared, and with a deep level of responsibility. As counter-intuitive as it sounds, we should not seek opinions and ideas of the stakeholders to guide the project, but rather seek out representatives of the interest groups who are willing to take the whole journey, sharing the responsibility for both successes and failures. With this approach, you’ll find people who are going to understand – at a depth, why things turn out one way or another. This is where people are engaged just enough that they feel they have been heard. They have handed over their opinions and ideas, but most people have no idea just how complex architectural problems are, and that some concepts must get lost in the design and building process. When the finished product inevitably doesn’t reflect their input, people feel deceived and unheard, and this breeds negativity – even if the opinions and ideas were worthless or not implementable. 112


It’s important that everyone knows that the project is aiming to be the best and futureproof, which means it cannot rely on current models of care or design paradigms. But this short paper is not the place to lay down a methodology for effective collaboration and project development. Consider engaging a change management expert and see for more guidance (Plsek & Wilson, 2001).

The Salutogenic method In 2010 a method was published especially for addressing the salutogenesis of mental health patients to give a good basis for decision making, wherever evidence is hard to locate or simply doesn’t exist (Golembiewski) (Article on p.62 q.v.) The method aims to make every decision support the SOC in some way. Generally speaking these will have a holistic effect on the coherence of the entire facility.

To do this all decisions, however minor, should be subjected to close scrutiny for how they assist the ability to manage, comprehend or find meaning. They should then be checked for how they might erode the sense of coherence by taking away manageability, comprehensibility and meaning.

Ideally the more important decisions should be referred to a collaborative committee so that the critical decisions can be ratified from other perspectives (Plsek & Wilson, 2001).

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Figure 9: Salutogenic theory treats the state of well-being as a continuum, with death at one end and a more meaningful, more fulfilled, more connected life at the other. The sense-of-self in this model is the core of experience. Beliefs are the anchors we use to connect to the greater world, but beliefs are plastic and changeable to suit any situation – or delusion. Only beliefs that are grounded in reality are nondelusional.

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In this model a state of paranoid psychosis is a contraction from greater social concerns because of a loss of meaning and comprehensibility.

The hierarchy of meaning “The absence of the things that make life manageable has obvious consequences, although they are not as significant as we tend to assume. Lack of food, water and shelter will be a source of stress that will make outcomes worse, but with their meaning and comprehensibility needs looked after; people can go a long time without basics. As Frank Lloyd Wright famously said, “give me the luxuries of life, and I’ll gladly go without the necessities.’” (Golembiewski, in review-b) (Article on p.159 q.v.)

Not all interventions and decisions are equal. There is a distinct hierarchy of meaning, with meaning and connections with society and the greater world as the foundational basis for meaning, followed by understanding and comprehensibility and finally by basic needs. This inverts Maslow’s well-known logic that basic needs are pivotal for maintaining human life and that self-actualisation a final luxury once all other needs are in place.

The mental health unit is also a forum for the competing needs of the various users: the clinical, legal, non-clinical, patients and visitors. Each has a claim on limited resources such as space, sunlight and proximity to the centre of the building/s. But more 115


importantly still, clinical and legal staff can claim the basic freedoms of patients. These freedoms are essential to the maintenance of a sense of meaning, yet all too often psychiatric facilities are designed to make manageability for the staff extremely efficient, while taking power from patients. This is all too easy with architecture, which has a long tradition of amplifying power to some and denying it to others (Jan Golembiewski, 2010b)(Article on p.62 q.v.) Such games must be avoided because it works against the very raison d’ etre of the unit: to empower and enable patients enough that they can handle life on their own once they leave. Great care should be taken to make sure that the patient’s well-being and sense of meaning is always protected. In the context of the mental health facility, this principle harks back to the Hippocratic oath “I will apply measures for the benefit of the sick according to my ability and judgment; I will keep them from harm and injustice.” (Edelstein, Temkin, & Temkin, 1987), p. 6)

Manageability This is what hospital architecture does best. Support for manageability means providing the basics to support life; food, shelter, medication, security, activities to occupy the mind etc. (Golembiewski, 2012b) (See article on p.183- q.v.) it is also the focus of a lot of the treatment; managing pain, managing patients etc. But at every step, the role of the unit in managing on behalf of patients should be rolled back to allow patients to manage on their own. It may be impractical, but giving the less critical patients access to a kitchen and groceries could be an important step in enabling independence. “The feeling that a person is in control of his or her environment and life circumstances is very 116


fortifying” (Golembiewski, 2010, p. 107) (In this thesis, p.82). Things that support manageability for patients will include provisions for their health, security and comfort, and even more importantly, provisions for the patients to make decisions for themselves and as far as possible, to take action accordingly.

Comprehensibility Comprehensibility is the way an individual understands the situations they’re in. It is information of every kind. In a mental health facility context, that means knowing why they are there, how to negotiate the facility and its routines and how to do things, including how to leave. It also means knowing about the diagnoses and medications they’re being given, their rights etc. and the context of the greater world, including the formal laws or informal social mores of the world.

Comprehensibility is more important than manageability, because it’s much easier to cope with adversity if people can understand their circumstances: if people know what is going on and why.

Psychiatric patients often have a very hard time understanding the basis of how things work and why things are like they are. In fact, it is widely hypothesised that attempts to rationalise beliefs about how things work are the basis of delusions. (D. Freeman, Garety, Kuipers, Fowler, & Bebbington, 2002; Garety & Freeman, 1999; Garety, Kuipers, Fowler, Freeman, & Bebbington, 2001; Startup, Freeman, & Garety, 2008)

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Things that may improve comprehensibility for patients are clear way-finding, simple typologies, lots of relevant information, lessons, transparency in methods of care and decision making and as little ambiguity as possible. Ambiguity may be fun for healthy people, but it is generally dangerous for psychiatric patients (Osmond, 1957). A doorknob should look like a doorknob and a shower like a shower.

Meaning Only a rich sense of meaning will be of assistance when manageability and comprehensibility is lost. With meaningfulness, one can face dire circumstances – starvation, pain, illness and the worst demonstrations of human antipathy and feel confident, that in the long run everything will turn out for the best (Antonovsky, 1987; Frankl, 1963). In psychotherapy, it is only when meaning is established that there is ever release, resolution and recovery (Clarkson, 2006), thus it is reasonable to assert that the fostering of meaning is the single most important role of the mental health facility. It is also the hardest task to accomplish because efforts cannot be prescriptive. Meaning is deeply personal and the product of an individual journey.

One of the great problems of health facility design and management is the problem of suicide. The creation of meaning is the only way suicidal ideation can be reliably treated. If anti-ligature fittings, CCTV and constant monitoring work at all, it is only while a patient is locked into a unit. As long as patients are free to leave, suicidal patients can always throw themselves in front of a passing car. When a patient discovers something to live for, suicidal thoughts will lose their power to turn into action. 118


To foster meaning, emotional connections are very important. Meaning is built on anything that is of greater importance than the individual self; friends, family, society, the planet, pets – all these are likely areas of concern on which meaning can be fostered. Religion can also fit into this group, but belief is infinitely plastic – in other words, belief is infinitely flexible and adaptable to current circumstances. Unless belief is grounded and validated by some level of external reality, it loses its purpose and is as worthless as any delusion. What belief is useful for is to create real and meaningful links with the greater society, world and cosmos. Remember that one of the fundamental reasons that the principles of salutogenics work, is because they enable action rather than paralysis. If I believe God loves me because I care for the environment, I will actively care for the environment, and those positive actions form the basis of an affectively positive connection with the environment. A basis for meaning.

Delusional beliefs don’t do this. Delusional beliefs support passive or negative behaviours. If I were to believe that it doesn’t matter, I can’t make a difference anyway; I would be suffering from a passive delusion. If I were to believe that a random shopper was evil, and the best thing I could do is to slay her (such an event took place recently in Tenerife) this would be a negative delusion (Golembiewski, in review-b) (Article from p.373 q.v.)

External reality is, for the best part, very unforgiving. People can be very savage – especially to people who behave strangely like many mental patients do (Goffman, 119


1963). But there are ways that patients can connect with external reality meaningfully, with little risk of failure.

This is not the place to detail all the ways of encouraging meaningful connections to the external world, but here are some ideas:

To encourage pet ownership Many patients with mental illnesses have pets – especially dogs, and in the context of mental health recovery, pets should be considered as more important than any contributor to manageability or comprehensibility (Beck & Katcher, 1983; Katcher & Beck, 1983; Searles, 1960). When designing a unit, it is wise to provide at least some rooms – separate if necessary – that welcome pets.

Arts The arts form important and traditional associations – they can be a meaningful way of linking mental patients with society. This is particularly relevant because there is a common perception that mental patients are frequently geniuses. Regardless of whether or not this is true, everything that could encourage artistic and literary endeavours should be encouraged: poetry, music, painting, drawing, sculpture, dance and performance are all wonderful for promoting a sense of meaning. And if you are concerned (like many others are) about handing patients carving tools, bear in mind that the use of woodcarving tools are increasingly common even in forensic mental health units (yes, where patients are sectioned because of extreme psychiatric violence) in New 120


Zealand, and the impacts on improved mental health and behaviour are really good. I’ve also heard concerns that patients will paint on walls and write obscene and threatening material. My answer to those concerns it to let them, and even to encourage it, but give the patients washable materials! That way the invective and obscenities can be washed clean before the next patient takes the room.

Meaningful activity It’s hard to find meaningful activity for patients who cannot even look after themselves, but an effort should be made. One of the most meaningful things a patient can do is share their recovery by helping out the more critical patients (Alomes, 2009). There was a short period between 1850 and 1860 when less critical tasks used to be routinely given to patients. Patients used to milk cows and work gardens, and the products of their labours used to end up on the tables in the evening, by all accounts, it was a spectacularly successful (E. T. Hall, 1975; Yanni, 2007).

Meaning takes time and effort to build, but can vanish in minutes. The thing that is most damaging to meaning is meaninglessness. Meaning is incrementally destroyed by any reason that someone may want to hate the world and society: cruelty, meanness, broken promises, deception, stonewalling, and contempt. Unfortunately sedation and seclusion fit into this category. This is not to say anti-psychotics are bad. In most cases they are essential. But the use of sedation as a management tool puts the management needs of staff before the patient’s need for meaning.

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Conclusion: an example of how a finished salutogenic unit might look and function. A number of examples and explorations of these ideas are included in (Jan Golembiewski, 2010b; Golembiewski, 2012a, 2012b, 2012e, 2013, in review-a, in review-b, in review-c, in review-d) (reproduced throughout this thesis), and every facility will be different, but to conclude this article, I would like to present the phenomenology of a patient’s experience of a new salutogenic psychiatric unit.

Frank is brought in a police van. It’s 2am. He’s been through this before because the past few years he has spent more time in short stay mental health facilities than out. He has been diagnosed with chronic Bipolar (type I) with frequent substance induced psychotic episodes. Frank is aware that he was smoking cannabis earlier in the night, but he’s furious because he didn’t do anything wrong – until the police arrived. It’s just that someone tried to steal his car and beat him up and stripped him as a final humiliation.

When the van door opens, Frank hurls abuse at his captors, the police. But he steps out somewhere unexpected. It’s not a prison cell, nor a mental health facility; it’s nice. It looks like the back veranda of a country home. The lights are low, and there are a couple of people sitting, chatting on a sofa having a drink and a cigarette. One gets up and meets Frank at the bottom of the steps. “Hi. I’m Lloyd,” He says.

“Those x*$# pigs! Roughed me up!” Frank replies.

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“Yeah. Looks like it.”

“When we picked him up, he was vandalising a car in a parking lot…” one of the policemen start to report. Frank doesn’t realise that the staff at the salutogenic unit have all the information the police can give already. They were contacted twenty minutes ago, and that’s why they are out here on the veranda at 2am!

“Put it in all your report, and kindly leave. This feller is naked, unhappy, and needs to relax.” Lloyd says to the policeman, who is slightly affronted but gets back into the van, and drives off. Lloyd leads Frank onto the veranda. “Do you want a dressing gown? A drink or a cigarette?” Lloyd asks. Veranda, nice person, dressing gown, cigarette, drink? Have I gone to heaven? Frank thinks to himself as he volunteers an arm for Lloyd to dress him.

Over the next fifteen minutes, Frank debriefs to Lloyd and Zaha on the sofa, with a glass of lemon, lime and bitters (not his personal choice – but that’s what was there) while he is introduced to the e-cigarette for the first time. “…Not allowed to smoke real ones here,” Zaha explains, handing Frank the e-cigarette. “But this is much the same. It’s still smoking, and it’s still nicotine, only you can use it indoors, and it’s not cancerous. Have it, it’s yours.” Frank is asked if he has pets or anything he has to collect from home in the morning…

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Soon Frank is led to his bedroom. The short corridor has a polished hardwood floor, with a long and deep runner rug to muffle footsteps. Paintings (some donated by an art school and some by other guests, he is told) hang off a picture rail. His room has a big, heavy wooden door with a brass handle. Inside, the room is simple. A heavy wooden bed with old-fashioned sheets and blankets is made up. The window has open louvers and a mosquito screen. There is a heavy wooden desk, with paper, crayons and pens laid out on it (they are washable, but John hasn’t been told that). The dimmed wall-mounted wash lighting casts a warm yellow glow. A fern sits in a small pot on the table. There are picture and dado rails, and an abstract painting hangs from them. As a precaution against suicide attempts, a few of the features – the curtains, the picture rail and the toilet roll holder in the bathroom are suspended by strong magnets, but the unit is still new, and nobody has tried yet, so these features just look normal, fancy even.

The story continues…so long as the designer is willing and belief can be sustained – materialised even, into something incredibly meaningful.

This is a snippet of my vision of how psychiatric units will look and function in the future: always cognisant that the healing process of mental illness involves humanity, aesthetics and everything else to foster a sense of meaning, comprehensibility, manageability and total coherence.

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MENTAL ILLNESS AND THE URBAN ENVIRONMENT

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Determinism and Desire: Some neurological processes in perceiving the design object.

In press, The International Journal of Design in Society, Year/Volume: 2013 Issue: 6

Winner CG Publisher’s research excellence award, 2012

Abstract

The environment moderates behaviour using a subtle language of ‘affordances’ and ‘behaviour-settings’. Affordances are environmental offerings. They are objects that demand action; a cliff demands a leap and binoculars demand a peek. Behavioursettings are ‘places;’ spaces encoded with expectations and meanings. Behavioursettings work the opposite way to affordances; they demand inhibition; an introspective demeanour in a church or when under surveillance. Most affordances and behavioursettings are designed, and as such, designers are effectively predicting brain reactions.

Affordances are nested within, and moderated by behaviour-settings. Both trigger automatic neural responses (excitation and inhibition). These, for the best part cancel each other out. This balancing enables object recognition and allows choice about what action should be taken (if any). But when excitation exceeds inhibition, instinctive

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action will automatically commence. In positive circumstances this may mean laughter or a smile. In negative circumstances, fleeing, screaming or other panic responses are likely. People with poor frontal function, due to immaturity (childhood or developmental disorders) or due to hypofrontality (schizophrenia, brain damage or dementia) have a reduced capacity to balance excitatory and inhibitory impulses. For these people, environmental behavioural demands increase with the decline of frontal brain function.

The world around us is not only encoded with symbols and sensory information. Opportunities and restrictions work on a much more primal level. Person/space interactions constantly take place at a molecular scale. Every space we enter has its own special dynamic, where individualism vies for supremacy between the opposing forces of affordance-related excitation and the inhibition intrinsic to behaviour-settings. And in this context, even a small change – the installation of a CCTV camera can turn a circus to a prison.

This paper draws on cutting-edge neurological theory to understand the psychological determinates of the every day experience of the designed environment.

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Determinism and Desire Some neurological processes in perceiving the design object.

Watching children on a 6th floor balcony, I couldn’t help but notice the way they searched for objects to throw over the balustrade. The promise of such a large fall yells: “Jump. Jump. JUMP!” It is only when an inhibitory reflex kicks in that a battle with a self-preservation instinct ensues. The winner is a holistic sense-of-self, of inner coherence, and the urge is diverted. And the children harmlessly throw apples over the edge in place of themselves.

The precipice, the apples – every opportunity the environment provides, calls for action. But why? This article presents a framework of neurological mediators of perception and action in an attempt to establish a cross-sectional theory of desire.

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A taxonomy of the neuro-correlates of perception, action and desire.

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Affordances; the heart of perception and the automation of action.

We don’t just perceive a compilation of colours and shapes (‘sense data’), then figure out what it all means, and then act on that knowledge as a serial process. The perception of the actions that an object allows (Gibson, 1979), occurs with the first phase of perception, prior even to the recognition of features such as colour and shape (Yantis, 2000). This is an evolutionary necessity. An animal that is slow to react when threatened will be the first to be eaten, and action must therefore commence before perception even reaches a declarative (conscious) stage (Stephen Kaplan, 1992). When we hear a loud roar, a range of automatic actions take place; our legs may start running and we may grab a weapon. The blood pressure and heart rate increases, plasma levels of adrenaline increase and our senses are piqued (Ekeberg, Kjeldsen, Greenwood, & Enger, 1990). All this occurs even before we know where the roar has issued from.

The instinctive reach for tools and escape paths is just one of many hints informing us that perception revolves around opportunities to act, for better or for ill. These opportunities are called ‘affordances’ and are a central premise of Gibson’s Ecological Theory of Perception (Gibson, 1979; Withagen, de Poel, Araújo, & Pepping, 2012).

Action-opportunities (objects) are the primary stimulants for attention (the first phase of perception), but even so, they are subject to pre-existing environmental restrictions (Yantis, 2000). These issue from behaviour-settings. Individuals have a sense of 130


contextual awareness, a sense of what is possible and what is the right thing to do in most given circumstances, and these are deliberately embodied in the physical milieu. Because the perception of behaviour-settings is automatic, people in good mental health rarely ‘act now and think later:’ such impulsiveness is unusual and is frequently a sign of psychiatric illness (American Psychiatric Association, 2000) or the immature conduct that you’d expect in children and adolescents (Quay & Quay, 1965).

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Behaviour-settings: the context of affordances and the automation of inhibition.

A behaviour-setting is an environment that highly correlates with the behaviour that is expected to take place there, that is the standing patterns of behaviour (mores,) that take place in a congruent milieu (Barker & Wright, 1954). The behaviour-setting of a football field invites the affordance of ball play, but restricts the play to specific rules (Lhermitte, 1986). Most behaviour-settings are designed to reflect the mores that will take place within.

A behaviour-setting restricts the possibilities of an affordance within it. For example, the affordance of an apple in a store (a behaviour-setting) is different to the same apple at home. At home you can just pick it up and eat it without breaking with convention. Behaviour-settings restrict behaviour to the limits previously learned, so it should come as no surprise that the inhibitory reflexes imposed by behaviour-settings will tend to reflect normative limits of social acceptability. The behaviour-setting of a church, for instance, demands an introspective demeanour and the behaviour-setting imposed by surveillance demands introspective self-monitoring (Foucault, 1977). Behaviour in keeping with the milieu is a primary automatic response and is neither creative nor individualistic. This doesn’t mean that behaviour-settings are bad – or even good. Just that they exist ubiquitously and that they modify the potential behaviour that an affordance will trigger. 132


Normally healthy adults are particularly good at voluntarily resisting the temptation to act. This inhibitory phase of perception extends the automatic inhibition provided by the behaviour-setting. But some people have neither choice to act, nor to resist action. They must act – even against specific and authoritative instructions. These people include children, whose frontal lobes are not yet fully developed, but even more so patients with organic brain damage (Lhermitte, 1986; Lhermitte, Pillon, & Serdaru, 1986).

During a clinical study investigating the effects of organic brain damage on behaviour, one patient (a 52 year old housewife who had been given a partial frontal lobectomy to remove a cancerous tumour) attempted to give her doctor an injection, just because a syringe was handy. Another patient (a 51 year old engineer who had also had a lobectomy for cancer) picked up a gun, and because it was unloaded, found the appropriate cartridges. The doctor had to intervene to confiscate the weapon (Lhermitte, 1986). Like the patient with the syringe, the man would have had no choice but to shoot the doctor. This bizarre behaviour, absolutely lacking in autonomy, is caused by the excitatory presence of a perceived opportunity. The perception of opportunity was involuntary in both the cases mentioned above. They are examples of how the constant stream of action and thought that we humans are engaged in is completely co-opted by affordances if the organ that is responsible for inhibiting impulses and enabling alternate actions ceases to function. The same impulse to act occurs even in healthy individuals, but what is bizarre about the attempted actions of the lady with the syringe and the man with the gun, is the absence of normal neural reactivity, a product of the very same organ that also moderates the functions of self-reference (Northoff & Bermpohl, 2004; 133


Northoff et al., 2006) and creativity (Dietrich, 2004; Dietrich & Kanso, 2010). In other words, reactivity, self-awareness and creativity are all closely linked.

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Creativity and awareness: the deliberate extension of affordances and behaviour-settings.

Not all action is automatic, especially for healthy adults. Given a context, we have two choices; we can act as we please within the tight behavioural limits set for us by learning. That means we can act on the automatic action cues imbedded within affordances as they are modified by the automatic initiatory limits prescribed by behaviour-settings (see Figure 10). But we can also break convention and extend those limits. So if a person has learned to adopt a certain demeanour in church, this will be the automatic mode of action when in church. But, by an act of wilful defiance, a person may dance down the isle. This is a creative act, originating in the prefrontal cortex, the seat of creativity (Golembiewski, 2012a). Creative acts of this kind will extend the limits of automatic activity, by modifying associated schemata (Johnson Abercrombie, 1960); once you have danced down the isle once, it will be hard to return to the demure demeanour that was once automatic.

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Automatic limbic processes Affective / hedonic pre-judgement – + 1a. Narrative/affective monitoring Automatic (mesostriatal) processes 1b. Latent restrictions from behaviour settings (inhibition) Behaviour limits

}}

3. Opportunities of Affordances (excitation) – +

Creative (frontal) reprocessing 2. Expanding possibilities of behaviour settings (excitation) 4. Choice to react against affordances (inhibition)

5. Potential range of final action (mediated by the striatum)

Figure 10: The Choices We Make.

In this model, excitatory and inhibitory forces compete to establish the range of potential action. The mesencephalon is the source of automatic responses and the frontal cortex the source of creative reprocessing. 1. Behaviour limits are automatically set. 2. These are consciously and defiantly extended. 3. The initial excitation of affordances is also automatic. 4. This is already inhibited (to some degree) due to the behaviour-setting (1) but may be consciously restricted further. The result is the scope of action that may take place.

•

If affordances are negative, this inhibition is normally so complete that no action takes place (see factors of saliency: worth).

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•

When patients have frontal damage, the behaviour-setting limitations and affordances are automatic.

•

Automatic responses are learned from creative responses.

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What drives engagement? The factors of saliency.

The levels of perceptual engagement that affordances trigger are uneven. The reason is that the level of perceptual engagement (activation potential) that they capture is uneven and subject to competing forces. Live studies on monkeys, where sensors were wired directly to monkey neurons (for obvious reasons not repeated on humans) isolate three factors that contribute to how much engagement an affordance or behaviour-setting will trigger (Schultz, 1998; Schultz, Apicella, & Ljungberg, 1993; Schultz, Dayan, & Montague, 1997). All three factors are types of attentional salience; and the higher the salience, the more likely the attention of a subject will be engaged 18. The three factors are described below from numbers 2-4. The first factor was discovered by experimentation on humans.

Opportunity: People instinctively find themselves attracted to an opportunity to act just because it’s an opportunity to act. There may be the attraction of a nice smell, a beautiful hue, a lovely texture (an individual may find themselves touching, looking, reacting appropriately) (Gibson, 1979).

18

The terms prominence, significance and worth are used in place of the more common,

but less specific term; salience. 138


Prominence: This is the prominence of the physical qualia of the object or setting. Noisy, sudden sounds, flashing lights and bright colours etc., are highly prominent and therefore demand reaction. High contrasts and perceptual simplicity contribute to perceptual prominence (Ljungberg, Apicella, & Schultz, 1992).

Significance; the importance of the whole concept that is being recalled. There are three things that increase the significance of an affordance or setting according to importance: a) anything that helps build meaning, b) anything that contributes to understanding, and c) anything that may needed to sustain existence (Golembiewski, 2009a; Jan Golembiewski, 2010b). In other words, we react to affordances that are important. If your work demands that you react in a certain way, you do so.

Worth, This is a quantitative measure of desirability. The promise of positive experience generates a much greater impact than the threat of a negative one (Mirenowicz & Schultz, 1996; Schultz, 1998). This is the graded pleasure principle. There’s a big difference in human reaction to bland food and delicious food, even though the two may be equally healthy.

The presence of an affordance may be informed by any of the above four saliency factors. For example, someone may pick a rose because it’s there to be picked (opportunity) it catches their eye (prominence), they want to gift it to someone they love (significance) or because that rose is a particularly beautiful (worth). Beyond initial

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attention, another set of neurological processes commence, these involve an enormous range of neurotransmitters and processes that are beyond the scope of this article.

The salience of sensory opportunity As a driver of engagement, sensory opportunity may be unique to humans. Certainly humans have rich taxonomies for every kind of sensation and are easily absorbed in sensory experiences of all kinds. We hoard opportunities for sensory exploration in the same way that a squirrel hoards acorns. Sensory opportunities are not a quantitative measure of anything. They are the potential quality of an experience. Affordances of this kind are invitations to explore and interact with the world in a sensual way (Gibson, 1979). A sensory opportunity may be found in the quality of a curve in a body (not only because the curve is prominent or bright or significant). It is found in the texture of a cashmere sweater, but also in the roughness of a fence-post.

From birth, babies will actively engage with the perceptual environment. They will imitate expressions (Meltzoff & Moore, 1977), grasp a graspable object, and with age they will want to touch textures, run fingers down Brancusi’s sculptures, absorb themselves in colours and scents, feel the curvature and warmth of surfaces, immerse themselves in tastes, experiment with sounds, etc. They will want to squeeze bubblewrap and juice cartons, just to hear them pop. They light sparklers to see the sparks fly off in all directions; they burn incense to scent the air, and climb snowy mountains, just to feel the rush of zooming down again. None of these engagements are especially

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useful. But they are enjoyable, and possibly even fortify one’s mental health (Golembiewski, 2009b, 2011b).

With familiarity, sensory affordances appear to be temporarily extinguished (there are limits on how much bubble-wrap one can pop). Anecdotally it appears that sensory pleasures are renewed unless they are recast in a negative light, so the desire to eat fish, for example might be repeated, but may be extinguished after a night of food poisoning. Designers deliberately use sensory affordances all the time, and undoubtedly it makes their projects more successful. From the crackle of pop-candy to the sweet-water fountains of Rome, little sensory treats are difficult to resist, but do enrich experience in a positive way. The architect, Louis Kahn appeared to be aware of this, and made his use of affordances to create behaviour-settings explicit, using the terms availabilities in a similar way to the way Gibson used affordances, and the term agreement to describe the congruency of behaviour-setting, affordance and mores. It was his view that the milieu should be designed in agreement with the mores that would take place there (Kahn, 1971).

The salience of prominence Prominence or as architects say, ‘spectacularity’ is a quantitative measure of the difference between qualia and expectations. It is a measure of novelty - the unexpected. As such, salience is subject to extinction with familiarity. Someone dressed in orange will catch your eye, but if you see them in orange all the time, then they take on background status (they become less salient). Technically, the dopamine neurons that 141


are activated by prominence lose their activation potential with familiarity (Berns, Cohen, & Mintun, 1997; Mirenowicz & Schultz, 1994). Familiarity is comfortable and is an essential feature of a behaviour-setting, but one that gradually extinguishes prominence (Schultz, 1998).

One very important fact about prominence is that, in the dopamine neurons that mediate saliency, it has a short bursting (phasic) action which temporarily dominates the underlying rhythmic ‘tonic’ action that moderates other forms of saliency (Jan Golembiewski, 2010a; Golembiewski, in review-d; Grace, Floresco, Goto, & Lodge, 2007). Prominent perceptions may therefore displace other perceptions and thoughts along with all other contents of the working memory (Lavie, 2010; Theeuwes, Kramer, Hahn, & Irwin, 1998)

19

. In real terms this will mean that prominent perceptions take

possession of the mind and generate enormous but temporary interest, in the same way that a tiger would, if you suddenly discovered one in your home. It is as if the brain only recognises prominence as potentially important, and closes perception off to it once it has been fully assessed and found to be benign.

The importance of prominence for architects and other designers is that prominence gets a lot of attention quickly. But it is difficult to maintain interest unless other saliency

19

It should be remembered that working memory is a hotly debated construct with

several competing models, none of which has universal acceptance. (Miyake & Shah, 1999) 142


factors support it. The focus of human attention travels logically from an initial phase of exploration of novelty and difference, to familiarity and the exploration of further opportunity, to significance and worth. With greater familiarity, the exploration of potential opportunity will also be extinguished, leaving only significance and worth.

This truism has frustrated many an egotistical designer. An architect may design a prominent and forward-thinking building, only to see it rejected and all of its great innovations ignored. Big exceptions occur when the project is somehow identified as being genuinely important. This happens whenever the building serves mores, in which case prominence is at least remembered as people go about their business. For example, someone working next to Sydney’s Opera House may see it from their window daily, so the initial shock of the new – the curves, bright white tiles and stylistic ambition – is maintained by a generalised engagement with the Opera House. The interest we have in new and delightful designs will only remain as long as those designs continue to be useful and/or foster meaning and serve worthy mores.

The salience of significance Significance and worthiness are essentially two axes of the same concept. In the commercial world, this is the ‘what’s in it for me?’ question that drives many a marketing effort. Worthiness is a quantitative value (where something stands in the spectrum between good or bad) and significance is what the worthiness qualifies. As an example, cuisine can be described according to whether it is delicious or bland (worthiness) but what is significant is that it will feed you. Significance is the potential 143


for an affordance to enrich or diminish the quality of our lives. ‘What’s in it for me?’ Well, with this example, you’ll get fed.

Significance A: Meaning. Things that imbue life with the richness of meaning are significant even if they don’t serve any direct function as such. These things often transcend the pedestrian notions of good or bad because they are essential. These are the things we live and die for. And like all other forms of saliency, can be attributed to both object/affordances and places/behaviour-settings. One needs to look no further than religious artefacts and places for evidence of the importance of these settings and the mores that surround them. Take the Temple Mount for the Jews, the Church of the Holy Sepulchre for many Christians and the Al-Aqsa Mosque for Islam. Places and artefacts need not be religious or even commonly acknowledged to be deeply meaningful. Meaning is also very personal (Antonovsky, 1987; Golembiewski, 2012b).

Significance

B:

Comprehensibility.

Another

dimension

of

significance

is

comprehensibility. We engage with things that help us understand the situations we find ourselves in, for example, some people may find astrology interesting as it gives them insight into people and behaviour and even into themselves. The desire to find out more is the basis of a rich personal ontology and provides a foundation for independence (Antonovsky, 1987).

Significance C: Manageability. Manageability, the things that make a person’s existence manageable right now may also be significant (Antonovsky, 1987). But here 144


we have a caveat; you must have a simultaneous corollary need. Things that enable manageability alone are in themselves not very enriching, yet they are essential – but in an opposite way to meaningful ones. Affordances that contribute to manageability are basic shelter from the weather, food etc. Manageability is frequently the only consideration designed into the built environment, particularly in institutional design (Jan Golembiewski, 2010b). And while things that enable existence are important, they are of no interest when the need does not present itself (preparations for future needs being a product of comprehensibility) (Golembiewski, 2009a). How much consideration does one give to an anorak during mid-summer? It doesn’t register as an affordance at all. Yet, in mid-winter it becomes very important indeed as it yells ‘put me on!’

The salience of worth At first glace, affordances that appear to be positive draw more attention than negative ones. Technically, this appears to be due to one of the functions of the medium spiny striatal dopamine neurons. Empirical studies of these neurons show that, in healthy adult populations, they are reliably more easily excited by positive stimulus than negative (Northoff et al., 2004; Schultz, 1998). The judgement of worthiness is among the first of a series of automatic reactions. And in general terms, positive affordances are far less subject to reactionary inhibition. For example, smiles, laughter, warm fuzzy feelings and cause automatic and unrestricted engagement beyond the a-priori automatic restrictions imposed by the behaviour-setting. Put another way, the choice to engage in positive experiences is a normal feature of robust mental health, but so too is the ability to restrain oneself to be appropriate in a given context. In many psychiatric conditions, 145


this positive bias is far less apparent or is even inversed in fact ‘affective flattening’ or catatonia, are common in clinical pathologies (American Psychiatric Association, 2000; Golembiewski, 2012a).

Figure 11: Excitability of Negative, Positive and Neutral Stimulus for Catatonic, Paranoid and Healthy People. (from Golembiewski (2012a) and based on data from (Northoff et al., 2004)), shows results from a clinical study of three groups. The first group: C) were akinetic catatonic patients, three of whom were diagnosed with schizophrenia, and seven with bipolar disorder. The second group: P) had seven paranoid schizophrenic patients and three bipolar. In the third group: H)

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there were ten people who had never been diagnosed with a mental disorder.

The numbers (graphed) show the net excess of neural excitatory reactions after all concurrent inhibitory reactions has been subtracted. All groups were exposed to negative stimulus (pictures of horrific things; black), positive stimulus (pictures of lovely things; white) and neutral stimulus (grey card; grey). As you can see, in the negative condition, there was such a minor excess of excitation in the healthy group that it was not chartable (0.63%). The patients however, were unable to balance negative perceptions. On the other hand, positive perceptions were not so strongly balanced out (although some inhibition had taken place – not graphed). The healthy group had about double the positive reaction than the paranoid group and about a third greater positive reaction than the akinetic catatonic patient group. This demonstrates how negative affordances are balanced out in healthy people as opposed to psychiatric patients.

Unless negative affordances are very prominent, an individual will react against them, effectively reducing their activation potential to nearly nothing (here only 21 more excitatory neurons fire than inhibitory ones. In psychiatric conditions the excitation is much higher - as much as 1385 among the paranoid group. See Figure 11.)

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An interesting correlate is that when healthy people start perceiving something with a negative sentiment, they avoid further exploration and continue to reject the affordance, behaviour-setting and all it entails (Golembiewski, 2012a). This pervasive bias is automatic and therefore requires conscious and creative intervention to reverse. For example, neighbours may complain about the construction of an absolutely glorious and useful building because the construction meant cutting down a beautiful forest on the site. To get the neighbours to appreciate the building is going to be difficult, as they have decided to explore the ‘affordance’ no further. One very important thing to note here, is that a very small design change can have a disproportionate effect on the ‘worth’ of an affordance or behaviour-setting. A neutral space can very easily adopt the negative associations implied by objects therein; a CCTV camera or surface dirt.

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Using theory in praxis: determinism

Intuitive observations of behaviour around affordances and behaviour-settings have traditionally played a major role in the design industries, but observations have seldom reached into neuroscience to find explanations. For affordances, determining how an object will be engaged with is relatively simple; an object is perceived for what it offers. Thus a Zippo® lighter is attractive because of its sensory opportunities; it is graspable, flickable and pocketable. It provides an opportunity for discrete engagement (a plaything in a pocket), even when circumstances (behaviour-settings, mores) prevent the lighter to be used. The Zippo® may also have significance; it is presentable, meaning it serves a need for meaning (social status), and also for the occasional function (manageability) need for fire.

The main complication with affordances is that they are subject to change given different behaviour-settings. An apple says, ‘Eat me!’ when it is in a bowl on a kitchen bench. It says, ‘Pick me!’ when hanging, ripe from a bough. And it says, ‘Buy me!’ when it is displayed in a supermarket.

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Figure 12: Jeff Koons (1985). Three Ball 50/50 Tank (Two Dr. J Silver Series, One Wilson Supershot). MOMA. New York. Glass, painted steel, distilled water, plastic, and three basketballs, (154 x 123.9 x 33.6 cm).

In Three Ball 50/50 Tank and in others, Koons explored how affordances shifted with new settings in his works.

But behaviour-settings not only represent complications for affordances, they also complicate design problems. The manipulation of human behaviour through design is called determinism. For small objects (affordances), this is done intuitively and with relative success, but for big objects – buildings in particular, the variables are more complex and success is far harder to predict.

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The concept of architectural determinism has fallen to disrepute and the term is usually considered dismissive due to a history of disappointment (Broady, 1966; Lang, 1980). There are a number of reasons why authors criticise deterministic thought – for the fact that it privileges the power of the environment and neglects psychology – the individual and social reaction with the environment. This introduction of a neuropsychological basis for design determinism attempts to redress this shortcoming.

In brief, typical criticisms of determinism include the following:

Sometimes deterministic failure is put down to normative effects such as beliefs of the designer:

Determinists are accused of overestimating the value and power of the their own ideas – for example, the innovative vertical corridors in the Pruitt-Igoe complex were thought by reviewers to be fabulous, but many of the people who lived in the complex were far less enthusiastic (Franck, 1984; Lang, 1980). In other words, the mere presence of opportunity within the environment does not ensure that will be noticed, appreciated or even used (Lang, 1980; Newman, 1996).

Determinists are accused of a naïve belief that environmental effects on behaviour are always direct (Franck, 1984). For example, Hellmuth, Yamasaki and Leinweber (later reincorporated as Hellmuth, Obata, Kassabaum Inc.) the architects of the Pruitt-Igoe complex provided common rooms for suites of several apartments in the belief that they 151


would create informal communities. The stark reality is that the provision of a common room doesn’t create a community. The common room is just a space until mores match it. And a space without positive mores has a tendency to turn to a negative space (Jacobs, 1961). In this case, Pruitt-Igoe was famously criticised for a lack of passive surveillance and defensive opportunities (Newman, 1996).

Determinists are accused of believing that people are passive in their interactions with the environment and are not driven by their own autonomous goals and choices (Franck, 1984).

They are also accused of assuming that the environment is an immutable entity that will not be modified by inhabitants (Franck, 1984).

Determinists may also be cynical of knowledge that they don’t have – for example an architect who doesn’t know anything about colour theory might dismiss it without exploring its potential.

There is a possibility that deterministic design may fail because designers employ faulty or inappropriate psychological theories. These are input errors:

The psychology used by determinists may have been developed to explaining a phenomenon, but for unknown reasons may not be applicable for predictive design. Psychological theory is largely derived from empirical studies that are performed in 152


controlled circumstances, which may not reflect reality in a holistic way. People don't necessarily behave as they do in a psychological experiment (Philip, 1996).

Input errors may occur because a designer has embraced part of an unresolved debate. The psychological literature on behaviour contains unresolved debates, incomplete models and oxymorons, which may occasionally be contradictory (Lang, 1980).

Sometimes the motivations, values and competence levels of populations are not properly considered when designing behaviour-settings. This may affect the usability of designs (Lang, 1980).

All of the above factors play a part in limiting the effectiveness of deterministic design; after all, there are many ways to judge success or failure and many more ways that something may be right or wrong about a design. But possibly the most significant factor is that a behaviour-setting must be congruous with the mores that take place therein, and whilst architects can design the milieu, they cannot design mores. In other words, when designing a behaviour-setting, architects may design just one side of a complex interaction; the other side is largely social and neurological and cannot be ‘designed’ – certainly not in the way that buildings can be. As Louis Kahn may have said, the building is not in agreement (Kahn, 1971). This is not to say that revolutionary ideas cannot work. It’s just that any new scheme still needs to be matched with mores in order to be fully functional. Wherever the customary mode is abandoned, any effort to

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make a scheme engaging will encourage users to make the commitment to adapt to the new space and way of doing things.

Of course both the physical environment and behaviour is subject to adaption. But accordingly, behaviour patterns are only likely to change incrementally when transferred to a new but familiar milieu. But if the design is congruent with a major shift in the mores, then radical innovations may also be embraced.

In support of this hypothesis, many of the well-accepted examples of (socially) successful radical architecture are matched by equally radical social change. Niemeyer and Costa’s city of Brasília reflected the major social, industrial and political changes of Brazil that occurred during the highly popular reformist presidency of Kubitscheck. Even before the foundation stone was laid, the city had been long awaited. The construction of the new capital was a fundamental election promise, reflecting a decision that had been written into the constitution six generations earlier (Avila, 2008). Similarly another modernist and innovative city that has been continually praised, is Chandigarh, planned by Le Corbusier, which was built to re-house the Punjab capital after Lahore was lost to Pakistan during the partition of India. India’s first Prime Minister, Nehru, personally oversaw the project seeing it as a symbol of India’s new independence and self-determination (Lang, 2005). But not all ambitious rationalist schemes of similar genres and scales are so well received.

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The twentieth century saw a list of great architectural ideas being bulldozed (and occasionally blown up) there are many reasons for the failure of architectural determinism, as outlined earlier, but especially when inhabitants’ don’t engage with the new schemes. Remember, here we present engagement as a neurological problem, not an abstract one.

The archetypal example of failure was the aforementioned Pruitt-Igoe public housing development in St. Louis. This development was originally praised for its innovations – especially for the creation of common balcony areas, each servicing twelve apartments of 1-4 bedrooms each. These would run off the common areas to either side or immediately

above

or

below.

These

were

intended

to

create

‘individual

neighbourhoods’ within the larger monolithic building (Lopez, 1956). Apart from these common spaces, there was no common horizontal circulation within the buildings.

The relative successes and failures of Pruitt-Igoe are still hotly debated with fashionable opinions swinging one-way and then the other (see (Freidrichs, 2011) for comparison). With a project as iconic and complex as Pruitt-Igoe, it’s hardly a surprise. Even so, it’s reasonable to assert that projects like this that could benefit from greater insight into the neuropsychological systems that underlie the desire to engage and perceive.

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Conclusions

Affordances and behaviour-settings are at once designed objects and are also designed physical interventions to the human neuropsychology. Put in simple neurological terms, affordances automatically trigger excitatory reactions, and behaviour-settings automatically trigger inhibitory ones. Beyond these, the range of potential behaviours that are associated with these design-objects can be expanded or contracted through choice by engaging the creative centre of the brain. This action has the benefit of fostering individuality and a sense-of-self, which is incidentally one of the major factors in combating a range of important mental health problems (Kean, 2009; Sass & Parnas, 2001; Searles, 1966).

Affordances are relatively intuitive to design because they are simple. As long as there are provisions for one or more forms of salience, the affordance (the object) will be in the running to engage people. But the design of behaviour-settings is a wicked problem and is much more difficult. The problems are open ended and you can always ‘do better’ (Kunz & Rittel, 1972). Furthermore the problem isn’t improved by the complexity of human/object interactions; the congruency between humans and their habitats is easy to misread. Certainly, behaviour-settings will predetermine the limits of affordances. But it is a mistake to think that people will be content with prescribed behaviour patterns. The strong correlations between the way people behave and the milieu where the behaviour takes place does not mean that architecture determines 156


behaviour – even if it appears that way. Equally, it is mistaken to say that mores determine human behaviour. A behaviour-setting still inhibits behaviour when only one person is present. We don’t stop being social beings just because nobody else is around. Behaviour-settings will continue to suggest mores when people are not present at all. When a shop is opened up in the morning, shoppers will behave very much as they did the day before, even though there was nobody there to continue the behaviour overnight.

Behaviour-settings are more than the limitations on how a space can be used. A cathedral may offer enough space to play football, but this behaviour is not suggested by the architecture (curiously sports stadiums have been used as churches during events such as World Youth Day, but how these exceptions have been achieved are a study of their own). Behaviour-settings do not only limit behaviour, they suggest it also. Effectively, every behaviour-setting is an affordance also.

However it is considered, a behaviour-setting is a dynamic and organic relationship between designed place, the mores that it enables and the neurology and psychology of the users. A new setting can change those mores, but only incrementally, as much as people will individually allow. The adoption process can be sped up if the mores are already in a state of positive flux. Under these conditions, people are more willing to change.

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GENERAL HOSPITAL DESIGN

There is a growing interest in my work on salutogenics and mental health research, because most of the research into health facility design is limited to studies involving direct evidence. These studies, though very valuable, only serve to prove or disprove very specific hypotheses in a very controlled setting. Typically, such a study will involve the modification of one element of the environment and then records of hospital stays or consumer satisfaction will be gathered. There is a growing frustration with this approach. Designers, researchers and commissioning bodies need and want more. They need to understand the psychological implications of their decisions. Traditionally it has been difficult to apply such knowledge and even more so to assess outcomes. The indepth knowledge provided by an understanding of neurological mechanisms is therefore refreshing, especially as this fine-grained approach is backed up by a broad-brush methodology, which picks up the pieces to allow a holistic approach to design.

An understanding of some of the mechanisms involved in mental illness is applicable across the board. With this in mind, I was invited to present the following paper on general hospital design as an invited plenary address at the Design and Health Australasia Symposium: Global Perspectives, Local Identities, UTS, Sydney 29th March 2012. 158


The neurological basis of salutogenic healthcare design.

In Press: World Health Design, 5(4) October 2012

This paper was received a highly commended award in the 8th World Congress for Design and Health (2012), in Kuala Lumpur, Malaysia.

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Abstract

Objectives The theory of salutogenics has a basis in the empirical testing and ideas of Antonovsky, which state that health outcomes improve when a sense of coherence is fostered. A sense of coherence in turn, depends on the net resources that support meaning, comprehensibility or manageability. The reason that manageability is important for health is obvious, but why abstractions like meaning and comprehensibility are important is more difficult to understand.

Methods Salutogenic abstractions are traced to back to current neurological models to locate the endocrinal and neural mechanisms that underpin them.

Results Meaningfulness, comprehensibility and manageability functionally correlate with triune brain theory. Meaning is managed by the neomammalian frontal cortex; comprehensibility by the hippocampus and amygdalae within the paleomammalian limbic region and the association cortices; and manageability by the reptilian brain: the mesencephalon and primary perceptual cortices. In general, the slower, but more evolved frontal functions take precedence. But the paleomammalian organs continually monitor the comprehensibility of phenomenal events. If events fit within a positive 160


narrative, the neomammalian processes are allowed to continue, but if things ‘look bad,’ instincts regulated by the reptilian brain take over. The result includes a wide range of deleterious somatic and behavioural changes.

Conclusions Healthcare architecture is not a neutral container for healthcare facilities. All architecture embodies narratives that may either support or work against a state of good health. A salutogenic approach to design attempts to include support for meaning, comprehensibility and manageability, and to avoid their antithesis – meaninglessness.

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The neurological basis of salutogenic healthcare design.

Architecture mediates almost all experience and moderates a great deal of behaviour. For the best part, the moderation effect that architecture plays is qualitatively even. The ubiquity of vertical walls and orthogonal layouts with very similar features for similar typologies guarantees this. Is there a qualitative difference in a right turn over a left one? Does it mater whether a window is a sash-cord or a casement? Either way the actions these decisions prescribe are radically different, but on a qualitative level, the experiences are nearly identical.

But architecture can be genuinely manipulative, and herein lies the qualitative differences in the phenomenology of architectural experience. Sudjic (2006) describes how architecture is used as a weapon, to defeat an enemy before a shot has ever been fired; Snodgrass (1990) describes architecture that is used as a vehicle for religious and spiritual revelation; and Jencks (1999) makes a solid attempt to relate how architecture can thrill its visitors. But when it comes to healthcare design, architecture is rarely so focused on psychology. Somehow architecture all too often loses its considerable manipulative power as it becomes subservient to its parts: future expansion, structure, models of care, functional programme, efficiencies, sightlines, infection control and the needs of a diverse group of users. There’s no question; all these things are critical, but to 162


let functional and structural issues lead design is to let the cart lead the horse. So is it possible to harness the considerable manipulative power of architecture for better health outcomes?

Architecture – a building, or better still, an entire environment can amplify emotions, especially when they are already vulnerable. Sudjic (2006) proposes that the endless gallery leading to Hitler’s chambers in Albert Speer’s Neuen Reichskanzlei, and the grandiosity and sheer scale of his suite so amplified the helplessness of the 1939 president of Czechoslovakia, Dr. Emil Hácha, that he not only surrendered his nation, but also suffered a cardiac arrest in Hitler’s presence.

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Figure 13: The Neuen Reichskanzlei in 1941. A grandiose gallery leading to Hitler’s chamber takes up most of the building. Photograph by Heinrich Hoffmann.

From a medico-legal paradigm, it seems impossible to prove that the Neuen Reichskanzlei (Figure 13) had anything to do with the state of Dr. Hácha’s heart, but from a salutogenic perspective, the relationship is un-missable. The same can be said for architectural interventions that are designed to improve health outcomes – correlations don’t mean causation. But architects and healthcare planners should not be dismissed so 164


easily. Reviews of healthcare design research show there are now thousands of relevant studies, many of which have been shown to make a substantial difference in health outcomes (Ulrich et al., 2008). But these studies invariably focus on single details, frequently drawing on abstract aetiological mechanisms such as the general concept of ‘stress’. The salutogenic methodology is both more holistic and more specific: for Antonovsky (1987) the stimulation we call stress isn’t just noise, it’s information. And our ability to cope with the flood of information – be it good or bad – is ultimately what determines our generalised state of health.

The theory of salutogenics has a basis in the empirical testing and ideas of Antonovsky (1987), which find that health outcomes improve when a sense of coherence is fostered. A sense of coherence (SOC) in turn, depends on the net resources that support meaning, comprehensibility or manageability. Put simply, all of these things help us make the best of life’s circumstances. They help us cope.

Almost all healthcare interventions (medicine, care, architecture) focus on Manageability: the physical resources needed to keep on going. It’s paradigmatic that this is virtually all healthcare is obliged to do: to treat the sick and keep them warm, fed and dry while they recover from a point of critical illness or injury.

Comprehensibility is a function of knowledge. Information about the life situations people find themselves in builds a sense of comprehensibility. For healthcare information will include facts about the nature of the illness, how long a stay will be, 165


what treatments are available, who will be involved and how, information about side effects and what resources will assist in recovery. In the healthcare sector, things are improving for comprehensibility and there are a few ‘islands in the sun,’ but information communication is something which health facilities have traditionally been bad at (Cleland, Ross, Miller, & Patey, 2009; Wistow, 2012).

Meaningfulness enriches and gives quality to life. It is the sum of all the best reasons people have to keep on living (Antonovsky, 1987; Jan Golembiewski, 2010b; Golembiewski, 2012b, 2012e).

Generally speaking, hospitals don’t consider the

fostering of meaning to be their role, but when people are beleaguered with anxiety about their state of health and about the future, it’s hard to imagine that any other psychological interventions could be more significant than developing reasons to hang in there and believe that everything is going to be okay in the long-run (Antonovsky, 1987, 1996; Jan Golembiewski, 2010b; Golembiewski, 2012b, 2012e). A caveat is due here; salutogenic needs do change with the intensity of pathology – comprehensibility is more important (in the short term) than meaningfulness whenever ‘things are not looking good’ for a patient, and they know it - in cases of primary myocardial infarction (cardiac arrest), for instance (Bergman, Malm, Ljungquist, Bertero, & Karlsson, 2012), and we shall soon see why.

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The neurology of salutogenic healthcare design The reason that manageability is important for health is obvious and doesn’t need further elaboration here, but why abstractions like meaning and comprehensibility are so important can be difficult to understand.

The brain can be seen as an organ that perceives, creates and manages meaning. The most basic level of this is manageability. Even the most simple of creatures need to manage the needs of survival: sustenance, protection and reproduction. The bulk of the relevant processes to manage these needs are automatic in most creatures. The areas of the brain that are wired for manageability are within the reptilian complex; a simple system that implements a simple formula; if it’s food, eat it, if it’s danger, flee and if it secretes sex hormones, mate it (Bargh & Dijksterhuis, 2001).

Comprehensibility is a step more complicated because it involves perception, that is, a cognitive, interpretive step. And this presents a problem: how is sense-data interpreted. The internal representations we have of external objects cannot be true to reality. This is firstly because reality offers a richness that humans simply cannot experience: humans don’t even share the same sensory range as one another (some have better high frequency hearing, others are colour blind etc.), and certainly we have very different sensory ranges to other animals. Bats can hear pitches of up to 115kHz, and humans only about 17 kHz, humans can feel light of 300-400 tHz range as heat, but poecilia reticulata (the common freshwater guppy) can see and taste the same spectrum. But what humans lack in terms of sensory ability, we make up for in cognitive ability. We 167


have an extraordinary ability to identify the differences between just about everything, and this information is stored in vast lexical ontologies. At a glance we can tell the difference between a Nokia and an iPhone, between a painting by Modigliani and one by Picasso or a song by Jimi Hendrix and a religious hymn. Not all this information is immediately relevant, but it is our nature to store and use such information as needed. Information becomes critical only when required: “I need medical attention – where’s Emergency?” Or “If I take this medicine will I get side effects?”

The cerebral cortex is used for associations, in other words, the links between pieces of information – the basis of comprehensibility. Learning is the generation of these links, and knowledge is their retrieval. Although learning takes place over a globally distributed network (Baars & Franklin, 2007), the main place that somatic (sensual, physical) associations are paired with meanings is in the primary perceptual cortices (Grossberg, 2009). A paleomammalian (limbic) organ called the thalamus mediates the somatic nervous and sympathetic nerve impulses and distributes them to the appropriate perceptual areas of the brain. These are then associated with one another and more abstract meanings in the higher perceptual association cortices and with actions in the motor cortex (all are subsections of the cerebral cortex).

Comprehensibility doesn’t have to reflect ‘truth’. Comprehension can be delusional. Delusional subjects generally have relatively low SOC scores, due to poor manageability and meaningfulness scores. But recovery from delusional states only reduces SOC scores further – particularly for comprehension, implying that the 168


underlying SOC is challenged by having to comprehended the world afresh (Bergstein, Weizman, & Solomon, 2008).

Meaning is an order more complex again, and in this evolutionary step, the anterior hemisphere of the cerebral cortex swells to make a distinctly neomammalian shape, one that is far more defined in humans than in any other species – it is the neomammalian complex, incorporating a highly developed anterior cingulate cortex (ACC) and prefrontal cortex (PFC). These organs process choice, insight, creativity, the sense-ofself and other complex cognitive processes to establish appropriate actions for situations for which there are no ready responses (Dietrich, 2004; Northoff et al., 2006). The use of the neomammalian complex definitively separates humans from all other animals, and makes us what we are: more human 20.

Like other advanced mammals, the folds of the neomammalian complex contain a thick network of dopamine neurons. What differentiates ours from those of all other animals is that most of the neural receptors in the human frontal cortex are of the D1 type with higher densities of D2 type receptors deeper, in the paleomammalian regions (see the top section of Figure 15). In contrast, D2 receptors remain ubiquitous throughout the entire

20

Note that some neuroscientists question the validity of the free-will concept, but neu-

roscientists who do believe in the freedom of will usually link the concept to creativity, and the ‘most human’ of organs, the prefrontal cortex (Searle, 2001).

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mesofrontal region in other mammals – from the reptilian middle brain right through to the prefrontal cortex (Nichols, 2010; Prante, Dörfler, & Gmeiner, 2010). The difference is not subtle. The D1 receptor is excitatory, meaning that when it fires, it activates the neo-mammalian complex. This means that some perceptions will activate the centre of consideration, thoughtfulness and creativity. D2 is inhibitory, so when it fires, it restricts activations in the same region. This enables faster judgements, but at the expense of consideration, thoughtfulness and creativity. This explains what we all know already; that humans are naturally more considered in their actions than any other animals. Animals, on the other hand, are more instinctive.

Each evolutionary iteration of the brain must process increasingly complex information, but like a computer the more complex information is, the slower it is to work through. Unfortunately evolutionary theory doesn’t favour slow reactions, so to maintain quick reflexes, the more evolved areas don’t replace the primitive ones. The more developed layers of the brain fold around the more primitive, and mechanisms have been developed that allow the primitive/instinctive areas to spring back into action whenever speed is required. In advanced mammals, reflexes are regulated by the amygdalae (used to monitor emotional context) and the hippocampi (to monitor schemata and narrative context). Together these set up thresholds for automatic inhibitory responses and excitatory overrides, so if a surprise occurs, appropriate instincts will be already approximately set for appropriate action in a given situation (Golembiewski, 2013) (see Figure 14).

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#Automatic#limbic#processes# Affective$/$hedonic$preCjudgement – + 1a.$Narrative/affective$monitoring Automatic#(mesostriatal)#processes 1b.$Latent$restrictions$from behaviour$settings$(inhibition) Behaviour#limits

}}

3.$Opportunities$of Affordances$(excitation) – +

Creative#(frontal)#reprocessing 2.$Expanding$possibilities$of$ behaviour$settings$(excitation) 4.$Choice$to$react$against affordances$(inhibition)

5.#Potential#range#of#final#action (mediated#by#the#striatum)

Figure 14. The reptilian complex (orange) mediates instinctive ‘event management’ responses – there is either instinctive/learned action or none. Paleomammalian organs (the hippocampi and amygdalae) monitor experience for narratives that impart an affective or hedonic value (i.e., “it’s good or bad for me”) the sense of “where I am in this story” roughly corresponds to the salutogenic notion of comprehensibility (green). In positive circumstances, the neomammalian complex (blue) is engaged and is able to expand the possibilities of action or restrict them according to a person’s own sensibilities and context. (Image from (Golembiewski, in review-c))

Behaviour settings are pre-set expectations of behaviour in a given environmental setting. Affordances are perceived opportunities to act (Barker & Wright, 1954; Gibson, 1979; Golembiewski, 2013).

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Sometimes surprises are good and welcome – jokes for instance, and the automatic reactions include laughter, smiles and happy feelings. These are good and don’t need to be managed. But a negative shock will solicit screaming (sounding an alarm to others) and even more basic self-protection instincts: the release of stored energy to enable flight, and the defensive withdrawal of blood from the periphery of the body (to prevent certain death, should a snake or bear bite a limb). All of these reactions commence in the reptilian complex, and their activation inhibits the activation of the neomammalian complex (Golembiewski, 2012a).

The withdrawal of peripheral circulation protects the body from physical shocks. It is a primary function of the hypothalamus, the pineal gland and adrenal cortex. Together, these secrete hormones, which inhibit peripheral circulation by metabolising quickly to cortisol (Steptoe & Kivimaki, 2012). It’s fast, but not an ideal solution because cortisol has a number of undesirable side effects: It overrides healthy limits on blood sugar, blood pressure and heart rate (the tip of the iceberg: there are other negative side effects also). In non-emergencies, cortisol synthesis doesn’t occur and essential hormones are produced from the same primary compound (cholesterol) instead. These maintain happiness and appropriate healthy bodily function; they include progesterone, dihydrotestosterone (DHEA) “the joie de vivre hormone” (Gluck & Edgeson, 2010), testosterone and oestrogen, to name only a few (see lower section of Figure 15).

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Key


CREATIVITY

D1

Hypothalamus

The “automatic” pathway

Ventral tegmental area Oxytocin

Hippocampus

GABA

ACTION

Nucleus accumbens

Adrenocorticotropic hormone

Posterior pituitary Anterior pituitary

Corticotropin releasing hormone and Arginine vasopressin

Premotor/motor cortices

Glu

D2

Parahippocampal gyrus

Amygdala

Prefrontal cortices

D1

The “free-will*” pathway

Anterior caudal cingulate

Chemical Neuronal-Excitatory Neuronal-Inhibitory (’shuts down’ target) Neuronal-Axon (base)

Adrenal gland

FEELINGS Oxytocin Cortisol

References: Swenson, R. (2006) Review of clinical and functional neuroscience Steptoe, A. and M. Kivimaki (2012) Nature Reviews Cardiology Rossato, J., L. Bevilaqua, et al. (2009) Science Oei, N. and I. Veer, et al. (2012) Social Cognitive and Affective Neuroscience Goldman-Rakic, PS. (1987) Handbook of Physiology Golembiewski, JA. (2012) Medical Hypotheses

Other hormones

Figure 15: The automatic vs. creative action pathways – the thresholds for conscious choice and deliberate behaviour are moderated by the combined amygdalae and the hippocampi in the limbic region of the brain. If circumstances are perceived as going beyond a reasonable threshold of control, these organs trigger the hypothalamus to override neomammalian processes. Associated feelings occur in parallel - negative events triggering cortisol – a hormone associated with non-specific anxiety. Cortisol bypasses normal hormonal regulation.

It is important to note that cortisol is not stress and stress is not cortisol, although the two are commonly confused. Cortisol can be a useful medicine when used wisely. 173


Cortisone (synthesised cortisol) is used to suppress the immune system (during allergies or asthma attacks, for instance). But in natural circumstances, cortisol is a by-product of automatic self-preservation systems that only kick in when:

a) The neomammalian complex is bypassed. This area is used to process the primary salutogenic resource: meaning. b) People find themselves in situations, which they associate with lurking danger (a hippocampal function, which correlates to another salutogenic resource: comprehensibility). c) The environment is perceived as being aversive (a function of the amygdalae, which also correlates to comprehensibility). Note that amygdalae don’t have a ‘neutral’ function. Neutral stimuli are emotionally ambiguous, so they are polarised into negative or positive following narrative cues from the hippocampi. d) Automatic behaviours commence before cortisol even reaches the bloodstream. These include instinctive and learned behaviours, but the problematic ones are only noticed in negative circumstances: they are stereotypical behaviours, screaming, fleeing, sudden violence, confused thinking patterns and perseverance (when in excess, all of these are associated with mental illness) (Golembiewski, 2012a) (See p. 358- q.v.). It begins to become clear that the failure of comprehensibility triggers the reflexes in the reptilian brain to produce cortisol and other unwanted reactions. This is apparently a

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‘last-ditch effort’ to maintain the last and most primitive of the salutogenic resources: manageability.

If asked if Dr. Hácha’s experience in the Neuen Reichskanzlei could have caused a heart attack, there is no doubt that the building was an essential factor in rapidly increasing his vulnerability. The design of the Neuen Reichskanzlei worked (as intended) to defeat adversaries. The narrative of immense power was written into the masonry. And when this was combined with the generalised negativity that Dr. Hácha must have sensed as he approached his nemesis, his creative and adaptive resources would have been reduced. Instead of using his neomammalian brain to test creative solutions, the negativity inherent in his situation (reinforced by the architecture and social milieu) must have triggered alternative automatic behaviour pathways, thereby reducing his thoughts to testing established fears for himself and his country. It’s easy to imagine Dr. Hácha thinking thoughts along the lines of: ‘Perhaps they have invaded already, and they are keeping me here so I’m not there to rule my country in its hour of need?’ (Note the paranoid thinking). Meanwhile, on a physiological level, Dr. Hácha’s cortisol levels will have soared, causing his blood pressure to increase. When extreme this reaction can cause transient myocardial ischemia, an atypical cause of cardiac arrest: the heart stops because of the sudden swelling of the heart tissues (Steptoe & Kivimaki, 2012).

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Figure 16: A patient reads the morning paper on one of the many

abundantly green spaces of the Khoo Teck Puat Hospital in Singapore. (Designed by CPG Consultants Pte Ltd and landscaped by Peridian Asia Pte Ltd – photo credit CPG Consultants Pte Ltd)

Thus architecture can be a powerful weapon. But can it be an equally powerful ally? The hippocampi/amygdalae coupling sets up automatic response thresholds that are already likely to be low for people entering a healthcare setting, so as healthcare designers, our first task is to maintain comprehensibility (Bergman et al., 2012). To do this, the embedded narratives within the environment must be managed. That means taking great care that the typology and patient experience is recognisably and indisputably positive. The first step is to distance the style of the new facility from those ubiquitously seen in medical dramas. That means design teams should look for 176


functional alternatives to white walls, vinyl floors, strip lighting, typical services and even the design of surgical scrubs and nurses’ uniforms (Richardson, 1999). Bring in masses of glorious plants and fresh air like in the Khoo Teck Puat Hospital in Singapore (Figure 16), and consciously design the soundscapes, lighting, and patient experience. Perhaps the most alarming features of modern hospitals are the monitors, which set off alarms when a patient’s vital signs are irregular. There is no question that these machines are essential, but the alarms no longer need to sound right by a patient’s bedside. Current technology allows the alarms to be routed directly to communications devices that are carried by medical staff. Healthcare lighting should be natural and electric light should be low -glare, and be of a ‘warm’ temperature (Tammes & Burnett, in review). Windows should look out to gardens and plants and art should adorn patient rooms. Many interventions of this kind have already been studied and found to be useful, even on their own, once again see (Malkin, 2008; Ulrich et al., 2008) for handy reviews.

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Figure 17: When in a state of robust health, a person’s attention is primarily focused on the aspects of life that provide meaning; family, friends, the world around etc. and not only focused on survival. In this diagram blue represents the locus of attention, and green peripheral attention.

The next step is to enrich meaning. Meaning is to be found whenever humans engage in concerns beyond their own (even if these are very abstract); the well-being of family and friends, in the greater good of society, in protecting animals and the environment, even in protecting the security of the cosmos (Figure 17). Designing environments that foster meaning isn’t easy because what makes life worth living is intrinsically personal, but design decisions that should be avoided are more universal. At the top of this list, 178


unsurprisingly, is meaninglessness. Meaninglessness causes bizarre and frightening expressions such as mutism, emotional shutdown or severe mental illness (Golembiewski, 2009b, 2012b; Reach Out, 2009; Searles, 1966). As mentioned earlier, it can also be traced to physiological breakdown as demonstrated by Dr. Hácha’s heart attack. Meaninglessness must be avoided in all scales from typology to detail. Yet meaninglessness is ubiquitous in traditional hospitals: Kafkaesque corridors that go on and on, rooms without windows, machines that make alarming sounds and have flashing lights (the staff appear to ignore them and never explain what they are for). Large wards, where patients may feel like objects not people. More important still are the subtleties of approaches to care: Staff that don’t look you in the eye, don’t seem to care, or have mean dismissive or haughty attitudes are measurably deleterious (Gottman, 1996). Unsurprisingly, evidence suggests that the same innovations that improve health outcomes also improve social relations (L. Larsen, Adams, Deal, Kweon, & Tyler, 1998). It doesn’t always take much to change these details, and the differences will be very profound.

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Figure 18: A meercat photographed in the ambulatory waiting room of the Royal Children’s Hospital, Melbourne. In this project, the architects (Bates Smart and Billard Leece) up the ante: hospitals can be places to be enjoyed. (Photo credit: John Gollings.)

It seems ironic, but hospital stays are shortened by better hospital experiences. Thus, designers are wise to concentrate on making a patient want to stay. The ‘-care’ in the term: ‘healthcare’ is axiomatic for better health because care supports the amygdaloid/ hippocampal coupling. If the environment says, “everything possible is being done to help and it’s all going to be okay,” then the scene is set for the ideal health-building behaviour and thought patterns to kick in. Furthermore, unhelpful by-products such as cor180


tisol will be reduced, meaning the endocrine system can naturally regularize.

Ultimately, the healthcare designer has to juggle two narrative concerns. On one hand vigilance is needed to avoid any typologies, symbols and settings that may be associated with negative outcomes. On the other hand, the team should look for opportunities to imbed positive experiences for all the facility users. Not only are all good things expected to improve the outcomes for patients, but to improve the environment for the entire facility including the staff and guests.

Already some industry leaders are pushing far beyond the statutes and guidelines to make exceptional hospitals by focusing on the patient and staff experience. Simple concepts like comfort, cosines, joy and aesthetics have had no place in traditional twentieth century hospitals, yet they are the psychological bricks and mortar of all healthy buildings, whether or not they are healthcare facilities. The architects who designed the Royal Children’s Hospital in Melbourne, Billard Leece Partnership and Bates Smart, put in a giant touch screen – like a huge iPod, for kids to play with. There’s a multi-level aquarium, a great adventure playground and even a meercat enclosure. CPG Architects ensured that Khoo Teck Puat Hospital in Singapore departed from the twentieth century hospital paradigm by introducing an abundance of greenery, fresh air and 100 varieties of butterflies. The payoff is that patients feel that things are going to be better than expected, and surely they are right.

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A BROADER APPLICATION OF THE SALUTOGENIC METHODOLOGY IN MENTAL HEALTH SERVICES

After completing ‘Start Making Sense’ (from page 62), I could see that the salutogenic methodology may have application outside the walls of the mental health facility, even for treating mental health disorders. To test and see if it was acceptable to the many people involved in mental health services delivery, I presented the following paper to the Australian Rural and Remote Mental Health Symposium in Canberra, 2nd November 2009. It was subsequently published in the Australian Journal of Emergency Management, 27(2), 42-47.

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Moving from theory to praxis on the fly: Introducing a salutogenic method to expedite mental health care provision in disaster situations.

Presented to the Australian Rural and Remote Mental Health Symposium in Canberra, 2nd November 2009. Subsequently published in the Australian Journal of Emergency Management (2012), 27(2), 42-47.

Abstract

Not a lot is known about most mental illness. Its triggers can rarely be established and nor can its aetiological dynamics, so it is hardly surprising that the accepted treatments for most mental illnesses are really strategies to manage the most overt symptoms. But with such a dearth of knowledge, how can worthy decisions be made about psychiatric interventions, especially given time and budgetary restrictions?

This paper introduces a method, extrapolated from Salutogenics; the psychosocial theory of health introduced by Antonovsky in 1987. This method takes a normative stance (that psychiatric health care is for the betterment of psychiatric patients,) and applies it to any context where there is a dearth of workable knowledge. In lieu of guiding evidence, the method identifies reasonable alternatives on the fly, enabling rational decisions to be made quickly with limited resources. 183


Figure 19: The principles of salutogenic theory based on the model by (Antonovsky 1987).

An emergency psychiatric response is the sort of time critical intervention that might not be well informed by enough evidence to proceed quickly but must regardless. Whatever the nature of the emergency, it is the very nature of catastrophe that they catch people unprepared; in recent history we’ve seen bushfires, floods, earthquakes, tsunami’s, storms, volcanoes, landslides and winds the events are diverse in nature, but the effect on people is consistent and devastating.

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Figure 20: The San Francisco Earthquake. Source: Records of the Office of the Chief Signal Officer. (1906) National archives and Records Administration (Public access).

It is the nature of emergencies that they are sudden and catastrophic (Galambos, 2005). A swift turn of events means that some people lose their lives and other lives are put on tenterhooks. The initial damage tends to be physical and material, but mental health issues follow close behind. Whatever the emergency event: be it tsunami, bushfire, storm, flood or earthquake, the initial impact of the disaster only spells the beginning of the catastrophe. Because of supply interruptions provisions for basic needs such as communication, shelter, food, sanitation and water as well as health services and social networks, matters tend to deteriorate after the initial shock. It is at this early stage when mental health issues begin to compound a disaster.

It is a conceit to think of mental and physical health as separate issues. Although they are distinct, the two are intimately related. One will exacerbate the other

21

21

. That is,

This is true in situations where the emergency was an unusual occurrence. In

situations where emergencies are regular and expected, such as in the North East of NSW, which is subject to frequent flooding, events cause some psychological stress, but probably don’t trigger mental illness as such. (Little 2009)

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mental stress tends to make physical illness worse and vice versa. For this reason it is imperative that service providers address mental issues as quickly and appropriately as possible after a catastrophic event, just as they will food, shelter and sanitation.

Delays in the provision of all forms of emergency care can be caused by indecision about what is suitable action. The question of appropriateness always calls for normative decisions based on subjective opinion – and those opinions are difficult to justify in life and death situations – especially when providing a limited resource to one person might mean someone else will go without. The outcome, sadly, is that decisions sometimes aren’t made and this only makes matters worse. It is for the psychological comfort of the decision makers that they (we) want to rely on evidence to make decisions. Evidence based decisions are easily justified and move the burden of decision making to scientists elsewhere. And fair enough. There’s little doubt that empiricism is the most suitable way forward in the circumstances where empirical evidence exists and is available at hand (Galambos 2005). This is, sadly, rarely the case.

The scientific method is very specific and conclusions can only be proven if they are drawn in isolation from any confounding variables that might otherwise influence the data. Not just is this clinical approach divorced from reality, but also more significantly, the findings tend to be incremental and as such there isn’t enough empirical data to answer most basic real world problems. I am an architect and I specialise in mental

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health design 22. Like emergency services provision, there is a huge onus on evidence to generate any innovations in this area of the profession. As with emergency services provision, evidence is time consuming to locate and analyse, and in many cases it turns out to be irrelevant in any case. There are few clients who are willing to encumber their design bills with much time for research, and yet, decisions need to be made constantly because architectural problems are incredibly consequent. One minor change here will affect something else elsewhere. Like the problems that face providers for emergencies, the problems we face are incredibly complicated and open ended, often with no clear solutions. Thus we usually have two ways forward. To continue to do things the way they have always been done – even if we suspect those methods are dated or plain wrong. Or we have to take risks and improvise. But I have been faced with these problems and have tried both methods and found them both deficient – So I developed a methodology that allows reasonable decisions to be made on the fly. And the same methodology can be easily adapted to enable quick and appropriate decision making for various logistical tasks in emergency situations.

22

I also have some experience with emergency services provision; I was part of

Bangun, a UNSW effort to assist survivors of the 2004 Boxing Day Tsunami. (Golembiewski, Ho & Wong 2004)

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Firstly it is important to understand that every provision means the denial of something else because resources are always limited in some way. It’s like going and ordering at a restaurant. Out of the twenty dishes presented you’ll only get to choose one. If the choice is yours, there’s a fair chance it will be the best choice. If the choice is left to someone else – your spouse for example, you might be disappointed. The defence that ‘beggars can’t be choosers,’ is unhelpful. It is not the spirit of fine dining to be classed as a beggar! Significantly, the more victims of emergencies can be spared a similar attitude the better.

Aaron Antonovsky’s salutogenic theory (1987) demonstrated that the distinction between sickness and health is indistinct and a person’s level of well-being will be somewhere on the continuum between death and a theoretical state of perfect health. Antonovsky found that a person’s state of health reflects a person’s sense of coherence. The more a person feels they understand and make a contribution to the world around them the stronger their resistance to illness.

Antonovsky breaks down a sense of coherence into three domains of importance. A strong sense of coherence is supported by feelings of comprehensibility, manageability and meaningfulness (Jan Golembiewski, 2010b) (See p.62 q.v.) Ultimately a SOC builds a dynamic feeling of confidence that one’s internal and external environments are predictable and that there is a high probability that things will work out as well as can reasonably be expected (Bahrs et al., 2003). These categories can be extrapolated to find easy application in emergency situations as a salutogenic method. When applied to 188


emergency care, comprehensibility is the matter-of-fact understanding of the situation a subject finds him or herself in. In a disaster situation this can mean information: who, why, what, where, how and when. Manageability, the next of the principles of salutogenic theory extrapolates to mean action and empowerment and in an emergency situation it will be the things that enable survival, things like food, water, communication, shelter and things that can be done to lessen the impact of the disaster. Meaning is the most illusive of all the salutogenic principles, yet it is in many ways the most important. Meaning always comes into question during disasters, yet it is the hardest issue to address. Meaning is the subject of the big question; “but why?” If meaning can be sustained, then survival in the most difficult and horrific circumstances becomes possible (Frankl, 1963). This kind of survival gives others hope. It is the stuff of miracles, and it through these miracles that meaning is fostered in others.

A salutogenic methodology for emergency care ensures that the best interests of the victims of disasters are always maintained with a holistic perspective, even when dealing with the minutiae of service provision. It is an approach to understanding the individual’s needs holistically and in such a way that the effort isn’t likely to interfere with the psychosocial needs of the subjects. This method is intended to be used by communication officers through to people at the cold face because it is simple to remember and easy to apply. It’s just a matter of keeping three things at the forefront of mind: Comprehensibility, manageability and meaningfulness, and having an idea of how these concepts work on the ground. With more complex projects (such as architecture or emergency service provision,) each decision can be analysed with respect to the three 189


salutogenic categories to see how elements relating to a sense of coherence can be incrementally supported. It is important to remember that this method is designed for use on the fly and mistakes are okay, to make an error of judgement using a salutogenic theory is better than having no theoretical basis whatsoever.

Comprehensibility is maintained when people are kept abreast of what’s happening. In the case of the Victorian fires, there was a need for information about where the fires were heading and at what velocity. Information is also needed about the emergency response. When will help arrive? People need to know who is dead and who survived. They need to know about the safety of their family, friends, pets and livestock. They need to know if their homes are in danger or if there is anything left of them. These are all very profound issues and quality information is an extremely important tool for the maintenance of a sense of coherence. The inverse is also true. Rumours and lies are harmful (Freyd, Klest, & Allard, 2005). And so too can be ‘shielding’ survivors from the truth (although this is a complex issue in itself because the truth is rarely definitive and hope must also be maintained as much as possible.) It might be really tough to tell a mother that her child has died, but if it is absolutely and unavoidably true, there is no protecting her from that fact. Yes, sympathy is called for and it might be ‘the last straw, ‘ but it is an inevitable last straw, and at the very least it shouldn’t come with added ugliness from deceit and distrust (Meyer, 1969).

When information is given in an emergency, accuracy and honesty is imperative. Under promising allows expectations to be exceeded, carrying a strong message of hope and 190


that everything is working out as well as possible. Disappoint on the other hand might be taken as betrayal. The art of making promises has implications for higher levels of coherence. When stressed, people might be excused for making unreasonable demands. They might, for instance, extract promises that are difficult or impossible to keep. Who, after all, wants to deny someone who is desperate and might have his or her life in danger? Who wouldn’t prefer to lie and say, ‘don’t worry. Everything will be fine?’ But a hastily made guess that ‘someone will be there to help in a couple of hours,’ can start doing damage at 120 minutes and 1 second (Alomes 2009). The reason is because the promise suddenly becomes questionable, and at his point meaning starts to erode (Golembiewski, 2009a, 2009b).

Whether it is the provision of food, water, shelter, blankets or medical services, most aid and emergency provisioning focuses on improving manageability – usually helping people to help themselves. Its critical, but the obviousness of this area of concern tends to dominate emergency provisioning. Needs – physical ones are the squeaky wheel of emergency care. Information and material support enables people to act. And when people act, and feel that they can do something, their overall sense of coherence improves. This is good for health outcomes, and having people move from stunned/disabled mode to being an active participant in the rescue effort means another hand (with local knowledge) at the helm.

The absence if the things that make life manageable has obvious consequences, although they are not as significant as we tend to assume. Lack of food, water and 191


shelter will be a source of stress that will make outcomes worse, but with meaning and comprehensibility needs looked after, people can go a long time without basics. As Frank Lloyd Wright famously said, “give me the luxuries of life, and I’ll gladly go without the necessities.”

Meaning is the most difficult aspect of the salutogenic theory to understand and to provide for, but it is nevertheless the most important. Meaning is the glue of life. It is what makes lives whole and fulfilled. In psychotherapy, it is only when our life’s narratives are revealed to be meaningful that there is release and resolution (Clarkson 2006). Meaning is the force that binds social groups together and is a major purpose of religious belief (Durkheim, 1975; Obeyesekere, 1981). All aesthetics, literature, art, and all other ubiquitous abstracts of human endeavour relate to and contribute to meaning. Meaning gives people the power to withstand inhuman conditions, starvation, illness, and extreme conditions (Frankl 1963). There are theories about why and how meaning gives people such tenacity, but it is not the purpose of this paper to go into these debates (For more information, see (Golembiewski, 2011a, in review-d) (see article on p.204).

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Figure 21: Meaning trumps concerns for hunger and comfort. Source: Ponting, H. (Rights expired).

Whilst meaning is associated with arts and the complexities of culture, there is no suggestion that reading poems will be of any use to someone who has just lost their family in a bushfire (on the other hand, it might happen to be just what’s needed!) In emergency situations meaning can be defined as whatever is of critical importance to the subjects. It means concern for life, for the people they care about, and sometimes for significant cultural constructions like religion, history and tradition. Meaning is what 193


creates the desire to stay alive. And the desire to stay alive keeps people alive. Meaning comes from anywhere and everywhere, but there are some sources that are especially potent. Sometimes the emergency effort itself can contribute meaning; after all, being needed is a big one. Emergencies are situations where the people who are needed, are needed to the extreme. Thus involvement in the rescue operation is a good way to help people through their grief and hardship. This is true to the extent that fire-fighter’s have commonly been found to be arsonists, lighting fires, so they can fight them and feel significant as humans. By fighting fires, the arsonists found camaraderie and intense personal narratives, both of which are critically important contributors to a sense of meaning (Australian Institute of Criminology, 2005).

Under normal circumstances meaning is a stable constant for most people. It waxes and wanes a bit, but in circumstances of extreme displacement it becomes mobile. Meaning is based on a personal ontology – a holistic foundation of connections, meaningful associations and distinctions and narratives that are created throughout a person’s entire life. As things are found to ‘make sense’ they contribute to this holistic body of knowledge and order. And things that don’t make any sense and cannot be understood directly challenge a person’s ontology, causing severe disturbances until everything makes sense again (Golembiewski, 2012b) (see article on p. 183). In emergency circumstances meaning can be a double-edged sword. The power of meaning to do good by maintaining a person’s psyche can suddenly come under fire. The elusiveness of meaning means that it is particularly susceptible to inversion. Meaning can suddenly become meaninglessness – especially in extreme circumstances. And meaninglessness 194


undermines a salutogenic framework like nothing else can. This causes bizarre and frightening expressions such as mutism or emotional shutdown (Reach Out, 2009). In fact, there is every possibility that the atomisation of an ontological framework is the root cause of every single case of mental illness – especially the psychoses (Golembiewski, 2012b; Searles, 1966).

The capacity for the ontology to flip makes the protection of meaning the single most important function of the emergency caregiver. The well-accepted model proposed by Maslow (the hierarchy of needs model,) places meaning as a ‘higher’ need that can only be considered once the stability of ‘lower’ needs such as shelter or food is established. This truism is false. Rather it is the ontology the ‘highest need,’ that is the foundation upon which everything is known. The ontology is the product of self-actualisation. Without a strong ontology, a person loses the capacity to think, feel, or even act. But people can go without basic needs or make do indefinitely if the struggle is meaningful. There is meaning in place and even in the narrative of hanging in there against the odds.

Of course the maintenance of someone else’s body of wisdom and experience isn’t possible because we still have no means to occupy somebody else’s mind. So how can we help? We can be on the lookout. As we know that emergencies trigger ontological challenges we can encourage people to find direction when they most need it. Getting survivors active and involved in the emergency effort when they look like they might otherwise take a turn for the worse can be a good idea. We can be encouraging, helping the survivors of disaster understand that all that is humanly possible will be done and 195


that the things will work out as well as can reasonably be expected. It is important, however not to overplay this, as dashed promises or misinformation are often the tipping point to despair (Alomes 2009). In catastrophes, the survivors must be allowed to feel that they can trust the providers and care they are getting. Consider the anger after Hurricane Katrina when misinformation about looting caused the mobilisation of armed troops with orders to shoot. The McLeod Commission noted that the greatest failure of the bushfire response was the misinformation that the response team disseminated in good faith (McLeod, 2003).

Frequently ontological shifts mean that old spiritual models will be dismissed. In these circumstances missionaries for various faiths can do a lot of good, even as they prey on the victims of disaster. Rigid belief systems offer support when it is most needed, like a crutch, but have a tendency to fail people down the track (Antonovsky 1987). In emergencies missionary activity can be a double edged sword of its own – often missionaries are very experienced and generous caregivers who ask nothing in return, but cultural suitability of service provision is an issue that cannot be overlooked. Culture is a very important source of meaning and is a context for our life’s narratives.

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Figure 22: Nero fiddles while Rome burns. Quo Vadis. (1924). (Rights expired)

When Nero famously played the fiddle while his city burned, was he mad or was he reaching for the thing that gave him meaning and a sense of control at a time of extreme disempowerment and inevitable death? In emergency situations even empirically tested and well-accepted theory and information may not apply. Catastrophes both change the normal order of things and the speed with which decisions have to be made. So it is 197


essential that people who are to go out and face emergencies are equipped to make clever decisions on the fly. An extrapolation of salutogenics (a salutogenic method,) is a fine tool for such circumstances, because it is easy to guess how little efforts might be amplified once projected onto a simple salutogenic framework; how does an action affect manageability, comprehensibility and the sense of meaning? Is the sum force on the coherence continuum likely to be life supporting or not?

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2.

QUESTION TWO: WHAT IS SCHIZOPHRENIA?

This second question is largely answered by a single paper “The Riddle of Psychotic Perception Revealed…” (p.204).

This section should be read with the following however, because the aetiology cannot be easily separated from the syndrome. Thus the first papers in the third section “Are diverse factors proxies…” (p.336-) and “Common Psychotic Symptoms can be Explained…” (p.358-) should be taken to address both research questions.

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SCHIZOPHRENIA AND PERCEPTUAL EXPERIENCE

The question about the relationships between schizophrenia and the environment are complex and answers have to be built on both a robust understanding of schizophrenia and also the built environment. Both are complex in their own right, but lines of enquiry are further complicated by the unknowable common mechanism: the human mind. In the case of built form, the idea that buildings are form and space created by people out of material stuff is very tempting but is only half the story – and probably not even half because architecture is not only to protect people from bad experience (the weather, dangers etc.) but also to improve experience.

Experience is a composite process in that it draws on all previous experience to establish an a-priori framework of understanding. Experience is therefore a unique analogue process that affects everything we perceive. In as much as our experiential referents differ, we cannot experience the same space in the same way. It is common to discuss the quality of experience among friends, precisely because experience is not universal and yet a social experience is one that is shared. “It’s beautiful, don’t you think?”

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Even the experience of a single building draws on knowledge that has been gathered on approach. Short of arriving in a coma, we cannot separate the experience of the interior spaces from the experiences of the exterior as we draw near. If we arrive with the building in full view, we have the opportunity to access it typographically. We get a sense of what it is and what it will be like when it is still a postage sized representation on the back of the retina. If we arrive in the back of a paddy wagon, we will be delivered to an unloading bay, and presumably rushed through an uncomfortable and frightening arrivals process that denies normal opportunities of assessment. We arrive with the distinct impression that out safety is in immediate jeopardy, because we don’t know where we are.

Perceptual experience is sequential and composite. Under normal conditions we will see first, then we will usually see and hear by this stage we will have greater faculties of sight, perhaps we will get a sense of depth in parallax and perspective. We might also have a glimpse of some textural qualities. The first sounds will be deep or loud ones. Later we will smell, then feel and perhaps at some later stage again taste. Although the opportunities for sight will generally come much earlier than those for smell or taste, the latter senses do not shut out the first. Perception becomes more complex as it becomes increasingly polymodal. Complex as polymodal perception is, it is anything but rich without the backup of a deep ontology.

Physically our perceptual abilities are very limited. Out of the potentially infinite array of available information, we genuinely perceive only the tiniest sample of the stimulus 201


that we are exposed to. Let’s consider the sight, the primary modality for humans. When we see, we do so over a very limited focal range, depending on how close an object is, the range might be as short as a couple of centimetres (reference needed). We also only truly see whatever is in an arc of about 1.5° (E. T. Hall, 1990). This limited information is restricted to the capacity of the human eye, the fovea allows us to see finest details but even then we can’t see objects or textures smaller than about 0.1 mm3 without assistance. The cone sampling rate drops precipitously with increasing retinal eccentricity (D. Williams, 1986). Furthermore, with increased eccentricity, the lattice becomes more irregular (D. Williams, 1986). By the periphery, the eye sees very little – some colour information and a sense of ‘presence’ generally – but not enough detail to distinguish shapes. Thus the images we receive from the periphery are highly abstract, and whatever is in the foveal area is specific. Effectively we don’t get to see a lot with any certainty, but memory and ontology fills the gaps maintaining the sense of consistency. This reduces the perceptual demands on the brain. We maintain a notional ‘visual image’ of what is behind our heads also. This is maintained by auditory haptic and olfactory supplementary information. But our other senses aren’t much better. We hear unevenly – with a better horizontal range than vertical. The human capacity for hearing tone seldom reaches its limits of 20hz – 17khz. Even then, we can only focus on one sound at a time. Humans cannot hear volumes less than 1dB and have difficulty detecting sounds less than 10dB, and even then, those sounds need to be in the middle of the human spectrum to be heard at this level.

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Ultimately, the information we gather from the environment has little new information and is supplemented by what we expect already. By ‘expect,’ I mean information that fits within a normal range of expectations given similar criteria in the past, these sensory inputs are constructed from meaning, instinct and memory. The mechanism is identical to the one used to draw meaning from writing and language. A symbolic representation draws on the ontology to find and express meaning. The sensory inputs only relate to the physical as a point of reference, like a written word triggers the meaning response, but doesn’t embody it. (Meaning is only ever an approximation (Popper, 1970)) Thus architecture, like all else, as it is experienced, exists primarily in the mind. Occasionally architectural expressions use our relative inability to perceive; the architecture of adventure rides in theme parks for example. When sight is suppressed with darkness and sound masked by sound-scapes, the architectural environment can shift and change in order trigger false a-priori decisions about the likely narrative – the likely content of the ride.

The sense of concreteness and reality that is associated with architecture obviously has some reality beyond experience – but my concern is not for what is, but how it is constructed from our ontological models of physicality, which is confirmed using the perceptual systems: Constructs of memory, meaning and desire. These intangibles are highly subject to change, to reinterpretation.

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The riddle of psychotic perception resolved: the integrated findings of an in-depth analysis of current hypotheses for schizophrenia.

The following paper presents a hypothesis for schizophrenia that draws together many disparate strands of evidence. It is currently being read a third time by Psychological Bulletin, after significant changes to the last draft.

Abstract

After generations of enquiry, and currently around 6150 papers being published annually (mostly focusing on the minutiae of the syndrome) there is a normative expectation that the pathogenesis of schizophrenia will never be unearthed.

This in-depth review of all the prominent hypotheses of schizophrenia reveals that none can account for the heterogeneous presentations of the syndrome, especially one that ‘reaches beyond the categorical definitions to recognize the ‘constellation’ of schizophrenia features’ as the DSM-IV instructs. But by integrating and developing these hypotheses (including competing ones like the glutamate vs. dopamine hypothesis rivalry), the reams of data appear to congeal into a remarkably coherent metahypothesis. For the first time since the DSM-IV diagnostic criteria was published, a 204


comprehensive and holistic explanation of all the symptoms and signs (as well as other findings known to the scientific community) is presented.

The role that the striatal D1/D2 heteromers have in modulating saliency and mediating both bottom-up and top-down perception is expanded, bearing in mind that the switching of the striatal D1/D2 heteromers from a low affinity state (D2Low), to high (D2High) is already putatively the root of schizophrenia. Here links are found that associate top-down attention with presynaptic tonic dopamine synthesis and the function of D2High. Bottom-up attention, on the other hand, is given to powerful phasic synthesis – the action of D2Low.

All attentional modes are essential to healthy perception and the functions that depend on perception, and as bottom-up attention subsides and top-down attention increases, eight very closely related syndromes can be identified, each with a distinct presentation and psychogenesis. These converge roughly into the main schizophrenia subtypes.

The meta-hypothesis that emerges from this review is highly triangulated and supported by robust published evidence.

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The riddle of psychotic perception resolved: an in-depth analysis of aberrant salience hypotheses for schizophrenia

By its narrowest definition, psychosis is a delusional and/or hallucinatory experience (American Psychiatric Association, 1994). Psychosis (thus defined) occurs in a number of conditions, but when psychotic symptoms are particularly bizarre and enduring, they characterize the most prominent symptoms of schizophrenia (Schneider, 1959). Next to schizophrenia, other psychoses simply aren’t as bizarre. The causes of schizophrenia have never been resolved and debate abounds from disciplines as diverse as linguistics and genetics about what mechanisms may be involved. A Medline review reveals 6146 articles since last year alone23. All heuristically use normative hypotheses, but these are fragmented and their findings ad-hoc: they study one facet of the disorder or another and produce new hypotheses to explain their findings – the few comprehensive hypotheses are notable exceptions. These are discussed below but their explanations invariably fall far short of plausibility considering quite how bizarre, debilitating and heterogeneous schizophrenia is. This paper traverses several prominent hypotheses and integrates diverse streams of data to present a cogent meta-hypothesis to draw together all the diagnostic criteria listed in the DSM-IV to a single molecular dysfunction.

1. Topics: schizophrenia, period: 2011-2012 206


This model first picks up on a number of perception-based hypotheses. These conceive perception as an input and behaviour as an output. Psychotic symptoms are thus output errors, caused by the dysfunction either within perception, working memory, or any number of other areas of cognition, depending on the model. One class of hypotheses with an enduring legacy is that symptoms are caused by an inability to filter out (attenuate) perceptions of little or no importance resulting in a tendency to make irrelevant observations (Frith, 1979; Gray et al., 1991; Kapur, 2003). More recently, one of these hypotheses has gained particular attention; because it links dopamine – a known active agent in psychosis, to the front end of the perceptual process, that is perceptual saliency (Heinz & Schlagenhauf, 2010; Howes & Kapur, 2009; Kapur, 2003; Kapur, Mizrahi, & Li, 2005; Schwartz, Wiggins, Naudin, & Spitzer, 2005). In the aberrant saliency models, a salient event is a perception marked by significance (something of importance relative to other percepts). In elaborating his hypothesis, Kapur posits that the importance or saliency of the event is tagged by the stimulation of the D2 receptors within the striatal dopamine neurons. The tagging process ensures that selective attention is directed to the percept that has been tagged as important.

Salient events (those that have been tagged as important) should reflect normal perception and the gamut of common reality as experienced by healthy people. Dopamine-saliency hypotheses propose that a functional oversupply of dopamine may harness attention independently of cue and context (Kapur et al., 2005). As an example, Kapur refers to Bowers & Freeman (1966), who recall a patient describing his symptoms thus: 207


‘I developed a greater awareness… my senses were sharpened. I became fascinated by the little insignificant things around me.’

Aberrant saliency is presumed to cause disorganized thought, hallucinations and subsequent delusions. The pathogenesis is explained by a competing hypothesis, which is similar in many details: Fletcher & Frith’s Bayesian attenuation failure hypothesis (2009). In this model, normality is a state where familiar events go unnoticed – in other words they are attenuated. That is, people get so used to normality that they fail to notice it. However, when there is an attenuation failure, normal experiences appear uncanny, and essential cognitive processes are aborted and left unresolved. Essentially Kapur, Fletcher & Frith are in agreement here.

While the prima facie evidence appears to bind dopamine, saliency and psychosis into a tight relationship, these hypotheses are bereft of details and need exploration. This is especially important because the hypotheses are used to advocate specific treatments and account for serious conditions such as schizophrenia. But before we can discuss the implications of a dysfunctional system, a better understanding about the nature of the healthy system is needed, and for the purposes of this article, four research questions have been posed.

Firstly, we need to ask exactly what saliency is. How much do we know about the neurological and perceptual processes involved in directing attention to important

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information? Only once these questions have been covered, can we ask questions that are more pertinent to the aberrant saliency model.

Secondly, if aberrant saliency is the basis for florid psychotic symptoms (hallucinations, delusions, etc.) as both Fletcher & Frith (2009) and Howes and Kapur (2009); Kapur (2003); Kapur et al. (2005) assert, then what are the deficit symptoms – the distinct lack of responsiveness that was once thought to be at the core of the schizophrenic diagnosis (Bleuler, 1950; Parnas, 2011)?

Thirdly, must aberrant salience (the mis-tagging of important events) equate to overstimulation – or even dopamine oversupply? Certainly, this is what Fletcher & Frith and Kapur both propose (Fletcher & Frith, 2009; Kapur, 2003; Kapur et al., 2005), yet about a third of schizophrenia cases don’t respond to dopamine antagonists (H. M. Jones, 2004), and how can this be explained?

Lastly, is aberrant saliency restricted to saliency, as the concept is traditionally defined? That is, solely to stimulus-led perception, or does it also affect intention-led perception? In other words, does it only affect attention that is stimulated by bottom-up, unsought stimuli – or are there other events that may also trigger saliency responses - even when stimuli are not unanticipated?

The answers to these questions will help us not only to better understand schizophrenia, but will shed light on the processes of perception more generally. 209


Healthy salience

The concept of salience is based on the assumption that we selectively attend to a limited number of competing streams of information by filtering out or de-prioritizing irrelevant information (Milstein, Dalley, & Robbins, 2005). In this general framework, saliency is the measure of the influence that a singleton (a technical term for a single potential percept, prior to it actually being singled out and declaratively perceived) has in gaining attention. At most, a single percept can dominate thought. It can, quite literally, ‘take possession of the mind’ (James, 1890, p. 404). At a minimum, the percept may remain latent; that is, beyond the threshold of declarative consciousness (Duckworth, Bargh, Garcia, & Chaiken, 2002; Hassin, Bargh, Engell, & McCulloch, 2009; Hassin, Bargh, & Zimerman, 2009). In between these two points, a singleton might make a partial incursion on working memory, occupying one or more ‘places’ of what is often reckoned to be a limited capacity system. (The capacity is dependent on the model for working memory that you find most compelling. Most models allow four to seven items in active awareness (Cowan, 2005) and others extend working memory to a further ‘behind the scenes’ implicit level of awareness (Baars & Franklin, 2003; Hassin, Bargh, Engell, et al., 2009).)

The factors of saliency Saliency refers to those properties of a singleton that attract selective attention – that is the directed awareness of the perceiver. But saliency is not a unitary concept. In vivo 210


studies of monkeys reveal that at least three factors will capture attention (Golembiewski, 2013) (Article reprinted from p.126). Because all three are referred to as salience, a new taxonomy is proposed to distinguish exactly why information is tagged as important:

Prominence

High contrasts of the singleton against the setting (noisy, sudden sounds, flashing lights and bright colours etc.) are highly prominent and demand reaction (Ljungberg et al., 1992). As a subject learns about the presence of a prominent object, the initial burst of saliency immediately begins to wane - eventually to the point of extinction (Berns et al., 1997; Mirenowicz & Schultz, 1996). It appears that prominence is moderated automatically through the glutamatergic and cholinergic neurotransmission systems (Carlsson, 1995; Corringer, Changeux, Bronner, Edelstein, & Smit, 2008) these then gate the secondary dopaminergic system (more about that below).

The kind of arousal that prominence evokes is highly automated, instinctive and is central to orientation reflexes (Ward, 2008). This form of salience must be noncognitive because it generally survives states of hypoarousal such as vegetative comas (Laureys, 2005; Schiff et al., 2002) it will also activate both excitatory and inhibitory synapses of layer 2/3 of pyramidal neurons even in vitro – the result being a rhythmic oscillation in the gamma frequency – one that is widely recognised as relating to sensory processing (Feldmeyer, 2010). 211


Significance

This form of salience is highly cognitive. It is the potential importance of the concept (schemata) that is being recalled. There are three things that increase the significance of a singleton: a) anything that helps build meaning, b) anything that contributes to understanding, and c) anything that may needed to sustain existence (Jan Golembiewski, 2010b; Golembiewski, 2011b) (Articles on p. 62 and p.296 q.v.) In other words, we react to perceptions that are significant concepts, not only prominence.

Worth

Salience has a pre-cognitive affective or hedonic bias (Barrett & Bar, 2009). Monkeys responded to stimuli according to their desirability. The promise of a rewarding experience generates a much greater impact than the threat of a negative one (Mirenowicz & Schultz, 1996; Schultz, 1998). Worth should further be broken down into affective and hedonic subcategories. Affective worth is how a singleton makes you feel, whereas hedonic worth relates to an expectation of reward or sensual punishment. Worth appears to be mediated by the amygdala, and its function appears to remain either intact or slightly under engaged in schizophrenia (Anticevic et al., 2012; Becerril & Barch, 2010). This contrasts with affective psychoses like bipolar disorder, in which a large body of literature reports over-engagement of the amygdalae (S. B. Perlman et al., 2012).

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❊

A fourth saliency factor should also be added to the list. This factor was not identified using the same series of animal experiments, possibly because it is peculiar to healthy humans.

Opportunity

This is response to stimuli just for the sake of it, sometimes just because we are active beings and need to do something. This is engagement – just for sensory variation, for stimulation, but not necessarily for affective or hedonic gratification. It seems that no other animals have a go at things without good reason or choose to avoid a favourite food, just to try something different. Such behaviour is very compelling for humans, and is therefore undeniably salient on some highly intellectual level, yet it doesn’t fit into the categories mentioned above. Nor does it behave the same way: opportunity is engagement with experience; it is not led by saliency cues and is not normally coercive (except perhaps as it builds habits through Hebbian processes). Opportunity is the salience of choice. The choice to try something off-putting, for no reason other than the fact that it’s possible.

The modes of perception and attention. The psychological canon allows for two modes of selective attention (see Table 2.) There is top-down attention, which is the deliberate focus of declarative resources; and 213


bottom-up attention, which refers to the attention that is brought to a subject by the interruption of top-down attention. As attention turns to attend to the interruption of an unexpectedly salient singleton, top-down intent changes. We abandon our prior engagements and focus on the rude intruder. What is it? Does it have relevance? How does it fit into what I know (the ontology)? If the transfer of focused attention to a new stimulus is automatic and unavoidable, then intent plays no part and is thus called bottom-up (Theeuwes, Atchley, & Kramer, 2000). This use of the term ‘bottom-up’ is thus a bit ambiguous, because it refers to the top-down attention that is given to bottomup stimuli. To resolve this ambiguity the terms listed in column 2 of Table 2 are used.

Mode

Action

Saliency factors

Raw

Potentially fills perception with undefined richness.

Bottomup

Identification and experience of novelty, aberrance, data mismatches.

Prominence (stimulates gamma band inhibitory and excitatory oscillations) and if strong enough, NDMA triggers the D1 receptors Prominence: mismatch detection (when D1 has been already activated.) Worth (negative) – not dopaminergic Opportunity

Active

Top-down/ feed-forward

Bottom-up/ feed-back

Canonical term

Top-down

•General engagement, occupation of interest, turns opportunities into actions and brings attention to bottom-up stimuli that are neither anticipated, nor beyond the range of probability. •Brings attention to ‘non-critical’ interests such as aesthetics. •The basis of most experience. Recognition of expected targets, data matches. ‘The bingo’ experience. Experience that is intended or worse than anticipated.

Significance Worth (positive)- not dopaminergic

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Table 2: The modes of attention. Introducing a new taxonomy. The canonical terms: bottom-up and top-down both miss the basis of most experience, and the term ‘bottom-up’ is unclear about whether it refers to a precognitive or cognitive phase of perception.

Raw attention

If there is such a thing, in its purest form, bottom-up attention must be a non-cognitive observation of unprocessed perceptual stimulus. Theoretically, in this raw state, nothing could be salient, because it would completely lack any kind of definition or ontological associations. Even so, automatic bottom-up attentional processes continue to monitor prominence, even during vegetative states, anaesthesia, deep sleep, and in vitro (Feldmeyer, 2010; Laureys, 2005; Schiff et al., 2002) implying that this raw data feed bypasses cognition. This form of bottom-up attention is referred to as raw attention.

Bottom-up attention

The cognitive attention given to anything that is not driven by intention, such as prominence and negative feedback, is widely known as bottom-up attention.

Singletons that are picked up by bottom-up attention are those that stand out as different from expectations (for example, you crack an egg and it smells bad – you weren’t expecting it, but you notice). In bottom-up attention, saliency is primarily a response to 215


the unexpected, the undefined, misplaced and unanticipated, in other words mismatches between singleton-data and related schemata; Functionally this means that bottom-up attention is a response to difference and novelty, and this is how the term is normally used (Theeuwes et al., 2000).

Mismatch identification appears to be a Bayesian process, meaning that singletons are noticed when they don’t fit expectations, and are otherwise ignored (Clark, 2012 - in press; Friston, 2003; Stephan, Penny, Daunizeau, Moran, & Friston, 2009). In another body of literature, another feedback mechanism called error related negativity (ERN) is also proposed. This is a feedback loop specifically for negative affective or negative hedonic feedback – ERN occurs when an event is worse than expectations (Falkenstein, Hohnsbein, Hoormann, & Blanke, 1990; Holroyd & Coles, 2002). ERN is Bayesian too – but it isn’t driven by bottom-up attention because the negative event happens within the general range of expectations – ERN therefore fits in another category: active attention. An example of a bottom-up Bayesian mismatch detection is when you see a red poppy in a green field or a tiger on your lawn, the former is inconsequential, the latter critical.

Bottom-up attention isn’t only given to external stimuli; it’s give to any unanticipated stimuli. Bodily (somatogenic) signals like hunger, tiredness, pain etc. would normally stimulate endogenous bottom-up stimuli because they are unsolicited: we do not usually ask ‘am I hungry, tired or in pain?’ because we will feel hungry or tired spontaneously.

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Initially these signals are received using raw attention, but are modulated with bottomup attention.

It must be noted that top-down attention can be directed to somatogenic stimuli, therefore while somatic and other bottom-up experience is normally bottom-up, it may occasionally be modulated by top-down intention.

Top-down attention

Top-down attention is the mode of attention where percepts are anticipated. For example, if I am hunting for truffles I ignore stones, but when I see something that matches my expectation of a truffle, it will elicit recognition salience: a ‘bingo!’ response. The top-down mode of attention has an exclusive domain of interest: the known. It is only concerned with recognizing significance saliency and only the correspondence between a singleton and expectations (Coull, 2005). Unlike bottom-up attention, top-down attention is not Bayesian, because of its tight focus. Because topdown attention assesses only matches against intentions, top-down attention yields only positive feedback (you don’t have an interest in things that you weren’t looking for – these can only be noticed by other modes of attention.) This sets up a confirmation bias (Nickerson, 1998). Things that are actively sought trigger top-down recognition reactions easily, yet negative outcomes are referred to the bottom-up system, and will only be regarded if it is salient in its own right (usually prominent) or significant in some way. 217


There are two levels of top-down attention; focal and incidental. If we want to do something, we may focus on it intensely, in which case intention is highly deliberative. In such cases saliency is only used for positive feedback. On the other hand, the attention we give simple and well learned tasks is incidental. Here top-down attention that is incidental is reclassified as active attention.

Active attention

When a bottom-up singleton interrupts a deliberate (top-down) action, it comes as a distraction. But such encroachments are not regular (and may even be rare, depending on one’s lifestyle) because they depend on bottom-up stimuli, which may or may not be present. Despite this, we are not totally driven by intent (as other animals might be). In real terms, for humans, there is a large and undefined grey-area that separates the topdown and bottom-up modes of attention. If bottom-up attention is limited only to detecting prominence, and top-down attention covers only significance, then what of the rest? What of ERN? When things are noticed when they are worse than expectations but are generally within the range of unconsidered probability – such as when someone reaches into a fire and gets burned? Another whole range of experience is awareness on the edge of latent automaticity, which is nevertheless still noticed. When we do any routines we know well – such as drive, we do so automatically for the best part, yet we remain more or less aware as we do so.

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There are many opportunities that we choose to engage in, just because they are there. Likewise, events are noticed but neither because we are looking for them, nor because they are prominent. Active attention is a term to describe the middle ground between bottom-up and top-down. It may be environment led, yet without the sharpness of novelty. Active attention is where top-down intention directs a ‘fuzzy’ search or where bottom-up attention reveals something that you had an interest in, but had not been looking for. Active attention is not driven by saliency, and isn’t a mode of attention in its own right, but complex combinations of bottom-up and top-down processes, which are led by habits of engagement, by choice and simply by the availability of resources. And as such, active attention doesn’t sit comfortably with the assumed dynamics of the canonical model of attentional salience.

Attention is an expansive resource that doesn’t retreat and become passive when it’s not engaged in any clear intent or with salient environmental stimuli. If anything, the opposite: Active attention is the awareness that accompanies the continual activity of the mind and body, on the lookout for something to do, to experience and to think about. Indeed, studies have demonstrated that when environments are depleted of natural stimuli and opportunities for active attention, even healthy people start to hallucinate them (Grassian, 1983; Weckowicz, 1957) or fabricate them using whatever material is available – even human faeces (Osmond, 1958).

The behaviour that takes place around active perception is largely automatic and involves stereotypical actions that are associated with whatever an object suggests – or 219


affords the perceiver, thus objects of engagement are called affordances (Gibson, 1979; Withagen et al., 2012). An example is when you find yourself eating a cookie that you found when doing something altogether different. It wasn’t an intentional act, but neither was it unintentional, it was just automatic.

Active-perception is very basic and instinctive because it links opportunity directly to action and in evolutionary terms, this is the primary role of perception. Simple creatures must act according to opportunities offered to them, but they don’t have the cognitive apparatus to intellectualize or otherwise make that action declarative (Bargh & Dijksterhuis, 2001). Active perception is evident in children too:

‘From birth, babies will actively engage with the perceptual environment. They will imitate expressions (Meltzoff & Moore, 1977), grasp a graspable object, and with age they will want to touch textures, run fingers down Brancusi’s sculptures, absorb themselves in colours and scents, feel the curvature and warmth of surfaces, immerse themselves in tastes, experiment with sounds, etc. They will want to squeeze bubblewrap and juice cartons, just to hear them pop. They light sparklers to see the sparks fly off in all directions; they burn incense to scent the air, and climb snowy mountains, just to feel the rush of zooming down again.’ (Golembiewski, 2013) (p. 126 q.v.)

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Parallel model of bottom-up and top-down selective attention Salience Prominence

!

Bottom-up attention

Significance

★

Worth

Top-down attention

Intention

✓

Working memory

Feedback

An integrated model of active attention Salience ! Prominence

Active awareness

★ Significance

BU TD

☺ Opportunity Worth

Working memory

Attention +

–

Figure 23: Here the traditional parallel model of attention is contrasted with an integrated model that incorporates active attention. Saliency is mediated by the active nature of awareness, not by a property of the stimulus. Saliency isn’t unitary as commonly thought either. The various factors of saliency show different patterns of behaviour although they ultimately end up using a top-down or bottom-up pathway to achieve declarative awareness.

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Systems that depend on attention Perception is the most tangible link between the shared reality and personal experience. A lot depends on it and this brief section cannot even address all the facets of the psyche that are affected by attentional dysfunction, much less do them justice. Even so, it’s important to sketch out the interconnected systems of perception, automaticity, the sense-of-self and learning are needed because the most characteristic symptoms of schizophrenia can be explained as dysfunctions of these downstream functions all of which require attentional salience to function (see Figure 24).

The ontology (schemata)

Automaticity

Hebbian (‘dumb’) learning

Senseof-self

Perception

Learning

antiHebbian (considdered) learning

Raw perception

Figure 24: Perception is informed by new raw data and also by

learned schemata stored in memory (the ontology). This is constructed using a ‘dumb’ but efficient Hebbian processes ‘cells that fire together wire together’ (Shatz, 1996). New knowledge isn’t learned this way, but associations are strengthened. This process creates the automatic ontology – processes that can be enacted without much consideration. 222


New knowledge is processed through anti-Hebbian processes in which aberrance is detected and considered thoughtfully. The whole ontology is used to process all perception, but the ontology itself is opaque – it is perceived as something else – ‘the self’.

Perception

Even with robust attentional salience, perception is never perfect. Raw perceptual data is filtered and interpreted by our gross perceptual mechanisms. The sensory world is experienced through the available senses, so it is neither directly nor fully experienced. Human sight is the experience of reflections or luminosity of a narrow bandwidth (400790 tHz) of vibrations, 1-400 tHz is experienced as warmth (Gibson, 1979; Matlin, 1988), and the 17Hz-17kHz range as sound and pressure (Moore, 1997), but bats hear frequencies up to 115kHz (Heffner, 1983) and guppy fish can see light down to 300tHz (E. J. Smith et al., 2002). To sense these and other frequencies, humans have to use specialized equipment (such as radios or hyperspectral cameras), which translate frequencies into our native sensitivity range of visible light and audible sound.

The next task ‘of the brain… can seem impossible: it must discover information about the likely causes of impinging signals without any form of direct access to their source’ (Clark, 2012 - in press, p. 6). Sensations must be iteratively interpreted and experienced through cortical processes. Information from the sensory organs travels to a series of perceptual cortices which process information of increasing complexity and abstraction. 223


The later cortices (such as V4 and V5) are globally integrated to enable the processing of unknown, unpredictable and abstract stimuli. All the senses have lower-order processing areas and share the higher order ones – although even primary inputs are shared to some degree (Foxe et al., 2002).

A bottom-up process is required to modulate raw perceptual data of the environment (including the body), but these stimuli can only be known and used in translation; that is through the top-down process of learning: decoding and recoding, creating and remodelling schemata. The heavy reliance on top-down processes doesn’t mean that what we experience isn’t real – but it does mean that experience is highly mediated and a partially inferred best guess (Sanders, 2004). The implications of this are broad:

1. The fact that all perception is in some way translated into electrical and chemical impulses before it is reinterpreted as sensory perception should modify the way we understand hallucinations. In a profound way, all we know is, in some way hallucinated. I don’t suggest that healthy experience is just as unreal as psychiatric hallucinations, but wish to point out that the qualifier of ‘hallucination’ is the departure from common and grounded sense of reality, and not the extension of experience into fantasy.

2. Perception will be distorted if the ontology (which informs perception) is dysfunctional.

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3. The ontology is informed by personal experience, structured into schemata (including lexical schemas) and is fact-checked through a cultural lens. These form the basis of perception. This is reflected in the DSM-IV:

‘Ideas that may appear to be delusional in one culture (e.g., sorcery and witchcraft) may be commonly held in another. In some cultures, visual or auditory hallucinations with a religious content may be a normal part of religious experience (e.g., seeing the Virgin Mary or hearing God's voice). In addition, the assessment of disorganized speech may be made difficult by linguistic variation in narrative styles across cultures that affects the logical form of verbal presentation.’ (American Psychiatric Association, 1994, p. 285).

4. The imperfect match between perception and experience means that all people have the capacity to be fooled by what they believe they perceive. This leads to one of the most commonly accepted hypotheses for hallucinatory experience – the illusion-hallucination continuum (eg, Brébion et al., 2000; Frith & Done, 1988; Harvey, 1987; Johns et al., 2001). While direct studies of this phenomenon do demonstrate significant illusion/hallucination correlations, and therefore a possible role in psychosis, the effect size is still too small to explain psychotic symptoms (Aleman, Böcker, Hijman, de Haan, & Kahn, 2003; Woodward, Menon, & Whitman, 2007).

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5. The higher the reliance on top-down and active attentional processes are (that is, the higher the top-down vs. bottom-up sampling rate is), the more likely that perception will be distorted from reality, because sampling loses its factchecking facility and negative feedback tends to get ignored, creating a confirmation bias. This perspective is known in philosophy as the intellectualist position (A. D. Smith, 2007).

Theorists who take an intellectualist stance on perception have an easy time understanding hallucinatory experience, because, for them the problem is resolved by asserting that top-down attention leads perception, therefore, a dysfunctional top-down attentional system will cause hallucinations. These models don’t acknowledge the possibility of direct perception. Intellectualist models only outline the higher order experience of knowing (a top-down function): they understand perception as a cognitive process that employs raw perception only as feedback.

Current intellectualist models argue along the following lines: The brain is modelled as an organ that assigns meaning to raw perception. On one hand, raw perception is sensed, but sensory information remains meaningless until it is associated with schemata within ontology. Clark (2012 - in press) and Fletcher and Frith (2009) emphasize that this follows an anti-Hebbian, Bayesian logic in order to maintain efficiency. In their models, singletons are only noticed when they are aberrant, at which point learning must take place. Grossberg (2009) is interested in the cytoarchitecture of perception. His model is Hebbian and distinctly not Bayesian, but is no less 226


intellectualist. He proposes that the very laminar structure of the neocortical neurons match raw data to schemata by matching predictive representations of the world with raw bottom-up stimuli. The model Grossberg proposes is that neither top-down intentions nor raw bottom-up stimuli will trigger a neuronal excitatory reaction (recognition salience) on their own, except in psychosis (Grossberg, 2003b). It is when two inputs: a tonic top-down intention and the other, a raw bottom-up singleton come together, that a saliency signal is transmitted horizontally (from one neuron column to another) through dendrites and vertically (to other brain regions) through axonal connections. In this model, intent quite literally works in a top-down fashion, because it stimulates the first layer of the neocortex. This tonic stimulation primes perception to receive appropriate input. Bottom-up perception works the opposite way around, from the sixth layer upwards. This tonically primes the neuron too, but the excitatory potential of the neuron is only achieved when both top-down and bottom-up stimulation occurs.

On their own, intellectualist approaches are limited. A distinction is not made between knowing and experience. Intellectualist approaches must face a very valid criticism; ‘I think is not I am, unless by thought I can equal the world’s concrete richness.’ (Merleau Ponty, 1943), This is not a critique of the reductive efficiency of Descartes, Bayes, Hemholtz or their inheritors (like Clark, Fletcher, Frith, Friston or Grossberg), but a critique of the lack of richness of experience that such approaches imply.

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As it happens, an automatic form of perception continues when top-down attention ceases, even in conditions such as a vegetative coma (Laureys, 2005; Schiff et al., 2002; Zeman, 2003), when sleep-walking (Plazzi, Vetrugno, Provini, & Montagna, 2005) or even in vitro (Feldmeyer, 2010). This means that raw perceptual processes are independent of any form of top-down attention, confirming Grossman’s assertion that attention and perception work in parallel. Habitual engagement (active attention) integrates the two. In this model, raw awareness provides a non-cognitive backdrop to experience: a richness and fullness instead of a perceptual vacuum. During active perception, raw sense data is not disposed of, just because it’s understood, nor is it disposed of merely because it is not. On the contrary, these conditions are when we may really start to enjoy experience. When we look at a painting and discover the subject, the richness in how the figures are presented doesn’t evaporate. The active-attention model accepts the intellectualist models of perception, but also the concept of direct perception, thereby lowering the threshold for experience. The active attention model proposes that experience becomes declarative iteratively, exactly as perceptions are engaged with and acted on iteratively. At the most fundamental (pre-cognitive) level, action is automated, not necessarily by attention, but by habits that have formed direct associations with perceptual activations and actions: given familiar singletons, it isn’t necessary to recognize them before actions commence. We do not see a flat, hard surface and think; ‘hey – I can walk on that.’ We just walk (Bargh & Dijksterhuis, 2001; Gibson, 1979). The factors of salience will determine how much attention a singleton is given as a parallel process (See The factors of saliency p.210).

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In agreement with Clark, prominence (mismatches between expectations and experience) is a factor. But other factors (significance, worth and opportunity – see p. 212-213) also capture attention, and all are important. The mechanics of opportunity are especially interesting in the context of active attention because we do engage through action, but our awareness of such engagement may be implicit (Hassin, Bargh, Engell, et al., 2009).

The associations that intellectualist models emphasize are plastic and changeable and thus are intrinsically vulnerable. Grossberg recognizes this and insists that a resonance between the raw data of reality and intentions is essential to create stability of meaning, to prevent it from being re-written with every new perception (Grossberg, 2003b). Meaning cannot survive (long) when sensory cortical inter connectivity is lost, even if bottom-up sensory perception continues. Dementia within the association cortices causes the singletons of perception to vanish, leaving behind nothing but a full, but unintelligible jumble of sensory indistinctness. In some cases, patients with specific dementia in the higher visual cortices cannot even distinguish between the categories of visual information – between colours, lines and shapes, much less pick out contents of a view, even though the raw visual information is still omnipresent (Sacks, 2010).

The sense-of-self

The sense-of-self is normatively considered irrelevant or only of peripheral interest to perception, but this viewpoint is difficult to defend. All the modes of attention serve a 229


single perspective, and this is experienced as the locus of the sense-of-self; I am the centre of my experience. There are many possible reasons for this, including (at a minimum):

1) Because all the organs of perception report to a single brain (although nominally to different parts of the brain);

2) Because perception is served, and serves a single and personal ontology;

3) Because the actions perception triggers all occur within a single physiology (Braund, in preparation);

4) Because all of these functions unite a single sense of identity and ego (Shoemaker, 1968).

5) Because we have narratives of existence (R. A. Jones, 2010)

6) Because we act on self-knowledge and a sense of coherence emerges from these actions (Deci & Ryan, 1991);

7) We find anything that contributes to meaning, comprehensibility and manageability perceptually significant and salient (Antonovsky, 1987)

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The holism these interconnected and interdependent systems generates normally taken for granted, but it is vulnerable. The person (as philosophically conceived here) is an ego-centric composite of a body, perceptual system and ontology, and for the best part, the sense-of-self doesn’t atomize when these constructs do – blindness, injury and ignorance are all undoubtedly risk-factors, but for the best part, the phenomenological sense-of-self is relatively robust in these domains. An experiment was conducted where the visual first person perspective was challenged, in this study the participants’ eyes were masked and all sight was channelled through monitor glasses with a wireless closed circuit video feed. The camera was put at a fixed angle in the corner of the room, creating the illusion that ‘my body is there – not here.’ Even in these circumstances, the sense-of-self was generally maintained; when participants wrote, the writing faced the camera, not the body, but the participants had a choice – they could also choose to engage their proprioception rather than visual modality, meaning that their writing faced their bodies (Mizumoto & Ishikawa, 2005). This suggests that the self-perspective is maintained by all the senses and can survive major disruptions. What is more vulnerable is the ability to reflect on the narratives and actions that we associate with the constructs of self, identity and self-agency. These narratives are sometimes oppositional: ‘I am x because I am not y’ (Festinger & Carlsmith, 1959). They are sometimes affirmative: ‘I am x because my actions are x-like’ (Bem, 1967). Both arguments rely on perception for the basic information to know what x and y are, and on narratives to contextualize x and y. Within these narratives, the sense-of-self is established relative to actions and thoughts, whether they are oppositional or reconciliatory.

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I contend that both positions are valid, certainly in terms of contemporary neuroscience, because the more deliberate actions are, the more resistance: neural excitation and inhibition occur together, except during highly automated tasks, which are far more parsimonious, and don’t necessarily engage attention at all (Bargh & Dijksterhuis, 2001). Sometimes excitation and inhibition are in equal measure, in which case the balance suggests that no actions take place, but the greater the excess of excited neurons, the more spontaneous action occurs (Golembiewski, 2012a) (see p.358 q.v.) It might be resistance to action (inhibition) that is recognized as self-agency, rather than actions themselves, whether successful resistance as in Festinger & Carlsmith’s model or unsuccessful as in Bem’s. If this is the case, active attention will be insufficient to maintain a sense-of-self.

Learning

The human search for comprehensibility and meaning appears to be endless. Every unexpected singleton is met with top-down questions about why, who, what and when – even when dreaming we are constantly trying to figure things out. This process involves linking singletons to the lexical and motor schemata that are most challenged by the new singleton (robin fits with birds, superhero side-kicks; with rhymes bobbin and coffin; with names and other people called Robin like Robin Hood, with similar names such as Robert and so on.) This is a logical process that has been adopted to simulate intelligence in computing and has been adapted for very diverse models of learning (Baars & Franklin, 2003; Clark, 2012 - in press; Grossberg, Carpenter, & Ersoy, 2005; 232


Johnson Abercrombie, 1960; McClelland, McNaughton, & O'Reilly, 1995; Rumelhart, McClelland, & UCSD PDP Research Group, 1986). If concepts defy knowing, they may still be placed into abstract schemata. Concepts like God, love and infinity are unknowable, but nevertheless have many associations across the global neural network. Abstract schemata are sometimes less grandiose but no less vague. If a singleton doesn’t initially appear to be of personal significance (i.e., few significant associations), it may be bundled with other concerns for someone-else to deal with.

Regardless of whether their nature is specific or abstract, concepts and their associations become schemata and are useful for defining other singletons (Johnson Abercrombie, 1960). This is an intrinsically antiHebbian process, because it wrestles apart automatic associations and creates finer and finer distinctions within the ontology. But there is also ‘dumb’ learning, which follows Shatz’ (1996) aphorism to describe Hebb’s rule of synaptic plasticity; ‘cells that fire together, wire together.’ Where real learning creates associations, Hebbian learning reinforces them through long term potentation (ie, usage). The mechanisms are highly complex, but recent reviews link automatic functions to the strength of associations in the striatal association area (Ashby, Turner, & Horvitz, 2010). Under normal circumstances, Hebbian and antiHebbian systems work together. Whereas the anti-Hebbian system is primarilly used for initial learning (as described by Clark and others), the associations that are generated are strengthened by Hebbian processes, the oppositeis also true; disuse leads to synaptic loss and sometimes dementia.

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Schemata that have been committed to memory for long periods are known to lump together with similar concepts, if they can be recalled at all. This is demonstrated when people are given several stories and asked to relate them after only a short period and again after a long one. The phenomenon does not occur if subjects consider the stories regularly; instead, the stories develop details and a new character of their own (Johnson Abercrombie, 1960). This can be taken as preliminary evidence that the longer elements of the ontology are left without focal attention, the more tacit they become. The more focus they receive, on the other hand, the more explicit (Gulick, 2006). Tacit knowledge is difficult to express because meanings are personal and hermetic, and the communication of knowledge requires explicit knowledge, not vague concepts. For example, someone who has forgotten their primary school science may say ‘light works because of electricity.’ The person is not wrong, but the information lacks specificity and isn’t very useful. Without regularly scanning knowledge for errors using a system similar to the one described by Clark or Friston (Clark, 2012 - in press; Friston, 2003), knowledge must become more tacit.

Tacit awareness of well known schemata and routines appears to be an ideal level of awareness to allow associated actions to take place automatically.

Automation

Attention isn’t needed to trigger automatic actions such as well-learned motor behaviours. No deliberate attention needs to be given to walking, unless you are still a baby, 234


and the skill is new. Having said that, intention (a distinct top-down form of attention) can both trigger and inhibit automations. Automation is mentioned here because attention is variously helpful, destructive, or irrelevant to automatic performance at seemingly unpredictable times (Willingham, 2001). Giving focal attention to automatic tasks can cause ‘choking,’ the unintentional inhibition of that activity (Baumeister & Showers, 1986; Dijksterhuis & van Knippenberg, 2000; Willingham, 2001).

Attention is an inhibitory response to a singleton. It pauses or arrests both automatic actions and cognitive processes while the singleton is attended to. It will shortly be demonstrated that there are two pathways that moderate attention: one is directly inhibitory and the other excitatory – yet, because of their functional routes, they both end up inhibiting automations – to differing degrees. The lower declarative awareness levels associated with the troughs in tonic dopamine activity and associated with active attention (see Figure 27), is likely to be the ideal level of awareness to enable automatic tasks. This latent level of awareness allows automatic actions to be so efficient (Ashby et al., 2010). Greater awareness, particularly bottom-up awareness (the phasic bursts in Figure 27), as it invades working memory inhibits (that is, interrupts or even terminates) actions whether they are automatic or not, by exciting the possibilities that the action may precipitate and a range of alternatives (Dijksterhuis, Aarts, Bargh, & van Knippenberg, 2000). This is presumably a function of the ACC and frontal cortex through the activation of NMDA/D1 excitatory afferents (more about that shortly). But even too much top-down attention can do the same (the peaks of tonic action in Figure 27), not because the ACC and frontal cortex are excited but the opposite: because the 235


inhibitory D2 neurons bring awareness directly to the automatic functions, thereby lifting awareness out of the ideal latent state. The classic example is with professional sports players – when they ‘think too much’ they ‘choke’ – the automatic fluidity of their actions fail (Willingham, 2001).

Automatic actions can be deliberately triggered by top-down intention (Ashby et al., 2010), but for the best part, automatic actions are excited directly by affordances. This sometimes even occurs in states of very low arousal as mentioned above; for instance sleep-walkers will engage in automatic behaviours that relate to real and hallucinated objects and environments: they have been known to drive, cook and occasionally act in violent ways, especially if disturbed (Plazzi et al., 2005). When imaged using single photon emission computed tomography (SPECT), sleepwalkers show profoundly decreased regional blood-flow to the frontoparietal cortices, confirming that there is no self awareness in this state (Bassetti, Vella, Donati, Wielepp, & Weder, 2000).

The typical sleepwalking patterns suggest a relevant issue for this argument; automatic activity can be stimulated by top-down intention or simply by well-established links between actions and the raw electro-chemical representations of perceived opportunity; effectively bypassing all cognitive architecture (including the frontal cortex and ACC). The implication is that intent is implicit within knowledge and that once knowledge is established, it becomes an automatic reflex (Heidegger, 1981). For example, the knowledge that an apple is edible prompts an intention to eat it (Bargh & Dijksterhuis, 2001). Any attention given to automatic actions has an inhibitory effect, but this is 236


processed in parallel. For healthy people, inhibition balances latent ‘intentions’, thereby moderating automatic actions to make them context appropriate.

The same cannot be said for schizophrenic or bipolar (I) patients, who don’t sufficiently inhibit affordances, meaning that stereotypies and other automations go unchecked (Golembiewski, 2012a) (reprinted here from p.358). For this reason, the inhibitory properties of salience (when applied to automatic functions) must be considered as an essential element of robust mental health.

The attention that healthy people give to their environmental context, automatically establishes latent restrictions on behaviour – even on automatic behaviour. For example, in a church or a temple, people automatically tone down their behaviour, unless they have not learned the behavioural associations associated with the milieu (babies for instance). This effect is known in environmental psychology as the influence of the behaviour setting (Barker & Wright, 1954; Golembiewski, 2013). It is this latent form of inhibition24 that prevents actions from occurring whenever an affordance is present. A person will automatically assess the context, and will act only within the restrictions imposed by the context unless they wilfully choose to be deliberately defiant, or if they suffer a mental pathology of some kind.

24

. The inhibitory effect of the behavior setting should not be confused with latent inhi-

bition, a decrement in learning about notionally familiar circumstances (Lubow, 1973) that became a pivotal part of the hypothesis of Gray et al. (1991). 237


The neural architecture of healthy attention

Neurotransmitters and receptors The neural processes involved in attention have been of interest for some time and scientists have identified a range of systems and subsystems that may be involved. Within this general field, the very lateralization into two dissimilar hemispheres has been identified (Toga & Thompson, 2003). Four neurotransmission systems are also of interest: acetylcholine, noradrenalin (norepinephrine), glutamate, and dopamine. There is also a lot of research into specialized neural architecture, including larger scale region analysis and the study of neurons and their components. All of these specialist interests are growing fields, except perhaps lateralization, which, for all its promise, no longer attracts the interest it did twenty five years ago (McGilchrist, 2010). In this chorus of opinions, the striatal dopamine system is consistently singled out as the force that shifts attention from one thing to another (Coull, 2005). Striatal dopamine is also linked to salience perception (like in the above hypotheses (Fletcher & Frith, 2009; Howes & Kapur, 2009)), to bottom-up attention (Hickey, Chelazzi, & Theeuwes, 2010; Holroyd & Coles, 2002) and to reward salience – the way that attention is drawn to rewarding stimuli (Berridge & Robinson, 1998, 2003; Bromberg-Martin & Hikosaka, 2009; Mirenowicz & Schultz, 1994). The striatal dopamine pathways have also been empirically linked to attention system more broadly and this will be discussed in further depth shortly.

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The noradrenalin systems appear to support the dopamine function by selectively inhibiting activity that is not task specific (especially somatosensory inputs) and by the moderation of baseline levels of arousal (Coull, 2005), the cholinergic system, on the other hand, appears to sustain interest beyond the initial turning of selective attention (Aston-Jones, Rajkowski, & Cohen, 1999; Coull, 2005) It also serves a very important role in communicating somatosensory impulses to the brain (Corringer et al., 2008) along with glutamate (Carlsson, 1995). While all these processes are highly relevant to the topic of attention, only dopamine, acetylcholine and glutamate appear to be active in the early phases of perception. Because our interest here is particularly in the earliest phase of attention - selective attention, the other transmission systems will not be discussed further here.

A viable functional model is that salience is not unitary, and that most somatosensory inputs are moderated by glutamate, acetylcholine or both and that these moderate prominence. Cognitive saliency (significance and opportunity), on the other hand, is almost certainly moderated primarily by dopamine. The saliency of worth is moderated not by receptors, but by association organs – the left and right amygdalae.

The glutamatergic attentional system appears to monitor prominence, but glutamatergic activations don’t normally invade awareness unless an event is prominent enough to trigger the N-methyl D Aspartate (NMDA) receptors (Kleckner & Dingledine, 1988). At this point the dopaminergic (cognitive) attention system becomes engaged in bottom-up attention. People are profoundly unaware of glutamatergic activity until the NMDA 239


receptors are activated, at which point the ‘winner takes all’ and working memory is at least temporarily dominated by this new stimuli (Ward, 2008). The activation of the NMDA receptors requires both a surge of voltage and particular connections, meaning the receptor gates any activity that continues below the receptor ionization threshold (Kleckner & Dingledine, 1988). Until this point, glutamatergic activity will continue while a subject is utterly oblivious, meaning the deliberate blockade of NMDA receptors can even be used to induce non-associative anaesthesia (Marek et al., 2010).

The cognitive (dopaminergic) and somatic (glutamatergic) selective attentional systems are well integrated through networks of interconnected striatal neurons known as mosaics (Cepeda, André, Jocoy, & Levine, 2010; Fuxe, Marcellino, Guidolin, Woods, & Agnati, 2010; Gerfen, 1992; Gerfen, Baimbridge, & Thibault, 1987; Shen & Surmeier, 2010). The functions of these can realistically only be understood in simplified terms because mosaic patterns are often inconsistent and their distribution patterns are heterogeneous (Gerfen, 1992). But within the mosaics, there are specific dissimilar interconnections known as heteromers, which occur where two dissimilar receptors are collocated (whether they are on separate neurons or the same doesn’t appear to matter (Seeman, 2008a)). Relevant heteromers to the study of psychosis include NMDA/D1 and D1/D2. These are of further interest because some have been found to be up- or downregulated in a broad range of mental illnesses (Pei et al., 2010). As we shall see, the D1/D2 heteromers are almost certainly involved in the moderation of cognitive saliency (Seeman, 2010).

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There are a number of dopamine receptor types and these fall into two families: the D1 (excitatory) and D2 (inhibitory). But the ones that have been singled out as being responsible for saliency tagging are the striatal D2 receptors, although the literature rarely differentiates one type of saliency against another. The reasons for identifying the striatal D2 receptors, according to Ginovart and Kapur (2010), are because psychotic patients read far more significance into the environment than is evident to the greater majority, and it is primarily these D2 receptors that are blocked by all anti-psychotic medication. Thus, the prevailing hypothesis is that a psychotic episode is caused by a functional over-availability of dopamine or of the D2 receptors (Laruelle & Abi Dargham, 1999).

Seeman and others have also identified a particular formation of heteromers that render the D2 receptors far more reactive. These are the D2High receptors. These are thought to be responsible for psychosis for two reasons: not only are there more D2High receptors in animal models of psychosis and in vitro studies of psychosis, but these receptors are very easily stimulated and require very little dopamine to fire (Ginovart & Kapur, 2010; Samaha, Seeman, Stewart, Rajabi, & Kapur, 2007; Seeman, 2010; Seeman & Kapur, 2000; Seeman et al., 2006). The other formation of the same receptors is D2Low. This requires an order of magnitude more dopamine to fire (Seeman et al., 2005).

The conversion between D2High and D2Low (and vice versa) is caused by the presence of an activated coupled D1 receptor. D1 is sensitive to a number of chemical agents including nicotine and a range of psychostimulants. It is also activated by inputs from 241


other neurons especially NMDA gated glutamatergic ones which are sensitive to the same stimulants (Cepeda & Levine, 2000; Novak, Seeman, & Foll, 2010; Seeman, 2010; Seeman, Guan, & Hirbec, 2009). If the D1 receptor is stimulated before the coupled D2, then the D2 receptor is in a D2Low state. In other words it is far less susceptible to stimulation. If the D1 receptor does not fire before the D2, then the state is D2High at the time it fires. It would appear that in psychosis, the D1 receptor is not properly activated, leaving an unusual amount of D2High receptors to synthesize the dopamine in the striatum.

There are a number of tell-tale signs that the D1 receptors are not properly activated in schizophrenia. In humans, the identification of receptors activation in vivo is very limited, but it has been known for some time that the axons of the human prefrontal (PFC) and anterior cingulate cortices (ACC) are particularly abundant in D1 receptors. These are 4-7 times more abundant in this region than any other receptor types and in humans more so than in any other animals (Goldman-Rakic, Castner, Svensson, Siever, & Williams, 2004; Nichols, 2010; Okubo et al., 1997). But these neurons are significantly diminished in schizophrenia when compared with controls (Akil et al., 1999; Okubo et al., 1997). The anterior dopamine pathway (the ACC and frontal cortex) is under-activated during attentive tasks in schizophrenia, relative to healthy controls and other types of psychosis (MacDonald et al., 2005). These findings consistently correlate to the negative symptoms scales of schizophrenia (See review, Goldman-Rakic et al., 2004; Javitt, 2009; Okubo et al., 1997). Another signature of under-activation of D1 receptors in schizophrenia is an overabundance of D2High heteromers. In this state, 242


the D1/D2 heteromers contain an un-activated D1 receptor. The overabundance of D2High has not been adequately measured in schizophrenic patients and controls, but in animal models of psychosis they are found to increase by 250% for amphetamine induced psychosis 180% for phencyclidine induced states and up to 900% for certain gene deletions (Seeman, 2008a).

But where do concepts of attention fit into this neurological model? I speculate that the D2Low receptors mediate bottom-up attention because they only fire occasionally (how often do we see an aberration in the environment – a tiger on the front lawn?) and because the activated D1 receptors enable the ACC and frontal areas to consider matters insightfully, as one must to understand the significance of aberrant events

25

. D2Low is

excitatory, so its reaction is stronger – perhaps strong enough to turn attention from a top-down focus to a prominent but possibly unimportant singleton. Finally D2Low draws more dopamine, so it doesn’t leave a functional oversupply in the striatum.

25

. Unfortunately, the exact dynamics of the frontal activation is complex and

unclear (Dietrich & Kanso, 2010) so here the abstract paradigm of generalized frontal activation (areas along the rostral axis from the striatum – notably the ACC and PFC) as have been shown in the majority of the studies on insight) has to be used as a proxy for a subject that cannot yet be resolved. 243


Salient cue Layer I (dendrite)

r II ye La

Striatal cell

D2 Excitation

/III

D1

Learning

Neocortical cell

Bottom-up attention

Neocortical cell

Active and top-down attention

Layer VI (axon)

D2Low configuration Salient cue Layer I (dendrite)

Striatal cell

D2

Inhibition Familiar routines

D1 D2High configuration

Figure 25: a D1/D2 heteromer in the striato-frontal pathway. Heteromers are bistable – they modulate two functional outcomes (Fuxe et al., 2010). The D1/D2 heteromer modulates sensitivity to dopamine, and is subject to change rapidly from a high affinity state (D2High) to a low one; D2Low. The transformation is triggered by external stimulation (either through direct chemical stimulation or through indirectly through interneuronal connections (Seeman, 2010)). It is hypothesized here that the D2Low configuration allows greater declarative awareness to be brought to events by engaging the frontal neocortex. This is useful for figuring things out, considering implications, developing normative stances on ideas, and other learning tasks. The D2High, on the other hand, limits the same awareness, enabling the conditions for automatic action (Dijksterhuis & van Knippenberg, 2000). 244


Consequently, the D2High receptors are probably responsible for top-down and active attention, because these modes of attention are continuous, and usually follow wellestablished routines. These are the modes of attention that are used constantly in normal life (we’re always active, playing with the sugar, seeking out something, etc.). As a result, they require less dopamine to fire, but they must fire more or less constantly. Such a pattern has been repeatedly demonstrated in animal experiments.

In-vivo studies of macaca fascicularis monkeys and a number of rat species were conducted by implanting microelectrodes directly onto the target dopamine neurons in the striatum. Regardless of species, the studies repeatedly demonstrate two ranges of dopamine firing in the striatum, in keeping with the above hypothesis. On one hand, there is the occasional phasic burst, which is activated by unexpected rewards (Grace et al., 2007); and a low level rhythmic tonic action which remains more or less active unless it is interrupted (Grace, 2000; Schultz, 1998) (see Figure 26 and Figure 27). Logically, the phasic burst must be modulated primarily by D2Low receptors because they fire only occasionally, and only when the stimulus is unexpected. The tonic action, on the other hand, fires in a continual but low amplitude rhythmic pattern (between 730hz) (Grace et al., 2007; Seamans & Durstewitz, 2008). The implication is that tonic action is modulated primarily by D2High receptors.

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1. Unexpected reward Reward 2. Conditioned reward Pavlovian Conditioning 3. Conditioned (no reward) Time (Seconds)

0 Tonic waveform

1

2

Phasic burst / tonic depression

Figure 26: In vivo studies of Pavlovian conditioning in macaca fascicularis monkeys. Here microelectrodes inserted into the axons of mesocortical dopamine neurons (Ljungberg et al., 1992) demonstrate three ranges of dopamine activity; a saliency response to an unexpected reward without Pavlovian stimulus; the tonic ‘background’ pattern and a ‘tonic depression’, or a gap in the normal tonic pattern, as seen in condition 3 when the Pavlovian response occurs, but the reward is not given, thereby appearing to tag disappointment. (Data taken from Schultz, 1998; Schultz et al., 1997)

Heinz, Romero, Gallinat, Juckel, and Weinberger (2003); Heinz and Schlagenhauf (2010) and Grace (1991); Grace et al. (2007) have noticed that both tonic and phasic dopamine activation patterns are affected by saliency, but their findings vary from paper 246


to paper. What is striking is that all their studies appear to be sound. It seems the reported inconsistent findings reflect the non-unitary nature of salience, not poor methodologies. Salience can be simultaneously increased in phasic bursting and decreased in tonic actions and vice versa, notwithstanding the interrelationships that clearly exist between the two.

There can be no doubt that tonic and phasic mechanisms are very interconnected: a) They occupy the same neural pathways and stimulate the same neurons (Schultz, 1998). They are thus only distinguishable by amplitude and oscillatory frequency (Grace, 1990, 1991). b) Whenever either receptor type fires, dopamine is generated as a response (Strange, 1992), thereby incrementally increasing the baseline levels of dopamine supply.

There are also patterns that do the opposite of phasic bursts. These are called tonic depressions. They are gaps in the otherwise regular rhythmic tonic activity, and they occur whenever a time-related event is conditioned and set to occur but doesn’t happen. This is most likely due to harmonic desychronization of α-activity (Klimesch, Doppelmayr, Russegger, Pachinger, & Schwaiger, 1998). For example in Figure 26 when the monkey in condition 1 is given an unexpected reward, there is an obvious phasic burst. In condition 2, the monkey is given a reward but only after a Pavlovian conditioning signal, which the monkey has already learned means a reward is coming next. In condition 3, the monkey is given the same signal, setting up an expectation, but the reward never appears. Instead, there is a gap in the tonic waveform exactly when the 247


reward was due (Schultz, 1998). Similar findings have been widely replicated using other methods and subjects, including humans (Grace et al., 2007).

It appears that tonic depressions are mismatch induced; meaning that tonic dopamine also occasionally processes mismatches, but only occur when they are between topdown expectations and how those expectations pan out in reality. Expectation mismatches in a top-down process cause tonic depressions (condition 3); just as positive

Awareness Low High

mismatches produce phasic bursts (condition 1) in a bottom-up process.

b f h d

a D2High

D2Low

e c g

Figure 27: Proposed features of dopamine reactions: D2High is proposed as the mediator of tonic dopamine wave patterns, and D2Low, the mediator of phasic bursting. These actions bring attention from a latent state (the grey background) to declarative awareness (white background).

It’s not known what moderates the baseline levels of declarative awareness, but being an organic phenomenon, it’s not likely to be lin248


ear. A number of studies point to α-frequency desychronization (Klimesch et al., 1998) – this is modulated both by higher cortical arousal and also by amygdala function (W. R. Perlman, Webster, Kleinman, & Weickert, 2004), thereby implicating worth-saliency in the modulation of baseline awareness.

•

Tonic dopamine firing makes low amplitude, regular (α - β frequencies).

•

Phasic bursts are irregular, stimulus induced and of high amplitude. These are gated by afferents from the glutamatergic NMDA receptors.

•

Tonic depressions are periods with no activity at all. This desychronization could be a harmonic effect of α-frequency desychronization, which also follows expectations (Klimesch et al., 1998).

•

The waxing ‘intent’ period of top-down attention.

•

The attenuation of tonic excitation.

•

The attenuation of phasic bursts. 249


•

Waxing interest – the active attention phase.

•

A body of evidence suggests that the discharge phase of dopamine activity is dependent on Ca2+ (calcium ions) (Grace, 1990; Grace et al., 2007).

Saliency and meaning: it’s all in the neurons Kapur et al. (2005, p. 61) hypothesize that ‘the normal process of context-driven novelty and salience attribution is usurped by an endogenously driven assignment of novelty and salience to stimuli… without cue or context.’ This line of thought attempts to escape the obvious fact that these saliency signals occur within specific neurons, and that they bring attention to the singletons that are associated with those neurons. It seems axiomatic that in schizophrenia there is some confusion about what is salient and what is not, but this process cannot be random as Kapur et al. suggests.

Even if aberrance is identified using an anti-Hebbian, Bayesian logic, it is still through Hebbian learning processes that the ontology is constructed; ‘Cells that fire together, wire together’ (Shatz, 1996, p. 604). If this aphorism of Hebb’s rule of neural plasticity is valid, then the connections that are stimulated by a saliency event is not random at all, but a distinct and meaningful association, even if that meaning is indecipherable to anyone but a single psychiatric patient. Meanings need not be rational for instance: they may be phonically (rhyme, alliteration etc.) associated (a phenomena known as clang or jargonaphasia), or associated through irrelevant narratives (or delusions). 250


A compelling model for how neurons are specifically associated with meanings (discussed in the section on learning on page 232 in this article) is conceptually described by Grossberg (2009) and confirmed by Feldmeyer (2010). The specifics both authors relate are somewhat different, but this is only to be expected because when analysing cells, scientists are forced to use idealized models to understand a heterogeneous reality (Gerfen et al., 1987). The concept is that the outer dendritic layer (I) of the neocortex process perceptual stimulus, whereas the inner axonal layer (VI) processes top-down associations. As these match, the arbors of the middle layers (II-III, IV, V) connect to other cells horizontally and diagonally across a distributed network (Baars, 2005). Grossberg asserts that under normal circumstances, neither top-down, nor bottom-up perceptual processes are sufficient to stimulate a recognition response in the cell, but when both top-down and bottom-up stimuli match, an event potential spreads to associated cells through the arbors.

This model is conceptualized for physical perception, but endogenous perception (identified as aberrant by Kapur et al, 2005), is no different. The phonological loop and the visuo-spatial sketchpad (the resources of endogenous perception identified by Baddeley, 2003) are hypothesized to use the same mechanics, and largely in the same areas of the brain (Grossberg & Kazerounian, 2011).

Even with the most basic level of bottom-up perception, perception requires an endogenous chemical (such as acetylcholine) or electrical signal to function as a proxy to represent an external sensation (see perception, p.223). This means that the most 251


basic divisions in perceptual processes: between bottom-up top-down or between endogenous vs. exogenous are not dissimilar. They’re only differentiated by whether they are the subject or object of observation (and this permits confusion if the sense-ofself were to unravel, as it frequently does in schizophrenia (Kean, 2009; Sass & Parnas, 2001)). The difference is relative – where the proxy for the object is processed in the cortical dendrites, whereas the subject (self-perspective and intentions) is processed in the axons.

The higher-order our awareness becomes, the more abstract. Indeed, we can even become aware of our intentions, meaning that even intentions may be regarded as a bottom-up phenomenon (dendritic stimulation), whereas, in lower-order perception, intentions are the basis of top-down (axonal) perception.

Dysfunction of the attention system: aberrant salience Both Fletcher and Frith (2009) and Howes and Kapur (2009); (Kapur, 2003; Kapur et al., 2005) agree that the upregulation of dopamine and the correlated upregulation of perceptual salience causes the positive symptoms of schizophrenia

26

. Frith didn’t

always have this view. In 1978, Frith first floated the idea that schizophrenia may be understood as a shortage of perceptual attention – a kind of cognitive blindness that

26. Technically Fletcher and Frith use a different terminology: they write of attenuation failure rather than aberrant salience, but these are the same.

252


stunts the cognitive component of perception (Frith, 1979; Joseph, Frith, & Waddington, 1979). But because an empirical basis for the hypothesis was weak and further studies only produced equivocal results, the hypothesis was subsequently withdrawn (Frith, 1987; Frith & Done, 1988). Even so, the idea continued to find support in modified hypotheses, such the neurophysiology hypothesis of schizophrenia (Gray et al., 1991) and the attention deficit model for recurrent complex visual hallucinations (Collerton et al., 2005). In keeping with Frith’s reversal, the aberrant salience hypothesis and the Bayesian attenuation failure hypothesis do not take the view that attention in schizophrenia is deficient, rather, that it is in surplus (Fletcher & Frith, 2009; Kapur, 2003). But Frith’s reversal is somewhat justified.

Distinctions between modes of attention allow for both a deficit and a surplus to coexist. This may partly explain the division in the schizophrenia diagnostic criteria, where on one hand, diagnosis by the more florid of the so-called positive symptoms (Symptoms A1: delusions, and A2: hallucinations, etc.) appear to be caused by attentional superfluity, whereas the negative signs (Symptom A5: absences of normal behaviours – akinesia etc.) appear to be caused by attentional deficits, and others such as catatonia (Symptoms A3 and A4: disorganized speech and gross disorganization) appear to be caused by both.

I propose that the core symptomatology of schizophrenia depends on Frith’s paradox. It also solves a number of other prominent riddles: schizophrenia can be understood as a functional surplus of top-down and active attention due to a presynaptic and subcortical 253


upregulation of dopamine and the simultaneous deficit of bottom-up attention because of a shortage of striato-frontal activations which would be triggered by phasic (postsynaptic) dopamine.

Because of the known reliance on glutamatergic NMDA receptors to stimulate D1 receptors (Seeman, 2008b), this model directly explains another prominent paradox. It is the problem of the glutamate hypothesis. The blockade of glutamatergic NMDA receptors (using NMDA antagonists like ketamine or phencyclidine) mimics the negative signs of schizophrenia like no other psychotropic intervention (Javitt, 2009), yet no significant losses of glutamate are found in schizophrenia (losses range from 0% to -5%) (Tamminga, Holcomb, Gao, & Lahti, 1995).

This hypothesis also solves another question that has plagued researchers for decades: the combined tonic surpluses when added to the phasic deficits would explain why striatal dopamine synthesis is found to be only moderately upregulated in schizophrenia 27

(Fusar-Poli & Meyer-Lindenberg, 2012) even though all anti-psychotics work by

reducing dopamine synthesis (Ginovart & Kapur, 2010).

27. A meta-analysis of 11 studies of dopamine synthesis capacity, covering cases of first episode chronic, and catatonic schizophrenia showed that the average upregulation of dopamine synthesis in schizophrenia was a moderate 14%, but with a telling variation – at the lowest, three datasets showed very insignificant upregulation over the normal 254


Converging evidence also points to the same finding: tonic D2 receptor activity is generally increased in schizophrenia – and to a significant level28 (d=0.79) (where 0 would mean that patients were matched to controls), yet these increases are not ubiquitous (Howes et al., 2012). The heterogeneity in the data suggests that in some cases presynaptic D2 activity is decreased – this is presumably in the aforementioned rarer presentations of catatonic schizophrenia – the condition most resistant to medication.

Finally this hypothesis will also explain why anti-psychotic medications are ineffective in about 30% of patients with schizophrenia (H. M. Jones, 2004). (Note that while this

level 0%, 0.02% and 0.05% (Av =101.3) all were for cohorts with catatonic schizophrenia. On the other end of the spectrum, upregulation reached as much as 40% in one study, but this outlier was found to be non-significant during post-hoc analysis. The other studies showed an average upregulation of 15.4% over a total of 81 cases of schizophrenia (undifferentiated by presentation), the only study looking at first episode schizophrenia exclusively, measured 18% upregulation above controls (Fusar-Poli & Meyer Lindenberg, 2012).

28. Data from a meta-analysis of SPECT and PET studies of drug-naive patients with matched controls. 255


observation lends support for the argument that schizophrenia is two syndromes (Crow, 1980). This logic is untenable because the functional surplus of striatal D2 receptors inevitably downregulates over the course of schizophrenia, and this represents a deterioration of the syndrome, not another nosology.)

To take this hypothesis further, the above outline of what (little) we know about the healthy attentional system should prove a good starting point. The next step is to drill down to the specifics of salience, to make informed predictions about what aberrant saliency should mean.

256


The emergence of symptoms

Level A

Biochemical, neuronal

Level B

Neuropsychological processes

Level C

Psychological syndromes

Level D

Behavioural symptoms and signs

Interneuronal interactions: D1-D2 heteromers Excitatory receptors Inhibitory receptors The modes of attention and combinations of: top-down attention superfluity top-down attention deficits active attention superfluity active attention deficits bottom-up attention superfluity bottom-up attention deficits Dependent systems: Perception Epistemological processes Automaticity The sense-of-self Contextual inhibition Tunnel focus Undermined automaticity Confirmation bias Hebbian degradation of the automatic ontology Positive feedback distortion Subcortical confinement Deficits in bottom-up attention Behavioural negativity DSM-IV Class A symptoms: (A1) Delusions (A2) Hallucinations (A3) Disorganized speech (e.g., frequent derailment or incoherence) (A4) Grossly disorganized or catatonic behaviour (A5) Negative symptoms, i.e., affective flattening, alogia, or avolition Class B symptom: Social/occupational dysfunction

Table 3: Translations. Linking symptoms biological dysfunctions through the modes of attention.

So far this paper has discussed the molecular biochemistry, and how it affects attention through neuronal interactions (See level A of Table 3). These interactions are then 257


linked to psychological processes; the modes of attention (top-down, bottom-up and active. See level B). The next section of the paper explores the psychological syndromes that the molecular dysfunctions, combinations of imbalances of the modes of attention and dependent cognitive processes generate (Level C). A number of important cognitive processes are directly affected including: attentional focus, perception, the ontology (epistemological processes), automaticity, the sense-of-self and contextual inhibition. Finally this hypothesis is putatively held to explain behavioural symptoms and signs of schizophrenia - the ‘constellation’ as the DSM-IV refers to it (American Psychiatric Association, 1994, pp. p. 274, 277), thereby linking the effect of molecular neurotransmission to specific symptoms (level D).

Which came first is a chicken and egg argument, and it is still difficult to say which came first. Some symptoms correlate with an up-regulation of top-down and active attention and others because of the down-regulation bottom-up processes, but at its most parsimonious, all the symptoms; positive and negative, acute or chronic and rare or common are caused by confluence of these two interdependent dysfunctions and eight interdependent but distinct syndromes this confluence causes. The patterns equate roughly to the three main schizophrenia subtypes. There is the paranoid type (295.30) which is where tunnel focus, undermined automaticity, and confirmation bias syndromes are dominant because of a surplus of striatal dopamine; there is the disorganized type (295.10) which manifests because of Hebbian degradation of the automatic ontology, positive feedback distortion and subcortical confinement syndromes. These are predominantly the combination of upregulated dopamine along 258


with bottom-up attentional deficits; and there is the catatonic type (295.20), which manifests because of bottom-up attention deficits and behavioural negativity syndromes. The psychogenesis of the catatonic type is when bottom-up attention is in severe deficit, especially when dopamine is no longer upregulated.

(Cantor-Graae, Nordström, & McNeil, 2001; Davidson & Heinrichs, 2003; Goldman, Hien, Haas, & Sweeney, 1992; J. A. McGrath et al., 2009; Parnas, Handest, Jansson, & Sæbye, 2005)

259


D,E,F B A,C A1 A2 A3 A4:

Behavioral negativity

bottom-up attention deficits

Subcortical arousal

Positive feedback distortion

Degradation of automaticity

Confirmation bias

Undermined Automaticity

Tunnel focus

Diagnostic tool

Catatonic

100% 100%

2 2

1 2

0 2

0 2

0 3

0 3

0 3

1 1

0 2

Not not better accounted for by other diagnoses (D,E, F)

100%

2

3

2

2

2

1

1

2

3

1 2 3 1 1 3 1 2 2 0 0 2 0 0

3 0 0 1 1 2 0 3 0 0 0 0 0 0

1 1 2 1 1 3 1 3 2 0 0 2 0 2

3 0 0 2 2 2 0 3 0 0 0 0 0 0

1 0 1 1 1 2 2 1 1 1 1 1 2 2

0 0 1 0 0 1 0 1 2 2 2 2 0 3

2 0 2 0 0 1 0 2 3 3 3 3 1 1

0 0 0 0 0 2 0 0 3 3 3 3 0 0

0 3 1 3

0 3 0 0

3 2 1 2

0 3 0 0

1 1 1 2

2 1 3 0

1 1 2 1

0 2 2 0

0

0

2

2

2

0

1

2

2 2 3 3 3 0 0 3 2 2 2 0 0 0 0 0 0 0

2 2 3 3 2 2 3 1 2 2 0 0 0 0 0 0 0 0

2 2 2 2 0 3 0 0 3 1 3 2 0 0 3 3 3 2

1 1 1 1 1 1 1 1 3 3 0 3 3 0 3 3 2 2

1 1 1 1 1 1 1 1 2 2 3 0 3 0 3 3 2 2

1 1 1 1 1 1 1 1 1 3 0 0 1 1 1 2 1 1

2 2 3 3 3 3 3 2 1 1 2 3 1 1 1 1 1 1

0 0 0 0 3 0 2 0 0 0 1 1 1 1 1 1 1 1

3 3 0

0 0 0

0 0 0

0 3 3

0 3 3

2 1 1

1 1 1

0 0 0

0 0 0 0 3 0 2 2 1 0 2 1 2

0 0 0 0 2 0 3 0 3 3 2 3 0

0 3 3 3 3 0 0 3 0 0 0 1 2

0 1 1 1 2 3 3 0 3 3 3 3 1

2 2 2 2 2 2 3 0 1 3 2 1 3

1 1 1 1 2 1 1 1 0 1 1 2 0

1 1 1 1 1 1 1 1 1 2 1 1 2

0 3 3 3 0 0 0 3 0 1 0 2 2

Positive Symptoms Distortions or exaggerations of inferential thinking (A1: delusions) 89% Erroneous beliefs/misinterpretation 275-276 3% Bizarre 82% Persecutory; being persecuted, followed, tricked, spied on, ridiculed. 275-276 87% Referential; environmental cues (press etc.) are directed at the patient. 275-276 78% Somatic; Loss of control over mind and body 275-276, 279 25% Grandiose or religious 55% Distortions or exaggerations of perception (A2: hallucinations) 274-275 73% Auditory 82% Two or more voices or running commentary Visual 41% Multimodal no data Monomodal no data Olfactory or gustatory 15% 15% Tactile 13% Somatic 275, 279 19% Thought insertion 21% Thought withdrawal 11% 25% Delusions of control 24% 53% Distortions of language, thought disorder (A3: disorganized speech) 274-276 76% Derailment no data Tangenitality no data loose associations to incoherence spectrum 53% Distortions behavioral monitoring (A4: grossly disorganized or catatonic behavior) 274-275 58% Childlike silliness no data Unpredictable agitation no data Difficulties in goal-directed action, Activities of Daily Living no data Deshevelled appearance no data dress in an unusual manner (e.g., wearing too much on a hot day) no data inappropriate sexual behavior (e.g., public masturbation) no data unpredictable and untriggered agitation (e.g., shouting or swearing) no data Catatonic behaviours - a marked decrease in reactivity to the environment 11% Catatonic stupor (total lack of responsiveness to environment) no data Catatonic rigidity (maintaining a rigid posture and resisting efforts to be moved) no data Catatonic negativism (active resistance to instructions or attempts to be moved) no data Catatonic posturing (the assumption of inappropriate or bizarre postures) no data Catatonic excitement (purposeless and unstimulated excessive motor activity) no data Negative Symptoms Affective flattening Alogia (manifested in brief, laconic, empty replies) Initiation of goal-directed behavior (avolition, apathy)

275, 277 275, 277 275, 277

Associated features and disorders (Unspecified, not for diagnosis) gross impairment in reality testing (loss of insight) Loss of ego boundaries Depersonalisation Derealisation Attention dysfunction (Poor concentration) Anhedonia (loss of interest or pleasure) Dysphoric mood (depression, anxiety, or anger) Disturbance to sleep patterns Lack of interest in eating as a consequence of delusional beliefs Psychomotor abnormalities (e.g., pacing, rocking, or apathetic immobility) Confusion, disorientation, memory impairment Suicide risk Comorbidity with substance abuse

980 923 152 1175 1091 1031 1103 980 1175

Notes

Reference

Minimum term of active phase Social or occupational dysfunction (Criterion B)

Sample

General criteria

Symptom

A5:

Putative explanation Disorganized

Frequency

DSM page

Paranoid

Castle etal. McGrath etal. Goldman etal. McGrath etal. McGrath etal. McGrath etal. McGrath etal. Castle etal. McGrath etal.

3,4,5 DSM-III/DIP 5 DSMIII/DSMIV 10 DSM-III DSMIII/DSMIV DSMIII/DSMIV 4 DSMIII/DSMIV DSMIII/DSMIV DSM-III/DIP DSMIII/DSMIV

1067 McGrath etal.

DSMIII/DSMIV

1079 McGrath etal. DSMIII/DSMIV 1079 McGrath etal. DSMIII/DSMIV 350 McGilchrist etal. RDS (Spritzer etal.) 1043 McGrath etal. 8,5,4 DSMIII/DSMIV 911 McGrath etal. 5,4 DSMIII/DSMIV 911 McGrath etal. 5,4 DSMIII/DSMIV 1031 McGrath etal. DSMIII/DSMIV 5,4 RDS (Spritzer etal.) 350 McGilchrist etal. 1007 McGrath etal. DSMIII & DSMIV 6 ICD-10 151 Parnas et al. 887 McGrath etal. 923 McGrath etal.

DSMIII/DSMIV DSMIII/DSMIV

1103 McGrath etal.

DSMIII/DSMIV

55% 1127 McGrath etal. 34% 923 McGrath etal. 69% 935 McGrath etal.

DSMIII/DSMIV

50% 980 75% 151 no data no data 29% 980 44% 1031 73% 980 no data no data no data no data 45% 1139 40-60% Metaanalysis

Castle etal. Parnas etal.

DSM-III/DIP 1 Unspecified

Castle etal. McGrath etal. Castle etal.

7 DSM-III/DIP DSMIII/DSMIV DSM-III/DIP

McGrath etal. Cantor-Graae etal.

DSMIII/DSMIV 9 Mixed

260


Table 4: The symptoms of schizophrenia, as listed in the DSM-IV, incidence and putative explanations. (The notes on the data appear in appendix 3, p.293). The putative explanations are detailed thus: 0=little/no importance to the pathogenesis of the symptom, 1= Possibly or somewhat involved: 2= This syndrome can be responsible for the symptom.

261


In untreated schizophrenia, there is frequently a moderate to high increase in striatal dopamine synthesis (Metadata of 11 studies show a minimum of 0% increase, a maximum of 40% and an average of 14% higher levels than healthy controls (Fusar-Poli & Meyer-Lindenberg, 2012)). This surplus can be explained by a deficit of D2Low activations, because D2Low consumes about ten times more available dopamine, so when the heteromers are switched to a high affinity mode, there will be a natural surplus of dopamine, of D2High and a deficit of D2Low. Many environmental conditions may cause this switch, including the deactivation of interconnected cortical NMDA receptors, the presence of corticosteroids or certain gene morphologies (Seeman et al., 2006). The surplus dopamine is consumed by presynaptic activations of the highly reactive D2High receptors. As these fire, they engage in the mechanisms of the striatum: the well-learned habits, schemata and routines of active attention as well as positive top-down saliency cues. Some of these naturally follow intentions. But the rest take place without any real intentions to match them against. Both create symptoms that are particularly noticeable in paranoid type schizophrenia.

Paranoid schizophrenia subtype (295.30) The following syndromes: tunnel focus, undermined automaticity and confirmation bias are all common in paranoid type schizophrenia: and these have the best overall prognosis (Deister & Marneros, 1994; Kobayashi, 2001) this is because all these syndromes maintain intent, and by doing this, a thread of meaning (however bizarre) is kept. This prevents the deterioration into the disorganized type or catatonic subtypes,

262


which occur when meaning is abandoned (see the specific subheads dealing with these subtypes on p. 267-on page 284 below).

Tunnel focus Where intentions exist, the attention they harness is intensified, especially as bottom-up distractions are weakened. This non-bizarre symptom is particularly prevalent in early and in paranoid psychosis, and whilst it is very common, is not unique to schizophrenia. Top-down superfluity creates a single but intense range or ‘tunnel focus’ of interest that defies distraction (Chadwick, 1992). The maintenance and single-mindedness of thoughts is significantly higher in schizophrenic groups than controls (Leonard et al., 2012).

Undermined automaticity As mentioned earlier, focused attention undermines automatic actions, regardless of whether the attention is bottom-up or top-down (Baumeister & Showers, 1986; Dijksterhuis & van Knippenberg, 2000; Willingham, 2001) Only active attention completely spares automatic functions. When top-down intention brings too much focus to activities, intended regular routines will become more difficult, frustrating, time consuming and prone to error (Semkovskaa, Bédard, Godboutc, Limogec, & Stip, 2004). Too much attention to functions that should be automatic, such as speech and behaviour can make them seem mildly disorganized. A phenomenal example is familiar to healthy people when trying to remember (a top-down process) a word or name that is 263


‘in the tip of the tongue’. An example is taken from a first person account: ‘… I was left with a nagging, pulling sensation in the middle of my brain…’ (Hayne & Yonge, 1997, p. 316)

Confirmation bias This syndrome occurs when surplus dopamine is consumed to register recognition saliency events. If there are any intentions, these ‘bingo,’ ‘this is important’ and ‘just as I expected’ cues will be matched up with intentions to set up a confirmation bias (Nickerson, 1998). Because Hebbian learning is not disrupted in schizophrenia (Morris, Griffiths, Le Pelley, & Weickert, 2012), patients will readily learn irrelevant associations. The results of this nonsense become part of the automatic ontology and are reinforced by Hebbian processes.

These new associations only make tunnel focus worse, because the weakest points of evidence will be enough to constitute proof. And a deficit of bottom-up attention (due to the downregulation of D2Low) means that there is a shortage of inhibitory negative feedback to keep judgments context appropriate or maintain any standards of evidence. The habit of jumping to conclusions has been found (in a meta-analysis) to occur in 4070% of studies of delusional patients (Garety & Freeman, 1999). This symptom gives rise to paranoid and grandiose delusions (A1), and when it gets severe, it can present as derailment – a particular form of disorganized speech (A3) also.

264


The over-focus on prior expectations has been found in a series of experiments that were conducted to establish where miscommunication between schizophrenic patients and others occurred. The studies (which I won’t detail) found that patients relied so heavily on prior expectations that they failed to regard obvious sensory evidence. Predictably, it was noticed, that this effect correlated strongly with the severity of the florid symptoms (Chambon et al., 2011).

Confirmation biases are also commonly reported in phenomenal accounts. Here is an example of the exaggeration of unrelated information in the formation of paranoid delusions:

‘A little girl… looked at me and then said to her mother, “Is that man possessed by the Devil Mummy?” Her mother also looked at me and replied, “Yes dear”. This coincidence just when I was thinking this very thought, was enough to “prove” to me…’ (A case of paranoid schizophrenia, in Chadwick, 1993, p. 244)

Derailment – a symptom of disorganized speech can also begin to occur due to intense tunnel focus. The following account about Phil; a patient known to have a delusion involving Stephen Hawking and bikies. This is a third person recount account of a psychiatric interview. Grace is an intern; the author is presumably a registrar:

‘So, could you, please, just tell me what’s been troubling you over the last couple of days?’ 265


Phil was slow to answer. ‘Nothing at all… They can stay out of trouble… If they’re in time.’

‘Sorry,’ Grace said. ‘When you say “They”, who do you mean? Who is it that can stay out of trouble?’

‘Bikies.’ Phil was silent for ten seconds, then finished with, ‘everyone really. Because of Stephen King.’

‘Do you mean Stephen Hawking?’ Grace asked.

‘Yes, Stephen King,’ he nodded. He paused, then continued, ‘He’ll put the bikies in another time force if they make trouble…’ (From a case of schizophreniaprobably disorganized type, in Pridmore, 2010, p. 17)

In this account, Phil’s attention has narrowed to the point that he can only focus on subjects that relate to his delusion. This is principally a symptom of tunnel focus. The questions posed by Grace are unable to steer Phil from his rut-like delusional course. An association that would normally be very loose, the relationship between Stephen King and Stephen Hawking appears to be indisputable and absolutely settled. For Phil, they are one and the same because top-down saliency cues are triggered by the phonic similarity (jargonaphasic) between the names. Here you can see the effect of a

266


confirmation bias. To anyone else, this evidence would be far from acceptable they apparently share no more than similar names and careers as famous authors.

Pridmore’s recount also gives some insight into the nature of paranoia. Paranoia, once again is a state of exceptional focus given to the unacceptable evidence of loose associations. If negative ideas are the subject of over-intense focus, these will lead to a state of paranoia, because evidence to prove that people are conspiring against you will become ubiquitous and thought patterns will inevitably lead eventually to catastrophe (D. Freeman & Freeman, 2008; D. Freeman et al., 2002; D. Freeman, Pugh, & Garety, 2008).

In some cases, positive, egoistic ideas may be overvalued, especially if bottom-up attention has not completely atrophied. This may present as grandiosity and religiosity.

Disorganized schizophrenia subtype (295.10) Because the causal mechanisms of all of these syndromes are very similar, it is difficult to perfectly distinguish one syndrome from another. Certainly this makes distinguishing the schizophrenia subtypes complex. Not all disorganized symptoms are caused by the following syndromes (as demonstrated immediately above), but the following syndromes will make disorganization the main presentation of schizophrenia.

267


Hebbian degradation of the automatic ontology Whenever there are no intentions, but there is still a surplus of dopamine and D2High, the confirmation bias will still continue, but the ‘bingo’ signals (recognition salience) will be aberrantly matched to irrelevant routines, habits, schemata and ways of thinking (hunches, superstitions, suspicions, and magical thinking patterns), instead of meaningful associations. Naturally, these will also be subject to Hebbian reinforcement. The outcome is that the quality of the ontology deteriorates, and habits will become entrenched.

Positive feedback distortion A lack of new knowledge from bottom-up channels causes experience to become increasingly stereotyped, but doesn’t mean experience is dismissed as being absurd or bizarre. On the contrary, it is taken to be highly salient because of the confirmation bias and the decline of negative feedback. The conditions that are created are exactly analogous to the Larsen effect (the bizarre positive feedback patterns that occur when an amplifier amplifies it’s own signal) (See Figure 28). This distortion amplifies stereotypical thought patterns, behaviours and even physical actions. (Even motor functions are maintained in the greater ontology (Donchin & Shadmehr, 2002)). The results are genuine thought and gross motor disorders (A3, A4). Normally there are three mechanisms to prevent this positive feedback pattern, and the D2Low channel moderates all of them. The first is the bottom-up enrichment of the ontology with new understanding. Another is that the D2Low channel balances positive feedback with 268


negative feedback – a fact-checking mechanism to ensure that perception always adequately reflects raw reality (Holroyd & Coles, 2002). The last mechanism is that the channel is inhibitory and therefore ‘gain’ (the amplification of intent) is reduced.

A classical sign of poor negative feedback processing is in addictive behaviours, particularly gambling; a gambling habit will be fed by the expectation of wins and the failure to notice losses (Fletcher & Frith, 2009). Gambling is a common co-morbidity in schizophrenia (Desai & Potenza, 2009), but it is largely mitigated by a loss of interest in profits because of the advance of avolition and anhedonia and by confusion about the process and reasons to gamble in the first instance (alogia).

As this positive feedback loop develops, the lexical ontology (speech and thought) will start to take on skewed and hermetic meanings and conventions. Nuances may well become primary meanings. Neologisms may need to be developed to explain the profoundly important but deeply personal experiences a patient has. Associations may lateralize, meaning that the associations of such irrelevancies as rhyme or meter may become more important than the traditional target concept (e.g. Rail may be taken to mean jail, simply because they rhyme) (Chaika, 1977, 1982; Chaika & Lambe, 1989). Jargonaphasia

The effects of positive feedback distortion can be seen in the Oberrealschul Student case (presented by Kraeplin):

269


‘The patient I will show you today has almost to be carried into the room, as he walks in a straddling fashion on the outside of his feet. On coming in, he throws off his slippers, sings a hymn loudly, and then cries twice (in English), “My father, my real father!…” The patient understands perfectly, and has introduced many phrases he has heard before into his speech… He speaks in an affected way’ (Spitzer, Gibbon, Skodol, Williams, & First, 2004, pp. 495-497).

Input

(+) feedback

intent

O !

Hebbian

Hebbian

O

(+) feedback

R intent & habit

R

intent

(+) feedback

Input

Input

R

Hebbian

O

AntiHebbian (-) feedback

hypothesis checking

A

Bottom-up perception

A Top-down perception

A Hallucinatory conditions

Figure 28: Raw perception (R) is ultimately our primary link with the outside world and the purpose of our ontologies (O) is to understand what raw perception is telling us about the world we live in and to make that information useful. But what we see in raw perception is mediated by what we know already: We match our perceptions with intent - what we expect to perceive. If things seem to match (✓), a positive salience cue fires and our attention (A) is brought to the fact (positive feedback). Meanwhile the saliency event enforces the expec270


tation in a Hebbian way. With well learned routines and expectations, there isn’t much need for fact checking, but bottom-up perception steps in when perception doesn’t meet expectations. It stimulates attention and excites the cognitive apparatus that is needed to identify what is wrong. This approach is inefficient, but it yields real information, and builds the ontology in a meaningful (antiHebbian) way. Hallucinatory conditions occur when new information stops enriching the positive feedback loop. Representations of reality are always lost in translation, but when perception is based on intent, and intent is based on perception, losses are compounded while the stereotypical qualities of perception are amplified. Without raw enrichment, the ontology will shrink into ever more limited repertoire of stereotypical patterns.

Subcortical confinement When D2Low receptors are really depleted, a patient may effectively loose all frontal and ACC connectivity, thereby confining their awareness to over stimulated subcortical functions.

Excitatory receptors are needed to trigger event potentials in the parts of the brain that are used to process ideas (normal arousal), and the deficit of excitatory dopaminergic receptors (D2Low) in schizophrenia means this won’t happen, especially as the ACC is further subject to the inhibitory activations of D2High. In order to enable automatic 271


actions, the main cause of awareness (the phasic surges of bottom-up attention) must be quickly inhibited. This is done through the same critical pathway – the striatal D2High receptors. When these fire, they do create a limited awareness – particularly if they follow top-down intentions, but they also limit the engagement of the higher-order cognitive areas because they are inhibitory.

Importantly, a large number of neurons are activated nevertheless, because rather than have a small amount of excitatory neurons branch laterally to activate the frontal cortex and ACC, a much larger amount of inhibitory neurons shut it down. This creates the opposite of the ‘flight of ideas,’ inflated ego, euphoria, dysphoria and other signs of expansiveness of a manic episode (American Psychiatric Association, 1994), but the large amount of activations still creates an event potential of sorts, although wholly within the striatum (Figure 29).

The striatum isn’t used for insight or to make the abstract leap from symbols to meaning. This involves higher-order areas; the ACC and areas of the frontal cortex (Dietrich & Kanso, 2010) the striatum is, however strongly implicated in automaticity and the other structural elements of thought: it is better connected to manage the welllearned routines of lexica, grammar, schemata and other procedural resources than more rostral areas are. The striatum has inputs and outputs to the sensori-motor cortex for mediating movement; the association cortex, to mediates environmental stimuli and behavioural responses; the inferior temporal visual cortex which mediate the visuospatial sketchpad of working memory; the ventral striatum (including the nucleus 272


accumbens) that receives input the amygdala and hippocampus: these modulate emotions and narratives (Rolls, 1994).

It is conceptually bizarre that awareness can shift to focus on the building blocks of thought, without awareness of meaning, because for most of us the opposite is the only way we think. For most people meaning comes first, and the means to communicate meaning, action or even thought follows automatically. But in terms of evolutionary theory, the opposite must be the case – because if people stop to consider an impending danger, they may well just get eaten (Dijksterhuis & van Knippenberg, 2000).

More than any other syndrome, this syndrome addresses the inability of severely regressed schizophrenic patients to understand other people’s thoughts, abstractions like identity and first person accounts report that even their own thoughts become unintelligible (Kean, 2009). These symptoms (classed as theory of mind (ToM) dysfunctions) are already of interest and are well known to occur in schizophrenia and autism spectra disorders. Until now, no hypothesis has been presented that makes sense of these dysfunctions (H. Gallagher & Frith, 2003). In support of this hypothesis, ToM studies universally find activations of the most anterior region of the ACC – the paracingulate cortex (H. Gallagher & Frith, 2003) or, in the case of severely regressed schizophrenia – deactivations in this region (Brune et al., 2008).

A lot can be gleaned from first person accounts into this bizarre syndrome, and so the insights from just spending dedicated time with patients is telling. Searles (an old273


school psychiatrist who sat with his patients for an hour a week, for years on end) counted dozens of other old-school therapists who discovered that schizophrenic patients were frequently unable to escape concretistic thought. And he personally observed: ‘I had worked with schizophrenic patients for several years before I came to realize that a schizophrenic individual has, subjectively, no imagination. The moment that something that we would call a new concoction of fantasy, a new product of his imagination enters his awareness, he perceives this as being actual and undistinguished from the world around him.’ (Searles, 1962, p. 37) This passage pre-empts and distils this hypothesis beautifully because it is the imagination – the ability to think abstractly that is paradigmatically so important about the ACC.

When you know what you are looking for, direct examples abound. When reading the following extract, you cannot help but be aware of the lack of meaning; despite of a cohesive logic in in linking the cross-section of associated schemata (i.e.. Metabolism → illness → distemper → cats → my cat → colour of my cat → black and white → goldfish → clown (fish) → down (rhyme)): jargonaphasia

‘…Speeds up the metabolism. Makes your life shorter. Makes your heart bong. Tranquilizes you if you've got the metabolism I have. I have distemper just like cats do, ‘cause that's what we all are. Felines [pause]. Siamese cat balls. They stand out. I had a cat, a manx, still around somewhere. You'll know him when you see him. His name is G-I Joe. He’s black and white. I had a little goldfish

274


too like a clown [pause]. Happy Halloween Down…’ (Chaika & Lambe, 1989, pp. 411-412)

Sometimes the inability to raise ones awareness from the processes and schemata that underlie thought and action are noted by patients with rare flashes of lucidity29:

‘I’m concentrating so much and trying to listen to what they are saying and I lose track of the conversation’ (Chapman, 1966, p. 237)

‘…While I was blinking at a traffic signal light, remembering in it something familiar, something which had a meaning I couldn’t recall, a wave cascaded on the beach. A physical sensation, it arose in the back of my head and drifted forward in a pleasant way, like a light gentle wash of sea froth. The waves fell, disappeared into the sands, and left on the beach a thought. I remembered suddenly the purpose of traffic signals and what the red and green lights meant.’ (B. J. Freedman, 1974, p. 336)

7. Occasional coherence indicates that schizophrenic symptoms may constantly fluctuate with availability and consumption of dopamine. 275


Synthesis of 10 DA molecules

1 x D2Low

10 x D2High

+

{

-

{

Synthesis of 10 DA molecules

Normal arousal

Activates more cells

=

More cells activated

Atypical = arousal

~

Figure 29: The subcortical confinement syndrome. D2Low is excitatory, so it excites target neurons, and D2High inhibitory, so they terminate the excitatory sequence, but D2High is about 10 times more sensitive to dopamine and therefore, 10 times more neurons will fire to synthesize the same dopamine. The result, in terms of numbers of cells activated, may be approximately equivalent, or even higher. The differences are the location of these cells and what they do. In D2Low conditions, excitation is in the ACC (and other more rostral areas), whereas in the D2High condition (being presynaptic) are situated within the striatum, with afferents to the ACC and beyond.

The catatonic subtype of schizophrenia 295.20 Dopamine isn’t always upregulated in schizophrenia. Sometimes psychotropic intervention has been effective in consuming excess dopamine, and in other cases, time has taken its toll and hyperdopaminergia has naturally settled. When this happens, the symptoms that are driven by excess dopamine will also settle and the distinct absences of normal behaviours become more obvious. But because these symptoms are caused by 276


deficits of D2Low and bottom-up attention, they are expected to underlie all cases of schizophrenia, even if they are subtle not immediately obvious alongside other more florid symptoms.

Deficits of bottom-up attention: The decrease of bottom-up attention will mean a decreased ability to notice things including attention to somatic impulses, affect and social connection. Not only are these symptoms very common in schizophrenia (Andreasen, 1985; Manscreck & Maher, 1991), it is also a feature of other psychoses including bipolar type I disorder and the dementias (American Psychiatric Association, 1994; Spitzer et al., 2004).

‘The patient sits with his eyes shut, and pays no attention to his surroundings… In the hospital he was almost dumb, was cataleptic, gave his hand stiffly and jerkily, and almost entirely refused to eat. His expression was generally indifferent, though sometimes cheerful, and visits from his relations made no impression at all on him.’ (Kraeplin, the Oberrealschul Student case. Subsequently re-diagnosed as schizophrenia - disorganised type. In Spitzer et al., 2004, pp. 495-497)

It is hard to ascertain from the third person perspective why patients like the Oberrealschul Student may have such an indifference to other people, the environment or even somatic needs (such as hunger). This inability is not because of distracting ‘noise’ as many theorists propose (eg, Corlett, Frith, & Fletcher, 2009; Heinz & 277


Schlagenhauf, 2010; Howes & Kapur, 2009; Juckel et al., 2006)(See appendix II, p. 289), but because unsought perceptions will not attract attention and therefore they must simply go unnoticed or will appear distant, unconnected or irrelevant when bottom-up attention is grossly deficient. This condition becomes so extreme that patients may fall over obvious obstacles and the instinct to block the fall may not be triggered (McDiven, 2011).

Because bottom-up attention also mediates negative feedback (Clark, 2012 - in press; Holroyd & Coles, 2002) any unsolicited feedback (from other people or from the environment or from bodily experience) will go unnoticed. Without reality testing, perceptual errors can compound, causing experience itself to diverge from the common experience of reality. Many authors speculate that this or similar ideas

30

(Collerton et

al., 2005; Friston & Frith, 1995; Grossberg, 2000, 2003b; Stephan, Friston, & Frith,

30. A related concept is the corollary discharge error (CDE) model for hallucinations, which that was first described by Feinberg (1978), and further popularized by Frith (1979- and onwards) This model claims that an individual carries a record; ‘the efference copy’ of all endogenous actions, and once actions are complete, the record is ‘discharged.’ Errors in this process are perceived as hallucinations. The problem with this model is that it attempts to explain bizarre hallucinations as if they were simple illusions, and goes no further in explaining other bizarre symptoms of schizophrenia. 278


2009) can explain hallucinations, but not for schizophrenia because schizophrenic hallucinations can become very bizarre in a very short period and this cannot be explained by lack of feedback or breakdowns in feedback processing or other similar hypotheses.

What deficiencies of negative feedback will cause, is reckless, disinhibited or otherwise antisocial behaviour to go unchecked, and this is important because it sets up a definitive symptom of schizophrenia (symptom class B) the loss of social contact. An obliviousness of social cues often results in the habit of invading other people’s personal space.

A well-known area of schizophrenia research involves testing for Mismatch negativity deficits. These are usually tests of auditory bottom-up attention. In mismatch negativity studies, a repeated sound is interrupted with an unexpected discordant sound. So a tune is interspersed with aberrant notes, etc. A meta-analysis identifies (on an average taken over 32 studies) one standard degree of deviation between bottom-up attention in schizophrenic patients against healthy controls (Keshavan, Tandon, Boutros, & Nasrallah, 2008). Interestingly, and predictably, dopamine-blocking (antipsychotic) medications don’t appear to improve this inability to notice aberrant notes (Michie, 2001).

The reason that anti-psychotics cannot be used to treat mismatch negativity deficits or any other dysfunctional bottom-up phenomena is because the blockade of dopamine 279


receptors cannot improve bottom-up attention, because bottom-up processes are mediated by D2Low receptors. As it is, this configuration of the dopamine heteromers already requires far more dopamine to fire, meaning that less available dopamine will either make no difference, and may even make this symptom worse. Although D2Low has a much lower affinity for dopamine, its affinity to known antagonists are equal (Seeman, 2008a; Seeman et al., 2006). Nicotine, on the other hand is known to stimulate both D1 and prime the NMDA gateway receptors that gate its activation (Aramakis & Metherate, 1998; Seeman, 2008a) – it could be that the comorbidity between schizophrenia and smoking is because smoking is literally self-medicating.

The bottom-up deficit syndrome will also present as a decline of emotions and the overall sense of holism. Somatogenic, affective and hedonic impulses will all recede, resulting in an affliction of disconnectedness. Patients lose awareness of basic bottomup experiences such as hunger, pain, physical discomfort, tiredness or awareness of basic and obviously disagreeable experiences; they may dress in many layers in hot weather, go naked in the cold, eat putrid food and express other signs of anhedonia, until the associated urges become overwhelming. Most of these symptoms are well observed in schizophrenia and they fall under the general diagnostic categories that best define disorganized schizophrenia: A4, gross disorganization and A5, negative or deficit signs (American Psychiatric Association, 1994).

The flattened affect that is so characteristic of schizophrenia is caused by poor somatogenic awareness also. The cliché, ‘taking time to smell the roses,’ refers to a 280


known correlation between bottom-up attention and feelings of joy. When talking of family or friends, most healthy people subtly perk up (Pridmore, 2010). But this reactivity is restricted in many cases of schizophrenia as it is in depression, although it’s rarely restricted in other psychoses (American Psychiatric Association, 1994). Again, one of the known side effects of antipsychotic medications is the progression of anhedonia (S. Williams, 2002a; Wise, 1982). This stands to reason, because, once again, if emotions were mediated by bottom-up attention, the medications that decrease dopamine supply can only make the condition worse.

When bottom-up attention is debilitated over an extended period, the deficit signs – the notable absences of normal behaviour in schizophrenia – will start to manifest. Stimulus-driven perceptions will wane; negative outcomes and other unintended percepts will be discarded. Somatoparaphrenic syndrome might ensue, where patients don’t recognize their body parts and bodily processes (Coltheart, Langdon, & McKay, 2007). Symptoms like this are distinctly bizarre, and may be classed as somatic delusions (A1) or as hallucinations (A2). The biological (somatogenic) signals that depend on bottom-up attention (hunger, tiredness etc.) will go unnoticed until they have reached extreme levels of intensity, manifesting as severe self-neglect. Examples are most obvious among schizophrenic patients who live rough (Pridmore, 2010). A metaanalysis of studies of schizophrenic homeless people suggests that about 11% of all schizophrenic patients live on the streets (Folsom & Jeste, 2002). This figure, derived largely from US data, is 11-12 times higher than the US national average (including the schizophrenic homeless). It is conceivable that this isn’t only due to gross 281


disorganization, but also because bottom-up events are so much more intense ‘in the rough’ and this could be an attempt to maintain some form of bottom-up awareness.

Behavioural negativity Many of the disorganized symptoms are hypothesized to be the product of excessive inhibition of automatic functions and routines, resulting from excesses of focal attention inhibiting them. But automaticity has a complex relationship with attention, and while low levels of attention enables automaticity, too much automaticity is an unwanted symptom.

People automatically inhibit their behaviour according to their contextual awareness or behaviour setting (see automation, p. 234). But the awareness of the behaviour setting is bottom-up, and this will be diminished in schizophrenia, bipolar disorder and some other illnesses31. Healthy people always limit their behaviour to some degree – but they tend to limit unwanted, negative behaviour completely – except where circumstances are well beyond expectations, when they will scream or flee.

8.

This symptom occurs in schizophrenia, but is more marked in bipolar psychosis

because the amygdala, the organ that monitors positivity and negativity is overactive in this disorder (S. B. Perlman et al., 2012) in this condition, negative affordances appear to trigger psychosis (Golembiewski, 2012a) whereas positive ones do not. In schizophrenia there is less distinction. 282


The kinds of negative behaviours that would be stopped in healthy people, but not in psychosis include stereotypy, perseveration, and other unwanted habits and negative routine thinking patterns. When exposed to negative stimulus, healthy controls show balanced inhibition against activation (meaning no automatic action) and far less inhibition than psychiatric patients did for positive stimuli, when the total inhibitory activations were subtracted from the excitatory ones. The resulting activation of excitatory and inhibitory neurons in each area was recorded and published (Northoff et al., 2004) and analysed, post hoc by (Golembiewski, 2012a) (see article from p.358). When patients become aware of these automatic actions, they won’t always recognize their own role in them, giving rise to non-bizarre delusions.

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Summary: Solving the aberrant salience riddle

When formulating a comprehensive hypothesis for schizophrenia, an important argument that has been raised by sceptics of schizophrenia diagnosis should be addressed: How can a singular psychogenesis be discovered for something that cannot even be defined, bearing in mind that the set of observables used for diagnosis are so broad that at some point in the past, syphilis, scurvy, pellagra and hyperthyroidism have been included (Berrios et al., 2003; Boyle, 2002; Hoffer, 1970)? Even the DSM-IV notes that the diagnostic guidelines are insufficient tools to tackle the task. To lead clinicians toward grounds for consensus, the DSM-IV stipulates a number of explicit taxonomic conditions and exclusions (criteria C-F). But this is not enough: the DSM-IV instructs ‘individuals with appropriate clinical training’ to reach beyond the categorical definitions, and to recognize the ‘constellation’ of schizophrenia features, that is, not to construct a diagnosis out of the symptoms, like ingredients in a ‘cookbook’ (American Psychiatric Association, 1994, pp. xxiii, p. 274, 277).

It is tempting to ignore this advice and deal with schizophrenia in parts. But the applicability of such hypotheses are limited to the features they address. The hypothesis presented in this paper is not intended to dismiss the others, but to follow through on their leads and selectively integrate them in a holistic way.

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In order to present an authoritative and comprehensive hypothesis for schizophrenia, this paper has addressed each diagnostic criterion within the DSM-IV. And has done so inductively, by first recognizing the ‘constellation’ of schizophrenia as instructed. In doing so, a strict adherence to the DSM-IV (American Psychiatric Association, 1994) was essential because schizophrenia is not defined by its pathology, but by the correlations between its presentation and the diagnostic criteria. Without the DSM-IV (or an equivalent protocol), a definition of schizophrenia is invalid.

By focusing in on a single set of relationships starting on a molecular level and ending in specific symptoms, this meta-hypothesis triangulates hundreds of findings against each other, against every one of the diagnostic criteria listed in the DSM-IV and against other observations that are otherwise largely held to be ubiquitous. These include many symptoms and signs that have (despite the avalanche of papers being published) hitherto remained mysterious and unexplained.

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Appendix I: The psychotic spectra continuum

The DSM-IV, currently divides delusions (A1) and hallucinations (A2) into bizarre and non-bizarre subcategories, with bizarreness currently carrying more diagnostic weight, although both occur in schizophrenia. The DSM also notes that disorganized speech (A3) can be relatively normal, provided it is not ‘severe enough to substantially impair effective communication.’ (American Psychiatric Association, 1994). This division of symptoms into bizarre and non-bizarre is likely to change next year with the release of DSM-V (Tandon & Carpenter, 2012). This is unfortunate, because the hypothesis for schizophrenia presented here explains why experience can be so bizarre in schizophrenia, but not in the continuum of psychotic experience, and therefore an important diagnostic nuance will be lost.

The psychotic continuum into healthy populations is well known (Hanssen, Bak, Bijl, Vollebergh, & van Os, 2005; Johns et al., 2004; Nuevo et al., 2012; van Os, Hanssen, Bijl, & Vollebergh, 2001; van Os, Linscotta, Myin-Germeys, Delespaula, & Krabbendam, 2009). In a meta-analysis of random interviews of the general population, a mean 3.1% report psychotic symptoms (van Os et al., 2009), but this finding is subject to enormous variance. In Nepal, for instance, 45.8% of 8822 subjects have at least one psychotic symptom (Nuevo et al., 2012). Hay (1994) reports numbers that are higher again (potentially 60% of randomly interviewed subjects) if culturally encoded religious and numinous experience is to be counted as hallucinatory or delusional – although 286


these are specifically excepted by DSM-IV criteria (Saver & Rabin, 1997). When compared with the experiences of schizophrenic patients, these numbers are low, but this is due in part to a fallacious quantification: Few people (with or without mental illness) believe that their experiences are hallucinatory or delusional, and neither are they necessarily be aware of their speech disorders. Because inductive methods (selfreporting) are typically the method used to assess psychotic spectra symptoms in the community, it’s fair to assume that the data gathering takes place while the subjects are feeling comfortable, secure, well and with their consent. In contrast, the diagnosis of symptoms during the first meeting with a clinician is going to be deductive, enforced, and generally occur at a time when a lot is at stake.

While this should be a concern for the authors of the DSM-V and for clinicians, it is mentioned here to point out that the symptoms listed in the DSM-IV as not being psychotic per sé. Delusions are extremes of belief and hallucinations employ the mechanisms of normal perception (such as the phonological loop and visuo-spatial sketchpad). It is not the presence, but the nature of the symptoms that should be a concern for clinicians, because the difference between psychotic experiences and those of the community (and also from those of other mental illnesses) are quantitative and qualitative and not absolute. In dementia with Lewy bodies for instance, hallucinations are very common, possibly more so than in schizophrenia, yet the underlying pathology is putatively with decreased dopamine synthesis (Gold, 2009). As it happens, these hallucinations are quite distinct from schizophrenic ones; they tend to be visual and are rarely threatening (Collerton et al., 2005) whereas schizophrenic patients tend to suffer a multisensory and 287


threatening hallucinations, for example, someone appears on the TV to directly abuse the patient (Chadwick, 1992). Schizophrenic delusions may be both bizarre and nonbizarre, but they are usually polythematic. The monothematic delusions common in other conditions are rare in schizophrenia. This means that schizophrenics will believe a diverse range of things (John Nash, a Nobel laureate mathematician, believed that he would become Emperor of Antarctica, that he was the left foot of God on Earth, and that his name was really Johann von Nassau), but dementia patients or patients with a cerebral lesion is more likely to have monothematic delusions like Capgras’ (the belief that a close other has been replaced by a stranger) (Coltheart et al., 2007).

Other fundamental differences in the experiences of schizophrenic vs. healthy controls are that in schizophrenia, a high proportion of hallucinations and delusions are emotionally negatively charged (Garety et al., 2001). A study by Honig et al. (1998) with 18 schizophrenic patients and 15 controls, point out that negativity is ubiquitous (100% vs. 53%), fear is very common (78% vs. 0%) and interference with daily life is also ubiquitous (100% vs. 20%). Another difference is closely related: the feeling of being out of control. All healthy subjects report that they maintain control during hallucinations, against a mere 12% of schizophrenic patients. Another qualitative difference is that half the schizophrenic patients experience voices in the third person – whereas only a quarter of healthy hallucinators report third person voices.

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Appendix II: Refuting noise theories

The DSM-IV lists ‘problems with focusing attention or distractibility due to preoccupation with internal stimuli’ a non-diagnostic associated feature of schizophrenia (American Psychiatric Association, 1994, p. 279). This informs the heuristic belief that symptoms are a product of neural noise (Fletcher & Frith, 2009; Heinz & Schlagenhauf, 2010; 2009; Rolls, Loh, Deco, & Winterer, 2008). The hypothesis presented here locates a preoccupation with internal stimuli, but rejects the notion that this is a distraction preventing focused attention. In fact distraction possibly plays no greater part in schizophrenic perception (at least for paranoid subtypes) than it does in healthy perception.

‘Noise’ hypotheses are apparently well supported by evidence, but this reflects a common flaw in experiment design and analysis and is not an inclusive picture of all available evidence (perhaps a confirmation bias?) Nearly 2000 articles report distractibility in schizophrenia, and predictably, most found a pattern of misattribution of attention to irrelevant stimuli (E.g., Martins Serra, Jones, Toone, & Gray, 2001; Moran, Owen, Crookes, Al-Uzri, & Reveley, 2008; Oades, Zimmermann, & Eggers, 1996). When questioning these findings, a similar experiment ruled out the possibility that this effect was caused by learning difficulties – only strengthening the distractibility hypotheses (Morris et al., 2012). But no studies addressed the possibility that attention given to irrelevant stimuli may have been deliberate – and caused by an admixture of 289


the feeling that no information is irrelevant and a general disinterest in being psychologically tested. Both are natural products of tunnel focus (q.v.) To clarify this issue, other experiments demonstrate that the undue attention given to distracters in the abovementioned papers may be a feature of greater focus, not greater distractibility.

Indeed, not all abilities are subject to loss in schizophrenia. While bottom-up attention tags mismatches, top-down attention tags matches, whether they are true or not. If tasks are well defined, avoid unexpected (bottom-up) challenges and complications that will require creative and insightful solutions, tasks should be easier for patients with increased top-down attention than for controls, after all, paranoid schizophrenics should be less distractible than controls. A task was given to a group of schizophrenia patients and two other control groups; a clinical control group, which included patients with bipolar, personality and severe affective disorders (some of them also showed psychotic symptoms); and another healthy control group. The task was simple: to match two patterns, where distracting fuzzy marks surrounded the target. Subjects were instructed on the task and told to ignore the distracter stimuli. In experiment test 87% of the schizophrenic cohort outperformed the best result shown by the combined controls. Meanwhile, the differences between the two other control groups were insignificant (Dakin et al., 2005). In another experiment, pairs of words were given in succession; some had no correlation, others were genuine pairs. Paranoid schizophrenic patients performed especially well at picking the pairs, particularly when the words were pertinent to paranoia (victim, killer; secret, spy). Chronic schizophrenics with no positive symptoms (catatonic subtype) performed particularly badly (Brennan & 290


Hemsley, 1984; Hemsley, 1987). Once again, those with positive symptoms maintained exceptional focus.

In a third study, schizophrenic patients outperformed controls in an experiment designed to assess and match physical force, by reciprocating the force applied by a lever. In this study, all subjects underestimated their own efforts, but schizophrenic patients underestimated by only 27.5%, whereas controls underestimated by 43.5% (Shergill, Samson, Bays, Frith, & Wolpert, 2005).

Not only do these results contradict the abovementioned distractibility studies, but these results also appear to be in conflict with widely cited studies that demonstrate deficits in attention drawn from Stroop tests and Wisconsin Card sorting tests. These tests measure a combination of top-down and bottom-up attention and cognitive ability, rather than measuring top-down attention alone. Naturally almost all the results show schizophrenic patients lagging far behind controls in performance and accuracy (Chan et al., 2010; Zihl, Gron, & Brunnauer, 1998). The Stroop test involves presenting the name of a colour (RED) in dissimilar (green) ink, and assessing performance of subjects with a battery of measures including time, accuracy and neuroimaging. The Wisconsin Card Sorting Test similarly offers a range of contradictory triggers. In this test, the patient must arrange cards, which can be sorted by any of four criteria, but with every match, there is also a mismatch. They are not instructed on a correct method, although they are told whether they are right or wrong. In other words, both tests are puzzles that assess higher-order processing (Damasio, 1994; Goldman-Rakic, 1991; Zihl et al., 1998). And 291


there is no question that higher-order functions are badly debilitated in schizophrenia (Damasio, 1994; Goldman-Rakic, 1991).

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Appendix III: Notes on data sources for table 3.

(Table 3 is on p.257)

1. The ubiquity of this symptom reflects that it is a minimum diagnostic criterion; failure to meet this means a schizophrenia diagnosis is invalid.

2. The nature of delusions typically changes in different cultural milieus (Ndetei & Vadher 1984).

3. It can be difficult to differentiate between delusions and hallucinations, because one is putatively thought to cause the other. The higher occurrence of delusions than the hallucinations that are thought to cause them may reflect the difficulty clinicians have in differentiating these symptoms.

4. It is not known how much crossover or under-reporting there is with this symptom and related symptoms (e.g. delusions with hallucinations).

5. These values are combined because it is impossible to assess these values separately (Chika, 1982).

6. How this was assessed was not reported. Several studies show better concentration among schizophrenic patients, many show worse. 293


7. This figure should not be lower than for subgroups.

8. This figure is very complex because of heterogeneity of substance, the ubiquity of abuse in the community, and cultural and other factors including increased negative automaticity and lack of negative feedback.

9. The authors found that the group with bizarre delusions was the same group that had other severe positive symptoms, and yet interrater confidence in what constituted bizarreness was not as high. For this reason the authors recommended against inclusion of this qualifier in the Opportunistic psychotic behaviour

A lot of the behaviour that is most feared by psychiatric clinical staff is opportunistic. The following two articles attempt to explain this phenomenon.

The first, ‘All common psychotic symptoms can be explained by the theory of ecological perception.’ Has been published in Medical Hypotheses, (2012: 78, 7-10. doi: 10.1016/j.mehy.2011.09.029)

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3.

QUESTION THREE: WHAT IS THE ROLE OF

THE BUILT ENVIRONMENT IN THE AETIOLOGY AND SYMPTOMS OF SCHIZOPHRENIA?

The third research question looks at aetiological issues and at symptoms, as they are an expression of and express the built environment.

If the above hypotheses and evidence aren’t enough to convince sceptics of the relationship between schizophrenia and the environment, then the following arguments may.

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Lost in Space: The role of the architectural milieu in the aetiology and treatment of schizophrenia.

In review for a special issue of Facilities,

Expected to be published in mid 2013.

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Abstract

Purpose: Psychological and epidemiological literature suggests that the built environment plays both causal and therapeutic roles in schizophrenia, but what are the implications for designers? Methodology: A translational exploration of the dynamics between the built environment and psychotic illness, using primary research from disciplines as diverse as epidemiology, neurology and psychology. Findings: The built environment is conceived as being both an agonist and as an antagonist for the underlying processes that present as psychosis. The built environment is implicated through several means: Through the opportunities it provides. These may be physical, narrative, emotional, hedonic or personal. Some opportunities may be negative, and others positive. The built environment is also an important source of unexpected aesthetic stimulation, yet in psychotic illnesses, aesthetic sensibilities characteristically suffer from deterioration. This paper focuses on the role the built environment plays in psycho-environmental dynamics, in order that negative effects can be avoided and beneficial effects emphasised in architectural design. Limitations and implications: The findings presented are based on research that is largely translated from very different fields of enquiry. Whilst findings are cogent and logical, much of the support is correlational rather than empirical. 297


Social implications: The WHO claims that schizophrenia destroys 24 million lives worldwide, with an exponential effect on human and financial capital. Because evidence implicates the built environment, architectural and urban designers may have a role to play in reducing the human costs wrought by the illness. Originality/value: Never before has architecture been so explicitly implicated as a cause of mental illness. This paper was presented to the Symposium of Mental Health Facility Design, and is essential reading for anyone involved in designing for improved mental health.

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Lost in Space: The place of the architectural milieu in the aetiology and treatment of schizophrenia.

The environment is repeatedly found to be a very significant factor in the psychogenesis of mental illnesses – especially with non-affective psychoses. This article is a theoretical discussion. It draws on the evidence that links the designed and constructed environment to psychosis – and translates this evidence in a way that helps to inform future design practice.

Mental illnesses aren’t homogenous. They share some similarities, but also have very significant differences. In some cases, interventions that promote well-being in one disorder may do the opposite in another (Pei et al., 2010). In fact, not only are mental disorders heterogeneous, the symptoms that they present are, too (American Psychiatric Association, 1994). Hallucinations, for example, range from very normal experiences through to utterly bizarre and frightening ones. Hay (1994) reports that as many as 60% of people will have experiences that could be classed as hallucinatory if religious and numinous experience were to be counted. ‘Normal’ hallucinations and those associated with dementia are often meaningful and are usually experienced in a single modality – a person may see or hear a deceased relative or angels for instance, but they rarely see and hear. Shizotypal experience, on the other hand, is far less common: it’s usually out of control, malevolent and is usually multimodal –the visual and aural experience of 299


having God appear on the TV to command them to commit suicide, for example (Chadwick & Birchwood, 1994; Golembiewski, in review-d; Honig et al., 1998).

Despite the complexity of mental illness, the current evidence available to direct design decision-making is mundane, predictable and offers little insight into the psychological and phenomenal impacts of prescribed designs. Psycho-phenomenology of design hasn’t had much attention since (Elliot & Bayes Friba, 1972; E. T. Hall, 1975, 1990; Osmond, 1958, 1966). But since then, designers haven’t kept up with the explosion of knowledge about the psychology and neurology of mental illnesses.

Other papers on the design of psychiatric design take a few distinct methodologies, and all have limitations, particularly when it comes to understanding findings. Some are based on post-occupancy studies of units that have been renovated (Eg. Hurst, 1960; Sloan Devlin, 1992; Vaaler et al., 2005). These cannot extend beyond the working principles of the design team and are further limited by the evaluation criteria of the post-occupancy assessors. Another methodology is based on expert opinions rather than identifiable empirical support (Eg. Davis, Glick, & Osow, 1979; Foley & Lacy, 1967; Gross, Sasson, Zarhy, & Zohar, 1998; Gutkowski et al., 1992; 1957, 1958, 1966).

Some researchers ask the patients when seeking design solutions. This approach is effective, with qualifications. Valid questions hover over the usefulness of patient opinions when patients are typically confused about basic reality. Also, all patient cohorts cannot be represented – the more critical patients who have ‘lost touch with reality,’ (the disorganised or catatonic type schizophrenic patients in particular) are 300


unlikely to give meaningful answers at all, whereas it may be hard to contain the opinions of patients with manic disorders. For this reason, patient questionnaires are rare. Where useful findings can be uncovered using this approach, they still lack insight into the dynamics of the environment on the syndrome’s aetiology. Instead they tend to gauge patient satisfaction with one choice or another (Middelboe, Schjødt, Byrsting, & Gjerris, 2001) (Eg. Barnhart, 1996; L. S. Larsen, 1992; Perkins, in this issue). As examples, Barnhart (1996) found that schizophrenic patients generally prefer garden settings than constructed ones and L. S. Larsen (1992) found that schizophrenic patents preferred garden settings that were extremely naturalistic, highly enclosed by shrubbery and extremely complex in contrast to controls who preferred more open gardens, less complexity and more manicured gardens.

Another approach in the literature is to inform design through models of health, illness, stress and psychosocial needs. These methods provide a welcome richness for designers because they focus on broad principles. But these methods are still limited to the specifics of the overarching models. Is a study on an Alzheimer’s unit applicable to schizophrenia for instance? The neurology, symptoms and apparent phenomenology of Alzheimer’s dementia is totally different from schizophrenia, so the applicability of Zeisel’s studies on the environments for Alzheimer’s patients (Zeisel, 2005, 2007; Zeisel & Raia, 2000; Zeisel et al., 2003) cannot be naïvely superimposed. Even so, some of the eight principles and sixteen dimensions of Alzheimer’s care of (Zeisel) remain relevant. This draws us toward another approach: the development of design principles that transcend the specifics of illnesses, and are based on models of sickness 301


and health. Examples include: Jan Golembiewski (2010b); (2012e, 2012f); S. Kaplan (1995); Lawton and Nahemow (1973), but where focusing on specific disorders may be too specific, approaches based on principles may be too generalised.

The approach taken here is not to address problem behaviour (ie. boredom, getting lost, wandering etc.) but to identify specific aspects of the built environment that appear to be aetiologically related to psychosis, so designers may understand how the built environment may actually foster or settle psychotic experience.

Background Attempts to alleviate the symptoms of schizophrenia by altering the built environment reflect widely held and well-supported hypotheses that perception is dysfunctional in schizophrenia (Fletcher & Frith, 2009; Kapur, 2003; Kapur et al., 2005; Searles, 1960). These beliefs are supported by the prevalence of hallucinations in 73% (n=980) of diagnoses (Castle et al., 2006) and by a general lack of responsiveness in others (69%, n=935 (J. A. McGrath et al., 2009)). Attempts to improve symptoms by altering environments are not uncommon but are usually guided by naïve models of perception. Changing finishes does not change the way things are perceived. A green-coloured bicycle is functionally no different from a peach-coloured one and likewise, peach or green paint on the walls of a day-room cannot change the walls in a meaningful way, even if it does make the place noticeably more cheerful to a healthy visitor. Yes, replicated evidence does suggest that interior decorations, if significant enough, may 302


improve mental health outcomes, lower vandalism rates, and shorten stays (Hurst, 1960; Sloan Devlin, 1992; Ulrich & Parsons, 1990; Vaaler et al., 2005). These outcomes are welcome, and these innovations may guide designers to make better choices, but because superficial approaches are unlikely to affect the psychogenesis that underlies psychotic states, there’s promise for much better results yet.

It’s heretical to suggest that the built environment has a causal effect on schizophrenia, but the facts are bare: when other known factors are discounted – ‘urbanicity’ at the time of birth correlates to an increase in schizophrenia incidence by 28-34.3% (above the null hypothesis) once genetic factors have been discounted (Kelly et al., 2010). Furthermore, epidemiological studies consistently point to a similar figure – assuming that all other factors are even. Data from meta-analyses suggest that urbanicity at any time of life correlates with a 48% increase in schizophrenia incidence. This number is one of the highest and most stable epidemiological factors for schizophrenia (van Os, 2004). Ultimately, this builds a compelling argument that the urban environment has a causal effect on psychotic conditions.

The idea that urbanicity is psycho-toxic has been tested, but the reasons are elusive. Ellet et al (Ellett et al., 2008) conducted ‘the Camberwell Walk Study,’ which found that even a few minutes of exposure to the urban environment has a significant negative impact on psychotic patients. A ten minute walk along the dilapidated but busy Camberwell High Street (South London) resulted in a significant effect on a battery of psychological tests, including Positive And Negative Symptoms Scores (PANSS) 303


(anxiety t (14) = –3.57 (p = 0.003); and paranoia t = –2.69 (p = 0.017, negative scores represent deterioration).

The finger points squarely at the urban environment, but what features of the environment are culpable? Is the urban environment itself a problem, or is it a proxy for something else? Can ‘urbanicity’ represent particular social mores, the prevalence of the built environment, for indoor living? For the psychic pressure of too many people? For richness of opportunity?

Attempts to identify specific environmental psycho-agonists have looked at how genetic influences are multiplied by environmental interactions (van Os, Kenis, & Rutten, 2010; van Os, Rutten, & Poulton, 2008) or social dynamics (Selten & Cantor-Graae, 2007). Collip, Myin-Germeys, and van Os (2008) suggests that the urban environment may represent a concentration of both these factors and more: an increased likelihood of exposure to whatever it is that a patient is sensitised to. This approach seems wise, but it still fails to identify anything specific. The key to identifying environmental psychoagonists (at the level of detail required by designers) is in the relationship between perception and action.

304


Ecological perception: understanding the action/behaviour expressway. Mental illnesses are not defined by pathology but by behavioural symptoms. If the symptoms aren’t disingenuous, then symptoms must be the expressions of a state of mind and reflect natural responses to perceived stimuli, whether they are hallucinatory or real. Certainly delusions (the most prevalent symptom in schizophrenia (J. A. McGrath et al., 2009)) are best understood as being very genuine expressions of a state of mind that is informed by a perceptual bias (Garety & Freeman, 1999). But how can perception be so disordered that a patient can, in all honesty, mistake people for trees or genuinely believe that the TV is broadcasting personal messages to them?

In order to understand schizophrenic experience, we must first abandon naïve models of perception. Even a lot of scientific literature makes the mistake of assuming that perception is a process where colour, shape, texture and other qualia (sensory information; colours smells etc.) are separated and recombined in the mind to form the objects of knowledge, but this is not a tenable position. We simply don’t have the computing power to recognise every perception from all available data (Clark, 2012 - in press). Certainly such a process must occur in healthy perception wherever objects are unrecognisable, but in most instances, perception is direct and active. One of the best models for understanding this kind of perception is the Ecological Theory of Perception. This theory doesn’t immediately promise all the answers to the complex questions surrounding psychotic illness, but it does provide valuable insight into phenomenology – the presumed basis for psychotic experience. The principle is that we 305


perceive ‘affordances:’ opportunities to engage and to act in well-learned or instinctive ways (Bargh & Dijksterhuis, 2001). The cue-behaviour dynamic occurs in a very mechanical way – much as a transplanted heart will automatically start thumping when exposed to warm blood. We notice (and involve ourselves with) things we can directly recognise, manipulate and use (For empirical evidence, see Gibson, 1979). Meanwhile, colours, sounds and other raw sense data are easily missed or immediately forgotten.

Superficial changes do not affect the opportunities a space provides. People act when they recognise affordances, and while colour and shape information may make an affordance more or less recognisable, people don’t act on qualia (sense information) as such. The primary task of perception is to initiate action (Bargh & Dijksterhuis, 2001; Gibson, 1979). There are different types of affordances and each has its own lexica of action-responses. Although not all are relevant to architecture as such, they all become relevant to the dynamics within the designed milieu.

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Emotional affordances

Some perceptions have direct emotional (affective) meaning. This kind of engagement is very important for humans. Humour automatically solicits laughter, friendship solicits happiness, betrayal solicits anger, and disappointment solicits resentment etc. But psychotic conditions often prevent emotional affordances from eliciting a normal range of responses. This is particularly so for those with affective psychoses such as bipolar type 1 disorder or symptoms of paranoia (note that paranoid schizophrenia is a technical term that does not necessarily denote the presence of paranoia as such (American Psychiatric Association, 1994)). In fact, symptoms can be induced by exposure to circumstances that are rich in emotional affordances.

This was found using an image study. The subjects were 17 psychotic patients (catatonic schizophrenia, n=3; akinetic type 1 bipolar disorder, n=7; paranoid schizophrenia, n=3; and type 1 bipolar 1, n=7) and ten healthy controls. All subjects had their frontal cortices scanned using functional magnetic resource (fMRI) imaging methods at the same time as they were shown a series of pictures. Some pictures were generically negative and others positive. One finding was that the psychiatric patients showed very aberrant activation and inhibition patterns when compared to the controls (Northoff et al., 2004). Another was more specific: where the healthy controls perfectly balanced their neural excitations and inhibitions in response to the negative images, the patients’ neural reactions were out of control. Aberrant excitation correlates with 307


excessive thought and activity. And where healthy controls showed some control for the positive images, the psychiatric patients showed excessive inhibition, indicating that they were unable to ‘let go’ and enjoy a healthy experience. These dysfunctional perceptual reactions appear to explain a wide range of psychotic symptoms including stereotypy and negative thinking patterns (Golembiewski, 2012a).

Emotional affordances are, by and large embodied in the social environment (including pets), but they are also to be found within the arts. The emotional affordances are the product of aesthetic qualities such as beauty and sublimity. Since antiquity beauty has been recognised as a quality of architecture (Vitrivius, circa 15BC) – although the last century has largely disposed of this legacy. Other arts, including the visual arts and music remain very important sources for emotional affordances.

HEDONIC AFFORDANCES: Anything that is known to stimulate hedonic pleasure can become a hedonic affordance. These include substances; ‘recreational’ drugs and alcohol – and behaviours; gambling, sex, and sometimes theft and violence. In the context of health facilities, violent behaviour is a significant issue, but other habitual behaviours are largely prevented through lack of opportunity.

Among healthy people, the moderation imposed by neural inhibition renders many hedonic affordances acceptable but without healthy neural inhibition, the use of hedonic stimulants becomes a mental illness in its own right, commonly known as an abuse or addiction (American Psychiatric Association, 1994; Golembiewski, in review-b).

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Physical affordances

A very common symptom of schizophrenia is that patients will drink when a glass is offered, even if they aren’t thirsty. The symptom seems innocuous, but the subsequent overconsumption of water has been associated with acutely low sodium levels and there have been published hypotheses suggesting that this may be the cause of schizophrenia (American Psychiatric Association, 1994; Reeves, 2004; Wyatt et al., 1988). While this hypothesis is simplistic and untenable, the symptom draws attention the lack of control that patients demonstrate around physical affordances. Physical compulsions are common in a range of organic neurological disorders (Lhermitte et al., 1986). The presence of a syringe solicits a jab, a gun solicits a shot and flowers solicit smelling and picking (Lhermitte, 1986). Louis Kahn also observed that building materials have intrinsic affordances: a brick wants to be built into an arch (1982).

Environments may be rich or starved of affordances. If the affordances are negative, that might be a good thing. But if people are deprived of positive affordances, not only is a beneficial opportunity lost, but the absence of positive affordances could also contribute to the pathogenesis of the illness.

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Identification affordances

Another critical area where the designed environment plays a part in schizophrenia is in the formation of the sense-of-self. There is no consensus about what creates a holistic sense-of-self; but whatever it is, one of the most alarming phenomena in schizophrenia is that the sense-of-self is lost (Kean, 2009; Sass & Parnas, 2001; Searles, 1966). Symptomatically this is classed as a bizarre delusion that is particularly characteristic of schizophrenia (American Psychiatric Association, 1994).

A number of prominent theories emphasise the effect of personal choice in the formation of a sense-of-self, although there is considerable dispute about why we make those choices (Eg. Bem, 1967; Deci & Ryan, 1991; Festinger & Carlsmith, 1959). Arguments aside, our choices are universally accepted as being important in establishing a sense-of-self. But the sense-of-self is absent when choices are automatic. You don’t choose how to bring a cup to your lip, nor do you peg your identity on this action. You don’t choose how to drive either (once these basic functions have been learned), and if you did, it would be a signal to others that the way you drive is an important expression of self. While automatic choices may define others’ impressions of you, your sense-of-self is defined by the choices you choose to make and by those you choose not to.

The designed environment is possibly the most prominent context for personal choice making, in this regard it is likely to eclipse the social environment in importance – after 310


all, the designed and constructed environment is ubiquitous, whereas the social environment comes and goes. The constructed environment can therefore be understood as being an important domain for self-expression and therefore for the establishment of a sense-of-self. Choices abound in the negotiation of the built environment and many of them are definitively associated with the sense-of-self. Many of these choices revolve around affordances. What we choose to do, given the opportunity. The major product is what we call ‘home’ (Golembiewski, 2009b).

In a diminished environment, alternatives (and therefore choices) are restricted. The choice to sit in front of the television usually has little to do with choice, if there’s nothing else to do. Television may even be harmful because it trains passivity in the face of virtual opportunities and also a sense of unlikely narrative through the storylines of television shows, and this may structurally reinforce delusional patterns of thought (see below).

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Narrative affordances

Paranoid psychotic patients (the most common subtype of the psychotic spectrum) have a predisposition (a trait, perhaps) to believe that a narrative is being constructed around them in which they are the unwitting protagonist (S. Gallagher, 2007). These delusional narratives hold that all events ultimately relate to the self. Exposure to any place with strong symbolic loadings and omens of impending disaster or evil must stimulate these delusions – and such omens will be concentrated wherever people and their symbols are concentrated: whether it be the glint in someone’s eye, an unusual concentration of police or the odd name of a street.

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Figure 30: The odd name of a street may be enough to trigger paranoid thinking - Orpheus St, on the Camberwell walk – in an area with extremely high schizophrenia incidence.

Some environments might be particularly loaded with affordances that lend themselves to delusional narratives. This was demonstrated by the Camberwell Walk Study (Ellett et al., 2008) described on page 303. Camberwell is known for its extremely high incidence of schizophrenia – as much as 9 times the incidence of areas that are nearby (Kirkbride et al., 2006). My methodology was not scientific and cannot be reported as such, but I retraced the area where the study had taken place. My route took me across 313


an Orpheus Street (Figure 30), past the Pre-Loved store (Figure 31), and went past several signs from the Black Katz real estate agent (Figure 32). In one place there was a gathering of at least thirty police. These examples are just a few of many more odd and suggestive narrative cues that I experienced in my ten-minute walk. Other notable nonverbal omens I saw included stray dogs, graffiti, pits in the street, ladders leaning over walkways, Zeus brand motorbike helmets, and ominous posters for games and superhero movies, and a number of extreme an cultish looking places of worship.

Figure 31: The Pre-loved store, Camberwell 314


Exactly what triggers a delusional quest shall not be discussed here, but once it has commenced, there’s little doubt that the urban environment will contain more salient stimuli in which emotional, physical and narrative cues are present. Without robust inhibition, these will exacerbate delusional beliefs and hallucinations (for an explanation see Golembiewski, 2012a). It has yet to be tested, but this alone seems sufficient to explain complex patterns of schizophrenia incidence, particularly the increase in urban areas as compared to rural ones. A rural lifestyle is simply going to be less symbolically loaded, more regular, and more benevolent in general.

Figure 32: Black Katz real estate agents.

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Given the richness in urban narrative subject matter, it seems that a rural setting could be beneficial for patients, simply because of the decreased concentration of these agonists. The theory that the country is healthier than the city is one that dates back two hundred and fifty years, and has taken form in some archetypal asylums: the York Retreat and the Kirkbride units that were constructed in the nineteenth Century (Yanni, 2007).

But confusingly, circumstantial evidence demonstrates that schizophrenic patients appear to be attracted to the city. Healing though the country may be, schizophrenic patients show a tendency to drift into the 24/7 red light areas of the big metropolises, where they sleep rough in doorways, traffic islands and in areas often recognised for the highest levels of substance induced violence. Psychiatric migration isn’t huge; but schizophrenic people tend to flow to the centre rather than into the more calming environments of small towns and the country. A traditional (but still current) argument links this psychiatric migration to poverty (Read, 2010). But where city centres were once cheap, the opposite is usually the case now – yet wanderers still roll in. So another hypothesis is proposed: that the frenetic action of inner city life may provide comfort, even though quietness and security comforts most other people. And although frenetic city life may indeed increase the symptoms, it may also provide relief to a particularly troubling symptom: the loss of the ability to experience anything other than troubling delusions and hallucinations. Here I suggest that psychiatric migration is based on decisions a person makes, rather than following some sort of unconscious process. But to understand how the hustle and bustle of city life might provide relief from 316


hallucinations and delusions, it’s necessary to look at another aspect of perception: this time at selective attention theory. This theory also explains another gamut of psychotic phenomenology that is relevant to designers.

Selective attention The tendency to live rough in noisy and uncomfortable places suggests that schizophrenic patients may want or need more external stimulation. As just noted, this could provide relief from relentless delusional thought patterns because it stimulates bottom-up attention, one of the two kinds of attention in the perceptual psychology canon: Bottom-up attention is drawn to all stimuli that are unexpected and unsought. The opposite, top-down attention is given to expected or intended phenomena. Affordances (discussed above) are perceived only through top-down attention. Affordances are automatic actions that follow a known pattern of behaviour. For example, a glass of water affords the familiar action of drinking. Bottom-up attention can’t trigger behaviour, as its stimuli is not yet associated with set behavioural responses. For example, we recently had a morning in Sydney where the air was red as if it had been dyed (Figure 33). Nobody knew how to respond, so instead we enquired (turning on the radio, etc). Enquiry (rather than action) is triggered by bottom-up stimuli. Thus action-responses to bottom-up perceptions aren’t automatic. Events that draw bottom-up attention beg answers, not actions. Unusual opportunities, awe and unexpected experiences are brought to attention by bottom-up processes. 317


Figure 33: In 2009 Sydney awoke to a bright red sky. Nobody seemed to know why or what it meant. People asked one another, tuned to the radio and news and invented theories. Some alarmist people suspected it was the fallout from a nuclear holocaust. Photograph credit: Manske, Magnus.

Where top-down attention is stimulated very easily and requires little stimuli, bottom-up attention requires momentous events to draw attention. These include significant mismatches with normal expectations, sudden contrasts and jolts from prominent sense data and information (Golembiewski, in review-d; Theeuwes et al., 1998). 318


Both the bottom-up and top-down modes of attention appear to be moderated by dopamine (Grace et al., 2007), a neurotransmitter that is dysfunctional in schizophrenia, Parkinson’s disease, depression and most other mental illnesses. There are two different types of dopamine dysfunction. Put simplistically, too much dopamine causes an excess of top-down attention (so called ‘positive’ symptoms of delusions, hallucinations, disorganised speech and thought and grossly disorganised behaviour (American Psychiatric Association, 1994). A deficit of dopamine (in the simplest terms) causes symptoms associated with bottom-up attention failure – the so called ‘negative’ signs such as the noticeable absences of normal behaviour that are very difficult to treat pharmacologically – such as staring blankly or catatonia (Golembiewski, in review-d). For reasons that can’t be discussed here, dopamine is sometimes in short supply in one part of the brain and in surplus elsewhere, meaning that positive symptoms and negative signs frequently present together.

What this means in schizophrenia is that prominent, awesome or unexpected things tend to go unnoticed, even when they are plainly obvious. Bottom-up attention deficits are not easy to observe as an outsider, but may be the most severe and troubling symptoms of schizophrenia and other mental illnesses. These deficits present a whole host of problems, not least of all a tendency to not to notice the glaringly obvious (Broome et al., 2007). The inability to engage with awe (even if only occasionally) is possibly sufficient to cause depression, debilitate good judgement, erode a sense of well-being and contract the perception of time, so that it always feels like it’s running out (Rudd, Vohs, & Aaker, 2012). Other bottom-up perception abilities are even more critical; the 319


ability to listen to internal messages that tell us we’re hungry, tired, happy or miserable: the signals that guide us socially and monitor whether our behaviour is appropriate or not, etc.

Deficits of bottom-up attention seem to give rise to very worrisome symptoms. Social dysfunction, isolation, hunger and confusion can all be traced to this deficit. This hypothesis proposes that schizophrenic migration to the most stimulating parts of town may occur in order to stimulate bottom-up attention. To force real feelings – to have real experience.

Facility designers should be aware that patients with bottom-up attention deficits will be especially prone to accidents – they are prone to get lost and fail to notice aesthetic concerns such as time and beauty (Golembiewski, in review-d). Reflexively designers and faculty managers may want to restrict movement and behaviour to prevent accidents and harm (See Chrysikou, - in this issue). But equally so, environments that don’t challenge bottom-up attention with opportunities for discovery or aesthetic stimulation are in danger of causing further atrophy of bottom–up attention. So a careful balance is required – improved safety measures must be balanced with aesthetic generosity, and opportunities for discovery and to act in a fulfilling and positive way (See Perkins, - in this issue). Decision makers may want uniform and bright lighting, but should be warned that variation is important, especially as it reinforces diurnal rhythms.

The combination of top-down oversensitivity and bottom-up deficiency exacerbates symptoms, especially delusions because patients overvalue unimportant, but expected 320


perceptions (Chadwick, 1992; D. Freeman & Freeman, 2008) while missing contrary facts. This phenomena, known as a confirmation bias, is very common even outside of mental illness, but in paranoid states it is ubiquitous (Broome et al., 2007; Nickerson, 1998). Most people with face-to-face experience of schizophrenic and bipolar type I patients recognise this syndrome and recall patients who may be standing there, wearing two left shoes, claiming that they have re-cognised Einstein’s theory of relativity. The patient’s claims are reinforced by top-down oversensitivity (the false ‘eureka experience’). At the same time their bottom-up deficiency makes them oblivious to the fact that they are wearing two left shoes.

Where a patient’s delusions and hallucinations are often a worry for other people, they contribute to a sense of comprehensibility for the patient themselves – at least the patient is sure about what’s going on and why (even when they’re wrong) (Bergman et al., 2012). This knowledge may not be much use to negotiate the world, but it does add to an overall sense of coherence, and that is certainly beneficial (Golembiewski, 2012e) and delusions should not be treated as a problem, but as a coping strategy when formulating a model of care (the functional program) for a facility.

Bringing the theory to praxis: the architectural milieu When discussing opportunities to address schizophrenic dysfunction with architecture, a caveat is required. Any changes to safety, security and operational systems need to reflect and parallel changes to the model of care. Furthermore, support from all 321


stakeholders should also be in place (Plsek & Wilson, 2001). There can be no doubt that security and operational features are essential for the function of a psychiatric facility and arguments against their removal will include fears that opportunities for self-harm, violence and vandalism may increase. Having said this, the possibility that safety concerns are in conflict with health issues is also real (L. Bowers, Banda, & Nijman, 2010; Chrysikou, in this issue), and in the interests of good practice, must be discussed with all stakeholders in a frank and open way. Some patients are not at risk of suicide, and others are. Patients are individuals and so are their circumstances (For a review of specific factors see L. Bowers et al., 2010). Some provisions that are essential for one patient will be detrimental for another, and as such, a diversity of spaces and provisions should be designed for. Alternatively, units should be customised for the individual conditions that they are to treat.

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Addressing bottom-up attention deficits

If bottom-up atrophy can be successfully addressed, the deficit signs of schizophrenia will definitively show improvement. As it stands, pharmacological treatment for the deficit signs is “at best modest… results have been largely disappointing” (Buckley & Stahl, 2007, p. 93). This leaves a huge onus on alternative treatments, including improved environments. But how bottom-up attention may be stimulated in a positive way without stimulating top-down attention is a difficult problem.

Converging lines of evidence suggest deficits of bottom-up attention are partly caused by the built environment, but there’s little doubt that the same symptoms diminish an architect’s toolkit to deal with it. Bottom-up attentional deficiencies mean that design features may simply go unnoticed, and if they are, top-down attentional surpluses mean that features may only be noted only because they feed on-going delusions. For example, a red feature may be noticed, not because of the prominence of the colour in the context, but because red is interpreted to mean power or some other such delusion (Reina, 2010).

Eventually a tailored in depth longitudinal study will be needed to pinpoint more specifics of causal relationships that the built environment have with schizophrenia, but evidence is already strong enough to justify assuming causality. In the same way, WHO advises caution with mobile phones because they are linked to the recent glioma epidemic, although the mechanism has not yet been identified (WHO & IARC, 2011). 323


There is still every possibility that the removal of psychosis agonists and provisions intended to counteract deficit signs will not reverse schizophrenia, but because even insubstantial environmental changes improve outcomes, a targeted and informed approach should be tested because it may yield remarkable results. Interventions may work directly or assist natural recovery.

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Aesthetic and natural engagement:

Because positive bottom-up attention is engaged by aesthetics, it follows that good, beautiful, natural and especially awe-inspiring design is likely to be restorative.

Unfortunately, there’s no easy guideline that will ensure good and beautiful results, and just about any attempt to do so will incur extra costs in construction. This objective will also prove difficult to quantify because bottom-up attention is notoriously difficult to assess (Theeuwes et al., 2000) as are aesthetics, which are subjective. The objective of aesthetic appeal in architecture has a long tradition – perhaps older than man’s ability to build. It is the third of Vitruvius’ classical qualities of good building; “firmitas, utilitas, venustas,” that is, the importance of the delight that architecture can evoke (Vitrivius, circa 15BC).

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Figure 34: Aesthetic and Natural Engagement: It’s Morning. A patient reads the paper in one of the many abundantly green spaces at Khoo Teck Puat Hospital in Singapore (designed and photographed by CPG).

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Environmental generosity

When bottom-up attention atrophies, synaptic plasticity is reduced. In other words, the interconnections between neurons are thinned, leading to difficulties with learning, spatial cognition, information and logic handling, as well as other cognitive functions that lead to dementia (Schultz & Dickinson, 2000; Stephan, Friston, et al., 2009). Similarly, a socially and materially deprived environment has also been shown to cause synaptic atrophy – at least in rats, which are easier to observe and test ethically than humans (F. Hall et al., 1998). Whether these losses occur for humans or if they are associated with the psychogenesis of mental illnesses is still unknown, but should be considered. And any positive or neutral enrichment of the environment should improve synaptic plasticity. If this proves to be the case, environmental richness will directly assist recovery – once again, this is a hypothesis that is well worth testing.

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Figure 35: Boxed for native birds are attached to trees and the walls of Roseberry Park Mental Health unit (UK) designed by Medical Architecture. Image courtesy of Medical Architecture. The intent is to make the environment more positive and more generous.

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Dealing with top-down superfluity

Another approach to take in design intervention for psychotic conditions is to enrich spaces with positive affordances. Top-down attention is a mode that is concerned only for engagement. For this reason, designers should focus on what positive activity and entertainment the space can provide and they should avoid the opposite – negativity and passive environments.

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Figure 36: A photograph of a meercat, taken from an ambulatory waiting room in The Royal Children’s Hospital in Melbourne. This room, and the ones around it look into a meercat enclosure. A good method to channel excessive top down attention positively. The Royal Children’s Hospital was designed by Billard Leece and Bates Smart. Photograph by John Gollings.

The biggest scale of architectural intervention will be at the level of typology. Typology is the classification of function according to appearance; (a house that looks like a 330


house, a bank that looks like a bank etc.) the main function of typology is information: it informs people about the nature of the place they are visiting. As Kahn puts it, “rooms suggest their use without a name” (Kahn, 1971). Strong typology simplifies understanding, orientation and way-finding (Lynch, 1992). But not all typology is equal. Typology is symbolically and phenomenologically loaded, and so sensitivity needs to be given to types that may have negative meanings. Negative typologies may include prisons, hospitals, schools, courts, psychiatric facilities, seclusion rooms and other institutional buildings (Jan Golembiewski, 2010b).

Spatial arrangement within an environment is important because it has a direct effect on how people navigate and use the space. This becomes increasingly important as skills and cognitive abilities atrophy. For best effect, space should be logical, non-repetitive and well marked with memorable objects and functions.

Opportunities for engagement also exist at a smaller scale. We don’t regularly engage in walls, and although we do constantly engage with the floor, it’s only because the ground beneath us is as ubiquitous as the prevalence of gravity. For the best part, we use the ground automatically, not as a matter of active engagement. We may be more inclined to engage in architectural elements if they offered us something more, like if they have to be negotiated in some way. Aalto had people engage with the floor by bringing it up closer to the eye level of a seated person – he created step-down living spaces. Walls would come alive with washable crayons and licence to scribble. It’s true that given a chance, some paranoid patients will use the opportunity to write threats and draw 331


obscenities. But if these expressions were easily erased, even this kind of expression may still be helpful – at least it shows engagement and is a distraction from more harmful pursuits (Golembiewski, 2012e).

We engage with objects, particularly interesting ones (is not engaging a synonym of interesting?) more than we do with basic building elements. Our bodies are designed to interact with movable objects and moving parts. Light switches, venetian blinds, knickknacks and furniture are the sorts of ordinary moving objects in the built environment that we regularly engage with. Architectural elements like these are designed for our bodies and actively invite engagement. We fill our homes, hotels and workplaces with such things – probably because they fortify mental well-being. Ironically, the few places that are stripped of physical affordances are the places that need them in abundance - prisons and psychiatric facilities - because such facilities are designed with safety as a priority over healing. This is exemplified by the overuse of anti-ligature devices - showerheads that don’t direct the water properly, doorknobs that can’t be grasped, tap-less basins, and furniture that can’t be moved because it’s blindbolted to the floor. Institutional strip-lighting is recessed and secured and blinds are often secured behind tempered glass. It is not unusual for anything that moves to be controlled remotely by nurses. The intention behind the installation of these components is clear; to restrict possible affordances for self-harm, but the result is that the affordances of the environment are restricted to an absolute minimum.

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Top-down attention (the relevant mode for the engagement in affordances) is driven by the tonic dopamine system, which is thought to be overexcited in schizophrenia (Grace et al., 2007; Heinz & Schlagenhauf, 2010). This means that psychotic patients have a stronger drive to engage than healthy people do, even though the drive may be masked by catatonic symptoms or deficit signs (Northoff et al., 2004; Sass & Parnas, 2001) The ‘irresistible’ drive to engage is demonstrated in the emotional image study detailed on page 307. In this context, the removal of physical affordances is predicted to only frustrate patients and aggravate symptoms, if not the underlying pathology of the disorder. Given the removal of positive affordances, negative intentions are likely to become only more focused. It is important to note that even healthy people start having hallucinatory and delusional experiences when all affordances are taken away (Grassian, 1983; Weckowicz, 1957). To counter this, Osmond (1957, 1958) (an experienced clinician and one of the leading authors on the subject of the design of the psychiatric milieu) recommended movable furniture, the provision of equipment to play music, to write etc. Now we should go further: design teams should actively think about the creation of positive affordances: the provision of a multisensory environment filled with relatively harmless but fun toys, sports equipment, drawing tools, opening windows, doors that have a pleasing sound when closed, adjustable lighting, heating and ventilation etc. Sensory rooms have already been found to be successful in a psychiatric milieu for engaging patients and helping to manage undesirable behaviour (McGann).

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Conclusion Ascertaining what is ‘bad’ and what is ‘good’ in an architectural context is not particularly difficult, but it’s subjective and there’s no established scientific method for such assertions. Moreover, there will always be specific exceptions for particular patients, particularly if they suffer from paranoia. In such an ambiguous context, it is dangerously seductive for designers to rely on ‘neutral’ design options. However, neutrality in the design of psychiatric facilities will only serve to amplify the negativity or positivity of the environment. On a neurological level there’s no such thing as ‘neutral’ engagement – it’s either positive or negative. Thus exactly the same ‘neutral’ affordances can be taken either way, depending on whether circumstances are judged as aversive (D. Freeman & Freeman, 2008).

The image study described on page 307 used generic emotive photographs to solicit emotional responses. Designers can also use the same methods to elicit specific emotional responses – for example, use paintings or images with generically happy themes rather than resort to the safety of artistic abstractions. Ulrich identified views of trees as positive (Ulrich, 1991; Ulrich & Parsons, 1990), and current projects that employ these concepts have been spectacularly successful (see Figure 34). The ability to engage with plants to touch them and lie under them is likely to be an even stronger positive affordance, although there is a reticence to plant trees in or around psychiatric facilities due to a risk of self-harm. Other architects have been experimenting with the inclusion of animal enclosures in their hospitals, also with wonderful feedback (Figure 35 and Figure 36). But the beneficial potential of architectural care goes far beyond 334


trees, animals and emotive pictures. All positive affordances are likely to support the recovery from all mental illnesses, where negative ones appear to make the conditions worse. There are affordances everywhere, seats to sit on, apples to eat, windows to open, books to read. Most of these are positive, but care should be taken, because potential negative associations aren’t always obvious because of superstitious and symbolic encoding (eg. the thirteenth room along a corridor) or linguistic associations (eg. the association between Lucifer and Lucite; a brand of transparent acrylic used in skylights) etc.

Any opportunities that engage in personal choice are particularly important because they will contribute to a sense-of-self. But the most elusive opportunities are those that will have the strongest beneficial effect (if any effect can be evoked at all) – sublimity and abundant beauty. The response to unintended delight is one of the most profound atrophies in schizophrenia and one, what’s more, that is currently untreatable using pharmacological interventions.

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Are diverse factors proxies for architectural influences? A case for architecture in the aetiology of schizophrenia.

This article has been submitted to Cureus.

Abstract

The last half-century of epidemiological enquiry into schizophrenia can be characterized by the search for neurological imbalances and lesions, for genetic factors. The growing consensus that these directions have failed, means there is a growing interest in psychosocial models and developmental aetiological models. Another area of recent interest is in epigenetics – the multiplication of genetic influences by environmental factors.

In the flood of data that is being produced around the schizophrenia epidemic, one of the most consistent findings is that schizophrenia is an urban syndrome. Once demographic factors have been discounted, between a quarter and a third of all incidence can still be traced to urbanicity. This prospect has been taken to threaten the psychosocial, genetic and developmental models.

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This paper explains that the environment is an inextricable factor in all the above models, and sketches out the arguments for the built environment to be considered as a valid epidemiological factor. It maps all these models and demonstrates how they appear to miss the mark.

The reason the built environment hasn’t already become a de rigueur area of epidemiological research is possibly trivial – it just doesn’t attract enough science, and lacks a hero to promote it alongside other hypotheses.

Are diverse factors proxies for architectural influences? A case for architecture in the aetiology of schizophrenia

Ever since John Snow successfully combined statistics and mapping to identify the Broad Street pump as the source of London’s cholera epidemic of 1854, attempts have been made to do the same for other illnesses. Like the Broad St. Pump study, the research of Faris and Dunham into the incidence of insanity in Chicago also found a locus of concentration – the inner city slum area (Faris & Dunham, 1939). But neither pump, nor pathogen was found. Instead, the authors pointed to various ‘breeder’ factors: race, migration status, poverty and access to sunlight. To make sure this was not a case of the ‘cum hoc ergo procter hoc’ fallacy (for confusing correlation with cause), Faris and Dunham gave evidence to counter the ‘drift effect ‘ caused by downward (affected) social mobility. They found that parents of the ‘insane’ are equally likely to inhabit the 337


slums. The possibility that upward (unaffected) social mobility out of these areas may increase concentrations was not raised for many years (H. L. Freeman & Alpert, 1986).

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Figure 37: Cholera mapping. By charting of deaths in places of residence (black marks), John Snow revealed that cholera clustered

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around the Broad Street pump in the Barbican, London, 1854. Source: Snow, J. (Rights expired).

Social environment

Cholera

Urban environment

Living environment

Pathogen

Geographic environment

Figure 38: The epidemiology of the Broad St Pump charted the urban (in this case the public infrastructure; the streets and the pump itself) and the living environment (the quarters of the deceased) in order to trace the effect of an unknown pathogen to a known illness (cholera). The mapped areas are marked here in grey, and the finding – the pathogen in black. The interplay of other factors (background) were very significant; the social and geographic environments in particular, but knowledge of the contaminated water table and the way the 340


social environment clustered around it was only made clear after the cause of the cholera was identified.

Nearly a century later, similar methods are still being used to identify similar findings, albeit with better controls for drift. But even with new methodological approaches, tighter definitions (insanity has been restrictively redefined as schizophrenia) and different cohorts, studies are still identifying lack of sunlight and social dysfunction as ‘risk factors’. The problem is that effect sizes are universally small and therefore cannot identify causality. The multifactor hypothesis attempts to explain how small effect ‘risk factors’ will compound to cause the illness (van Os et al., 2010). In some instances, factors don’t only add together, they seem to multiply.

A well-documented example is a case of multiple factors compounding together is ecogenetic (genetic x ecological factors (van Os et al., 2008)). This involves the catechol-O-methyltransferase (COMT) gene and exposure to cannabis in adolescence (age being another factor which is at once social, biological and environmental). All people have the COMT gene, which is expressed in one of three functional states: Met/Met, Val/Met and Val/Val. Whichever functional state a person inherits makes very little difference in the likelihood of developing schizophreniform disorder as an adult. When isolated, cannabis use also represents a relatively small risk factor for adult schizophreniform disorders (OR 1.13, CI 95%). But individuals with the Val/Val polymorphism were found to have a high risk factor (OR 10.9, CI 95%), if they were a cannabis user during adolescence. This contrasts to the Val/Met variation (OR 2.5, CI 341


95%) and to Met/Met individuals who showed no additional likelihood of developing the disorder (OR 1.1, CI 95%), a risk factor that was statistically insignificantly lower than the factor of cannabis alone (Caspi et al., 2005).

As the authors of the COMT x cannabis x age study (quoted above) made explicit in their findings, statistical analyses that are used to identify causal relationships are at risk of cum hoc ergo propter hoc (correlation or false cause being taken as cause) fallacies being made in the interpretation of data. To protect against epiphenomenal confounding, there is an increasing obligation to link data with biological mechanisms that are known to be active in schizophrenia; this often involves atypical morphologies of dopamine or glutamate neurons. Scientists often go further, with animal studies that inevitably produce peculiar behaviour, which is declared to be an animal equivalent of schizophrenia. The fact that there are dozens of such models, and each quite different should be alarming (Kilts, 2001; Marcotte, Pearson, & Srivastava, 2001). This allows for post-hoc strategies, where the animal model of schizophrenia is developed – apparently to prove the hypothesis. These strategies don’t disprove the hypothesis, but neither do they prove them. An example is the developmental Vitamin D Deficiency Schizophrenia animal model, which was generated apparently to justify the Vitamin D deficiency model of diagnosable schizophrenia (J. J. McGrath et al., 2010; J. J. McGrath, Saari, et al., 2004). This model manifests “abnormal motor responses to psychomimetic agents… and (b) cognitive deficits” (Eyles et al., 2009, p. S252). Attempts to reverse engineer schizophrenia in animals run the risk of complicating data with comparison fallacies; the diagnosis of human schizophrenia is subtle and great care 342


has to be taken that it is not confused with other human psychoses (American Psychiatric Association, 1994), much less with induced psychoses of other mammals – even if they are primates. Furthermore, these strategies do not protect against other fallacies such as information biases. Epidemiological mapping always contains such biases, because inclusion criteria must be chosen prior to a study being undertaken. These inclusions will be based on what is already known or suspected, and on what is readily measurable. This means that larger factors may well be ignored because they haven’t yet been considered, are difficult to control, to identify, justify or are not prone to clustering and therefore to study.

One of the most widely replicated data in schizophrenia incidence is the influence of ‘urbanicity’ in the aetiology of schizophrenia. When tested against a null hypothesis and when controlled for other known factors, meta-analyses of epidemiological data show the influence of the urban environment as place of birth turns increases the odds of developing schizophrenia significantly, and can be traced back to 28-34.3% of all cases once genetic factors have been factored out (Kelly et al., 2010). This does not have to be taken as evidence that the urban environment has an effect on schizophrenia (this assumption would be fallacious), but is definitely a robust enough finding to dismiss the automatic scepticism that abounds when this possibility is addressed. Personally, I hypothesize that the urban environment has no effect on schizophrenia, per se – but rather that it exerts a negative salutogenic influence – in other words, it fails to protect against the forces that cause schizophrenia.

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Whilst ecological effects may be able to multiply a genetic predisposition, there’s no reason to reject the possibility that all other factors may also be subject to multiplication. This is speculated to occur in a social context, for instance, where risk factors for schizophrenia such as low IQ, poor hearing or immigration status are multiplied by social discrimination (Selten & Cantor-Graae, 2007)32. There are other areas where multi-factor compounding takes place, which may be obscure because of information biases. Of these, on occasion when it has been studied, the urban landscape has consistently and evenly been shown to have a dose-dependent, raised incidence of schizophrenia (Krabbendam & van Os, 2005). This appears to be causal because urban birth and upbringing precedes the development of the disorder (Krabbendam & van Os, 2005).

The effects of many urban factors have been noted to be significant; social cohesion (Kirkbride et al., 2008; Selten & Cantor-Graae, 2007), the quality of urban fabric (Curtis, 2008), urban density (Curtis, 2008), the ethnic makeup of the area (Coid et al., 2008), the geographical location (Torrey, Mortensen, Pedersen, Wohlfahrt, & Melbye,

32

Please note that the evidence of a poor IQ is weak – a recent meta-analysis appears to

demonstrate the opposite. A high IQ (prior to the prodrome) is positively correlated to the development of the syndrome – 93% of 1007 subjects had good/fair high school results (J. A. McGrath et al., 2009). 344


2001) etc., but like genetic factors on their own, each factor has a relatively small effect size, which appears to multiply collectively in the urban milieu.

The urban environment is a melting pot for many external factors, implying that multifactor relationships take place in the urban milieu. But the living environment (home) provides the principal filter for the ecological effects of urbanicity and the factors that urbanicity draw together: society, civic services, poverty, atmosphere, geography and collective identity. The living environment is also – and possibly more importantly, the melting pot for internal factors because it is the primary milieu for self-development and for behaviour, especially during childhood, or in a depleted social network, as is usually the case in schizophrenia. These personal development factors are very difficult to measure directly, but they have already been implicated in the expression of schizophrenia (Golembiewski, 2012a) (p.358- q.v.). It remains to be seen whether ‘urbanicity’ is a proxy for the built environment – and whether the etiological influence of the urban setting may be as it is mediated by the architectures of home, or work and of other places where day-to-day life takes place.

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Genetic factors

Social environment

Personal factors

Biological factors

Living environment

Schizophrenia

Historical pathology

Urban environment

Geographic environment

Atmospheric environment

Figure 39: The multiple factors of schizophrenia epidemiology appear to come together in schizophrenia itself rather than in any identifiable epidemiologically distinct milieu. Having said this, of all the ‘pathways,’ the living environment (grey) is the most implicated because it has important relationships with the social environment, the urban environment and other epidemiologically significant factors, such as geography. The high implication of the urban environment in the incidence of schizophrenia (28-34%) may be in how closely it relates to the living environment (and not vice versa).

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Genetic factors

Social environment

Personal factors

Schizophrenia

Figure 40: Factors that are mapped for the social defeat hypothesis (Selten & Cantor-Graae, 2007) pinpoint a single psychological mechanism (social defeat). This is the product of the compounding of genetic factors (racial appearance, hearing impediments), social factors (competition) and personal factors (use of illicit drugs, low IQ10, hearing impediments).

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Genetic factors

Personal factors

Biological factors

Schizophrenia

Atmospheric environment

Figure 41: Factors that are mapped for the vitamin D hypothesis pinpoint a biological mechanism (vitamin D deficiency due to long northern European winters). They also take account of some genetics (UV reflectivity of skin) and personal factors (dietary vitamin D).

The Vitamin D hypothesis reduces many environmental variables to the supply of vitamin D at various critical points of a person’s life: specifically to availability of sunlight, the most universal supply of ultra violet-B spectrum of light (UVB), which is 348


the precursor for vitamin D synthesis. For this reason, theorists predicted that people born in the northern winters, where and when there is virtually no sun, would make them susceptible to schizophrenia later in life. The hypothesis also suggests that the high incidence of schizophrenia among immigrants from Africa and the Caribbean is because the skin colour of these immigrants is dark and therefore reflects more UVB. In addition, in the cold European climates, the reduction of UVB is compounded by the need to wear heavier clothing. Other factors that affect vitamin D supply are dietary, that is, they follow the consumption of fish and mushrooms (which is naturally high in dietary vitamin D,) but also of vitamin D supplements (Kinney et al., 2009).

There’s no doubt, these associations tend to concur with the vitamin D deficiency hypothesis once outliers are excluded. But despite the linear graphs that Kiney et al present, the relationships are nonlinear and are marked by exceptions. The exceedingly high schizophrenia clusters in North West Ireland, where the risks at (17.4/1000) are among the highest in the world, appears to be one such exception (D. Freeman, 1994; Torrey, 1987). This population is presumably largely fair skinned and has a strong fishing industry (The Irish Department of Agriculture Fisheries and Food, 2009). It is speculated that exceptions like these must be complicated by increased genetic risks of an unidentified nature (i.e.. not skin colour genes) (Torrey et al., 2001). Other secondary elaborations that are used to round up the outliers (frequently by some of the same authors) is exposure to the feline parasite, toxoplasma gondi (Kinney et al., 2009; Torrey, Bartko, & Yolken, 2012; Yolken, Dickerson, & Fuller Torrey, 2009) and poverty, which is linked to an inability to provide youngsters with supplements (Kinney 349


et al., 2009). Genetics, infections and parasites are just a few of many factors that also appear to create a predisposition for schizophrenia that have no clear relationships with vitamin D. Poverty may have a lot to do with vitamin D deficiency, but surely this is very speculative.

Architectural factors are no less fuzzy. There are many architectural factors that may affect people to predispose them to schizophrenia – these should be looked at as seriously as fish consumption, and perhaps more seriously after all, the entire schizophrenia research community is shooting in the dark when it comes to schizophrenia aetiology and we should look seriously at all factors that show high incidence rates. What about the quality and tenure of housing, workplace and facilities for leisure – what direction do buildings face? Do they collect sunlight or reject it? Is the air quality good or is it ionised or polluted? Are surfaces hard or soft? Are living places comfortable or not? There are other ecological factors too; Are these environments prone to fungal or bacterial growth? Are pets, vermin or other animals present? And the quality of interior light: does the spectrum include UV? Is it bright enough to trigger cones, or do people get by only using rod-vision? With all of these other factors, add the effects of varying amounts of daylight, of temperature and humidity, and the question of how clusters occur become very difficult to resolve.

In order to clarify whether Vitamin D deficiency is epiphenomenal or causal, Eyles et al. undertook a study of vitamin D deprived rats. The researchers took a population of pregnant rats and removed Vitamin D from their diets and the diets of their pups. The 350


researchers were careful that the lighting was balanced, (light for 12 hours/day, dark for 12 hours) but with no ultraviolet spectrum to prevent natural synthesis of Vitamin D. Other rats were kept in similar conditions, but were fed with vitamin D supplements (Eyles et al., 2009). The results of this study were impressive, with the rats developing certain key morphologies that relate to schizophrenia: these include a sensitization to glutamate antagonists; minor distortions of brain shape; increased lateral ventricle volumes; reduced differentiation; diminished expression of neurotropic factors; and peculiar behaviours that are speculated to be ‘schizophrenic like.’ But the assumption that induced rodent psychosis is equivalent to schizophrenia is difficult to support. Even human schizophrenia is not a correlate of human psychosis and findings such as ventricle size are not diagnostic criteria. Certainly they are common correlates – and may even be directly due to vitamin D deficiency, but they, like so many other correlations are tendencies that are not ubiquitous (Rosa et al., 2010). Psychosis is but one set of defining symptoms, and one that is excluded if there is no marked decrease in social function (American Psychiatric Association, 1994). The rats that were subject to this study had no noticeable social dysfunction (Eyles et al., 2009) and were therefore definitively not schizophrenic. The study is once again suggestive, but proves only that the target has somehow been missed.

The complexity of data can be read a number of ways; either that the aetiology of schizophrenia is itself complex, with multiple compounding causal factors as suggested by (Muller & Dursun, 2010; Rutten & Mill, 2009; van Os et al., 2010; van Os et al., 2008), alternatively the same variation may point be because we are close to the target, 351


but still a little way off. Surely John Snow also noticed increasing incidence of illness and death as he approached Carnaby Street (Figure 37)? Compare Figure 40 and Figure 41 with the bigger picture presented in Figure 39. High, but not absolute correlations are expected from the social environment and from biological factors, but unless they show a 1:1 correlation, the high variation appears to be the reflection of correlations, epiphenomenal and co-morbid effects. If this is the case, the aetiology of schizophrenia may still be parsimonious and singular but somewhere that hasn’t been studied properly.

The physical built environment is sufficiently complex to be such an illusive target. Just because it cannot be as easily unravelled and analysed as the human genome and it can’t be put into a lab and studied under microscopes doesn’t mean it’s not the bull’s-eye we’re all looking for.

The effect the physical environment has on human psychology is often overlooked as a causal factor. The physical environment has a powerful influence on the social milieu and also on other possible aetiological factors, including civic, geographical, demographic, personal and other ecological influences. In fact, the physical milieu has an influence on nearly every factor that has ever been targeted in the search for an aetiology of schizophrenia so far – the primary exception being genetics. This idea has been scoffed at in the past33, and to this day, receives little scientific attention. The

33

Specifically, Professor John McGrath’s answers to my question after his presentation

at the Australiasian Schizophrenia Conference in Sydney, 22-24 Sept 2010 352


reasons for this are twofold; Firstly it is difficult to control environmental conditions for human subjects and therefore difficult to study. Secondly, environmental aetiologies reach outside of the traditional domain of psychiatry and into architecture, non-clinical psychology, anthropology and sociology.

Evidence of the etiological effect of the environment is in its infancy, but already preliminary findings are no less coherent than those of alternative hypotheses – and are possibly better. My paper ‘Lost in space: The role of the architectural milieu in the aetiology and treatment of schizophrenia.’ (Q.V.) starts to show some correlations and possible mechanisms.

The statistical variables raised by the vitamin D case can be explained by the physical environment: In this model, low levels of vitamin D is an indicator of reduced exposure to the sun because of being indoors. Even in a brightly lit milieu, light through glass is filtered of most UV. The idea that vitamin D deficiency is an indicator of environmental factors supported by other data – statistical data gathered in various boroughs of South London show extreme variation in the incidence of schizophrenia. From one borough to another contiguous one, incidence may increase by several times (Kirkbride, Fearon, et al., 2007). Even accounting for ethnicity and other demographic data, the increased odds ratio remains extreme (Kirkbride et al., 2008; Kirkbride, Fearon, et al., 2007; Kirkbride et al., 2006; Kirkbride, Morgan, et al., 2007).

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The same data can be used as evidence of a completely different hypothesis. And one that makes sense of a different set of data on the epidemiology of schizophrenia. Is it possible that schizophrenia is the product of general stimulation or environmental poverty? A childhood lifestyle characterized by housing estates and run-down neighbourhoods, with overworked and stressed parents and too much babysitting by the TV. But in spite of this variation, environmental poverty, like schizophrenia, can be found even in the most salubrious homes and well-manicured suburbs, in countries where sunshine – and therefore vitamin D, is bountiful. This paper poses the question: could a vitamin D deficiency in early childhood point to a lack of sunshine, which further implies (but doesn’t mean) a lack of stimulation? This would mean that the aetiology for schizophrenia is psychological and possibly sociological, but not biological, at least in the developmental stage.

Epidemiological studies of schizophrenia find that financial poverty and schizophrenia have a close relationship, but like vitamin D, the correlation reflects an impressive tendency, but still not a one to one relationship. The studies find the children of migrants have particularly high (Beebe et al., 2005) incidence of schizophrenia in later life. The data of (J. J. McGrath et al., 2010) suggests that this may be due to maternal and neonatal Vitamin D deficiency in the ‘new country’ (Eyles et al., 2009). Whilst this is a very worthy argument, the same data may mean that the kids are brought up with little more than a TV for company and stimulation while the parents try to get ahead in their new life.

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Schizophrenia is strongly associated with poor lifestyle, but the question about whether poor lifestyle is the product of schizophrenia or predisposed people to it dates right back to Dunham and Ferris.

McGrath asks “Is it time to trial Vitamin D supplements to prevent schizophrenia?” (J. J. McGrath, 2010) To this question, the answer must surely be yes, but this doesn’t have to be at the expense of taking care that the environments in which we rear our children are rich and rewarding.

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AUTOMATIC AND OPPORTUNISTIC PSYCHOTIC BEHAVIOURS

There is a prevalent normative view that the physical stuff of existence – literally the bricks and mortar around us has little to do with mental illness. This is a leftover from Descartes, who argued that the mind and body were intrinsically separated (Bolton, 2008). My own findings refute this logic.

An important step in relating the symptomatology of mental illness to the environment is directly addressed in the following paper.

In retrospect I have one problem with this article: the principle data source I cite (Northoff et al., 2004), doesn’t differentiate between bipolar and schizophrenia when the symptoms these syndromes express are the same (i.e.. Paranoia, catatonia). Whilst this is reasonable, I regret this lack of specificity and strongly suspect that schizophrenic automatic behaviours will not reflect the same negative bias. My reason is that the identification of experience as negative is currently figured to be a product of the amygdala, and amygdala function is considerably greater in bipolar patients than in healthy controls (S. B. Perlman et al., 2012; Watson et al., 2012), whereas in schizophrenia amygdala function is reduced or unchanged (Anticevic et al., 2012). This argument is followed in (Golembiewski, 2012d) (see article from p.159 q.v.) 356


Regardless, the paper is what it is: a useful tool for heuristically understanding the relationship between the environment and psychotic conditions.

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Common psychotic symptoms can be explained by the theory of ecological perception.

Originally published in Medical Hypotheses in 2012 (78, 7-10. doi: 10.1016/j.mehy.2011.09.029).

Abstract

The symptoms of psychiatric illness are diverse, as are the causes of the illnesses that cause them. Yet, regardless of the heterogeneity of cause and presentation, a great deal of symptoms can be explained by the failure of a single perceptual function: the reprocessing of ecological perception.

It is a central tenet of the ecological theory of perception that we perceive opportunities to act. It has also been found that perception automatically causes actions and thoughts to occur unless this primary action pathway is inhibited. Inhibition allows perceptions to be reprocessed into more appropriate alternative actions and thoughts. Reprocessing of this kind takes place over the entire frontal lobe and it renders action optional. Choice about what action to take (if any) is the basis for the feeling of autonomy and ultimately for the sense-of-self. When thoughts and actions occur automatically (without choice) they appear to originate outside of the self thereby providing prima facie evidence for 358


some of the bizarre delusions that define schizophrenia such as delusional misidentification, delusions of control and Cotard’s delusion.

Automatic actions and thoughts are triggered by residual stimulation whenever reprocessing is insufficient to balance automatic excitatory cues (for whatever reason). These may not be noticed if they are neutral and therefore unimportant whereas actions and thoughts with a positive bias are desirable. Responses to negative stimulus, on the other hand, are always unwelcome, because the actions that are triggered will carry the negative bias.

Automatic thoughts may include spontaneous positive feelings of love and joy, but automatic negative thoughts and visualisations are experienced as hallucinations. Not only do these feel like they emerge from elsewhere but they carry a negative bias (they are most commonly critical, rude and are irrationally paranoid).

Automatic positive actions may include laughter and smiling and these are welcome. Automatic behaviours that carry a negative bias, however, are unwelcome and like hallucinations, occur without a sense of choice. These include crying, stereotypies, perseveration, ataxia, utilization and imitation behaviours and catatonia.

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Common psychotic symptoms can be explained by the theory of ecological perception.

INTRODUCTION Psychiatric illness may strike anywhere and in any demographic. And even though some syndromes are somewhat treatable, they are often utterly debilitating. For generations researchers and clinicians have been attempting to grapple with these syndromes. The effort is impressive, and with more than 7000 peer-reviewed articles for schizophrenia alone being published per year, (Schizophrenia Research Forum, 2011) there is no shortage of high quality empirical data. But like the data, most hypotheses relate to a small aspect of a single syndrome – a single symptom perhaps. Very few hypotheses or studies look broadly at psychiatric disorders, despite the murky boundaries between the syndromes and the reoccurrence of common symptoms in diverse conditions. Take imitation behaviour for instance. This is common in conditions as diverse as biological lesions, schizophrenia, and Alzheimer’s disease. (American Psychiatric Association, 1994; Lhermitte et al., 1986)

Psychotic disorders: The effect of unmoderated Ecological Perception

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Ecological perception

Until mirror neurons were first explained using the ecological theory of perception, (Gibson, 1979; Rizzolatti, Fabbri-Destro, & Cattaneo, 2009) the theory had no traction at all in neuroscience or medicine, even though the theory has robust support and is relatively well accepted in the field of perceptual psychology. (Bargh & Dijksterhuis, 2001) But mirror neuron theory remains a relatively isolated curiosity in medicine, where naïve belief in serial and qualia oriented perception still dominates. As long as this belief is maintained, it is hard to imagine that the Descartian divide between the studies of ‘mental’ psychotic states and ‘physical’ stereotypies will be bridged or that the overlap of symptoms of psychiatric illness will ever be understood holistically.

The ecological theory claims that perception is action. (Gibson, 1979) A person doesn’t just interpret sense-data (qualia) to compile an array of conclusions – the senses work holistically to excite or inhibit the actions and thoughts that we find ourselves continually engaged with. A ‘delicious’ smell is delicious because it invites eating. A smell is repulsive when, prior to any subsequent rationalisation, an impulse to retreat is triggered. A chair isn’t a composite of visual and tactile information; it is foremost an opportunity to sit, the colour and shape of the chair may never even register.

Evolutionarily advanced animals are able to moderate action/thought perceptions with ‘self-control,’ a secondary process that allows a person to moderate (accept or 361


transform) perception/action. The ability to choose how we react forms the basis for autonomy (as much as there is such a thing.) (Searle, 2001) Simple creatures have no such discretion. For them perception does not suggest nor demand behaviour, it is indistinguishable from behaviour. A frog has no choice but to eat a moving object of a certain size, and a barnacle has no choice but to stick to a hard surface, at which point it begins to consume its own brain. (Bargh & Dijksterhuis, 2001)

Just as a cue for action is automatic, so too is self-control, at least for animals that have a frontal lobe which is developed enough to enable self-control. (Bargh & Dijksterhuis, 2001) In healthy adults, the force of self-control opposes undesirable automatic behaviour with an equal opposite. In most cases, reprocessing is so well balanced that people will not realize when they have ‘acted’ or ‘behaved’ (refrained from action). People sometimes notice after the fact: for example when they have just swallowed the strawberry that was meant to decorate a cake. People may also recognize the impulse ‘telling’ them to jump when they reach a cliff’s edge, but equally so, they recognize the impulse to self-control: the recoil of alarm at the thought of plummeting of a cliff, or the guilty thought: ‘I couldn’t resist,’ regarding the strawberry for the cake. As Gibson points out, the ecological theory makes sense of impulses triggered by perception: “Fruit says ‘eat me’”. (Gibson, 1979, p. 140) And a cliff says, “jump!”

An ecological hypothesis for the symptoms of psychiatric disorders Because the laws of physics govern action, they should also govern ecological 362


perception because perception is active. Newton’s third law is particularly pertinent in this instance; to discharge an action/perception, an equal and opposite selfcontrol/reaction is required. Perception always triggers action, although those actions may be transformed into alternative responses. Self-control can transform inappropriate action/perception impulses into alternative thoughts, feelings, desires or actions, just as energy can be transformed.

Stimulus may be desirable (positive), neutral or undesirable (negative). And untransformed actions should reflect these qualities. A raucous positive action may be permissible in specific contexts (a party for instance). It may be tempered to meet a social milieu, but the reprocessing of a positive stimulus need only be partial. Likewise for neutral stimulus – action resulting from positive or neutral stimulation will rarely be harmful and unwanted. Negative stimulus, on the other hand, needs complete transformation, lest unwanted, unintended and unmoderated actions and thoughts occur. Although organic brain damage (particularly to the frontal lobe) may prevent reprocessing, (Lhermitte, 1983, 1986; Lhermitte et al., 1986) a Bayesian system moderated by the dopamine system (Fletcher & Frith, 2009) also appears to be in place to restrict autonomous action in emergencies, (Das et al., 2007) allowing automatic behaviour free rein. (Cowan, 2005) Because automatic processes are fast and accurate, the evolutionary purpose for this bypass function is presumably to allow much faster fight and flight instincts when needed. (Stephen Kaplan, 1992)

Unmoderated reactivity is definitively automatic, regardless of whether a patient is 363


aware of their behaviour or not. Because all unmoderated actions originate outside of the autonomous domain, they will appear to originate elsewhere. If primarily physical, unmoderated reactivity will present as stereotyped behaviours. Unmoderated thoughts are experienced as hallucinations when thoughts (internal voices) and visualisations (imagery) are experienced without the context of autonomy. The experience of continual automaticity will erode a sense-of-self, because actions are genuinely not autonomous. The primary exceptions being cases of severe frontal damage, where the sense-of-self cannot exist at all (Northoff & Bermpohl, 2004; Northoff et al., 2006), but neither can choice (Lhermitte, 1986). Aside from these extreme situations, many of the bizarre beliefs and experiences that are common among psychiatric patients, and characterise schizophrenia are related to the loss of autonomy of thought and action. (See Table 5, on p. 368.)

When automatic reactions are predominantly physical, they will be classed as catatonic (DSM-IV 295·20). When excess automaticity primarily causes misidentification of action and thought, the paranoid classification is most appropriate (DSM-IV 295·30). If automatic behaviours interfere with normal trajectories of reason or behaviour, a disorganised classification (DSM-IV 295·10) will be applied. If perceptual reprocessing is overly applied to positive stimulus, schizoaffective disorder and affective flattening may be the diagnosis (DSM-IV 295·70). Thus, one solution addresses all the primary symptoms of psychiatric disorders.

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Evidence Reprocessing of action/perception is thought to occur over the entire frontal lobe of the brain. This area is subject to decreased connectivity in schizophrenia (Das et al., 2007), and is also the primary site for the processing of creativity, choice (Dietrich & Kanso, 2010) and the sense-of-self (Northoff & Bermpohl, 2004; Northoff et al., 2006). The function of the frontal lobe in reprocessing of information is evident because whenever there is frontal damage, some degree of unusual automatic behaviour is ubiquitous. A study of fontal lesions showed that 100% eventually eventuated in imitation behaviour or a more severe disorder involving loss of autonomy (4%, n=1), (n=29). (At the time the study was conducted, there was one exception, whom presented with headaches. This patient developed imitation behaviour shortly after the study period.) (Lhermitte et al., 1986)

The reprocessing of negative stimulus was imaged by Northoff and colleagues (Northoff et al., 2004). In this study, akinetic catatonic patients (DSM-IV 295·20, n=3; bipolar 1 DSM-IV 296·54c, n=7), psychiatric patients (paranoid schizophrenia DSM-IV 295·30, n3; bipolar 1 DSM-IV 296·54, n7) and healthy controls where exposed to emotionally positive, neutral and negative stimulus in the form of pictures (from the International Affective Picture System) while undergoing fMRI scans of their entire frontal lobes. For positive and neutral stimulus, all subjects showed processing imbalances (eccentricity) where excitation (+) exceeded inhibitory reprocessing (-). For negative stimulus, however, only the psychiatric cohorts showed any eccentricity. They were all unable to balance the negative impact of the stimulus over the areas the frontal 365


lobe (the orbitofrontal, anterior cingulate, medial prefrontal, lateral prefrontal, premotor and motor cortices). In contrast, healthy controls did this nearly perfectly (variation=0·63% n=21, p