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Review in Advance first posted online on January 4, 2010. (Changes may still occur before final publication online and in print.)
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Substance Use in Adolescence and Psychosis: Clarifying the Relationship Emma Barkus and Robin M. Murray Institute of Psychiatry, King’s College London, De Crespigny Park, SE58A4 London, United Kingdom; email:
[email protected],
[email protected]
Annu. Rev. Clin. Psychol. 2010. 6:13.1–13.25
Key Words
The Annual Review of Clinical Psychology is online at clinpsy.annualreviews.org
cannabis, alcohol, stimulants, personality, psychosis, schizophrenia
This article’s doi: 10.1146/annurev.clinpsy.121208.131220 c 2010 by Annual Reviews. Copyright All rights reserved 1548-5943/10/0427-0001$20.00
Abstract Adolescence is a time of exploration of the self, and this exploration may involve the use of alcohol and drugs. Sadly, for some, adolescence also marks the first signs of a psychosis. The temporal proximity between the onset of substance use and of psychosis has been the cause of much debate. Here we review the association of alcohol, cannabis, stimulants, and other drugs with psychosis, and we conclude that the use of cannabis and the amphetamines significantly contributes to the risk of psychosis.
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Contents
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INTRODUCTION . . . . . . . . . . . . . . . . . . 13.2 ARE THE RATES OF SUBSTANCE USE HIGHER IN THOSE WITH PSYCHOSIS THAN IN THE GENERAL POPULATION? . . . . . . 13.2 WHAT IS THE DIRECTION OF THE RELATIONSHIP BETWEEN SUBSTANCE USE AND PSYCHOSIS? . . . . . . . . . . . . . . . 13.4 Alcohol Use . . . . . . . . . . . . . . . . . . . . . . . 13.4 Cannabis Use . . . . . . . . . . . . . . . . . . . . . . 13.4 Stimulants . . . . . . . . . . . . . . . . . . . . . . . . . 13.5 Substances Acting on Glutamate . . . . 13.6 PSYCHOSIS ENDOPHENOTYPES AND THE EFFECTS OF SUBSTANCE USE . . . . . . . . . . . . . . . . 13.7 ARE RISK FACTORS FOR SUBSTANCE USE THE SAME IN THOSE WITH PSYCHOSIS AS IN THE GENERAL POPULATION? . . . . . . . . . . . . . . . . . .13.11 SUBSTANCE USE AND THE PRODROME FOR PSYCHOSIS . .13.12 SUBSTANCE USE AND THE NATURE AND OUTCOME OF PSYCHOSIS . . . . . . . . . . . . . . . . . .13.12 COGNITION IN PATIENTS WHO DO AND DO NOT USE SUBSTANCES . . . . . . . . . . . . . .13.13 CONCLUSIONS . . . . . . . . . . . . . . . . . . . .13.14
INTRODUCTION
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ARE THE RATES OF SUBSTANCE USE HIGHER IN THOSE WITH PSYCHOSIS THAN IN THE GENERAL POPULATION? The risk of substance use in patients with schizophrenia was reported to be 4.6 times that of the general population in the United States (Regier et al. 1990). A large study of patients suffering their first episode of psychosis in
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Adolescence marks a period of rapid change in an individual, not only biologically but also psychologically and socially. Individuals may try on different personas in order to explore their own personality and beliefs. Part of this process may include the use of recreational substances such as alcohol, cannabis, and other illegal recreational drugs. Indeed, it seems that within Western societies, particularly in Europe, the use of alcohol and cannabis are so
widespread that their use has almost become a rite of passage for teenagers and an accepted part of adolescent and student culture (e.g., Watson et al. 2000). However, for a minority, adolescence and early adulthood also mark the emergence of mental health difficulties. Here we focus on psychotic disorders; these are a group of illnesses marked by the presence of unusual belief systems which do not conform to societal norms (delusions), hallucinations (particularly auditory), and disorders of thought and cognition. These difficulties can coexist with marked depressive or manic (affective) symptoms. The pattern of symptoms expressed leads to a variety of diagnostic labels: schizophrenia, schizophreniform psychosis, schizoaffective disorder, and psychotic disorder not specified. Already the reader will have noted that both substance use, on the one hand and the first signs of psychosis, on the other, commonly begin in late adolescence and early adult life. Whether their co-occurrence is more than just chance has attracted much attention and is the subject of the current review. We employ the term “substance use” to refer to recreational use and use it to include alcohol as well as illegal recreational drugs; the terms “dependency” and “abuse” are only used when the articles cited differentiate between these specifically defined problems. The definitions of dependency and abuse according to the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (Am. Psychiatr. Assoc. 2000), are presented in Table 1.
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Australia found that 74% of patients had a lifetime prevalence of a substance use disorder, and 62% presented with current substance use disorders at baseline (Lambert et al. 2005). Many other studies also acknowledge that rates of substance use are higher in patients with psychotic disorder both at onset and in those who have had psychotic disorders for a longer period of time (e.g., Barnett et al. 2007). The environment in which studies are performed needs to be considered when assessing elevated substance use in psychotic patients (e.g., Coulston et al. 2007). For instance, drug use is associated with increased relapse and hospitalization. Therefore, studies conducted on inpatient rather than community samples are likely to select patients in whom drug use may be especially common due to the worse course of psychosis in those who use drugs. One must also realize that the type of drugs used by psychotic patients will reflect to a considerable extent those used by the general population since patients are subject to the same social influences as the rest of the population. Such social influences determine which substances are “trendy” at a point in time, and this will influence the drugs available to patients. Alcohol is abused commonly by patients with psychosis and by the nonpsychotic population, but certain classes of substance are more frequently abused by patients with psychosis. For instance stimulants, such as amphetamine, as well as cannabis and nicotine, appear to be especially likely to be used by patients with psychotic disorders (e.g., Addington & Addington 2001, Kavanagh et al. 2004, Lambert et al. 2005). In Norway, Ringen et al. (2008) reported rates of amphetamine and cocaine use in patients with psychotic disorders that exceeded those reported in the general population by 160%. However, other drugs, such as heroin or morphine, are not reported to be used more heavily by patients with schizophrenia. Part of the explanation may be the relatively low rates of use of such drugs in the general population and therefore lack of access. Alternatively, it may be that some but not all illicit drugs
Table 1 Substance use and substance dependency in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (Am. Psychiatr. Assoc. 1994) Dependence—at least three of: Tolerance Withdrawal Increased use Cut down use Time dedicated to substance Give up alternatives Continued use despite physical/ psychological harm Abuse—at least one of: Failing responsibilities Dangerous use Contact with legal services as a result of substance Problems with friends and family
have pharmacological characteristics that may explain the association between their use and psychosis. For example, substances such as amphetamine, cannabis, and phencyclidine (PCP) have been reported to lead to psychotic-like experiences in the experimental situation. This has been taken as evidence that these substances lead to changes in neurotransmitter levels that mimic the alterations that occur in idiopathic psychosis. There is substantial literature concerned with the use of nicotine in patients with schizophrenia. Almost all studies suggest there are higher rates of smoking in patients with schizophrenia compared to the general population (e.g., Ripoll et al. 2004, Roick et al. 2007), with some reports of a similar pattern in relatives of patients with schizophrenia (e.g., Smith et al. 2008) and in those who are psychosis prone (e.g., Esterberg et al. 2007). It has been proposed that nicotine may be used in excess in these groups because of its cognitive enhancing qualities (e.g., Levin et al. 2006, Ripoll et al. 2004). However, given the attention that nicotine has already received in the literature and the fact that nicotine does not induce psychotic symptoms, we do not consider it further in this review.
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WHAT IS THE DIRECTION OF THE RELATIONSHIP BETWEEN SUBSTANCE USE AND PSYCHOSIS?
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There are at least four possible explanations for an excess use of substances in those with psychosis: (a) substance use can cause psychosis; (b) there are common risk factors for both; (c) the development of psychosis makes the development of substance use more likely; and (d ) having both mental health difficulties and substance use problems makes it more likely that an individual will come to treatment for one and therefore the other may be more likely to be detected. We discuss the evidence for these, with a particular emphasis on whether substance use can contribute to the onset of psychosis.
Alcohol Use
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In many studies, the use of alcohol and drugs is combined under the term “substance use,” but some studies do report separate rates. In Sweden, the sale of alcohol is highly controlled; in patients with schizophrenia, alcohol consumption exceeds that reported for the general population (Cantor-Graae et al. 2001). An elevated level of alcohol use in patients with schizophrenia is also reported in other studies (Sevy et al. 2001, van Mastrigt et al. 2004). However, in an Australian first episode study, an alcohol-only disorder was one of the least frequently reported disorders (Lambert et al. 2005). Roick et al. (2007) reported lower rates of daily alcohol use in German patients with schizophrenia compared to the general population; additionally, in comparison with the general population sample, a larger proportion of patients did not drink at all. Lower rates of alcohol consumption by in-patients with severe mental health problems compared with general population rates have also been reported in the United Kingdom (Bernadt et al. 1984) and in community patients with schizophrenia compared to the general population (Brown et al. 1999).
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Cannabis Use Cannabis is the most frequently used illicit drug in the world both in the general population (United Nations Report 2008) and among patients with psychotic disorders (e.g., Kavanagh et al. 2004, Mueser et al. 1990). When considering the relationship between cannabis use and psychosis, the usual difficulties exist in
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Alcohol is much more freely available and its use more socially acceptable than that of other substances. There is little evidence to implicate alcohol in initiating the onset of schizophrenia, but as its use is often associated with that of other substances, it is difficult to totally rule it out as a mediating variable in the onset of psychotic symptoms (e.g., Baeza et al. 2009). In the general U.K. adult population, alcohol is associated with a twofold-increased risk for psychotic symptoms, even after controlling for other factors such as drug use ( Johns et al. 2004). Of course, long-term heavy alcohol use can lead to brain damage (such as Korsakov’s syndrome) that can produce psychotic symptoms. However, these symptoms tend to have the hallmarks of organic psychosis, being characterized by visual hallucinations and prominent cognitive difficulties. Heavy use of alcohol at an early age may lead to changes in the brain that are reflected in alterations in cognitive performance (e.g., White & Swartzwelder 2004). But alcohol-related psychotic symptoms tend to occur in those past the traditional younger risk period for the onset of psychosis. Hambrecht & H¨afner (1996) reported that heavy alcohol use followed rather than preceded the first signs of psychosis and pointed to alcohol being used for self-medication rather than causing the onset of psychotic symptoms. Other reports indicate that patients may use alcohol to alleviate negative symptoms and encourage social interactions (e.g., Hambrecht & H¨afner 1996, Salyers & Mueser 2001); the latter would not be surprising since this is one of the main reasons for drinking in the general population.
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interpreting the literature: Are those who are psychosis prone more likely to use cannabis or, regardless of underlying predisposition, can cannabis use cause or precipitate psychotic symptoms (e.g., Barkus et al. 2006, Degenhardt & Hall 2001, McGuire et al. 1995, van Os et al. 2002)? There is no dispute that patients with established psychosis who continue to use cannabis have a worse prognosis than those who stop (e.g., Grech et al. 2005, Kovasznay et al. 1997, Linszen & van Amelsvoort 2007). Neither is there any dispute that administration of -9-THC, the major psychoactive compound in cannabis, produces a transient psychosis-like state in healthy volunteers (D’Souza et al. 2004, Morrison et al. 2009) and can also exacerbate psychotic symptoms in patients with schizophrenia, despite them being clinically stable and medicated at the time (D’Souza et al. 2005). Evidence from longitudinal epidemiological studies of general population samples indicates that cannabis use is associated with elevated risk of subsequent psychotic symptoms and illnesses including schizophrenia (Andreassen et al. 1987, Arseneault et al. 2002, van Os et al. 2002, Zammit et al. 2002). Two recent metaanalyses (Henquet et al. 2005, Moore et al. 2007) conclude that cannabis use is a contributory cause of psychotic illness. It has been suggested that those who have a vulnerability to psychosis (individuals who are psychosis prone or express high levels of schizotypy) are more likely to have psychotic-like experiences in the immediate high after smoking cannabis (Barkus et al. 2006, Barkus & Lewis 2008, Henquet et al. 2006, Stirling et al. 2008, Verdoux et al. 2003). There are also some suggestions that cannabis use in early adolescence, before the age of 15 years, may have the most significant impact on the risk for future development of a psychotic disorder (Arseneault et al. 2002). Prior to the age of 15, many neurobiological and hormonal changes are taking place. Cannabis use in this time of rapid biological change may be more likely to lead to
alterations in neurobiology that increase psychosis risk (e.g., Adriani & Laviola 2004, Viveros et al. 2005). Of course, given the high rates of cannabis use in the general population, the incidence of psychotic disorders would be much higher if cannabis use alone caused psychosis. Rather, it is suggested that cannabis use interacts with other risk factors for psychosis, such as genetic vulnerability, and other environmental factors, such as obstetric insults and various social adversities, to contribute toward psychosis onset (Arseneault et al. 2004, Fergusson et al. 2006, Henquet et al. 2008, Semple et al. 2005).
Stimulants Curran et al. (2004) reviewed experimental and longitudinal studies concerned with stimulants and concluded there was evidence (a) that their use could lead to a transient psychotic state and exacerbate psychotic symptoms in medicated patients with schizophrenia (regardless of medication status), and (b) that individuals may become sensitized to the psychotomimetic effects of stimulants. Connell’s (1958) monograph provided evidence suggesting chronic use of amphetamine can induce a state that mimics paranoid schizophrenia. The ability of amphetamine to induce psychotic symptoms has also been shown in experimental studies (e.g., Featherstone et al. 2007, Hermens et al. 2009). Amphetamine increases striatal dopamine release in healthy volunteers, and patients with schizophrenia are more sensitive to these effects (e.g., Laruelle & Abi-Dargham 1999, Laruelle et al. 1996, Martinez et al. 2003). There is also limited evidence from longitudinal studies for amphetamine use predicting the onset of psychosis later in life (Andreassen et al. 1987, Zammit et al. 2002). However, given the relatively low rates of amphetamine use in the general population, it is difficult to determine the risk for psychotic disorders attributable to amphetamine use. Methamphetamine is a more potent form of amphetamine, and like amphetamine, it is
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used recreationally. Its use has been epidemic in Pacific countries such as Japan, Taiwan, and Thailand for many years (e.g., Ujike & Sato 2004). In the past decade, it has spread to the west coast of North America and is slowly moving east (Caulkins 2003, Jacobs 2002, Morgan 1998, Rawson et al. 2002), particularly in the homosexual community (Freese et al. 2002, Morgan & Beck 1997). Rates of methamphetamine dependency in the U.S. general population, aged 12 years and above, increased dramatically between 2002 and 2004 (NSDUH Report 2005). Its use can induce a psychotic state, and chronic use can lead to a picture almost identical to that of paranoid schizophrenia (Chen et al. 2003, 2005; McKetin et al. 2006). However, again there is evidence that the risk of psychotic illness is particularly high in those with a family history of the disorder and/or pre-existing schizoid and schizotypal personality (Chen et al. 2003, 2005). In recreational use, cocaine induces a confident and euphoric state. However, this can be accompanied by agitation that leads to paranoia; persistent use can lead to more florid psychotic symptoms (Mahoney et al. 2008). Although cocaine has been reported to be used in excess in some studies of patients with schizophrenia (e.g., Ringen et al. 2008), the Swedish Army study failed to find evidence that cocaine use confers a risk for the development of a chronic psychotic disorder (Andreassen et al. 1987, Zammit et al. 2002). Khat is a plant substance that has been used primarily in Africa and Arabian countries, although it is now also used in the United Kingdom and elsewhere by migrant workers. Khat contains an amphetamine-like substance (see Feyissa & Kelly 2008 for a review). Odenwald (2007) has reviewed evidence for its relationship with psychotic disorders. Although there were very few systematic studies, Odenwald felt there was sufficient evidence to suggest it can induce transient psychotic episodes and that those with an underlying predisposition to psychosis are more vulnerable to these effects. Ecstasy has a primary effect on serotonin but also interacts with the dopamine system (e.g.,
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Substances Acting on Glutamate In acute studies, ketamine is said to produce positive as well as negative symptoms of psychosis (e.g., Curran & Morgan 2000, Muetzelfeldt et al. 2008, Pomarol-Clotet et al. 2006), and these effects have been used to support a glutamatergic model of psychosis (e.g., Deakin et al. 2008, Stone et al. 2008). A number of studies have reported on the use of ketamine as a recreational drug, but to date there are no follow-up studies examining the risk of developing a psychotic disorder after recreational ketamine use. This may be owing to the relatively low rates of ketamine use in the general population, but the lack of such studies does seem an oversight given the frequency with which ketamine is cited as an experimental model of psychosis. Phencyclidine (PCP) was a popular recreational drug in certain parts of the United States during the 1980s and early 1990s, but it is not frequently taken today. However, PCP is frequently used as an animal model of psychosis and is thought to represent a model of the glutamatergic alterations that may take place prior to the onset of a psychotic disorder (e.g., Jentsch & Roth 1999, Mouri et al. 2007). In humans, PCP can induce a transient psychotic disorder that responds well to typical antipsychotic treatment (Carls & Ruehter 2006). In their summary of the effects of PCP, Jentsch & Roth (1999) consider that repeated (rather than acute) administrations of PCP produce a more accurate
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Steele et al. 1994). Reports have indicated that ecstasy can lead to psychotic symptoms either transiently or perhaps contributing to the onset of a psychotic disorder (e.g., McGuire & Fahy 1991, McGuire et al. 1994). However, given the small number of reported cases, this must be a rare event considering its widespread use in the rave and dance culture of the 1990s. A few reports suggest that the negative effects of ecstasy use on cognitive performance may be dependent upon the age of age exposure; i.e., use at a younger age is associated with worse outcome (Broening et al. 1994).
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behavioral and neurobiological model of psychosis.
Interest in establishing markers that are present prior to the onset of psychosis and that may be targets for treatment has increased recent work that attempts to identify objectively measurable risk markers for psychosis. The complexity of the genetic predisposition to psychiatric disorders has also led to resurgence in identifying endophenotypes. Endophenotypes are linked with the underlying vulnerability for the psychiatric condition and are generally thought to be nearer the action of genes than of symptoms. Gottesman & Gould (2003) have established criteria for an endophenotype. It should (a) cooccur with the illness in the general population; (b) co-occur with the illness within families; (c) be heritable; (d ) be present regardless of fluctuations in illness; and (e) be present in higher rates in relatives of those with the illness. These criteria demonstrate the biological proximity between the endophenotype and illness; however, for an endophenotype to be a useful model for psychosis, it should also be exacerbated by environmental factors similar to those reported in patients (Gould & Gottesman 2006). For psychosis, endophenotypes include cognitive or information-processing deficits that coexist with the disorder. A number of cognitive deficits can be considered endophenotypes for psychosis. The advantage of a focus on task performance is that translational models from animals to humans can be used to examine the relationship between substance use and psychosis endophenotypes, and, of course, in animal studies there is more accurate quantification of exposure to the substance. Table 2 summarizes acute and subacute/chronic studies for recreational drugs for three relevant endophenotypes. Spatial working memory, delayed memory, and working memory have sufficient supporting evidence to be considered endophenotypes
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for psychosis. Patients with schizophrenia have impaired performance in these domains (Driesen et al. 2008, Van Snellenberg 2009), as do their relatives (Conklin et al. 2000, Park et al. 1995), those from the general population who express schizotypy (Saperstein et al. 2006), and prodromal or at-risk mental state (ARMS) patients (e.g., O’Connor et al. 2009, Smith et al. 2006). One study has suggested that schizotypal traits in relatives of patients with schizophrenia mediate proneness to cognitive deficits in the domain of memory (Diwadkar et al. 2006). Working memory performance has also been related to the Val158Met polymorphism on the gene encoding for COMT. This enzyme is involved in the breakdown of dopamine, which has particular significance for the efficiency of prefrontal cortex functioning. This gene has been found to modulate working memory performance in patients, relatives, and healthy volunteers (Diaz-Asper et al. 2008) and is related to the blood-oxygen-level-dependent signal (measured with functional magnetic resonance imaging) in the prefrontal cortex during a working memory task (e.g., Egan et al. 2001, Sambataro et al. 2009). Both spatial and standard working memory may be sensitive to biological vulnerability for psychosis and substance use since they involve widely distributed brain regions (e.g., Henseler et al. 2009). Animal and human studies show that certain substances of abuse administered both acutely and chronically have an impact on performance in spatial and standard working memory. Substance use has also been reported to modulate the neural underpinnings of memory tasks (e.g., Moeller et al. 2004, Padula et al. 2007, Schweinsburg et al. 2008). Given that alcohol and other substance use has been associated with decrements in memory, it is difficult to hypothesize that particular neurochemical imbalances or brain areas are sensitive to environmental insult in the form of substance use. For example, low-dose administration of 3,4methylenedioxymethamphetamine (ecstasy) leads to detriments to memory performance and increased anxiety in the absence of depletion in serotonin levels or long-term neurotoxic
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Chronic/subacute dosing
Working and delayed memory Human studies Acute
Chronic/subacute dosing
Animal studies Acute
Groth-Marnat et al. (2007) Rosselli et al. (2001)
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– McKetin & Mattick (1997) Rapeli et al. (2005)
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Santucci et al. (2004)
Santucci (2008)
Morgan et al. (2009)
Lofwall et al. (2006)
Krystal et al. (2005)
Pitsikas & Boultadakis (2009) Enomoto & Floresco (2009)
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Mattay et al. (2000)
Mandillo et al. (2003) Aultman & Moghaddam (2001)
Pitsikas et al. (2008)
Morgan et al. (2009)
Rowland et al. (2005)
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– Hoff et al. (1996)
– Ornstein et al. (2000) –
Blokland et al. (1998)
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Ketamine
Bhattachary & Powell (2001)
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Kuypers & Ramaekers (2005) Dunmont et al. (2008) Rogers et al. (2009)
Able et al. (2006)
Chen et al. (2005)
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Braida et al. (2002)
Montgomery & Fisk (2008)
Fox et al. (2002)
Kuypers & Ramaekers (2007)
Ecstasy (MDMA)
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Mandillo et al. (2003) Li et al. (2003)
Rupniak et al. (1991)
Boyce et al. (1991)
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– –
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Phencyclidine
D’Souza et al. (2004) Morrison et al. (2009) Schweinsburg et al. (2008) Harvey et al. (2007)
Mishima et al. (2001) Robinson et al. (2007) Fadda et al. (2004)
Schweinsburg et al. (2008) Harvey et al. (2007)
Weinstein et al. (2008)
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Table 2 The effects of a number of substances on spatial working memory, standard working memory, and prepulse inhibition. References cited describe the detrimental effects of the substance on the endophenotype in animals and humans∗
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Mansbach et al. (1988)
Hijzen et al. (1991)
Martinez et al. (1999a) Byrnes & Hammer (2000)
Martinez et al. (1999a) Doherty et al. (2008)
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–
Mansbach et al. (1988) Bakshi et al. (1995)
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–
Johansson et al. (1995) De Bruin et al. (1999) Chan et al. (2008)
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Note: This list is not exhaustive but rather represents tasks with available evidence for both humans and animals.
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Animal studies Acute
Chronic/subacute dosing
Liechti et al. (2001) –
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Krueger et al. (2009)
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–
Pitsikas & Boultadakis (2009)
George et al. (2008)
Kumari et al. (1998) Hutchison & Swift (1999) –
Castner et al. (2005)
–
–
–
Dulawa & Geyer (2000) –
Geyer et al. (1984) Martinez et al. (1999b) –
Kehne et al. (1999)
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Heekeren et al. (2004)
– –
Morley et al. (2001)
Piper (2007)
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Trigo et al. (2008)
Geyer et al. (2001)
–
–
– –
Jentsch et al. (2000)
Baron & Wenger (2001) Hudzik & Wenger (1993) Jentsch et al. (1997)
Malone & Taylor (2006) Wegener & Koch (2009) –
Nagai et al. (2006)
Scholes & Martin-Iverson (2009) Kedzior & Martin-Iverson (2006)
– –
Da & Takahashi (2002) Wegener & Koch (2009) Hampson et al. (2003)
Varvel et al. (2005)
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Chronic/subacute dosing
Beatty & Rush (1983)
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effects (Baumann et al. 2007). This suggests that other monoamines are related to the cognitive and behavioral alterations associated with ecstasy use (Clemens et al. 2007). Prepulse inhibition (PPI) is an informationprocessing measure that is considered an endophenotype for psychosis; it is measureable in both animals and humans. PPI is the attenuation of the startle response with a preceding nonstartling stimuli. An eye blink is usually measured as a startle response in humans, and it is considered a physiologically basic reflex. PPI is thought to operate as a sensory gating mechanism to help to determine what stimuli in the environment can be ignored. PPI deficits are reported in patients with schizophrenia (e.g., Braff et al. 2001, Kumari et al. 2000, Weike et al. 2000), relatives of patients with psychosis (Cadenhead et al. 2000), patients with schizotypal personality disorder (Cadenhead et al. 1993), and psychometrically defined schizotypes (e.g., Perlstein et al. 1989, Simons & Giardina 1992). Disrupted PPI is also associated with other psychiatric and neurological disorders, such as obsessive-compulsive disorder (Swerdlow et al. 1993) and Tourette’s syndrome (Swerdlow et al. 2001), suggesting that PPI deficits may not have specificity for psychosis. However, an extensive animal literature on PPI and substances of abuse justifies its inclusion in this review. From Table 2, it can be seen that most drugs of abuse lead to deficits in PPI. However, there are one or two exceptions. Ecstasy is a drug that shows cross-species differences in its effects on PPI. In humans, administration of the drug tends to lead to increased PPI, whereas disruption of PPI is reported at comparable doses in rats (e.g., Vollenweider et al. 1999). This difference is thought to be due to the effects of ecstasy at the subtypes of serotonin receptors (e.g., Liechti et al. 2001). These data highlight the potential restrictions of cross-species translation in drug effects, whereby physiological differences lead to contradictory results in behavioral outcomes. However, it is interesting to note that ecstasy produces robust deficits in working memory, implying that the
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neurobiological and physiological mechanisms underpinning PPI and working memory are indeed very different. Acute human studies using cocaine and PCP are seldom possible at this time owing to restrictions imposed by ethical committees. Furthermore, recreational PCP users are understudied. The number of studies exploring the effects of these drugs chronically reflects the recreational use of these drugs in society: The degree of perceived problem use of a drug has driven the amount of research performed to examine its deleterious effects. Additionally, in animal studies, modeling of chronic dosing of a substance occurs neo- or prenatally, which does not correspond well to the effects of recreational drug use in humans. Many of the areas and substances outlined in Table 2 have references that report no effect of the substance on cognitive performance or subtle differences in other cognitive domains other than those discussed here (e.g., Abel et al. 2003, Bortolato et al. 2005, Colzato et al. 2009, Del Olmo et al. 2007, Ehrhardt et al. 1999, Oranje et al. 2002). These contradictory results could be attributed to methodological differences (such as the strain of animal used or task difficulty) or reflect the complexities in the interplay between ingested substances and individual differences in neurophysiology. One substance of use that reflects these complexities is amphetamine. Mattay et al. (2000) reported that the effects of acute administration of amphetamine on cognition were mediated by the COMT Val158Met polymorphism, with only those carrying the gene for the low-activity enzyme (Met) showing cognitive deficits following amphetamine administration; the other participants showed an improvement in cognitive performance following amphetamine administration. It has been hypothesized that dopamine turnover in the prefrontal cortex mediates working-memory performance by determining the efficiency of the response in the prefrontal cortex. This leads to an inverted-U response, whereby individuals have a resting-state high- or low-efficiency prefrontal response (according to their COMT Val158Met genotype), and the administration
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of dopaminergic antagonists will “push” them into a new position around the inverted U. This role of the prefrontal cortex has been supported by functional magnetic resonance imaging studies using working-memory tasks (e.g., Mattay et al. 2003, Tipper et al. 2005). Other studies have replicated the positive effects of amphetamine on cognitive performance in patients with schizophrenia (Barch & Carter 2005), those with schizotypal personality (Kirrane et al. 2000), and healthy volunteers (e.g., Zeeuws & Soetens 2007). However, the situation may be further complicated by the doses of amphetamine given: Arnsten (2006) suggests that the amphetamine-related improvements in cognitive performance may only occur at lower doses. Given that the studies reporting data on chronic or longer-term recreational use of amphetamine summarized in Table 2 report detrimental effects on cognitive performance, it is likely that continued exposure to the drug affects the dopamine system in a negative fashion. Additionally, given the dynamic nature of neurotransmitter systems, it is possible that continued exposure to amphetamines may lead to establishment of a new baseline of dopamine activity. Examining the effects of substances on endophenotypes for psychosis in healthy volunteers may help to elucidate the neurobiological effects of substance use on cognition, but this has limited value for determining the effects of these substances on a psychosis-prone brain. Extensive literature suggests that those who are prone to psychosis have structural and neurochemical differences that differentiate them from healthy volunteers. Chambers et al. (2001) suggest that in psychosis, the breakdown in connectivity between the prefrontal cortex and hippocampus leads to dysregulation of neurotransmitter input and outputs from the nuclear accumbens. The outcome of this dysregulation is a hypersensitivity to dopamine release and decreased behavioral inhibitory responses. This may increase the rewarding properties of drugs of abuse and help to explain why substance use is associated with psychosis. Although this hypothesis explains why patients with psychosis
are more sensitive to the effects of alcohol and cannabis (e.g., D’Souza et al. 2005), it does not explain why substance use is present in some but not all patients with psychosis, since Chambers et al. (2001) view this mechanism as being ubiquitously associated with psychosis risk.
ARE RISK FACTORS FOR SUBSTANCE USE THE SAME IN THOSE WITH PSYCHOSIS AS IN THE GENERAL POPULATION? Demographic variables associated with substance use in patients with psychotic disorders and in the general population include male gender and young age (e.g., Addington & Addington 2007, Barnett et al. 2007). Family discord is associated with the initiation of substance use in adolescents (e.g., Pedersen 1990) and is common in the families of people with schizophrenia, but of course the latter may be a consequence of the illness. Given that traits such as impulsivity are known to predict substance use in the general population, it is possible that these personality traits operate in a similar manner in those at risk for psychosis (e.g., Adams et al. 2003, Dervaux et al. 2001, Schmid et al. 2007). Furthermore, the expression of some personality traits, such as schizotypy, may be a premorbid expression of an individual’s vulnerability toward developing both a substance use disorder and psychosis. Schizotypy comprises attenuated psychotic symptoms including positive symptoms, such as unusual belief systems and perceptual experiences, and negative symptoms in the form of social withdrawal, anxiety, and depression (Raine 2006). Cannabis has received the greatest attention in the schizotypy literature. Some studies suggest that cannabis use elevates schizotypal characteristics (Bailey & Swallow 2004; Dumas et al. 2002; Mass et al. 2001; Nunn et al. 2001; Schiffman et al. 2005; Skosnik et al. 2001, 2006, 2007; Stefanis et al. 2004), but not all studies have found this association (e.g., Barkus et al. 2006; see Earleywine 2006 for a cautionary note). However, Van Os and colleagues (2002)
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reported that cannabis use per se increases the likelihood of experiencing psychotic symptoms, with a stronger effect in those with psychosis proneness at the baseline; i.e., the latter may be more sensitive to its effects (see also Barkus et al. 2006, Henquet et al. 2006, Verdoux et al. 2003).
SUBSTANCE USE AND THE PRODROME FOR PSYCHOSIS
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There has been much recent interest in identifying those likely to develop psychosis. The most significant aspects of the so-called prodrome for psychosis are deterioration in functioning, psychotic-like experiences, and expression of genetic liability, in the form of family history or schizotypal traits (Yung & McGorry 1996). Phillips et al. (2002) noted that reported rates of cannabis use were low in those attending a prodromal clinic compared to other services. but they were still significantly higher than those reported for the general Australian population. In the 12 months prior to the onset of psychosis, 18% of their sample met the criteria for cannabis dependency, 22% used cannabis once a month or more, and 13% used it less than once a month. These rates were similar to lifetime use, indicating there had been no change in cannabis usage. In the Calgary Early Psychosis Service, Addington & Addington (2007) reported that 51.7% of patients met criteria for a substance use disorder: 33% were cannabis related and 35% were alcohol related. Phillips et al. (2002) found that of those who made the transition to frank psychosis within a year, 37% were cannabis users compared to 29% noncannabis users; this difference did not reach statistical significance. However, in a study from the United States, those who had cannabis dependency or abuse were significantly more likely to make a transition into a psychotic disorder within twelve months (Kristensen & Cadenhead 2007). Hambrecht & H¨afner (1996) attempted to tease apart the temporal relationship between the first signs and symptoms of psychosis (these could be comparable to a prodrome). In 28% of their sample, drug abuse occurred at least a year before the
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SUBSTANCE USE AND THE NATURE AND OUTCOME OF PSYCHOSIS A number of studies have reported that age of first use of cannabis, cocaine, ecstasy, and amphetamine is significantly associated with age of onset of first psychotic symptoms (Addington & Addington 2007, Andreassen et al. 1987, ¨ Arendt et al. 2005, Barnett et al. 2007, Buhler et al. 2002, Cantwell et al. 2000, van Mastrigt et al. 2004, Zammit et al. 2002). Barnes et al. (2006) suggest that this effect is particularly related to cannabis use. However, not all studies report this association (e.g., Cantor-Graae et al. 2001, Sevy et al. 2001). Clinical psychiatrists have been much preoccupied with the distinction between substanceinduced psychosis and idiopathic schizophrenia. In reality, the former often progresses into the latter, with certain individuals more likely to make this step. Caton et al. (2007) followed up individuals diagnosed with substanceinduced psychosis. Twelve months later, 25% had received a diagnosis of primary psychoses. Those who made a transition to a primary psychotic disorder were more likely to have a family history of mental health problems, poorer premorbid adjustment, and less awareness of psychotic symptoms. Arendt et al. (2005) focused on 535 patients initially presenting with a cannabis-induced psychotic disorder. Within three years, 44.5% went on to be diagnosed with a schizophrenia-spectrum disorder. Mathias et al. (2008) summarize the literature to date. Variables that distinguished substanceinduced psychosis from primary psychosis were
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onset of the first signs of schizophrenia, for 35% both occurred at a similar time, and for 38% the symptoms of schizophrenia occurred before drug abuse. Cannon et al. (2008) reported that in their North American sample, history of any substance abuse was predictive of those who made a transition to psychosis in a 30-month follow-up, but substance use had poor sensitivity to discriminate converters to psychosis from nonconverters.
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presence of visual hallucinations, insight into cause of symptoms, better premorbid functioning, older age of symptom onset, and no family history of mental health difficulties. Another issue of great import to clinicians is whether individuals stop their drug use after being diagnosed with psychosis. Addington & Addington (2007) reported that in an early psychosis service, 51.7% of patients met criteria for abuse/dependency at baseline, but at 12month follow-up, this had dropped to 32.5%, a significant decrease. Three other studies have reported that after treatment, many patients show a substantial decrease in substance use (Addington & Addington 2001, Lambert et al. 2005, Sorbara et al. 2003). One study reported that 15 months after the onset of psychosis, one in five patients had stopped using any substances; those who continued substance use did not increase their use, and no patients initiated substance use (Wade et al. 2006). If psychotic patients are diagnosed with substance dependency rather than just use, they are more likely to be still using seven years later (Bartels et al. 1995). Lambert et al. (2005) reported that approximately one-quarter of their sample continued to meet the criteria for substance use disorder throughout treatment, with the majority using at the same rates established prior to the onset of treatment. There have been many reports that substance use by psychotic patients leads to increased hospitalization and remission (Cleghorn et al. 1991, Drake et al. 1989, Gerding et al. 1999, Lambert et al. 2005, LeDuc & Mittleman 1995, Møller & Linaker 2004), although a few studies have not found this (Mueser et al. 1990, 2000). Patients with psychosis who use substances have a poorer response to treatment (Cantor-Graae et al. 2001, Kavanagh et al. 2004) and a worse outcome, and, as noted above, those who continue to use cannabis have a worse clinical prognosis than do those who stop (e.g., Grech et al. 2005, Kovasznay et al. 1997, Linszen & van Amelsvoort 2007). An integrated treatment approach, using both pharmacological and psychological interventions, is necessary to manage
symptoms in patients with psychosis and substance use dependency (Drake et al. 2001, Hjorthøj et al. 2009). However, psychological interventions can only be engaged in changing behaviors, which occurs when the patient realizes his drug use needs to be addressed and expresses the readiness and motivation to change.
COGNITION IN PATIENTS WHO DO AND DO NOT USE SUBSTANCES The existing literature on cognitive performance in psychotic patients who do use substances compared to those who do not has produced mixed results. Some studies report relatively intact (or better) cognition in substance-using patients with psychosis ¨ et al. 2007, Kumra et al. ( Jockers-Scherubl 2005, Sevy et al. 2007, Stirling et al. 2005), whereas others report that those who do not use substances fair better (Allen et al. 1999, Liraud & Verdoux 2002, Manning et al. 2007, Pencer & Addington 2003, Serper et al. 2000). Many of these studies are confounded by differences in antipsychotic exposure, duration of illness, and age of onset. Additionally, the length of time patients have used the substance may have an effect on the results; for example, the effects of heavy alcohol use may only be evident in older participants (Mohamed et al. 2006). Comorbid cannabis use leads to the largest diversity in the findings (e.g., Coulston et al. 2007). Some evidence indicates that cannabidiol, one constituent of cannabis, is a cognitive enhancer (e.g., Bhattacharyya et al. 2009), and early data suggest that it may be neuroprotective against insults as severe as hypoxic-ischemia (Alverez et al. 2008). However, further research is necessary to isolate which cannabinoids may have a positive effect on cognition. Some authors suggest that those who develop psychosis after using cannabis or other illicit substances represent a distinct subgroup of patients who may have better long-term preservation in their cognitive capacity because their psychotic disorder has been more driven by environmental factors (i.e.,
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substance use) than endogenous factors (i.e., genetic vulnerability and/or neurodevelopmental impairment).
CONCLUSIONS
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The use of recreational drugs varies with geographic location and social fashions, and the risk factors that increase the likelihood of initiation and maintenance of substance use in patients with psychotic disorders mirror those reported in the general population. However, we do not fully understand why some people can use recreational drugs without significant adverse effects while others develop psychosis. Among possible mediating factors are schizotypy or psychosis proneness. Thus, the experiences that people have when using recreational drugs may reflect an underlying vulnerability to a psychotic disorder. However, the value of these initial drug-induced experiences in predicting the onset of psychotic disorders is yet to be established. Whether substance use causes the onset of psychosis is still debated. Clearly, the answer depends on the particular substance being used. For example, in the majority of
people who develop psychosis in the context of abuse of amphetamines, once the substance is withdrawn and the psychotic episode is treated, the psychotic symptoms cease in the absence of further use. However, in a minority, the psychosis continues or abates and then returns, and the picture changes to unrelenting psychotic disorder. The variables that differentiate those who go on to develop a persistent psychotic disorder after a substance-induced episode include family history of mental health problems and psychosis-prone personality (Chen et al. 2003, 2005). There has been a recent emphasis on cannabis use in both the epidemiological and clinical literature. There is now a widespread acceptance among psychiatrists that heavy use of cannabis increases the risk of psychosis, and continued uses worsens the outcome. However, future research needs to address the mechanisms underlying the epidemiological findings. In addition, further research is needed on the differing risks associated with the use of different illicit substances. Given the varying neurobiological effects of these substances, it seems unlikely that they will influence psychosis in the same manner.
DISCLOSURE STATEMENT The authors are not aware of any affiliations, memberships, funding, or financial holdings that might be perceived as affecting the objectivity of this review.
ACKNOWLEDGMENT EB would like to acknowledge the support of a NARSAD Young Investigator Award.
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