The mismatch negativity - Universitat de Barcelona

Clinical Neurophysiology 123 (2012) 424–458

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Clinical Neurophysiology journal homepage: www.elsevier.com/locate/clinph

Invited Review

The mismatch negativity (MMN) – A unique window to disturbed central auditory processing in ageing and different clinical conditions R. Näätänen a,b,c,⇑, T. Kujala c,d, C. Escera e,f, T. Baldeweg g,h, K. Kreegipuu a, S. Carlson i,j,k, C. Ponton l a

Institute of Psychology, University of Tartu, Tartu, Estonia Center of Integrative Neuroscience (CFIN), University of Aarhus, Aarhus, Denmark c Cognitive Brain Research Unit, Cognitive Science, Institute of Behavioural Sciences, University of Helsinki, Helsinki, Finland d Cicero Learning, University of Helsinki, Helsinki, Finland e Institute for Brain, Cognition and Behavior (IR3C), University of Barcelona, Barcelona, Catalonia, Spain f Cognitive Neuroscience Research Group, Department of Psychiatry and Clinical Psychobiology, University of Barcelona, Barcelona, Catalonia, Spain g Institute of Child Health, University College London, London, UK h Great Ormond Street Hospital for Sick Children NHS Trust, London, UK i Neuroscience Unit, Institute of Biomedicine/Physiology, University of Helsinki, Helsinki, Finland j Brain Research Unit, Low Temperature Laboratory, Aalto University School of Science and Technology, Espoo, Finland k Medical School, University of Tampere, Tampere, Finland l Compumedics NeuroScan, Santa Fe, NM, USA b

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Article history: Accepted 20 September 2011 Available online 13 December 2011 Keywords: The mismatch negativity (MMN) Central auditory processing Event-related potentials (ERP) Magnetoencephalography Auditory discrimination Neuropsychiatric disorders Neurological disorders Neurodevelopmental disorders The NMDA-receptor system

h i g h l i g h t s The mismatch negativity (MMN) indexes different types of central auditory abnormalities in different neuropsychiatric, neurological, and neurodevelopmental disorders. The diminished amplitude/prolonged peak latency observed in patients usually indexes decreased auditory discrimination. An MMN deficit may also index cognitive and functional decline shared by different disorders irrespective of their specific aetiology and symptomatology. MMN deficits index deficient N-methyl-D-aspartate (NMDA) receptor function affecting memory-trace formation and hence cognition in different disorders.

a b s t r a c t In this article, we review clinical research using the mismatch negativity (MMN), a change-detection response of the brain elicited even in the absence of attention or behavioural task. In these studies, the MMN was usually elicited by employing occasional frequency, duration or speech-sound changes in repetitive background stimulation while the patient was reading or watching videos. It was found that in a large number of different neuropsychiatric, neurological and neurodevelopmental disorders, as well as in normal ageing, the MMN amplitude was attenuated and peak latency prolonged. Besides indexing decreased discrimination accuracy, these effects may also reflect, depending on the specific stimulus paradigm used, decreased sensory-memory duration, abnormal perception or attention control or, most importantly, cognitive decline. In fact, MMN deficiency appears to index cognitive decline irrespective of the specific symptomatologies and aetiologies of the different disorders involved. Ó 2011 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

Contents 1. 2. 3.

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 425 The MMN as an index of decreased auditory discrimination accuracy (Table 1). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 431 The MMN as an index of shortened sensory-memory duration (Table 2) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 433

⇑ Corresponding author at: Cognitive Brain Research Unit, Cognitive Science, Institute of Behavioural Sciences, University of Helsinki, Helsinki, Finland. Tel.: +358 40 501 5740; fax: +358 9 191 29450. E-mail address: risto.naatanen@helsinki.fi (R. Näätänen). 1388-2457/$36.00 Ó 2011 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.clinph.2011.09.020

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4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15.

The MMN as an index of abnormal auditory perception . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The MMN as an index of increased backward masking (Table 3) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The MMN as an index of abnormal involuntary attention switching: either too weak (Table 4) or too strong (Table 5). The MMN attenuation caused by cerebral grey-matter loss or other structural change (Table 6) . . . . . . . . . . . . . . . . . . . The MMN as an index of pathological brain excitation/excitability (Table 7) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The MMN as an index of cognitive and functional deterioration (Table 8) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The MMN as an index of the level of consciousness (Table 9) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The MMN as an index of the progression/severity of the illness (Table 10) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The MMN in predicting illness course/drug response (prognosis) (Table 11) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The MMN as an index of genetic disposition to different pathologies (Table 12) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The MMN as an index of central auditory processing improvement or recovery (Table 13) . . . . . . . . . . . . . . . . . . . . . . . Concluding discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

1. Introduction Interestingly, central auditory processing is affected in a large number of different clinical conditions with very different aetiologies and symptoms such as schizophrenia, dyslexia, stroke, specific language impairment (SLI), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), epilepsy and autism, suggesting some shared aetiology in these different abnormalities (see also Gottesman and Gould, 2003; Bishop, 2009; Dolan et al., 1993; Hugdahl and Calhoun, 2010; Reite et al., 2009). These effects on central auditory processing in different clinical conditions and in ageing can now be objectively evaluated, and hence their degree of similarity determined, by using the electrophysiological change-detec-

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tion (or regularity-violation) response, the mismatch negativity (MMN; Näätänen et al., 1978; Näätänen and Michie, 1979) and its magnetoencephalographic (MEG) equivalent, the MMNm (Hari et al., 1984; Sams et al., 1985b). The MMN can be reliably (Pekkonen et al., 1995a,b; Escera and Grau, 1996; Tervaniemi et al., 1999; Escera et al., 2000b) recorded even in the absence of the subject or patient’s attention or behavioural task, e.g., in sleeping infants (Ruusuvirta et al., 2009), stroke patients even at a very early post stroke-onset period (Ilvonen et al., 2001, 2004) and in comatose (Kane et al., 1993, 1996; Fischer et al., 1999; Fischer and Luauté, 2005) and persistent-vegetative-state (PVS) patients (Wijnen et al., 2007).

Fig. 1. Grand average difference waveforms (9 subjects) for changes in duration, frequency, and perceived sound-source location for six different magnitudes of deviance at electrode Fz and referenced to the mean of the two mastoid electrodes (upper panel). The same waveforms referenced to the nose electrode and shown from Fz and the right mastoid (RM); lower panel. Sound onset is always at 0 ms (From Pakarinen et al., 2007).

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The auditory MMN response is mainly generated by a changedetection process occurring bilaterally in auditory cortices, in which the current auditory input is found to differ from the representation of the preceding auditory events, including regularities governing consecutive stimulus events (for reviews, see Näätänen et al., 2001, 2007, 2010, 2011b; Duncan et al., 2009; Winkler, 2007). For an illustration, see Fig. 1. In subjects performing some primary, e.g., visual, task, this preconscious auditory-cortex change-detection process reaches conscious perception by activating, with a brief delay (Rinne et al., 2000; see also Rinne et al., 2005, 2006), a right frontal-cortex process which, in turn, initiates further cerebral processes which may lead to conscious change detection (Näätänen, 1990, 1992; Näätänen et al., 2011b; Alain et al., 1998; Berti and Schröger, 2001; Deouell et al., 2007; Giard et al., 1990; Schröger, 1996; Escera et al., 2000a). Hence, the MMN is composed of overlapping contributions from auditory- and frontal-cortex processes (the supratemporal and frontal MMN subcomponents, respectively) (Giard et al., 1990). These two subcomponents of the MMN can be inferred from the data presented in Fig. 2 showing how ethanol selectively attenuates the MMN amplitude recorded over the frontal cortex, whereas the polarity-reversed MMN recorded at the mastoids (with a nose reference) is unaffected. This data pattern suggests that the frontally recorded MMN is composed of contributions from both the auditory and frontal cortices, whereas the mastoid ‘MMN’ gets a contribution from the auditory-cortex MMN generator only. Intracranial recordings in humans also support both auditory- and frontal-cortex MMN generators (Halgren et al., 1995a,b, 1998; Baudena et al., 1995; Kropotov et al., 1995, 2000; Liasis et al., 1999, 2000a,b; Rosburg et al., 2005, 2007). The MMNm, in turn, selectively reflects the temporal-lobe component of the MMN because the MEG is insensitive to the radially oriented frontal generators (Hämäläinen et al., 1993) of the MMN. Therefore, the MMNm is particularly well suited for detecting central auditory processing deficits specific for the temporal lobes. Consequently, the combined use of the electroencephalography (EEG) and MEG recordings helps one to separately determine to what extent the temporal and frontal MMN components are impaired (Hämäläinen et al., 1993; Näätänen, 1992). Further, these two components have their functional magnetic resonance imaging (fMRI) (Molholm et al., 2005; Celsis et al., 1999; Opitz et al., 2002; Schall et al., 2003), positron emission tomography (PET) (Tervaniemi et al., 2000; Dittmann-Balcar et al., 2001; Müller et al., 2002) and optical-imaging (OI) (Rinne et al., 1999; Tse and Penney, 2008) equivalents as well. Moreover, there is event-related potential (ERP; Paavilainen et al., 1991; Doeller et al., 2003; FrodlBauch et al., 1997; Escera et al., 2002), MEG (Levänen et al., 1993, 1996; Rosburg, 2003) and fMRI evidence (Molholm et al., 2005) for the attribute-specific organisation of the supratemporal MMN generator. Moreover, the MMN has its equivalents in other sensory modalities, too [the visual MMN; vMMN (Alho et al., 1992; Amenedo et al., 2007; Astikainen and Hietanen, 2009; Tales et al., 1999, 2002a,b, 2008; Tales and Butler, 2006; Maekawa et al., 2005, 2009; Berti and Schröger, 2004, 2006; Stagg et al., 2004; Stefanics et al., 2011; Heslenfeld, 2003; Pazo-Alvarez et al., 2003, 2004; Froyen et al., 2010; Iijima et al., 1996; Kenemans et al., 2003; Kimura et al., 2009; Czigler, 2007; Czigler and Csibra, 1990, 1992; Czigler et al., 2002, 2004, 2006a,b; Czigler and Pató, 2009; Nordby et al., 1996; Wei et al., 2002; Woods et al., 1992); the somatosensory MMN; sMMN (Kekoni et al., 1997; Shinozaki et al., 1998; Akatsuka et al., 2005; Kida et al., 2001; Spackman et al., 2007, 2010; Astikainen et al., 2001; Näätänen, 2009); and the olfactory MMN; oMMN (Krauel et al., 1999; Pause and Krauel, 2000)]. The vMMN has a parieto-occipital scalp distribution but there is no convincing evidence for a frontal component analogous to that in the auditory

modality. By contrast, the sMMN appears to have, similar to the auditory MMN, sensory-specific (somatosensory cortex) and frontal subcomponents (Restuccia et al., 2009; Spackman et al., 2010), consistent with its fronto-central, contralaterally predominant scalp distribution (Wei et al., 2002). Currently, it is not clear whether the auditory and somatosensory modalities share the frontal activation (generating the frontal MMN component) probably serving attention switch to stimulus change (Näätänen, 1992; Näätänen et al., 2002; Schröger, 1997). In addition, there is also an oMMN, with a long peak latency (about 500–600 ms) and parietally predominant scalp distribution (Krauel et al., 1999). The MMN can also be recorded in different animals [in monkey (Javitt et al., 1992); cat (Csépe et al., 1987, 1988, 1989; Pincze et al., 2001, 2002); rabbit (Astikainen et al., 2001); rat (Astikainen et al., 2006; Ruusuvirta et al., 1998, 2007; Roger et al., 2009; Tikhonravov et al., 2008, 2010); guinea pig (Kraus et al., 1994); and mouse (Umbricht et al., 2005; Ehrlichman et al., 2008, 2009)]. The MMN enables one to determine discrimination accuracy, usually with a good correspondence with behavioural discrimination (Sams et al., 1985a; Amenedo and Escera, 2000; Gottselig et al., 2004; Lang et al., 1990; Näätänen et al., 1993, 2007; Leitman et al., 2010; Kujala and Näätänen, 2010; Tremblay et al., 1998), separately for each auditory dimension (such as frequency, intensity and duration) as well as for the different speech sounds (Kraus et al., 1996), with the MMN vanishing at about the behavioural discrimination threshold (Sams et al., 1985a; Winkler and Näätänen, 1994; Winkler et al., 1993). Therefore, it permits one to form objective deterioration profiles covering all important auditory dimensions in different patient groups (Näätänen et al., 2004; Kujala et al., 2005a, 2006, 2007, 2010; Pakarinen et al., 2007, 2009, 2010). In addition, these MMN-based objective tests can be extended to all aspects of short-term auditory sensory memory, too, such as its

Fig. 2. The differential effects of ethanol on MMN at the frontal (Fz) and left and right mastoid (LM and RM, respectively) electrode positions. MMN was reduced at the frontal electrode but the polarity-inverted MMN recorded at the mastoids, suggesting the supratemporal MMN subcomponent, was not affected by ethanol (0.55 g/kg) whereas the frontal subcomponent was affected by ethanol. Adapted from Jääskeläinen et al. (1996b).

Table 1 The auditory MMN (MMNm) provides an objective index of affected auditory discrimination in: – ADHD (Alexandrov et al., 2003; Barry et al., 2003; Gumenyuk et al., 2005; Huttunen et al., 2007; Huttunen-Scott et al., 2008; Kemner et al., 1996; Kilpeläinen et al., 1999; Oades et al., 1996; Rothenberger, 1995; Rothenberger et al., 2000; Satterfield et al., 1988; Sawada et al., 2010; Wild-Wall et al., 2005; Winsberg et al., 1993) – Ageing (Alain and Woods, 1999; Alain et al., 2004; Amenedo and Diaz, 1998; Bellis et al., 2000; Bertoli et al., 2005; Cooper et al., 2006; Czigler et al., 1992; Fabiani et al., 2006; Gaeta et al., 1998, 1999, 2001, 2002; Gunter et al., 1996; Horváth et al., 2007; Iijima et al., 1996; Ikeda et al., 2004; Jääskeläinen et al., 1999a; Karayanidis et al., 1995; Kiang et al., 2007, 2009; Kisley et al., 2004a,b, 2005; Kok, 2000; Mager et al., 2005; Osawa et al., 1996; Pekkonen, 2000; Pekkonen et al., 1995a, 1996a, 2005; Schiff et al., 2008; Schroeder et al., 1995; Verleger et al., 1991; Woods, 1992; Woods and Clayworth, 1986) – Alcohol intoxication, acute (Ahveninen et al., 2000a; Jääskeläinen et al., 1995, 1996a,b, 1998, 1999a,b; Kähkönen et al., 2001, 2004) Alcoholism (Ahveninen et al., 2000a,b; Fein et al., 2004; Grau et al., 2001; Holguin et al., 1998; Kathmann et al., 1995; Marco-Pallares et al., 2007; Pekkonen et al., 1998; Polo et al., 2003; Realmuto et al., 1993; Rodriguez et al., 1998; van der Stelt and Belger, 2007; Zhang et al., 2001) – Alzheimer’s disease and dementia (Engeland et al., 2002; Gaeta et al., 1999; Katada et al., 2004; Kazmerski et al., 1997; Missioner et al., 1999; Pekkonen, 2000; Pekkonen et al., 1994, 1996b, 1999, 2001a,b; Riekkinen et al., 1997; Schroeder et al., 1995; Yokoyama et al., 1995) – Amusia(Congenital) (Moreau et al., 2009; Peretz et al., 2009) – Amusia (Caused by Stroke) (Kohlmetz et al., 2001; Särkämö et al., 2010b) Amyotrophic Lateral Schlerosis (ALS) (Gil et al., 1993; Hanagasi et al., 2002; Pekkonen et al., 2004; Raggi et al., 2008) Anaesthesis and sedation (Csepe et al., 1989; Heinke and Koelsch, 2005; Heinke et al., 2004; Koelsch et al., 2006; Astikainen et al., 2006; Yppärilä et al., 2002; Simpson et al., 2002; van Hooff et al., 1995, 1997)

– Asperger syndrome (Jansson-Verkasalo et al., 2003a, 2005; Korpilahti, 1995; Korpilahti et al., 2007; Kujala et al., 2005a, 2007, 2010; Lepistö et al., 2006, 2007) – Autism (Bomba and Pang, 2004; Ceponiene et al., 2003; Dunn et al., 2008; Ferri et al., 2003; Gomot et al., 2002; Kasai et al., 2005; Kemner et al., 1995; Kuhl et al., 2005; Lepistö et al., 2005, 2008; Näätänen and Kujala, 2011; Oram Cardy et al., 2005a,b; Roberts et al., 2008, 2011; Seri et al., 1999, 2007; Siegal and Blades, 2003) – Bipolar disorder (Hall et al., 2007, 2009; Takei et al., 2010) – Bipolar II disorder (Andersson et al., 2008) – Blindness (early) (Alho et al., 1993; Kujala et al., 1995a,b, 1997, 2000b) – Brain lesions (Alain et al., 1998; Alho et al., 1994; Auther et al., 2000; Deouell et al., 2000a,b; Hämäläinen et al., 2007; Jacobs and Schneider, 2003; Kaipio et al., 1999, 2000, 2001; Kohlmetz et al., 2001; Kotchoubey, 2007; Kotchoubey et al. 2003, 2005; Mäkelä et al., 1998b; Neumann and Kotchoubey, 2004; Polo et al., 2002; Reinvang et al., 2000; Tarkka et al., 2011; Woods and Knight, 1986); (see also Aphasia and Stroke) – Brainstem auditory processing syndrome (Kraus et al., 1993a) – CATCH-22 syndrome (Baker et al., 2005; Cheour et al., 1998a; Ceponiene et al., 2002) – Central auditory processing disorder (CAPD) (Bamiou et al., 2000) – Cerebellar degeneration (Moberget et al., 2008) – Childhood cancer and brain radiation (Järvelä et al., 2011; Lähteenmäki, 1999) – Chronic pain (Dick et al., 2003)


– Anhedonia (Giese-Davis et al., 1993) – Aphasia and stroke (Aaltonen et al., 1993; Alain et al., 1998; Auther et al., 2000; Becker and Reinvang, 2007; Csépe et al., 2001; Ilvonen et al., 2003, 2004; Jacobs and Schneider, 2003; Kohlmetz et al., 2001; Peach et al., 1992, 1993, 1994; Pettigrew et al., 2004a, 2005; Särkämö et al. 2010a,b; Wertz et al., 1998)

– Chronic primary insomnia (Wang et al., 2001) – Cleft palate (different forms of) (Ceponiene et al., 2000, 2002; Cheour et al., 1998a, 1999) – Closed-head injury (Kaipio et al., 1999, 2000, 2001; Polo et al., 2002) – Cochlear-implant (CI) users (Groenen et al., 1996; Kelly et al., 2005; Kileny et al., 1997; Koelsch et al., 2004; Kraus et al., 1993b; Lonka et al., 2004; Nager et al., 2007; Ponton et al., 1996, 2000, 2009; Ponton and Don, 1995, 2003; Ponton and Eggermont, 2007; Roman et al., 2005; Salo et al., 2002; Sandmann et al., 2010; Wable et al., 2000) – Coma (Daltrozzo et al., 2007; Fischer et al., 1999, 2000, 2004, 2006a,b, 2008; Fischer and Luauté, 2005; Guérit et al., 1999; Kane et al., 1993, 1996, 2000; Kotchoubey et al., 2003; Laureys et al., 2005; Luauté et al., 2005; Morlet et al., 2000; Naccache et al., 2005; van der Stelt and van Boxtel, 2008; Vanhaudenhuyse et al., 2008) – Conduct disorder (Rothenberger et al., 2000) – Craniosynosthosis (Huotilainen et al., 2008) – Deafness to musical dissonance ( Acquired) (Brattico et al., 2003) – Dementia (Schroeder et al., 1995; Yokoyama et al., 1995; Osawa et al., 1996) – Depression (He et al., 2010; Iv et al., 2010; Kähkönen et al., 2007; Lepistö et al., 2004; Ogura et al., 1991, 1993; Takei et al., 2009) (continued on next page) 427

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Table 1 (continued) – Developmental dysphasia (Holopainen et al., 1997, 1998; Korpilahti and Lang, 1994) – Diabetes mellitus (late phase) (Vanhanen et al., 1996) – Distractibility (Escera et al., 2000a; Gumenyuk et al., 2004; Kaipio et al., 2000, 2001; Kilpeläinen et al., 1999; Mager et al., 2005) – Down’s syndrome (Diaz and Zurron, 1995; Lalo et al., 2005) – Drugs –Antipsychotics/Neuroleptics: – Clozapine (Horton et al., 2010; Schall et al., 1999; Umbricht et al., 1998)

– –

–

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–

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– Haloperidol (Kähkönen and Ahveninen, 2002; Kähkönen et al., 2001, 2002; Pekkonen et al., 2002) – Olanzapine (Korostenskaja et al., 2005) – Risperidone (Umbricht et al., 1999) Alcohol: – (Hirvonen et al., 2000; Jääskeläinen et al., 1995, 1996a,b, 1998, 1999a; Kähkönen et al., 2001,2004,2005b; Kenemans et al., 2010) Acetylcholine: Tetrahydroaminoacridine (THA, Tacrine) (Engeland et al., 2002; Riekkinen et al., 1997) – (a) Muscarinic receptor antagonist: – Glycopyrrolate (Pekkonen et al., 2001a) – Scopolamine (Pekkonen et al., 2001a) – (b) Nicotinic receptor agonists: – Nicotine: (Baldeweg et al., 2006; Dulude et al., 2010; Engeland et al., 2002; Fisher et al., 2010; Harkrider and Hedrick, 2005; Inami et al., 2005, 2007; Knott et al., 2009; Martin et al., 2009; Pritchard et al., 2004) – AZD3480 (Dunbar et al., 2007) Benzodiazepines: – (Kivisaari et al., 2007; Murakami et al., 2002) – Triatzolam (Nakagome et al., 1998) – Lorazepam (Rosburg et al., 2004) GABA agonists/antagonists: – Bicuculline (Javitt et al., 1996) – Flumazenil (Smolnik et al., 1998) – Propofol (Heinke et al., 2004; Koelsch et al., 2006; Simpson et al., 2002) Monoamines – Review: (Kähkönen and Ahveninen, 2002) Adrenergic drugs: – Clonidine (Duncan and Kaye, 1987; Hansenne et al., 2003) – Atipamezole (Mervaala et al., 1993) – Noradrenergic agonist S 12024-4 (Missioner et al., 1999) Histamine: – Antihistamines: Chlorpheniramine (Serra et al., 1996) Dopamine: – Apomorphine (Hansenne et al., 2003) – Methamphetamine (Hosák et al., 2008) – Methylphenidate (Winsberg et al., 1993, 1997; Sawada et al., 2010; Verbaten et al., 1994) – Bromocriptine (Leung et al., 2007) – Domperidone (Leung et al., 2007) Serotonin: – Serotonin (Kähkönen et al., 2005a; Oranje et al., 2008) – Acute tryptophan depletion (Kähkönen and Ahveninen, 2002) – Dimethyltryptamine (Heekeren et al., 2008) – Escitalopram (Oranje et al., 2008; Wienberg et al., 2010) – Psilocybin (Umbricht et al., 2003) Neuropeptides/Hormones: – Vasopressin (Born et al., 1986, 1987a, 1998) – Oxytocin (Born et al., 1987a) – Cholecystokinin (Schreiber et al., 1995) – Desacetyl-alpha-MSH (Smolnik et al., 1999)

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– Hydrocortisone (Born et al., 1987a) – ACTH-related neuropeptides (Born et al., 1987b; Smolnik et al., 1999; Pietrowsky et al., 1990) – NMDA/Glutamate: – Ketamine (Ehrlichman et al., 2008; Heekeren et al., 2008; Javitt et al., 2000; Kreitschmann-Andermahr et al., 2001; Umbricht et al., 2002) – MK-801 (Javitt et al., 1996; Tikhonravov et al., 2010) – Phencyclidine (PCP) (Javitt et al., 1996) – Memantine (Korostenskaja et al., 2007) – Nitrous oxide (Pang and Fowler, 1999) – Glycine (Leung et al., 2008) – N-acetyl-cysteine (NAC; Lavoie et al., 2007) – Opiods: – Naltrexone (Jääskeläinen et al., 1998) – Opioid Dependence (Kivisaari et al., 2007; Näätänen, 2001) – Other/alternative therapies: – Hiba odour (Hiruma et al., 2002) – Purine nucleotides: – Adenosine (Hirvonen et al., 2000) – Caffeine (Rosburg et al., 2004) – Dyslexia (Ahissar, 2007; Ahissar et al., 2006; Alonso-Búa et al., 2006; Baldeweg et al., 1999; Bishop, 2007a,b; Blitz et al., 2007; Bonte et al., 2005, 2007; Bradlow et al., 1999; Bruder et al., 2011a,b; Corbera et al., 2006; Csépe, 2002; Czamara et al., 2011; Fisher et al., 2006; Froyen et al., 2008, 2009, 2010; Guttorm et al., 2005, 2001; Hämäläinen et al., 2008; Heim et al., 2000; Huttunen et al., 2007; Huttunen-Scott et al., 2008; Jansson-Verkasalo et al., 2010; Kujala, 2007; Kujala and Näätänen, 2001; Kujala et al., 2000a, 2001, 2003, 2006; Kurtzberg et al., 1995; Lachmann et al., 2005; Leppänen and Lyytinen, 1997; Leppänen et al., 1997, 1999, 2002, 2004, 2010; Lovio et al., 2010; Lyytinen et al., 2001, 2004, 2006, 2009; Maurer et al., 2003, 2009; Paul et al., 2006a,b; Pihko et al., 1999, 2008; Renvall and Hari, 2003; Richardson et al., 2003; Roeske et al., 2011; Schulte-Körne and Bruder, 2010; Schulte-Körne et al., 1998, 1999, 2001; Sebastian and Yasin, 2008; Shankarnarayan and Maruthy, 2007; Sharma et al., 2005, 2006, 2007, 2009; Stoodley et al., 2006; van Leeuwen et al., 2006) – Dysthymia (Giese-Davis et al., 1993) – Electromagnetic fields (Kwon et al., 2009, 2010) – Epilepsy (Boatman et al., 2008; Borghetti et al., 2007; Duman et al., 2008; Gene-Cos et al., 2005; Korostenskaja et al., 2010b; Liasis et al., 2000; Liasis et al., 2001; Liasis et al., 2006; Lin et al., 2007; Metz-Lutz and Philippini, 2006; Miyajima et al., 2011; Rosburg et al., 2005) – Frontal-lobe injury (Alho et al., 1994; Woods and Knight, 1986) – Herpes Simplex Encephalitis (Mäkelä et al., 1998a) – Hippocampus-Amygdala Partial Temporal-Lobe Resection (Hämäläinen et al., 2007) – HIV (Schroeder et al., 1994) – Huntington’s disease (pathological enhancement of discrimination) (Beste et al., 2008) – Hyperkinetic disorder (Rothenberger, 1995) – Hypnosis (Jamieson et al., 2005; Kallio et al., 1999) – Insomnia (Wang et al., 2001) – Intellectual disability (Ikeda et al., 2004; Nakagawa et al., 2002; Kaga et al., 1999) – Introvert/extrovert personality (Sasaki et al., 2000) – Landau–Kleffner syndrome (Honbolygó et al., 2006; Metz-Lutz and Philippini, 2006) – Language-learning impairment (LLI) (Benasich and Tallal, 2002; Benasich et al., 2006; Bradlow et al., 1999; Choudhury and Benasich, 2011; Kraus et al., 1996; Kujala, 2007; Marler et al., 2002; Pihko et al., 2007; Shafer et al., 2005; Uwer et al., 2002; Weber et al., 2005) – Late talkers (Grossheinrich et al., 2010) – Learning-disabled children (Banai and Ahissar, 2005; Bradlow et al., 1999; Kraus et al., 1996) – Left sylvian infarct in neonate (Dehaene-Lambertz et al., 2004) – Locked-in patients (Ragazzoni et al., 2000) – Meditation (Srinivasan and Baijal, 2007) – Mental work load (Kramer et al., 1995) – Mental retardation (Holopainen et al., 1998; Ikeda et al., 2004; Kaga et al., 1999; Nakagawa et al., 2002; Yokoyama et al., 1995; Zurrón and Díaz, 1997) – Migraine (de Tommaso et al., 2004; Korostenskaja et al., 2010a; Valeriani et al., 2008) – Multiple schlerosis (MS) (Gil et al., 1993; Jung et al., 2006; Santos et al., 2006) – Narcolepsy (Naumann et al., 2001) – Neglect (Hemifield inattention) and extinction (Deouell et al., 2000a,b; Tarkka et al., 2011) – Noise and distraction (Bertoli et al., 2005; Gumenyuk et al., 2004; Mikkola et al., 2010; Shtyrov et al., 1998, 1999; Simoens et al., 2007) – Noise, different types of (Kozou et al., 2005) – Noise, occupational (Mäntysalo and Salmi, 1989) – Noise, occupational, long-term exposure (Brattico et al., 2005; Kujala and Brattico, 2009; Kujala et al., 2004) – Obsessive–compulsive disorder (Towey et al., 1994; Oades et al., 1996) – Obstructive sleep apnea syndrome (OSAS) (Gosselin et al., 2006) – Opioid dependence (Kivisaari et al., 2007) – Parkinson’s disease (Brønnick et al., 2010; Karayanidis et al., 1995; Pekkonen et al., 1995c; Vieregger et al., 1994) – Perinatal asphyxia (Leipälä et al., 2011)

430

Table 1 (continued)


– Perinatal intracerebral hemorrhage (Leipälä et al., 2011) – Persistent vegetative state (Boly et al., 2011; Fischer and Luauté, 2005; Kotchoubey, 2007; Kotchoubey et al., 2003, 2007, 2008; Laureys et al., 2005; Wijnen et al., 2007; Zarza-Lucianez et al., 2007) – Personality differences (Matsubayashi et al., 2008; Franken et al., 2005) – Phonological deficit (Blitz et al., 2007) – Plagiocephaly (Huotilainen et al., 2008) – Post-traumatic stress syndrome (PTSS) (Cornwell et al., 2007; Ge et al., 2011; Menning et al., 2008; Morgan and Grillon, 1999) – Psychosocial stress (Simoens et al., 2007) – Prematurely born (with very low birth weight, VLBW) infants (Bisiachi et al., 2009; Cheour-Luhtanen et al., 1996; Fellman and Huotilainen, 2006; Fellman et al., 2004; Gomot et al., 2007; Holst et al., 2005; Jansson-Verkasalo et al., 2004, 2010; Leipälä et al., 2011; Mento et al., 2010; Mikkola et al., 2007, 2010) – REM-sleep deprivation (Zerouali et al., 2010) – Schizophrenia (Ahveninen et al., 2006; Baldeweg et al., 2002, 2004; Banati and Hickie, 2009; Bodatsch et al., 2011; Braff and Light, 2004; Brockhaus-Dumke et al., 2005; Catts et al., 1995; Davalos et al., 2003, 2005; Devrim-Ücok et al., 2008; Ehrlichman et al., 2008, 2009; Fisher et al., 2008, 2011; Grzella et al., 2001; Hermens et al., 2010; Hirayasu et al., 1998, 2000, 2001; Inami et al., 2007; Jahshan et al., 2011; Javitt, 1993, 2000, 2009a,b; Javitt et al., 1996, 1998, 1999, 2000, 2008; Jessen et al., 2001; Kasai et al., 2001, 2002a,b,c, 2003a,b; Kathmann et al., 1995; Kaur et al., 2011; Kawakubo et al., 2006, 2007; Kiang et al., 2007, 2009; Kircher et al., 2004; Korostenskaja et al., 2005; Kreitschmann-Andermahr et al., 1999, 2001; Lavoie et al., 2007; Leitman et al., 2010; Light and Braff, 2005a,b; Luck et al., 2011; Magno et al., 2008; Matthews et al., 2007; Michie, 2001; Michie et al., 2002; Minami and Kirino, 2005; Morlet et al., 2000; Näätänen and Kähkönen, 2009; Niznikiewicz et al., 2009; Oades et al., 2006; Oknina et al., 2005; Park et al., 2002; Potts et al., 1998; Price et al., 2006; Rasser et al., 2011; Rissling et al., 2010; Salisbury et al., 2002, 2007; Sato et al., 1998, 2002; Schall et al., 1998, 1999, 2003; Schreiber et al., 1992; Shelley et al., 1991; Shin et al., 2009; Shinozaki et al., 2002; Stone et al., 2010; Thönnesen et al., 2008; Todd et al., 2008; Todd et al., in press; Todd et al., 2003, 2008; Turetsky et al., 2007, 2009; Umbricht et al., 1998, 1999, 2000, 2002, 2003, 2006; van der Stelt and Belger, 2007; Verbaten and van Engeland, 1995; Wible et al., 2001; Wynn et al., 2010; Yamasue et al., 2004; Youn et al., 2003; for a meta-analysis of 32 studies, see Umbricht and Krljes, 2005) – Serotonin transporter gene variants, individuals with (Sysoeva et al., 2009) – Sensorineural hearing loss (Oates et al., 2002; Stapells, 2002) – Sleep (Atienza et al., 1997, 2000, 2002; Atienza and Cantero, 2001; Campbell et al., 1991; Cheour et al. 2000,2002; Martynova et al., 2003; Nashida et al., 2000; Nittono et al., 2001; Ruby et al., 2008; Sallinen et al., 1994, 1996; Sculthorpe et al., 2009) – Sleep deprivation (Gumenyuk et al., 2010; Raz et al., 2001; Sallinen and Lyytinen, 1997; Salmi et al., 2005; Wang et al., 2001; Zerouali et al., 2010) – Socially withdrawn children (Bar-Haim et al., 2003) – Somatisation disorder (James et al., 1989) – Specific language impairment (SLI) (Barry et al., 2008; Bishop and McArthur, 2004; Friedrich et al., 2004; Korpilahti, 1995; Marler et al., 2002; Pihko et al., 2008; Rinker et al., 2007; Shafer et al., 2007; Uwer and von Suchodoletz, 2000; Uwer et al., 2002; Weber et al., 2005) – Stroke (see Aphasia) – Stuttering (Corbera et al., 2005; Wu et al., 1997) – Temporal-parietal brain lesions (Alain et al., 1998) – Thalamic infarction (Mäkelä et al., 1998b) – Tourette syndrome (TS) (Oades et al., 1996; Rothenberger et al., 2000; van Woerkom et al., 1988, 1994) – Tune deafness (Braun et al., 2008) – Velo-cardio-facial (DiGeorge) syndrome (Baker et al., 2005)

431

R. Näätänen et al. / Clinical Neurophysiology 123 (2012) 424–458 Table 2 THE MMN shows abnormally short auditory sensory-memory duration in: Alzheimer’s disease (Pekkonen et al., 1994) Infants and children with cleft palate and CATCH-22 syndrome (Ceponiene et al., 2002; Cheour et al., 1997, 1998a, 1999) Late talkers (Grossheinrich et al., 2010) Chronic alcoholism (Grau et al., 2001; Marco-Pallares et al., 2007; Polo et al., 1999) Normal ageing (Cooper et al., 2006; Grau et al., 2001; Jääskeläinen et al., 1999a; Pekkonen et al., 1996a) Parents of children with specific language impairment (SLI) (Barry et al., 2008)

Table 3 The MMN provides an index of increased backward masking (affecting speech perception) in: – Chronic alcoholism (Ahveninen et al., 1999) – Dyslexia (Kujala et al., 2003) – Specific language impairment (SLI) (Marler et al., 2002)

duration, capacity and accuracy (Pekkonen et al., 1996a; Cooper et al., 2006; Polo et al., 1999; Grau et al., 2001). Furthermore, the auditory MMN can even index auditory long-term memory traces such as the language-specific memory traces, enabling one to correctly perceive the speech sounds of the mother tongue and other familiar languages (Dehaene-Lambertz, 1997; Näätänen, 2001; Näätänen et al., 1997; Pulvermuller et al., 2004; Shtyrov and Pulvermuller, 2007; Winkler et al., 1999c; Shtyrov and Pulvermüller, 2007). This linguistic MMN subcomponent is usually left-hemispherically predominant and generated posteriorly to the bilateral MMN subcomponent for mere acoustic change (Näätänen et al., 1997; Shestakova et al., 2002). The extensive MMN literature of clinical studies can be classified according to the kind of clinically useful information that can be obtained by using the MMN. The MMN can index: (1) Auditory discrimination accuracy (which is decreased in a number of clinical groups and affected by different drugs) (Table 1); (2) shortened sensory-memory duration (and hence possibly decreased general brain plasticity) (Table 2); (3) abnormal auditory perception; (4) increased backward masking (Table 3); (5) abnormal involuntary attention switching, either too weak (Table 4) or too strong (Table 5); (6) cerebral grey-matter loss and other structural changes (Table 6); (7) pathological brain excitation/excitability state (Table 7); (8) cognitive and functional decline (Table 8); (9) the level of consciousness (Table 9); (10) the progression of illness (Table 10); (11) future clinical condition (prognosis) (Table 11); (12) genetic disposition to certain disorders (Table 12); and (13) recovery/improvement as a function of time or treatment (Table 13). Moreover, recent studies using the vMMN (Iijima et al., 1996; Lorenzo-Lopez et al., 2004; Tales and Butler, 2006; Tales et al., 2002a,b; Kenemans et al., 2010; Tales and Butler, 2006; Tales et al., 2002a, 2008; Maekawa et al., 2011; Froyen et al., 2010; Chang et al., 2010; Qiu et al., 2011; Horimoto et al., 2002; Hosák et al., 2008; Kremlácˇek et al., 2008, Verbaten et al., 1994; Tales and Butler, 2006; Tales et al., 2008; Fisher et al., 2010; Urban et al., 2008; for a recent review, see Kimura et al., 2011) and sMMN (Restuccia et al., 2007; Akatsuka et al., 2005, 2007; Näätänen, 2009) have also provided clinically important results. The present review aims at covering all clinical MMN studies in the auditory modality published in refereed international English-

language journals. Almost all these studies report, with only a few exceptions, group-level results. 2. The MMN as an index of decreased auditory discrimination accuracy (Table 1) In several clinical conditions, the MMN amplitude is attenuated, usually indexing decreased behavioural discrimination accuracy (Javitt et al., 1998; Rabinowicz et al., 2000; Matthews et al., 2007). This amplitude reduction was usually found by recording the MMN to simple frequency or duration changes in sinusoidal tones, for instance, in schizophrenia (Todd et al., 2003; Javitt et al., 2000; Michie et al., 2000; see also Javitt et al., 1998). In schizophrenia, the duration MMN, in particular that to duration increment, was even more affected than that to frequency change (Michie, 2001; Michie et al., 2000; for a meta-analysis, see Umbricht and Krljes, 2005). The frequency MMN is attenuated in amplitude in several other clinical groups, too, such as children with developmental dysphasia (Holopainen et al., 1997, 1998; Korpilahti and Lang, 1994), dyslexia (Baldeweg et al., 1999; Renvall and Hari, 2003; Kujala et al., 2003, 2006; Sebastian and Yasin, 2008) and SLI (Mengler et al., 2005; Rinker et al., 2007). In children and adults with dyslexia, the MMN to frequency change but not that to duration change was considerably attenuated in amplitude (Baldeweg et al., 1999; Kujala et al., 2006). Furthermore, in keeping with this profile of MMN-amplitude reduction, the behavioural frequency but not duration discrimination was affected (Baldeweg et al., 1999). In addition, this frequency-MMN deficit strongly correlated with the severity of the reading problem. Subsequently, Lachmann et al. (2005)

MMN

MMN

Amplitude

– – – – – –

Time

Left hemisphere

Right hemisphere

3-5 days 10 days 3 months Fig. 3. MMN shows how frequency discrimination recovered to normal levels within 3 months from a stroke onset (averaged data of 8 patients). This MMN recovery was slower for right-ear stimulation (with the main part of the auditory input going to the damaged left hemisphere) (curves on the left) than with left-ear stimulation (curves on the right). During the MMN recording, the patient was watching video-films. Adapted from Ilvonen et al. (2003).

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Table 4 The MMN shows decreased involuntary attention switching in: – – – – – –

Alcohol intoxication (Jääskeläinen et al., 1995, 1996a,b, 1999b) Schizophrenia (Baldeweg et al., 2002; Catts et al., 1995; Matthews et al., 2007; Oades et al., 2006; Sato et al., 2003) Closed-head injury (Polo et al., 2002) Frontal-lesion patients (Alho et al., 1994) Right-hemisphere damage (unilateral neglect) (Deouell et al., 2000a,b) Children with major depression (Lepistö et al., 2004)

showed that the MMN-attenuation profile involving frequency and consonant–vowel (CV) syllable changes could disentangle different diagnostic subgroups of developmental dyslexia from each other. Moreover, Shafer et al. (2005) and Uwer et al. (2002) found that SLI children had attenuated MMN amplitudes for syllable change. Using the new multi-feature MMN ‘optimum’ paradigm (Näätänen et al., 2004), permitting one to obtain five different MMNs in 15 min, Lovio et al. (2010) found a widespread auditory discrimination deficit in children at risk for dyslexia. Their MMNs for consonant, vowel, vowel duration and intensity changes of syllables were diminished in amplitude. By contrast, Kujala et al. (2006), also using the multi-feature paradigm, found that in adult dyslexics, the frequency MMN was attenuated, whereas their location MMN was in fact enhanced in amplitude. This shows that not all changes in central auditory processing in dyslexia signify deteriorated discrimination. However, the MMN data may also suggest the presence of cognitive deficiencies associated with dyslexia, at least deficient phonotactic processing (Bonte et al., 2007). Furthermore, in children with autism, the MMN to duration change (Lepistö et al., 2005) and the MMNm to speech-sound change (Kasai et al., 2005; for recent corroborating results, see Roberts et al., 2011) were attenuated in amplitude. In addition, the MMN to CV-syllable change was prolonged in peak latency but only in those children who preferred non-speech analogy signals to speech (Kuhl et al., 2005). By contrast, the MMN to frequency change was enhanced in amplitude (Lepistö et al., 2005; Ferri et al., 2003) and shortened in peak latency (Gomot et al., 2002) in autistic children, consistent with their better-than-average pitch discrimination and musical abilities (Bonnel et al., 2003; Heaton et al., 2001). Very recently, it was found by Roberts et al. (2011;

see also Näätänen and Kujala, 2011) that in autistic children of 7–9 years, the MMNm peak latency for tone-frequency and vowel changes was delayed, in comparison with that of normally developing children of the same age, and, further, that this delay was considerably increased if the child also suffered from a delay in linguistic development. This might contribute to their speech-understanding difficulties and hence to their social isolation. In addition, in the Asperger syndrome, a condition belonging to the autism spectrum, the duration-increment MMN of children of about 9 years of age was attenuated in amplitude over the left hemisphere, whereas it was enhanced over the right hemisphere (Lepistö et al., 2006). Moreover, in this syndrome, the MMN amplitude was also attenuated for changes in prosody (Kujala et al., 2005a). Recently, a shortened MMN peak latency for frequency change and increased MMN amplitudes for duration and gap changes were found in Asperger adults by Kujala et al. (2007). In addition, the MMNs for frequency and duration changes were attenuated in amplitude in patients with a left-hemispheric stroke (Csépe et al., 2001; Aaltonen et al., 1993; Auther et al., 2000; Ilvonen et al., 2001, 2003; Pettigrew et al., 2005). These two MMNs showed somewhat different time courses of post-stroke recovery, however (Ilvonen et al., 2003) (Fig. 3). Importantly, the MMN recovery indexed that of speech perception, there being a correlation between the duration-MMN amplitude and the Boston Diagnostic Aphasia Examination Speech-Comprehension Test from 10 days to 3 months post-stroke onset (Ilvonen et al., 2003). Subsequently, Särkämö et al. (2010b) found that the MMNm recovery and behavioural discrimination could be expedited with music and speech stimulation. In addition, the MMNm recovery corre-

Fig. 4. Scatterplot of MMN amplitude at Fz versus age, for schizophrenia patients (open circles; dashed regression line) and normal control subjects (solid circles; solid regression line) (From Kiang et al., 2009).

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R. Näätänen et al. / Clinical Neurophysiology 123 (2012) 424–458 Table 5 The MMN shows increased involuntary attention switching in: – – – – –

Closed head injury (Kaipio et al., 2000) Ageing (Gaeta et al., 2001) Alcoholism (Ahveninen et al., 2000b; Polo et al., 2003) Children with major depression (Lepistö et al., 2004) Sleep disorder (Gumenyuk et al., 2010)

F3

Fz

F4

0.5 s

MMN

4.5 s lated with the recovery of behavioural speech-sound discrimination. In epilepsy, the MMN is also affected. The MMN peak latencies were abnormally long or no clear MMN response could be found for speech (but could for tones) in patients with benign childhood epilepsy with contra-temporal spikes (Boatman et al., 2008; Duman et al., 2008). Patients with such spikes with atypical features and learning difficulties also exhibit attenuated MMN amplitudes (Metz-Lutz and Philippini, 2006). In addition, in the Landau–Kleffner syndrome, an MMN was obtained for phoneme change but not for prosodic change (Honbolygó et al., 2006). By contrast, Miyajima et al. (2011), studying adult patients with temporal-lobe epilepsy, found that at fronto-central sites, their MMN amplitude for tonefrequency change was enhanced, interpreted by the authors as reflecting frontal-lobe hyperexcitability to compensate for temporal-lobe dysfunction indexed, according to the authors, by prolonged MMN peak latencies in patients relative to controls at both fronto-central and mastoid sites, consistent with previous reports (Lin et al., 2007; Borghetti et al., 2007). Furthermore, in the Miyajima et al. (2011) temporal-lobe epilepsy patients, the fronto-centrally recorded MMN persisted longer than that in controls, consistent with the results of Gene-Cos et al. (2005) who suggested that a prolonged MMN duration might point to difficulty in ‘the closure mechanism of the MMN process’. The MMN can also be used to evaluate the possible centralauditory-processing damage associated with a very premature birth. Studying very prematurely born children (mean gestational age 29 weeks) with a very low birth weight (mean 1115 g), Jansson-Verkasalo et al. (2003b, 2004) found that their MMN amplitude for consonant change at 4 years (from conception) was smaller than that of controls and, further, that the absence of the MMN at 4–5 years of age predicted naming difficulties at 6 years. However, if the MMN amplitude nevertheless was normal at 4 years, then there were no naming difficulties at 6 years. Moreover, the MMN enables one to also determine centralauditory-processing damage caused by long-term exposure to loud occupational noise. In workers exposed to such a noise for 2– 17 years, the MMN to syllable change was attenuated in amplitude (even though their peripheral hearing was not affected), in keeping with their increased speech-perception problems (Kujala et al., 2004). In addition, the Brattico et al. (2005) MMN data showed that long-term exposure to occupational noise altered the cortical organisation of speech-sound processing in these workers (in the absence of peripheral hearing loss) but did not alter that of nonspeech processing. In addition, the discrimination of auditory stimuli was generally slowed down, as indexed by prolonged MMNpeak latencies. Furthermore, by using the MMN, one can also monitor age-related changes in central auditory processing (Fabiani et al., 2006; Woods, 1992; Woods and Clayworth, 1986; Jääskeläinen et al., 1999a; Kiang et al., 2009; Cooper et al., 2006; Gaeta et al., 1998, 2001, 2002; Kisley et al., 2005; Pekkonen, 2000; Pekkonen et al., 1995a, 1996a). A particularly convincing characterisation of the MMN–age relationship was provided by Kiang et al. (2009) who carefully plotted the MMN and P3a amplitudes for tone-duration increment across adulthood for 147 normal subjects and 253 schizophrenic patients (Fig. 4). Along with an increasing age, the

Younger Males (mean 22 yrs) Older Males (mean 59 yrs) Fig. 5. MMN to frequency change (700 ? 600 Hz) was normal in older males with an inter-stimulus interval (ISI) of 0.5 s but was considerably attenuated, relative to that of younger males, with an ISI of 4.5 s, indexing faster auditory sensory-memory trace decay with aging (From Pekkonen et al., 2001a).

level of performance in different cognitive tasks is gradually decreased (Cansino, 2009). There is also evidence linking these MMN changes to cognitive deterioration (Kisley et al., 2005). Even in healthy elderly persons, the MMN to a short gap in the middle of a tone (Desjardin et al., 1999) was attenuated in amplitude, indexing their increased difficulties in correctly perceiving rapid speechsound patterns such as consonants (Bertoli et al., 2002, 2005). The MMN and MMNm are also affected by different drugs (Table 1).

3. The MMN as an index of shortened sensory-memory duration (Table 2) The MMN elicitation depends on the presence of the sensorymemory trace representing the preceding stimuli and their regularities at the moment of the delivery of a deviant stimulus (for a review, see Näätänen et al., 2007). Hence, by gradually prolonging the inter-stimulus interval (ISI), the MMN eventually vanishes, which enables one to assess sensory-memory duration in audition (a potential general index of brain plasticity; Näätänen and Kreegipuu, 2011). In young healthy adults, the trace duration, as estimated in this manner, approximates 10 s (Böttcher-Gandor and Ullsperger, 1992; Sams et al., 1993), but is gradually shortened with ageing. With short ISIs such as 0.5 s, the MMN amplitude for frequency change was very similar in elderly (mean 59 years) and young (mean 25 years) male subjects, suggesting that the memory-trace formation for sounds and, thus, perception (see Näätänen and Winkler, 1999) were not affected by ageing. By contrast, with a stimulus-onset asynchrony (SOA) of 4.5 s, the MMN amplitude of the elderly was much more attenuated than that of the young (Pekkonen et al., 1996a) (Fig. 5), indicating that in ageing, the auditory sensory-memory duration is shortened. Moreover, corresponding MMN data for frequency change in chronic alcoholics suggest accelerated age-related shortening of the memory-trace duration in these patients (Polo et al., 1999; see also Grau et al., 2001). The memory-trace duration is particularly short in patients with Alzheimer’s disease, of course. Their MMN was, however, normal with short ISIs (0.5 s), suggesting normal memory-trace formation/perception (see Näätänen and Winkler, 1999) even in these patients, but absent at long ISIs (3 s) (Pekkonen et al., 1994), indexing their extremely short sensory-memory duration. Interestingly, this data pattern is orthogonal to that observed in patients with schizophrenia in whom no normal-amplitude MMN can be obtained in any condition, not even with very short ISIs and wide frequency deviations (Javitt et al., 1998). This suggests that their memory-trace formation, and hence auditory perception

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Table 6 The MMN correlates with structural changes in: – Schizophrenia (Hirayasu et al., 2000, 2001; Kasai et al., 2003a,b; Park et al., 2002; Rasser et al., 2011; Salisbury et al., 2002, 2007; Yamasue et al., 2004; Youn et al., 2003; for a review, see van der Stelt and Belger, 2007) – Cleft palate (children with) (Ceponiene et al., 1999)

-4 µV

F4 +1 µV

350 ms

350-ms ISI 700-ms ISI 1400-ms ISI Fig. 6. MMN for tone-frequency change was of normal amplitude in 7–9 year old children with oral clefts when a short ISI (350 ms) was used but was considerably smaller than that of controls when the ISI was prolonged to 700 ms and to 1400 ms, suggesting an accelerated sensory-memory trace in patients (From Ceponiene et al., 1999).

(Näätänen and Winkler, 1999), is abnormal, consistent with clinical observations (for a review, see Näätänen and Kähkönen, 2009). By contrast, their sensory-memory duration, as judged from the ISI–MMN relationship in these patients, is unaffected (Javitt et al., 1998; see also March et al., 1999). The auditory memory-trace duration shows developmental changes also in the beginning of the life, but to the opposite direction, of course, being only 0.5 s in newborns, as judged from MMNs recorded during sleep (Cheour et al., 2002b), but is thereafter gradually prolonged during infancy and childhood. By using the Grau et al. (1998) MMN paradigm for effectively determining the sensory-memory duration, Glass et al., 2008a,b) found that this duration was about 1–2 s at the age of 2–3 years but was prolonged to 3–5 s by the age of 6 years (see also Gomes et al., 1999). This memory-trace duration is affected in some child patient groups, too. In children of 7–8 years with cleft palate, the MMN for tone-frequency change was of normal amplitude with short SOAs (350 and 700 ms), whereas the prolongation of the SOA to 1400 ms attenuated this amplitude much more than it attenuated that of control children (Ceponiene et al., 1999) (Fig. 6). Furthermore, an analogous data pattern was obtained in small infants with cleft palate, which was even more abnormal in children with the Catch-22 syndrome (Cheour et al., 1997, 1998a, 1999). In addition, a short auditory sensory-memory duration even in normal healthy children is associated with delayed linguistic development. Late talkers had a shorter sensory-memory duration than that of controls, as judged from MMN data for tone-frequency change as a function of the ISI recorded at the age of 4 years 7 months, even though the language development was normal by that age (Grossheinrich et al., 2010). Furthermore, the Barry et al. (2008) recent MMN data for tonefrequency change as a function of the ISI suggested a shorter auditory sensory-memory duration in parents of children with SLI than that in parents of normally developing children.

4. The MMN as an index of abnormal auditory perception In the foregoing, it was already mentioned that in patients with schizophrenia, no normal-size MMN can be obtained irrespective of experimental manipulations, not even with very short SOAs (Javitt et al., 1998). This suggests a fundamental abnormality in memory-trace formation, and thus in auditory perception (see Näätänen and Winkler, 1999), in these patients (Näätänen and Kähkönen, 2009). Moreover, a number of further studies in patients with schizophrenia (Oades et al., 1996; Hirayasu et al., 1998; Schall et al., 1999; Youn et al., 2003; Kasai et al., 2002a,b) showed that the frequency-MMN amplitude deficit tends to correlate with the severity of auditory hallucinations. In addition, Youn et al. (2003) found that the abnormality of the left–right MMN-amplitude asymmetry for frequency change of a tone correlated with the positive scores of the positive-and-negative syndrome scale (PANSS), in particular with its hallucination subscale. For corroborating MMNm data, see Thönnesen et al. (2008). Moreover, Fisher et al. (2008) found a smaller duration-MMN amplitude in patients with auditory hallucinations than in those with no hallucinations. In addition, the MMN amplitude for intensity change was also smaller in hallucinating than non-hallucinating patients. Furthermore, both patient groups showed an attenuated MMN amplitude for frequency change. This MMN deficiency however was differently distributed in frontal areas in the two patient groups. 5. The MMN as an index of increased backward masking (Table 3) Auditory masking refers to any observation such that information in a test auditory stimulus is reduced by the presentation of another (masking) auditory stimulus (Massaro, 1973). The perception of sequentially presented auditory stimulation may be hindered by backward masking, with a sound preventing the perception of an immediately preceding sound, apparently by affecting its memory-trace formation (Massaro, 1975), in particular when the later sound is stronger in intensity than the preceding sound (see Hawkins and Presson, 1986). Massaro (1975) concludes that backward masking occurs because the masking stimulus essentially overwrites the auditory image of the test stimulus and, therefore, terminates the perceptual processing of the test stimulus. Backward masking can be assessed both behaviourally and by using the MMN: a masker presented shortly after each stimulus of the oddball paradigm causes the MMN to deviants and the subject’s ability to discriminate them behaviourally to disappear in parallel (Winkler and Näätänen, 1994; Winkler et al., 1993). By using this type of paradigm, it was found by Kujala et al. (2003) that backward masking is enhanced in dyslexic individuals. Increased backward masking, as reflected by MMN-data pattern, was also reported in chronic alcoholism (Ahveninen et al., 1999). Importantly, this MMN deficit in chronic alcoholism correlated with the amount of their alcohol consumption and predicted their working-memory performance deficit (Ahveninen et al., 1999). 6. The MMN as an index of abnormal involuntary attention switching: either too weak (Table 4) or too strong (Table 5) As already mentioned, in addition to its auditory-cortex generators, the MMN also has a frontal (usually right-hemispherically predominant (Giard et al., 1990)) generator contributing, together with the auditory-cortex MMN generator (see Fig. 2), to the frontally and centrally recorded MMN amplitudes (Deouell, 2007; Giard et al., 1990; Rinne et al., 2000). The frontally recorded MMN amplitude is considerably attenuated, whereas the

R. Näätänen et al. / Clinical Neurophysiology 123 (2012) 424–458 Table 7 The MMN indexes pathological brain excitation/excitability in: – – – – – – –

Alcoholism (Ahveninen et al., 2000a; Pekkonen et al., 1998) ALS (with bulbar signs) (Pekkonen et al., 2004) Chronic primary insomniacs (Wang et al., 2001) Epilepsy (Miyajima et al., 2011) Huntington’s disease, Syndromatic Phase (Beste et al., 2008) Major depression, children with (Lepistö et al., 2004) Pediatric migraine (Valeriani et al., 2008; see, however, de Tommaso et al., 2004) – Schizophrenia (pathological microglia activation, indexing local disease process and neuronal death) (Banati and Hickie, 2009) – Stuttering (Corbera et al., 2005; see also Wu et al., 1997)

Table 8 The MMN indexes cognitive and functional decline in: – Ageing (Gaeta et al., 2002; Kisley et al., 2005; Schroeder et al., 1995) – Alzheimer’s disease and dementia (Engeland et al., 2002; Schroeder et al., 1995) – Amyotropic lateral schlerosis (ALS) (Raggi et al., 2008) – Autism (Seri et al., 2007; Roberts et al., 2008, 2011; Näätänen and Kujala, 2011) – CATCH-22 syndrome: children (for a review, see Ceponiene et al., 2002), adults (Baker et al., 2005) – Children with cleft palate (Ceponiene et al., 2002) – Chronic alcoholism (Polo et al., 1999) – Coma, survivors of (Kane et al., 2000) – Developmental dysphasia (Holopainen et al., 1997, 1998; Korpilahti and Lang, 1994) – Diabetes mellitus (advanced phase) (Vanhanen et al., 1996) – Down’s syndrome (Lalo et al., 2005) – Dyslexia (Bonte et al., 2007) – Epilepsy (Boatman et al., 2008; Liasis et al., 2000, 2001, 2006; Metz-Lutz and Philippini, 2006) – HIV (Schroeder et al., 1994) – Intellectual disability (Ikeda et al., 2004; Nakagawa et al., 2002) – Multiple schlerosis (MS) (Gil et al., 1993; Jung et al., 2006; Santos et al., 2006) – Parkinson’s disease (Brønnick et al., 2010; Karayanidis et al., 1995; Pekkonen et al., 1995c) – Persistent-vegetative-state (PVS), survivors of (Kotchoubey, 2007; Wijnen et al., 2007; van der Stelt and van Boxtel, 2008; Zarza-Lucianez et al., 2007) – Preterm children with very low birth weight (Jansson-Verkasalo et al., 2004, 2010) – REM-sleep deprivation (Zerouali et al., 2010) – Schizophrenia (e.g., Baldeweg et al., 2004; Hermens et al., 2010; Kawakubo et al., 2007; Light and Braff, 2005a,b; Rasser et al., 2011; Toyomaki et al., 2008) – Sleep deprivation (Raz et al., 2001) – Stroke and aphasia (Auther et al., 2000; Ilvonen et al., 2003, 2004; Pettigrew et al., 2005; Särkämö et al., 2009, 2010a,b; Wertz et al., 1998) – Velo-cardio-facial syndrome (Baker et al., 2005)

mastoid-recorded MMN (with nose reference) is unaffected in patients with schizophrenia (Baldeweg et al., 2002, 2004; Sato et al., 1998, 2002), suggesting dampened involuntary attention switching to auditory change and hence probably accounting for some of their withdrawal (negative) symptoms, as proposed by Näätänen and Kähkönen (2009) (cf. Fig. 2). Consistent with this, Matthews et al. (2007) found that the MMN at fronto-central electrodes for change in the interaural time difference, one of the two main cues for sound lateralisation, was attenuated in amplitude in patients with schizophrenia. This result was attributed by the authors to patients’ impaired ability to use temporal cues to sound lateralisation in natural settings, a deficit probably affecting, according to the authors, their ability to control the focus of attention effectively. The dampened bottom-up attention-switching function in schizophrenia patients might also contribute to their gradual cognitive decline because of the resulting reduction of cognitive and social stimulation (cf. sensory deprivation) (Näätänen and Kähkönen, 2009). For further supportive MMN evidence, see Hermens et al. (2010).

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A similar (but transient) dampening of involuntary attention switching can also be observed in acute alcohol intoxication (Jääskeläinen et al., 1995, 1996a,b, 1998, 1999b). Even a moderate dose of ethanol selectively weakened the frontal-MMN process, whereas the supratemporal MMN process (with most of it being separately observable in nose-referenced mastoid recordings) was unaffected (Jääskeläinen et al., 1996b) (Fig. 2). Furthermore, ethanol abolished the performance decrement caused by auditory distraction in a visual task (Jääskeläinen et al., 1999b), i.e., dampened the effects of auditory distracting stimuli on brain mechanisms controlling for environment-driven involuntary attention switches in audition (Escera et al., 2000a; Escera and Corral, 2007; Jääskeläinen et al., 1999b). This explains, in part, why alcohol increases accident risk in traffic (cf. Näätänen and Summala, 1976). In addition, the Alho et al. (1994) MMN data suggested decreased involuntary attention switching to auditory changes as a consequence of a frontal-lobe lesion (see Table 4). Conversely, the frontal involuntary attention-switching mechanism may also become too sensitive, in this way disturbing primary-task performance (Table 5). In patients with closed head injury suffering from dramatically increased distractibility, this mechanism is abnormally sensitive, judging from their very large frontally recorded MMN amplitudes at the presence of normal mastoid-recorded (nose-referenced) MMN amplitudes (Kaipio et al., 1999, 2000) (cf. Fig. 2). A subsequent study (Polo et al., 2002) did not confirm this finding, however, which might result from the abnormally fast vigilance decrement of these patients (Kaipio et al., 2001). Moreover, in children suffering from major depression, shortened MMN latencies and increased P3a amplitudes (an index of the occurrence of an attention switch; Squires et al., 1975; Escera et al., 2000a) might be associated with these patients’ increased distractibility and difficulties in concentrating on task performance, as shown by the Lepistö et al. (2004) MMN data for CV-syllable change. Analogous MMN evidence for increased distractibility was also obtained in chronic alcoholism (Ahveninen et al., 2000a,b) and ageing (Gaeta et al., 2001).

7. The MMN attenuation caused by cerebral grey-matter loss or other structural change (Table 6) The MMN is also attenuated by structural damage in the central auditory system and even elsewhere in the brain. In schizophrenia patients, a gradual loss of the left-hemisphere temporal grey-matter volume has been observed, which was reflected by attenuated MMN amplitudes for frequency change (Hirayasu et al., 1998). More recently, Salisbury et al. (2007) found, by using magnetic resonance imaging (MRI), that at first hospitalisation, schizophrenia patients’ left Heschl-gyrus volume did not differ from that of bipolar-disorder patients and normal controls and, further, that this was reflected by similar MMN amplitudes for tone-frequency change. However, in an 18-month follow-up, this volume was reduced in schizophrenia patients only, and the magnitude of the Heschl’s gyrus volume reduction in these patients strongly correlated with the parallel attenuation of their MMN amplitude. Also, Yamasue et al. (2004) found that in schizophrenia patients, MMNm deficiency for phoneme change in the left hemisphere correlated with the magnitude of the left planum-temporale grey-matter loss, suggesting that these structural abnormalities may underlie the functional abnormalities of fundamental language-related processing in these patients. In addition, very recently, Rasser et al. (2011) found that MMN-amplitude attenuation for frequency change in patients with schizophrenia (reflecting their impaired day-to-day functioning level) correlated with the magnitude of grey-matter loss in the left Heschl’s gyrus as well as in the motor and executive

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Fig. 7. Post Hoc correlation analyses of reduced gray matter measures – averaged over specific gyri defined on the Deformed ‘‘Montreal Neurological Institute’’ brain template – with reduced frequency mismatch negativity (MMN) peak amplitudes recorded at fronto-central electrodes in control subjects (blue) and schizophrenia patients (Red). Solid regression lines indicate significant correlation (P < .05, uncorrected) (From Rasser et al., 2011).

R. Näätänen et al. / Clinical Neurophysiology 123 (2012) 424–458 Table 9 The MMN can be used to on-line monitor the patient’s level-of-consciousness in: – Anaesthesis: depth and recovery (Heinke et al., 2004; Heinke and Koelsch, 2005; Koelsch et al., 2006; Yppärilä et al., 2002) – Coma (Kane et al., 1993, 1996, 2000; Fischer and Luauté, 2005; Luauté et al., 2005; Morlet et al., 2000; Naccache et al., 2005) – Persistent vegetative state (Kotchoubey, 2007; Kotchoubey, 2007; Wijnen et al., 2007)

regions of the frontal cortex while MMN reduction for duration deviants also correlated with grey-matter loss in the right Heschl’s gyrus (Fig. 7). It is possible that the MMN deficiency observed in schizophrenia can be linked to grey-matter loss occurring in these patients. Olney and Farber (1995) suggested that N-methyl-D-aspartate (NMDA)-receptor (NMDAR) hypofunction accounts for structural brain changes in these patients. The data reviewed by the authors showed, among other things, that a repeated treatment with an NMDA antagonist during a 3- to 4-day period induces a pattern of neurodegenerative changes distributed over several corticolimbic brain regions. The authors concluded that these and other findings signify that the persistent suppression of the NMDAR function lasting for a few days only can lead to relatively subtle but permanent structural changes that are distributed over the neocortical and limbic brain regions in a pattern roughly similar to the pattern of structural changes observed in schizophrenia (Bogerts, 1993). The fact that the MMN is an index of NMDAR dysfunction would then explain the relationship between MMN deficiency and greymatter loss (Salisbury et al., 2007; Rasser et al., 2011). The MMN can also reflect structural changes (craniofacial malformations) associated with cleft palate (for a review, see Ceponiene et al., 2002). In children with cleft palate of 7–9 years of age, it was found by Ceponiene et al. (1999) that the more posteriorly delimited the cleft was, the smaller was the MMN amplitude for tone-frequency change and the more severe was the cognitive defect. 8. The MMN as an index of pathological brain excitation/ excitability (Table 7) In some conditions, an increased MMN amplitude appears to index pathologically increased central nervous system (CNS) or central-auditory-system excitation/excitability. For example, in abstinent chronic alcoholics, the MMN for frequency change was abnormally enhanced in amplitude, which might be associated with their increased distractibility (Ahveninen et al., 2000a,b). In addition, in patients with persistent developmental stuttering, the MMN to phonetic contrasts was strongly enhanced in amplitude, whereas that to simple tone contrasts (both frequency and duration) was unaffected (Corbera et al., 2005). This might index abnormal excitability located specifically in the speech-sound MMN generation region (Näätänen et al., 1997). This MMN finding correlated with the patients’ subjective appraisal of their speechproduction problems. These results might indicate that proper speech production requires the presence of stable sensory reference provided by the speech-sound-specific memory traces of the left temporal cortex (Näätänen, 2001; Näätänen et al., 1997; Shestakova et al., 2003). In the same vein, an MMNm enhancement to tone-duration decrement found by Pekkonen et al. (2004) in patients with ALS with bulbar signs might result from cortical overactivity of excitatory neurotransmitter glutamate observed in ALS (Rowland and Shneider, 2001). Raggi et al. (2008), however, found MMN-amplitude decrement for frequency change in non-demented patients with sporadic ALS.

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Consistent with the Pekkonen et al. (2004) above-reviewed ALS results, at late, symptomatic, stages of Huntington’s disease, the MMN to frequency change was considerably enhanced in amplitude, along with behavioural improvement in an auditory signaldetection task, compared to the control group and Huntington patients in the early, presymptomatic, stage (Beste et al., 2008). This paradoxical effect, as contrasted to effects of neurodegenerative diseases in general, was attributed by the authors to toxic-level overexcitability of the NMDAR system (due to increased glutamate concentrations). In addition, very importantly, Banati and Hickie (2009); (see also Banati, 2003) found in patients in schizophrenic psychosis that MMN deficiency for frequency and duration deviants indexed pathological microglia (the main constituent of the brain’s innate immune system) activation, reflecting local ‘disease activity’ and neuronal death in these patients. The authors emphasised that this microglia activation is not a diagnostically specific pathological process but rather that this activation can serve as a generic marker that relates more directly to disease progression and may be correlated with other meaningful illness measures such as the MMN. Pathological brain excitation, as suggested by increased MMN amplitudes, can also be found in temporal-lobe epilepsy (Miyajima et al., 2011; Gene-Cos et al., 2005) even though MMN peak latencies may be prolonged, a possible sign of central-auditory-processing disturbance in these patients (Miyajima et al., 2011). Pathological excitation might also explain some results in patients suffering from post-traumatic stress disorder (PTSD), who showed considerably elevated MMN amplitudes for frequency change (Morgan and Grillon, 1999; Ge et al., 2011), whereas Menning et al. (2008) could not confirm these results.

9. The MMN as an index of cognitive and functional deterioration (Table 8) Baldeweg et al. (2004) found a relationship between the frontally recorded duration-increment MMN deficit and impairments in memory functions of patients with schizophrenia, which are evident in these patients (Sullivan et al., 1995; Jahshan et al., 2010). Subsequently, Light and Braff (2005a) obtained a strong correlation between the global-assessment-of-functioning (GAF) ratings and the fronto-central MMN amplitude for tone-duration prolongation in these patients. Furthermore, the MMN amplitude was highly predictive of the patients’ level of independence in their domestic life. This correlation was replicated in longitudinal studies 1– 2 years later, indicating a stable relationship (Light and Braff, 2005b). Subsequently, the relationship between the durationincrement MMN amplitude and patients’ functional status was also found by Kawakubo et al., 2007; social skills acquisition) and by Toyomaki et al. (2008; executive functioning). (For corroborating results with the frequency-MMN amplitude, see Rasser et al. (2011).) Interestingly, this relationship for duration-increment MMN amplitude is also present in normal healthy subjects (Light et al., 2007). For previous analogous results with the frequencyMMN amplitude in normal healthy subjects, see Bazana and Stelmack (2002) and Beauchamp and Stelmack (2006), and with the MMN amplitude for syllable change in children, Liu et al. (2007). For recent corroborating results, see Troche et al. (2009, 2010). In a similar vein, Jung et al. (2006) found that the MMN-amplitude attenuation for duration decrement in patients with MS indexed cognitive decline occurring in part of these patients, being larger in magnitude for greater cognitive loss. For corroborating results, see Gil et al., 1993) and Santos et al. (2006). Furthermore, MMN (MMNm) deficit indexes cognitive decline also in chronic alcoholism (Polo et al., 1999, 2003), stroke (Ilvonen et al., 2003;

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Table 10 The MMN can be used to monitor the patient’s state in: – Stroke: recovery (Ilvonen et al., 2003; Särkämö et al., 2010a,) – Schizophrenia: illness progression (Banati and Hickie, 2009; Bodatsch et al., 2011; Javitt et al., 2000; Oades et al., 2006; Oknina et al., 2005; Salisbury et al., 2007; Umbricht and Krljes, 2005; Umbricht et al., 2003, 2006) and temporary recovery (Shinozaki et al., 2002)

Särkämö et al., 2009, 2010a,; Auther et al., 1998, 2000; Pettigrew et al., 2005; Wertz et al., 1998), epilepsy (Boatman et al., 2008; Liasis et al., 2006), velo-cardio-facial (DiGeorge) syndrome (Baker et al., 2005), Down’s syndrome (Lalo et al., 2005), children with certain forms of cleft palate and those with the Catch-22 syndrome (Ceponiene et al., 2002) and, of course, in Alzheimer’s disease (Pekkonen et al., 1994; vMMN: Tales and Butler, 2006; Tales et al., 2008), dementia (Schroeder et al., 1995), intellectual disability (Nakagawa et al., 2002; Ikeda et al., 2004) and mild cognitive impairment (MCI) (vMMN: Tales and Butler, 2006; Tales et al., 2008). MMN-amplitude attenuation (at least for frequency change) can also index cognitive and functional degeneration in patients with an advanced stage of diabetes mellitus (Vanhanen et al., 1996), Parkinson’s disease (Karayanidis et al., 1995; Pekkonen et al., 1995b; Brønnick et al., 2010), HIV (Schroeder et al., 1994) and also in normal ageing (Gaeta et al., 2001; Kisley et al., 2005; Cooper et al., 2006). In addition, the MMN amplitude indexes decreased cognition in different subnormal states such as sleep deprivation (Raz et al., 2001), rapid eye movement (REM)-sleep deprivation (Zerouali et al., 2010) and in patients in the comatose (Fischer et al., 1999, 2006b) or PVS (Wijnen et al., 2007) state. Recently, Bisiachi et al. (2009) found smaller-amplitude MMN responses to tone-frequency change in newborns of less than 30 gestational weeks than in those with a longer gestational period. This amplitude strongly correlated with several maturational factors (gestational age, weight, length and cranial circumference). These results suggest, according to the authors, the role of the gestational age as the main factor explaining cortical functioning at the early age. 10. The MMN as an index of the level of consciousness (Table 9) In patients in the comatose state, no MMN can usually be recorded unless a latent recovery process has started, leading to the return of consciousness and cognitive capacities in the near future. Therefore, the MMN can be used as a tool in coma-outcome prediction (Kane et al., 1993, 1996; Fischer et al., 1999, 2004, 2006a,b; Luauté et al., 2005; Morlet et al., 2000; Fischer and Luauté, 2005; Daltrozzo et al., 2007; Vanhaudenhuyse et al., 2008). Moreover, the MMN peak latency measured at hospitalisation of survivors of coma caused by a severe head injury predicted, to some extent, their expressive language ability and visuo-spatial performance 1 year after the injury (Kane et al., 2000). Kotchoubey (2007) stressed that in using the MMN for the objective assessment of the patient’s remaining cognitive capacity, it is better to use complex rather than simple sound stimuli which may result in severe underestimation of the remaining capacity. For a meta-analysis of studies on the MMN in coma, see Daltrozzo et al. (2007). Recently, it was concluded by Vanhaudenhuyse et al. (2008) that MMN results in comatose patients converge to the conclusion that MMN is a very good predictor of recovery from coma, in particular in anoxic coma. In patients in the PVS, the frequency-MMN recovery occurred in parallel with the recovery of consciousness (Wijnen et al., 2007; Kotchoubey, 2007; Kotchoubey, 2007), showing a step-wise ampli-

tude increase when the patient crossed the boundary from unconsciousness to consciousness. In addition, in locked-in patients, the frequency MMN can give evidence for the presence of at least some level of consciousness (Ragazzoni et al., 2000). Moreover, the MMN can also index anaesthesia depth (for a review, see Heinke and Koelsch, 2005): a small-amplitude MMN was recorded to frequency change during deep sedation, whereas in complete unconsciousness, this MMN was absent. It, however, returned while the patient was recovering from anaesthesia (Heinke et al., 2004). Interestingly, an MMN type of response was also elicited by music-syntactic violations in deep sedation (Heinke et al., 2004; Koelsch et al., 2006), indicating that this kind of complex analysis following the rules of Western music can occur even in deep sedation. Very recently, it was found by Boly et al. (2011) that in the vegetative state, feed-forward processes are preserved whereas topdown processes are impaired. The effective connectivity was measured by using the MMN for tones presented in a roving paradigm (Baldeweg et al., 2004). The authors found that the only difference between patients in the vegetative state and controls was an impairment of backward connectivity from frontal to temporal cortices, suggesting that a selective disruption of top-down processes from high levels of a cortical hierarchy can lead to loss of consciousness in brain-damaged patients, and can clearly differentiate the vegetative state from minimally conscious state. In addition to its neuroscientific relevance, the present approach could, according to Boly et al. (2011), constitute a new diagnostic tool to quantify the level of consciousness electrophysiologically at the patients’ bedside. The MMN can also reflect effects of hypnosis (Jamieson et al., 2005; Kallio et al., 1999) and concentrative meditation (Srinivasan and Baijal, 2007).

11. The MMN as an index of the progression/severity of the illness (Table 10) In patients with schizophrenia, the MMN amplitude in particular to frequency change is attenuated concomitantly with disease progression (for a meta-analysis, see Umbricht and Krljes, 2005). Consistent with this, several studies (Salisbury et al., 2002, 2007; Umbricht et al., 2006; Devrim-Ücok et al., 2008; Todd et al., 2008) showed that the frequency MMN deficit was more robust in chronic patients than in first-episode patients in whom the effect was smaller in size or had not yet emerged. In addition, Shinozaki et al. (2002) found that a temporary recovery of acute symptoms of schizophrenia patients was accompanied by an MMN amplitude increase for tone-frequency change recorded at mastoids as polarity-reversed MMN (whereas the frontally recorded MMN did not correlate with this temporary recovery). In addition, Urban et al. (2008), using the vMMN, found that the reduction of its amplitude for motion-direction deviants was larger for a more severe state and longer duration of the illness of the patient. Moreover, MMN data also reflected clinical severity in patients with persistent developmental stuttering (Corbera et al., 2005), dyslexia (Baldeweg et al., 1999; Stoodley et al., 2006), PTSD (Menning et al., 2008) and in newborns and 6-month-old infants with cleft palate (with clinical severity being determined as the anterior–posterior extent of the cleft; Ceponiene et al., 1999, 2000a,b, 2002). In a similar vein, Moberget et al. (2008) found that patients exhibiting the most severe symptoms of ataxia, a sign of cerebellar cortical atrophy, produced smaller-amplitude MMN responses to tone-duration change than other patients. Studying stroke patients, Särkämö et al. (2008, 2009, 2010a, addressed amusia caused by a left or right middle cerebral artery


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Table 11 The MMN predicts: – Recovery from coma (Daltrozzo et al., 2007; Fischer and Luauté, 2005; Fischer et al., 1999, 2002, 2004, 2006a,b; Morlet et al., 2000; Naccache et al., 2005; Vanhaudenhuyse et al., 2008 (with the MMN being the best predictor of positive outcome, i.e., recovery without getting into the persistent vegetative state: Fischer and Luauté, 2005; Luauté et al., 2005); for a meta analysis, see Daltrozzo et al., 2007) – Recovery from the persistent vegetative state (Kotchoubey, 2007; Kotchoubey et al., 2007; Wijnen et al., 2007 (with the MMN recorded at hospilization also predicting the level of consciousness at discharge and even the extent of cognitive recovery during the next 2 years; Wijnen et al., 2007)) – Recovery from locked-in state (Ragazzoni et al., 2000) – Recovery from alcoholism (Kathmann et al., 1995; Pekkonen et al., 1998) – Social-skills learning in schizophrenia Kawakubo et al., 2007) – Social cognition in schizophrenia (Wynn et al., 2010) – Schizophrenia (first-episode onset) risk (Bodatsch et al., 2011; Stone et al., 2010) – Progression of schizophrenia (Bodatsch et al., 2011; Devrim-Ücok et al., 2008; Kawakubo et al., 2007; Kiang et al., 2009; Light and Braff, 2005b; Salisbury et al., 2007; Umbricht and Krljes, 2005; Umbricht et al., 2006) – Dyslexia (Blitz et al., 2007; Leppänen et al., 2010; van Leeuwen et al., 2006; Stoodley et al., 2006) – Language development (Choudhury and Benasich, 2011; for a review, see Stix, 2011) – Language development in prematurely born children (Jansson-Verkasalo et al., 2003b, 2004, 2010) – Drug-therapy outcome in schizophrenia (Horton et al., 2010; Javitt et al., 2008; Lavoie et al., 2007; Schall et al., 1999) – Working-memory performance decrement in chronic alcoholism (Ahveninen et al., 1999)

stroke. They found that amusia caused by a right-hemisphere damage, especially that to temporal and frontal areas, was more severe than that caused by a left-hemisphere damage. Furthermore, in amusic right-hemisphere patients, the severity of amusia correlated with weaker frequency-MMNm responses. Additionally, within the right-hemisphere-damaged group, the amusic patients who had damage in the auditory cortex showed worse recovery from amusia as well as weaker MMNm responses throughout the 6-month follow-up than did the non-amusic patients or the amusic patients with no auditory-cortex damage. Also, the amusic patients (both with and without auditory-cortex damage) performed worse than did the non-amusic patients on a number of tests of different aspects of cognitive performance (including working memory, attention and cognitive flexibility). These findings suggested, according to the authors, domain-general cognitive deficits as the primary mechanism underlying amusia without auditory-cortex damage, whereas amusia with auditory-cortex damage is associated with both auditory and cognitive deficits. In conclusion, because of the large number of different disorders affecting the MMN, it appears that the MMN provides a generic illness measure, useful for assessing illness severity, as suggested by Banati and Hickie (2009) for both the MMN and microglia activation.

12. The MMN in predicting illness course/drug response (prognosis) (Table 11) A striking finding was that the recovery of the MMN in a comatose patient strongly predicted, as already mentioned, the recovery of consciousness in the near future (Kane et al., 1993, 1996; Fischer et al., 2000, 2006a,b; see also Fischer et al., 2008; Luauté et al., 2005; Vanhaudenhuyse et al., 2008; for a meta-analysis, see Daltrozzo et al., 2007). In addition, the MMN in patients in the PVS recorded at hospitalisation predicted the magnitude of cognitive recovery even 2 years ahead (Wijnen et al., 2007; see also Kotchoubey, 2007; Kotchoubey et al., 2007).

Fig. 8. Grand-average difference waves showing the duration mismatch negativity in the frontal (upper row) and central electrodes (lower row) for converting (dashed line) and nonconverting subjects (solid line). AR-C = at risk – coinversion, ARNC = at risk – no conversion (From Bodatsch et al., 2011).

Table 12 The MMN shows increased genetic risk of: – Alcoholism (Rodriguez et al., 1998; Zhang et al., 2001) – Asperger syndrome (Jansson-Verkasalo et al., 2005; Korpilahti et al., 2007) – Dyslexia (Blitz et al., 2007; Friedrich et al., 2004; Leppänen et al., 2002, 2010; Leppänen and Lyytinen, 1997; Lyytinen et al., 2001, 2004, 2006; Maurer et al., 2009; Pihko et al., 1999; Richardson et al., 2003; van Leeuwen et al., 2006) – Language learning impairment (LLI) (Benasich et al., 2006; Choudhury and Benasich, 2011; Friedrich et al., 2004; Weber et al., 2005) – Schizophrenia in children (Schreiber et al., 1992), adults (Ahveninen et al., 2006; Bodatsch et al., 2011; Brockhaus-Dumke et al., 2005; Hall et al., 2007, 2009; Jessen et al., 2001; Magno et al., 2008; Michie et al., 2002; Shin et al., 2009), and in Individuals with the CATCH syndrome (with a higher risk in individuals carrying the COMT108/158Val than COMT108/ 158 Met allele) (Baker et al., 2005) – Specific language impairment (SLI) (Barry et al., 2008; Benasich and Tallal, 2002; Benasich et al., 2006; Friedrich et al., 2004; Weber et al., 2005)

Furthermore, in patients with schizophrenia, MMN data can predict future developments of the patient’s state and the efficiency of different treatments. For example, Umbricht et al. (2006) found that MMN deficiency at illness onset may index the presence of a more pervasive brain pathology and be observed only in a subgroup of patients, possibly in those with more precursors of schizophrenia or with an elevated risk of developing chronic schizophrenia. In addition, Kawakubo et al. (2007) found that the MMN in patients with schizophrenia was predictive of the acquisition of social skills during a 3-month social skills training programme. Importantly, it was recently found by Lavoie et al. (2007) that the deficient MMN amplitude for frequency change in patients with schizophrenia was corrected towards normal levels by a glutathione precursor, N-acetyl-cysteine (NAC), which improved their NMDAR function, supporting the role of the NMDARs in MMN generation. The MMN improvement was, however, found in the absence of any robust changes in clinical-severity indices, even though they were observed in a larger and more prolonged clinical study (Lavoie et al., 2007; Berk et al., 2008a,b; for supporting evidence,

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Table 13 MMN indexes central-auditory-processing improvement in: – Autistic patients (with frequency processing better than in Controls; Gomot et al., 2002) – Children with specific language impairment (SLI) receiving language and speech training (Pihko et al., 2007) – Cochlear-implant (CI) patients as a function of time since CI installation (Kraus et al., 1993b; Lonka et al., 2004; Ponton et al., 2000; Ponton and Eggermont, 2001) and training (Ponton et al., 2009) – Dyslexic children presented with consonant–vowel syllables with lengthened formant-transition duration (Bradlow et al., 1999) – Dyslexic children receiving audio-visual rehabilitation (Kujala et al., 2001) – Early Child development, mainly speech-sound learning (Alho and Cheour-Luhtanen, 1997; Alho et al., 1990; Carral et al., 2005; Cheour et al., 1998b, 2002a,b; CheourLuhtanen et al., 1996; Choudhury and Benasich, 2011; Draganova et al., 2005, 2007; Gomes et al., 2000; Gomot et al., 2000; Fellman and Huotilainen, 2006; Huotilainen et al. 2005, 2007; Kraus and Cheour, 2000; Kraus et al., 1992, 1993a, 1999; Kuhl, 2004; Kujala et al., 2004; Kushnerenko et al., 2002, 2007; Leppänen et al., 2004; Lovio et al., 2009; Lyytinen et al., 2001, 2006; Molholm et al., 2004; Novitski et al., 2007; Oades et al., 1996; Pang et al., 1998; Pihko et al., 2005; Tanaka et al., 2001; Trainor et al., 2001, 2003; Uwer and von Suchodoletz, 2000) – Early-onset blindness (Kujala et al., 1995a,b, 2000b, 2005b; Alho et al., 1993) – Epileptic patients with vagus-nerve stimulation (Borghetti et al., 2007) – Infants operated for craniosynosthosis (Huotilainen et al., 2008) – Patients with hearing aids (Rudner et al., 2008) – Patients with ultrasound hearing aids (Hosoi et al., 1998) – Schizophrenic patients progressing from the Acute to Post-Acute Phase (Shinozaki et al., 2002) – Sleeping infants exposed to auditory discrimination training (Cheour et al., 2002a) – Stroke patients as a function of time since stroke onset (Ilvonen et al., 2003; Särkämö et al., 2010a,) – Stroke patients receiving music or audio-book stimulation (Särkämö et al., 2010a,)

see Coyle, 2006; Schwieler et al., 2008). Hence, an MMN enhancement may precede improvement in clinical severity, which, according to the authors, highlights the possible utility of the MMN as a biomarker of treatment efficacy, and, therefore, also as a tool in drug development (see also Javitt, 2007, 2009; Javitt et al., 2008). Previously, in the Schall et al. (1999) study, the MMN predicted the outcome of clozapine therapy in patients with schizophrenia. Moreover, more recently, Horton et al. (2011) found that clozapine increased the MMN amplitude for tone-frequency change, with increasing doses being associated with increasing frequency-MMN amplitudes (but attenuated that for tone-duration increments and decrements). Very recently, it was found by Bodatsch et al. (2011) that in individuals with a high schizophrenia risk, the MMN for tone-duration decrement (but not for tone-frequency change) was lower in amplitude (resembling that of first-episode patients) in those patients who subsequently, during an observation period of 2 years, converted to the first-episode psychosis than that in those who did not convert to psychosis during that period (Fig. 8). This result was remarkable as these groups were thought to share a similar clinical risk of psychosis at baseline. The authors proposed that the duration-MMN reduction in their converters might reflect both structural and neurochemical alterations associated with the conversion to psychosis. Furthermore, such results do not, according to the authors, only contribute to the prediction of conversion and lead time to it but also contribute to a more individualised risk assessment and hence also to risk-adapted prevention. In addition, recently, Stone et al. (2010) found in subjects at risk of psychosis, an attenuated frontal-MMN amplitude for tone-duration increment and, further, that this MMN deficit was related to reduced thalamic glutamate plus glutamine and NMDA levels. Further, a phonological deficit in young elementary-school children, reflected by a reduced MMN amplitude to syllable change (but not that to simple frequency change), appeared to predict their dyslexia risk (Blitz et al., 2007). Also, in very prematurely born children, the MMN amplitude for consonant change at 4 years of age predicted, as already mentioned, naming performance at the age of 6 years (Jansson-Verkasalo et al., 2003b, 2004). Furthermore, Jansson-Verkasalo et al. (2010) found that the perceptual narrowing for non-native phoneme contrasts occurring in normal healthy infants from 6 to 12 months of age (Kuhl et al., 1991; Kuhl, 2004), reflected by attenuated MMNs for non-native phoneme contrasts in these infants (Cheour et al., 1998b), does not occur in very prematurely born infants who showed large MMNs even for non-native phoneme contrasts. This indicates that the ability to

discriminate non-native phonemes was preserved in prematurely born infants. Moreover, it was also found that the better this ability was preserved (reflected by larger MMN-amplitudes for non-native contrasts) at the age of 1 year, the worse was the performance in native-language tests at the age of 2 years. Thus, decline in sensitivity to non-native phonemes, as reflected by MMN attenuation for non-native phoneme contrasts, served as a positive predictor for further age-appropriate language development. Moreover, the Weber et al. (2005) MMN data showing a deficit of prosodic perception in 5-month-old infants suggested that the MMN might be taken as an early marker of SLI risk.

13. The MMN as an index of genetic disposition to different pathologies (Table 12) Some studies suggest that in schizophrenia there is a genetic contribution to its aetiology. An MMN-amplitude attenuation for duration increment was found by Michie et al. (2002) and that for frequency change by Jessen et al. (2001) in symptom-free first-order relatives of patients with schizophrenia but studies with larger samples have either not confirmed these findings (Bramon et al., 2004) or showed a trend only (Price et al., 2006). However, Hall et al. (2006) recently found a significant, although modest, genetic correlation between the duration-increment MMN-amplitude deficit and schizophrenia, and therefore suggested that the MMN is a potentially valid endophenotype in schizophrenia. By contrast, Ahveninen et al. (2006), using the MMN to tone-frequency changes in their study of twin pairs discordant for schizophrenia, obtained results suggesting, according to the authors, that MMN abnormalities in patients with schizophrenia might reflect predominantly state-dependent neurodegeneration. A similar conclusion was made by Magno et al. (2008) on the basis of their duration- and frequency-MMN amplitude results. In patients with the 22q11 deletion syndrome, the considerably increased rates of schizophrenia are attributed to the loss of one allele containing the catechol-O-methyl transferase (COMT) gene. Symptom-free carriers showed attenuated MMN amplitudes for both simple auditory (duration and frequency) and syllabic changes as well as corresponding decrements in behavioural sound discrimination (Baker et al., 2005). Moreover, these MMN and behavioural effects were stronger in subjects carrying the COMT 108/158Met allele on their single intact chromosome (associated with a greater risk of schizophrenia) than in those carrying the COMT 108/158Val allele (a smaller schizophrenia risk). The authors


concluded that because the MMN depends on the NMDAR function (Javitt et al., 1996), the MMN modification by the COMT Val 108/ 158Met polymorphism points towards abnormal dopamine–glutamate interactions in the MMN-generator system. Furthermore, children with a parent or sibling with dyslexia have an increased risk of dyslexia, and this is reflected by their attenuated MMN amplitudes to simple frequency (Maurer et al., 2003) or duration changes (Friedrich et al., 2004; Leppänen et al., 2002) or to phoneme-category change (van Leeuwen et al., 2006). Similarly predictive were the lack of a left-hemisphere MMN response to speech-sound change (Maurer et al., 2003) and the bilateral distribution of this MMN response (Maurer et al., 2009). Also, studying 6-month-old infants with a family history of language-related learning difficulties, Benasich et al. (2006) found that these infants had smaller mismatch responses (MMRs; the positive-polarity analogue of MMN; Maurer et al., 2003) than those of control infants with no such family history. In addition, as already mentioned, Barry et al. (2008) obtained MMN data suggesting that parents of children with SLI have a shorter auditory sensory-memory duration than that of control parents. Very recently, a major breakthrough in the research of the genetic background of dyslexia was made by Roeske et al. (2011) who found that a certain marker (rs4234898), located on chromosome 4q32.1, was associated with the MMN deficit for a CV-syllable change. Moreover, this MMN was also associated with a two-marker haplotype of rs4234898 and rs11100040, one of its neighbouring single-nucleotide polymorphisms. The authors concluded that their results suggest a possible transregulation effect on SLC2A3, the predominant facilitative glucose transporter in neurons, which might lead to glucose deficits in dyslexic children and could explain their attenuated MMN in passive listening tasks, as observed in this study. Moreover, in a very recent study of the same group, Czamara et al. (2011) obtained results pointing to an association between the late MMN for speech-sound change and rare variants in a candidate region for dyslexia.

14. The MMN as an index of central auditory processing improvement or recovery (Table 13) Spontaneous and training-induced improvement. A number of studies in normal healthy subjects (Atienza and Cantero, 2001; Kraus et al., 1995; Gottselig et al., 2004; Menning et al., 2000; Tremblay et al., 1997, 1998; Näätänen et al., 1993; for a review, see Kujala and Näätänen, 2010) demonstrated that the MMN reflects plastic neural changes associated with discrimination learning. Therefore, it is a very attractive tool for following up recovery and intervention effects in various patient groups, for instance, in stroke, coma, PVS or cochlear-implant (CI) patients or in children with developmental disorders. In stroke and other brain-injured patients, it would be important to determine the changes in perceptual abilities very soon after the damage. However, such patients are often unable to cooperate or to understand instructions, particularly if the neural network involved in speech perception is affected. Aaltonen et al. (1993), in an early study, found that the MMN to speech-sound change was abolished in posterior left-hemispheric stroke patients, whereas an anterior left-hemispheric stroke had no such effect. By contrast, the tone-frequency MMN was normal in both patient groups. Subsequently, as already mentioned, Ilvonen et al. (2003) followed up the recovery of left-hemisphere stroke patients, recording the MMN at 4 and 10 days, and then at 3 and 6 months after stroke onset. Language-comprehension tests (Boston Diagnostic Aphasia Examination and Token tests) were also administered in all but the first session in which the patients could not

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cooperate. The MMNs in the first two sessions were quite small in amplitude for sound-duration and -frequency changes, but became larger thereafter, disclosing normal-like amplitudes at 3 months post-stroke (Fig. 3). Furthermore, the duration-MMN amplitude increase correlated with the improvement in the Boston Diagnostic Aphasia Examination test scores from 10 days to 3 months. Subsequently, as already mentioned, it was found by Särkämö et al. (2010b) that the recovery of the MMNm and behavioural discrimination can be expedited with music and audio-book stimulation. Dividing their 60 middle cerebral artery stroke patients into music and audio-book listening and control groups, these authors recorded patients’ MMNm to frequency and duration changes in a binaurally delivered complex tone. (In addition, all patients received the normal hospital treatment and rehabilitation of stroke patients, of course.) It was found, as expected, that the MMNm amplitudes were, in general, smaller in the lesioned than opposite hemisphere. Importantly, the frequency-MMNm amplitude increased more in both music and audio-book groups than in the control group during the 6-month post-stroke period. In addition, the duration-MMNm amplitude increased more in the audio-book group than in the other groups. Moreover, the frequency-MMNm amplitude changes correlated with the behavioural improvement of verbal memory and focussed attention induced by music listening. The authors interpreted their results as demonstrating that the mere listening to music or speech starting soon post-stroke onset can induce long-term plastic changes in early sensory processing, as reflected by the MMNm enhancement, which, in turn, may facilitate the recovery of higher cognitive functions. These remarkable results encourage the use of music and speech stimulation in the rehabilitation of stroke patients in particular in the early poststroke period. The deficit of the auditory/language system may be inborn, as is the case in developmental dyslexia, SLI or in the autism spectrum. Because of the high prevalence of these disorders and their devastating effects on the individual’s academic success and thereby self-esteem, early identification and remediation methods should be developed. Recent evidence fortunately shows that the aberrant neural substrate of language deficits can be ameliorated with appropriate intervention. For instance, Pihko et al. (2007) found that language-impaired children at the age of 5–6 years benefited from language and speech exercises. Furthermore, this training also changed the neural processing of speech sounds so that the MMNm for syllable changes became stronger in the left hemisphere. In dyslexic first-grade children, intervention, judging from an MMN-amplitude enhancement, induced neural plastic changes and ameliorated reading difficulties (Kujala et al., 2001). These 7year-old school children were exposed to an audiovisual training programme with no linguistic items (Audilex Program; Karma, 1999) for 7 weeks. Their reading skills as well as the MMN elicited by tone-order reversals were assessed before and after this training period. After this period, the training group made fewer reading errors and tended to read faster than did the age-matched control group of dyslexic children. Moreover, the MMN amplitude for tone-order reversals was increased in the training group but not in the control group. These results consequently showed that reading deficits can be ameliorated with audiovisual training and, further, that the improvement of reading skills is associated with plastic neural changes of the central auditory system as reflected by the MMN enhancement. Furthermore, these positive training results were obtained by using no linguistic stimuli, which suggests that impaired auditory-perceptual processes other than deficient phonology may also contribute to reading impairments. Similar effects were also obtained with extremely low-birthweight children of 6 years of age (Huotilainen et al., 2011). These

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children were allocated to a 5-week training programme with Audilex (training group) or to a control group playing computer games. Before and after the intervention, auditory ERPs to sound changes were recorded and reading-related skills were assessed. The MMN responses to frequency and duration deviants increased in amplitude in the Audilex training group but not in the controlgame group. However, the reading skills were similar in the two groups after invention and 2 years later. As already mentioned, the shortening of the abnormally long MMN-peak latency and the MMN-amplitude recovery in drugresistant adult epilepsy patients after vagus-nerve stimulator implantation was recently found by Borghetti et al. (2007), suggesting a positive effect of vagus-nerve stimulation on central auditory processing in these patients. Drug-induced improvement. In Table 1, short-term effects of different drugs are reviewed. In addition, in the foregoing, some favourable drug effects in schizophrenia patients were already mentioned (NAC, Lavoie et al., 2007; clozapine, Schall et al., 1999; Horton et al., 2011). Moreover, very recently, Dulude et al. (2010) found that nicotine, relative to placebo, not only prolonged the peak latency of the duration MMN but also increased its amplitude in patients to a level comparable with that seen in controls. By contrast, the frequency MMN was not affected. The authors concluded that these preliminary findings demonstrate that acute nicotine can normalise temporal aspects of central auditory processing in patients with schizophrenia, an effect that might be mediated by the activation of a7 nicotinic acetylcholine receptors, the functioning of which is diminished in schizophrenia. The authors further concluded that these ameliorating effects of nicotine may have implications for understanding the increased tobacco smoking in schizophrenic patients and for developing nicotinic pharmacotherapeutics to alleviate sensory-memory impairments in schizophrenia. In addition, a positive effect of nicotine in both smoking and non-smoking normal healthy subjects on temporalinterval processing (indexed by an MMN-amplitude enhancement to ISI deviants) was recently found by Martin et al. (2009). Furthermore, very recently, it was found by Sawada et al. (2010) that in children of 7–13 years of age with attention deficit hyperactivity disorder (ADHD), the intake of osmotic-release methylphenidate (MPH) increased the MMN amplitude for tone-frequency change and simultaneously alleviated the severity of their ADHD symptoms. Central auditory discrimination and training in CI users. For profoundly deaf individuals, a sensation of hearing can be restored by a CI. CIs are currently the most successful and widely used sensory neuroprotheses. In a large percentage of those individuals fitted with a CI, a remarkable degree of language communication via the auditory domain is restored. Nevertheless, objective, nonbehavioural measures of auditory discrimination such as the MMN remain a potentially powerful, but as yet under-utilised, application for this population. The first MMN recordings from CI users were reported by Kraus et al. (1993b) who employed speech-syllable contrasts. For the group of individuals investigated in that study, Kraus et al. found that the MMN elicited from CI users was remarkably similar to that obtained from a group of normal-hearing listeners. These results suggested that despite the differences in peripheral input, the brain was processing basic speech units in a very similar fashion. Ponton et al. (2000; see also Ponton and Don, 1995, 2003; Ponton and Eggermont, 2007), recording the MMN evoked by a single contrast in stimulus duration from groups of normal-hearing adults and adult CI users, also found that MMNs of the two groups were quite similar. In a more detailed study in which subjects were separated into groups based on benefit gained by using a CI, Groenen et al. (1996) reported that whereas the group classified as good performers showed an MMN, poor performers failed to generate a

comparable response. Furthermore, Kelly et al. (2005) reported a similar failure to obtain the MMN from CI users defined as poor performers. In addition, Lonka et al. (2004), in longitudinally tracking the changes in the language function after a small group of deaf adults received a CI, reported that while the MMN was absent for approximately 12 months post-surgery, the response subsequently emerged, first for a large vowel contrast, and then later for more subtle vowel distinctions. Converging behavioural improvement in a speech-discrimination test was also observed during the follow-up period. Trautwein et al. (1998) and Ponton et al. (2000), who assessed the CI users with non-speech stimuli, obtained results that relate back to both speech performance and training. First, Trautwein et al. (1998) found that while psychophysical thresholds were superior to MMN-estimated discrimination thresholds for duration contrasts in the control group, the opposite was found for a group of adult CI users. Thus, in several individuals, there was neurophysiological evidence of discrimination based on the MMN, without the individual being able to behaviourally perceive the difference. Based on the apparent separation of discrimination at the level of sensation versus perception, Ponton et al. (2009) developed a protocol based on pre-training MMN evaluation to determine whether there was neurophysiological evidence of discrimination in the absence of perceptual discrimination. This knowledge was then used to develop a training protocol which resulted in significant improvements in frequency discrimination as well as combined consonant and vowel discrimination in a single highly trained adult implant user. As noted by Roman et al. (2005), there is a clear application of the MMN in clinical testing and training of CI populations. However, refinements are needed in methods and recording technique, to optimise the protocols for frequency discrimination and speech testing. Recently, music perception of CI users was also studied by using the MMN. Koelsch et al. (2004) found that CI users can perceive timbre, judging from the MMN elicited by timbre deviants in them (the timbre MMN: Tervaniemi et al., 1997; Toiviainen et al., 1998). Moreover, music-syntactic violations elicited an early right anterior negativity which might be interpreted as a music-syntactic MMN in CI users, which again was considerably smaller in amplitude than that in controls but nevertheless showed that CI users’ central neural mechanisms underlying music perception are activated by musical stimulation (even though they reported that they had difficulties in discriminating musical information and that they were in general frustrated by their inability to accurately hear music). Consistent with this, subsequently, Sandmann et al. (2010), by using the multi-feature MMN paradigm with six different levels of the magnitude of deviation for each feature (Pakarinen et al., 2007) (Fig. 1) found that CI users had difficulties in discriminating small changes in the acoustic properties of musical sounds. It was concluded by Sandmann et al. (2010) that this type of paradigm could be of substantial clinical value by providing a comprehensive profile of the extent of restored hearing in CI users. Moreover, an inverse relationship was found between the MMN amplitude and the duration of profound deafness; however, there was also evidence for experience-related plastic changes as a function of the duration of CI use (Sandmann et al., 2010). Ultrasonic hearing. Some profoundly deaf individuals can perceive ultrasound only, which occurs by bone conduction. Hosoi et al. (1998) found that in normal healthy subjects, ultrasound modulated by different speech sounds produces discriminable stimuli, which points to the possibility of developing ultrasonic hearing aids as an alternative for CIs for those profoundly deaf individuals who can sense ultrasound only. Hosoi and colleagues delivered ultrasound to the right sterno-cleidomastoid through a ceramic vibrator. Substantial N1m responses were elicited by both


audible air-conducted sound stimuli and bone-conducted ultrasonic stimuli. Further, when the (40 kHz) ultrasound stimuli modulated by vowels/i/ and/a/ were presented as standards and deviants, respectively, substantial MMNm responses were observed for deviants, indicating that the two sounds were discriminable. Moreover, the equivalent current dipole (ECD) for the MMNm was located within the auditory cortex, in the vicinity of the MMNm observed in a separate condition with the respective air-conducted stimuli. The authors also tested 53 profoundly deaf individuals behaviourally and found that 28 of them could detect ultrasonic stimuli and, further, that 11 of them could discriminate ultrasounds modulated by different speech signals. These results provide, according to the authors, the rationale for developing ultrasound hearing aids, which do not require surgery, for those profoundly deaf who can sense ultrasound. Improved discrimination in early blind individuals. A special case of enhanced central auditory function of compensatory nature can be encountered in early blinds. The MMN elicited by soundlocation changes was larger in amplitude in early-blind individuals than in sighted control subjects (Kujala et al., 1995a). (The MMN was recorded while subjects’ attention was directed to the tactile modality.) This suggests enhanced spatial auditory perception and discrimination in the blind. The result is consistent with behavioural data showing that the blind are more accurate than the sighted in detecting loci of origin of sounds (Lessard et al., 1998; Röder et al., 1999). The scalp topography of MMN response of Kujala et al., 1995a) did not differ between the two groups, however. It, therefore, behaved differently from the N2b (Näätänen et al., 1982; for a review, see Näätänen and Gaillard, 1983) response elicited by auditory targets in an active discrimination condition, which had a scalp topography in the blind that was posterior to that in the sighted (Kujala et al., 1992, 1995a,b). Thus, the MMN appears to be hard-wired in the central auditory system of the blind, reflecting plastic changes within the auditory cortex, whereas the generators of the N2b, associated with attentional processes in audition, may become part of the neural system normally subserving vision. This was supported by imaging studies suggesting occipital activity in the blind during auditory changedetection tasks (Kujala et al., 1995b, 2007, 2000b, 2005b).

15. Concluding discussion This article has shown that central auditory processing, as indexed by the MMN and the MMNm, is affected in a wide range of different clinical conditions and in ageing. Most of these effects are seen as indexing decreased auditory discrimination accuracy. In some cases, however, the duration of auditory short-term sensory memory, essential, for instance, in speech perception and understanding, is affected. This further decreases automatic discrimination when SOAs are prolonged. Moreover, these data also show effects on mechanisms controlling for involuntary shifts of attention (passive attention) or on those determining the characteristics of backward masking in different patient groups. Consequently, this article has shown that the MMN provides a unique window to the neuropsychology of central auditory processing, and hence a possibility for the objective assessment of auditory discrimination and sensory memory, in different patient groups, which previously could be mainly inferred from behavioural performance only. This is a major improvement, in particular when considering the special communicational and motivational problems with patients, deducting from the reliability of the results, and the fact that reliable behavioural measurements are not at all possible in some clinical groups and often in small infants. These new possibilities in particular involve the improved monitoring of the patient’s state and the prediction of its future

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development, for example, the prediction of coma or PVS outcome and even that of the extent of the cognitive recovery of these patients (during the next 2 years; Wijnen et al., 2007), or the monitoring of, and predicting, the progress of schizophrenia. Moreover, importantly, very recent results of Bodatsch et al. (2011) showed that the duration MMN can predict, in individuals in schizophrenia-risk group, conversion to first-episode schizophrenia and even when this would occur in the period of 2 years. In addition, another recent study (Banati and Hickie, 2009) suggested that the duration and frequency MMNs might enable one to online monitor local disease activity and neuronal death in patients with schizophrenia. Furthermore, in case of schizophrenia (see Lavoie et al., 2007; Horton et al., 2011; Javitt et al., 2008; Banati and Hickie, 2009; see also Berk et al., 2008a,b), and perhaps of other severe neuropsychiatric, neurological and neurodevelopmental disorders, too, the MMN can be used as an online index of treatment efficacy. As far as dyslexia is concerned, such a use of the MMN in assessing the effectiveness of different rehabilitation programmes is already well established (Kujala et al., 2001). In addition, in the foregoing, we reviewed results of Särkämö et al. (2010a) demonstrating how the MMNm can be used in evaluating the effectiveness of different auditory stimulus material in an attempt at facilitating stroke recovery. Some further clinically important uses of MMN data are, among other things, the possibility to determine the dyslexia risk in newborns and infants (Maurer et al., 2003; Leppänen et al., 2002; van Leeuwen et al., 2006; Friedrich et al., 2004), the magnitude of cognitive and functional deficit associated with different clinical conditions (Näätänen et al., 2011a) and the degree of severity of different conditions (in Schizophrenia: Umbricht et al., 2006; Devrim-Ücok et al., 2008; Todd et al., 2008; Light and Braff, 2005a,b; Salisbury et al., 2002, 2007; Stuttering: Corbera et al., 2005; PTSD: Menning et al., 2008; Cleft Palate: Ceponiene et al., 1999, 2000, 2002; Stroke and Aphasia: Ilvonen et al., 2003; Pettigrew et al., 2005; Särkämö et al., 2010b; Dyslexia: Baldeweg et al., 1999; Kujala et al., 2001). One might wonder why auditory discrimination is affected in such a large number of different clinical conditions (Table 1), which indeed points to a possible common pathology shared by these different conditions. A major part of this common pathology appears to be found in the deficient functioning of the NMDAR system, as there is very strong evidence indicating that MMN deficiency reflects deficient NMDAR functioning (Javitt et al., 1996; Näätänen et al., 2011a). For example, sub-anaesthetic doses of ketamine, an NMDAR antagonist, attenuated the MMN amplitude of healthy volunteers (Kreitschmann-Andermahr et al., 2001: MMNm; Umbricht et al., 2000, 2002), monkey (Javitt et al., 1996), rat (Tikhonravov et al., 2008, 2010) and mouse (Ehrlichman et al., 2008), and caused schizophrenic kinds of psychotic experiences in normal subjects (Umbricht et al., 2000, 2002; see also Sauer and Volz, 2000; Pang and Fowler, 1999). Furthermore, ketamine disturbed the performance in a memory task in normal subjects in a manner similar to that normally observed in schizophrenia, as shown by Umbricht et al. (2000). Importantly, it was found by Umbricht et al. (2002) that the smaller was the subject’s MMN amplitude for frequency and duration changes before ketamine administration, the stronger were the psychotic experiences caused by the drug. Therefore, the authors concluded that the MMN in the normal state of consciousness indexes the vulnerability to disruption of the NMDAR system in normal healthy subjects. Consequently, the MMN appears to index the functional state of the NMDAR-mediated neurotransmission even in subjects demonstrating no psychopathology and may therefore ‘‘become a useful tool in studies on NMDAR functioning in humans’’ (Umbricht et al., 2002).

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Consequently, the MMN attenuation observed in a large number of different clinical populations and conditions (Table 1) can, to a large extent, be accounted for by NMDAR dysfunction associated with different clinical conditions. For instance, as already reviewed, the dysfunction of the NMDAR system plays a central role in the brain pathology of schizophrenia and in particular in the cognitive deficit in these patients (Javitt et al., 1996; Coyle, 2006). Moreover, the cognitive decline occurring in several other neurocognitive abnormalities might also be accounted for, at least in part, by the dysfunctional NMDAR system (Näätänen et al., 2011a). Alzheimer’s disease, stroke, traumatic brain injury and even normal ageing are accompanied by widespread dysfunctions in the NMDAR system (Lipton and Rosenberg, 1994; Magnusson et al., 2010; Biegon et al., 2004; Dalkara et al., 1996; Izquidero, 1991; McGeer and McGeer, 2010). For example, Dhawan et al. (2010) recently found that middle central artery occlusion in rat resulted in widespread decreases in NMDAR density in brain regions extending far beyond the infarct area, including even regions contralateral to the lesion important to cognitive function. Dhawan et al. (2010), therefore, concluded that a persistent and widespread loss of NMDARs may contribute to cognitive and other neurological deficits in stroke patients, which cannot be localised to the side of infarction. Importantly, this NMDAR functional deficiency may hence account for, besides decreased discrimination accuracy, even the cognitive and functional decline occurring in a number of these conditions (Table 8) (for a review, see Näätänen et al., 2011a). It is, for instance, well established that the adequate functioning of the NMDAR system plays a crucial role in the initiation of longterm and working memories (Javitt et al., 1996; Newcomer et al., 1998). Therefore, the MMN and MMNm deficiency reflecting a deficient NMDAR function can also index cognition and its decrement in ageing and in different neurological and neuropsychiatric abnormalities (Näätänen et al., 2011a). Consequently, as an easily accessible non-invasive measure of the functional condition of the NMDAR system, the MMN (MMNm) might play an important role in future attempts at understanding what is common in the different neuropsychiatric diseases and abnormalities and what is specific to each of them (Umbricht et al., 2003). These conclusions are further supported by studies showing that pharmacological manipulations enhancing cognition also enhance the MMN (MMNm) response (Baldeweg et al., 2006; Dunbar et al., 2007; Inami et al., 2005; Fisher et al., 2010; Harkrider and Hedrick, 2005; Engeland et al., 2002; Knott et al., 2006, 2009) and vice versa (Pang and Fowler, 1999; Nakagome et al., 1998; Serra et al., 1996; Jääskeläinen et al., 1996a), and, further, that the MMN-cognition relationship holds even in normal adults (Light et al., 2007; Bazana and Stelmack, 2002; Beauchamp and Stelmack, 2007; Troche et al., 2009, 2010) and children (Liu et al., 2007). Optimising MMN protocols for clinical environments. Perhaps the most frequent issues associated with use of the MMN in clinical environments are time required to record enough data to obtain an identifiable response and the expertise required to identify when a response is present or absent. By definition, the traditional MMN protocol is very time consuming to obtain information regarding even a single stimulus contrast. In a standard paradigm, the standard stimulus is presented 80–90% of the time, with deviant stimulus presentations, which evoke the MMN, randomly interspersed through the sequence. The introduction of the multiple-deviant paradigm for tones (Näätänen et al., 2004; Pakarinen et al., 2007, 2010; Fisher et al., 2011; Grimm et al., 2008; Jankowiak and Berti, 2007; see also Vaz Pato et al., 2002; Deacon et al., 1998) and for speech (Pettigrew et al., 2004b; Pakarinen et al., 2009; Sorokin et al., 2010; Lovio et al., 2009) and music (Vuust et al., 2011) provided a method for rapidly acquiring information on a number of stimulus contrasts. This approach considerably in-

creases the amount of information that can be gathered within a specific time period. Equally as important are methods that would further reduce the amount of time required to acquire sufficient data that reach some objective criteria of identification. One such approach has recently been described by Rahne et al. (2008). In this modification to standard averaging, individual epochs to stimulus presentation are sorted on the signal-to-noise ratio (SNR) to each individual epoch. This epoch with the highest SNR, that is, the lowest background noise, is added first to average. Individual epochs are then added to the average in rank order based on the background noise in each epoch. Thus, averaging is continued until the SNR is optimised. Objective or statistical detection of these responses could then easily be achieved by using one of a number of online algorithms involving randomisation or bootstrapping analyses such as those proposed by, for example, Ponton et al. (1997) or Fujioka et al. (2005). Moreover, further progress to this end has been very recently made by Cong et al., 2009, 2010, 2011); Burger et al. (2007); Kalyakin et al. (2007, 2008a,b, 2009) and Marco-Pallares et al. (2005). Needless to say, a lot of work is still needed to bring the MMN methodology to clinics as a tool of everyday patient work in which reliable measurements have to be carried out at the level of individual patients (Bishop and McArthur, 2004; Boly et al., 2011; Taylor and Baldeweg, 2002; Lang et al., 1995), but studies as those reviewed in the foregoing have shown that this goal is both valuable and probably also attainable. Acknowledgements RN and KK were supported by Grant # 8332 from the Estonian Science Foundation. TK was supported by Grant # 128840 and RN by grant # 122745 from The Academy of Finland. CE was supported by grants from ICREA Academia 2010 and CSD2007-00012, EUI2009-04806, PSI2009-08063, and SGR2009-11. We wish to acknowledge Ms. Piiu Lehmus’ skilful and patient text-editing work. References Aaltonen O, Tuomainen J, Laine M, Niemi P. Cortical differences in tonal versus vowel processing as revealed by an ERP component called mismatch negativity. Brain Lang 1993;44:139–52. Ahissar M. Dyslexia and the anchoring-deficit hypothesis. Trends Cogn Sci 2007;11:458–65. Ahissar M, Lubin Y, Putter-Katz H, Banai K. Dyslexia and the failure to form a perceptual anchor. Nat Neurosci 2006;9:1558–64. Ahveninen J, Escera C, Polo MD, Grau C, Jääskeläinen IP. Acute and chronic effects of alcohol on pre-attentive auditory processing as reflected by mismatch negativity. Audiol Neuro-Otol 2000a;5:303–11. Ahveninen J, Jääskeläinen IP, Osipova D, Huttunen MO, Ilmoniemi RJ, Kaprio J, et al. Inherited auditory-cortical dysfunction in twin pairs discordant for schizophrenia. Biol Psychiat 2006;60:612–20. Ahveninen J, Jääskeläinen IP, Pekkonen E, Hallberg A, Hietanen M, Mäkelä R, et al. Suppression of mismatch negativity by backward masking predicts impaired working-memory performance in alcoholics. Alcohol Clin Exp Res 1999;23:1507–14. Ahveninen J, Jääskeläinen IP, Pekkonen E, Hallberg A, Hietanen M, Näätänen R, et al. Increased distractibility by task-irrelevant sound changes in abstinent alcoholics. Alcohol Clin Exp Res 2000b;24:1850–4. Akatsuka K, Wasaka T, Nakata H, Inui K, Hoshiyama M, Kakigi R. Mismatch response related to temporal discrimination of somatosensory stimulation. Clin Neuropshysiol 2005;116:1930–7. Akatsuka K, Wasaka T, Nakata H, Kina T, Hoshiyama M, Tamura Y, et al. Objective examination for two-point stimulation using a somatosensory oddball paradigm: an MEG study. Clin Neurophysiol 2007;118:403–11. Alain C, Woods DL. Age-related changes in processing auditory stimuli during visual attention: evidence for deficits in inhibitory control and sensory memory. Psychol Aging 1999;14:507–19. Alain C, Woods DL, Knight RT. A distributed cortical network for auditory sensory memory in humans. Brain Res 1998;812:23–37. Alain C, McDonald KL, Ostroff JM, Schneider B. Aging: a switch from automatic to controlled processing of sounds? Psychol Aging 2004;19:125–33. Alexandrov AA, Karpina NV, Stankevich LN. Mismatch negativity in evoked brain potentials in adolescents in normal conditions and attention deficit in response

R. Näätänen et al. / Clinical Neurophysiology 123 (2012) 424–458 to presentation of short-duration acoustic stimuli. Neurosci Behav Physiol 2003;33:671–5. Alho K, Cheour-Luhtanen M. Auditory discrimination in infants as revealed by the mismatch negativity of the event-related brain potential. Dev Neuropsychol 1997;13:157–65. Alho K, Kujala T, Paavilainen P, Summala H, Näätänen R. Auditory processing in the visual brain areas of the early blind: evidence from event-related potentials. Electroen Clin Neuro 1993;86:418–27. Alho K, Sainio K, Sajaniemi N, Reinikainen K, Näätänen R. Event-related brain potential of human newborns to pitch change of an acoustic stimulus. Electroen Clin Neuro 1990;77:151–5. Alho K, Woods DL, Algazi A, Knight RT, Näätänen R. Lesions of frontal cortex diminish the auditory mismatch negativity. Electroen Clin Neuro 1994;91:353–62. Alho K, Woods DL, Algazi A, Näätänen R. Intermodal selective attention II: effects of attentional load on processing auditory and visual stimuli in central space. Electroen Clin Neuro 1992;82:356–68. Alonso-Búa B, Dıáz F, Ferraces J. The contribution of AERPs (MMN and LDN) to studying temporal vs. linguistic processing deficits in children with reading difficulties. Int J Psychophysiol 2006;59:159–67. Amenedo E, Diaz F. Automatic and effortful processes in auditory memory reflected by event-related potentials. Age-related findings. Electroen Clin Neuro 1998;108:361–9. Amenedo E, Escera C. The accuracy of sound duration representation in the human brain determines the accuracy of behavioural perception. Eur J Neurosci 2000;12:2570–4. Amenedo E, Pazo-Alvarez P, Cadaveira F. Vertical asymmetries in pre-attentive detection of changes in motion direction. Int J Psychophysiol 2007;64:184–9. Andersson S, Barder HE, Hellvin T, Løvdahl H, Malt UF. Neuropsychological and electrophysiological indices of neurocognitive dysfunction in bipolar II disorder. Bipol Disord 2008;10:888–99. Astikainen P, Hietanen JK. Event-related potentials to task-irrelevant changes in facial expressions. Behav Brain Funct 2009;5:30. Astikainen P, Ruusuvirta T, Korhonen T. Somatosensory event-related potentials in the rabbit cerebral and cerebellar cortices: a correspondence with mismatch responses in humans. Neurosci Lett 2001;298:222–4. Astikainen P, Ruusuvirta T, Wikgren J, Penttonen M. Memory-based detection of rare sound feature combinations in anaesthetized rats. NeuroReport 2006;17:1561–4. Atienza M, Cantero JL. Complex sound processing during human REM sleep by recovering information from long-term memory as revealed by the mismatch negativity (MMN). Brain Res 2001;901:151–60. Atienza M, Cantero JL, Gomez CM. The mismatch negativity component reveals the sensory memory during REM sleep in humans. Neurosci Lett 1997;237:21–4. Atienza M, Cantero JL, Gomez CM. Decay time of the auditory sensory memory trace during wakefulness and REM sleep. Psychophysiology 2000;37:485–93. Atienza M, Cantero JL, Dominguez-Marin E. Mismatch negativity (MMN): an objective measure of sensory memory and long-lasting memories during sleep. Int J Psychophysiol 2002;46:215–25. Auther LL, Wertz RT, Miller TA, Kirshner HS. Relationships among the mismatch negativity (MMN) response, auditory comprehension, and site of lesion in aphasic adults. Aphasiology 2000;14:461–70. Baker K, Baldeweg T, Sivagnanasundaram S, Scambler P, Skuse D. COMTVal108/ 158 1653 Met polymorphism modifies mismatch negativity and cognitive function in 22q11 deletion syndrome. Biol Psychiat 2005;58:23–31. Baldeweg T, Klugman A, Gruzelier JH, Hirsch SR. Impairment in frontal but not temporal components of mismatch negativity in schizophrenia. Int J Psychophysiol 2002;43:111–22. Baldeweg T, Klugman A, Gruzelier J, Hirsch SR. Mismatch negativity potentials and cognitive impairment in schizophrenia. Schizophr Res 2004;69:203–17. Baldeweg T, Richardson A, Watkins S, Foale C, Gruzelier J. Impaired auditory frequency discrimination in dyslexia detected with mismatch evoked potentials. Ann Neurol 1999;45:1–9. Baldeweg T, Wong D, Stephen KE. Nicotinic modulation of human auditory sensory memory: evidence from mismatch negativity potentials. Int J Psychophysiol 2006;59:49–58. Bamiou DE, Liasis A, Boyd S, Cohen M, Raglan E. Central auditory processing disorder as the presenting manifestation of subtle brain pathology. J Audiol 2000;39:168–72. Banai K, Ahissar M. Psychoacoustics and working memory in dyslexia. In: Fourth conference on plasticity of the central auditory system and processing of complex acoustic signals, July 07–10, 2003. Plasticity and Signal Representation in the Auditory System, Prague, Czech Republic; 2005. p. 233–42. Banati RB. Neuropathological imaging: in vivo detection of glial activation as a measure of disease and adaptive change in the brain. Br Med Bull 2003;65:121–31. Banati R, Hickie IB. Therapeutic signposts: using biomarkers to guide better treatment of schizophrenia and other psychotic disorders. Med J Aust 2009;190:S26–32. Bar-Haim Y, Marshall PJ, Fox NA, Schorr EA, Gordon-Salant S. Mismatch negativity in socially withdrawn children. Biol Psychiat 2003;54:17–24. Barry JG, Hardiman MJ, Line E, White KB, Yasin I, Bishop DVM. Duration of auditory sensory memory in parents of children with SLI: a mismatch negativity study. Brain Lang 2008;104:75–88. Barry RJ, Johnstone SJ, Clarke AR. A review of electrophysiology in attention-deficit/ hyperactivity disorder: II. Event-related potentials. Clin Neurophysiol 2003;114:184–98.

445

Baudena P, Halgren E, Heit G, Clarke JM. Intracerebral potentials to rare target and distractor auditory and visual stimuli. III. Frontal cortex. Electroencephalogr Clin Neurophysiol 1995;94:251–64. Bazana PG, Stelmack RM. Intelligence and information processing during an auditory discrimination task with backward masking: an event-related potential analysis. J Pers Soc Psychol 2002;83:998–1008. Beauchamp CM, Stelmack RM. The chronometry of mental ability: an event-related potential analysis of an auditory oddball discrimination task. Intelligence 2006;34:571–86. Becker F, Reinvang I. Mismatch negativity (MMN) to tone duration and speech sound changes in aphasics. Brain Lang 2007;100:69–78. Bellis TJ, Nicol T, Kraus N. Aging affects hemispheric asymmetry in the neural representation of speech sounds. J Neurosci 2000;20:791–7. Benasich AA, Choudhury N, Friedman JT, Realpe-Bonilla T, Chojnowska C, Gou Z. The infant as a prelinguistic model for language learning impairments: predicting from event-related potentials to behaviour. Neuropsychologia 2006;44: 396–411. Benasich AA, Tallal P. Infant discrimination of rapid auditory cues predicts later language impairment. Behav Brain Res 2002;136:31–49. Berk M, Copolov DL, Dean O, Lu K, Jeavons S, Schapkaitz I, et al. N-Acetyl Cysteine for depressive symptoms in bipolar disorder-a double-blind randomized placebocontrol trial. Biol Psychiat 2008a;64:468–75. Berk M, Copolov D, Dean O, Lu K, Jeavons S, Schapkaitz I, et al. N-acetyl cysteine as a glutathione precursor for schizophrenia – a double-blind, randomized, placebocontrolled trial. Biology 2008b;64:361–8. Berti S, Schröger E. A comparison of auditory and visual distraction effects: behavioural and event-related indices. Cogn Brain Res 2001;10:265–73. Berti S, Schröger E. Distraction effects in vision: behavioural and event-related potentials indices. NeuroReport 2004;15:665–9. Berti S, Schröger E. Visual distraction: a behavioural and event-related brain potential study in humans. NeuroReport 2006;2:151–5. Bertoli S, Smurzynski J, Probst R. Temporal resolution in young and elderly subjects as measured by mismatch negativity and a psychoacoustic gap detection task. Clin Neurophysiol 2002;113:396–406. Bertoli S, Smurzynski J, Probst R. Effects of age, age-related hearing loss, and contralateral cafeteria noise on the discrimination of small frequency changes: psychoacoustic and electrophysiological measures. J Assoc Res Otolaryng 2005;6:207–22. Beste C, Saft C, Gunturkun O, Falkenstein M. Increased cognitive functioning in symptomatic Huntington’s Disease as revealed by behavioral and event-related potential indices of auditory sensory memory and attention. J Neurosci 2008;28:11695–702. Biegon A, Fry PA, Paden CM, Alexandrowitch A, Tsenter J, Shohami E. Dynamic changes in N-methyl-D-aspartate receptors after closed head injury in mice: implications for treatment of neurological and cognitive deficits. P Natl Acad Sci USA 2004;101:5117–22. Bishop DVM. Curing dyslexia and attention-deficit hyperactivity disorder by training motor co-ordination: miracle or myth? J Paediatr Child H 2007a;43:653–5. Bishop DVM. Genes, cognition, and communication. Insights from neurodevelopmental disorders. The Year in Cognitive Neuroscience 2009. Ann NY Acad Sci 2009;1156:1–18. Bishop DVM. Using mismatch negativity to study central auditory processing in developmental language and literacy impairments: where are we, and where should we be going? Psychol Bull 2007b;133:651–72. Bishop DVM, McArthur GM. Immature cortical responses to auditory stimuli in specific language impairment: evidence from ERPs to rapid tone sequences. DevSci 2004;7:F11–8. Bisiachi PS, Mento G, Suppiej A. Cortical auditory processing in preterm newborns: an ERP study. Biol Psychol 2009;82:176–85. Blitz U, Gust K, Spitzer M, Kiefer M. Phonological deficit in school children is reflected in the mismatch negativity. NeuroReport 2007;18:911–5. Boatman DF, Trescher WH, Smith C, Ewen J, Los J, Wied HM, et al. Cortical auditory dysfunction in benign rolandic epilepsy. Epilepsia 2008;49:1018–26. Bodatsch M, Ruhrmann S, Wagner M, Müller R, Schultze-Lutter F, Frommann I, et al. Prediction of psychosis by mismatch negativity. Biol Psychiat 2011;69:959–66. Bogerts B. Recent advances in the neuropathology of schizophrenia. Schizophr Bull 1993;19:431–45. Boly M, Garrido MI, Gosseries O, Bruno M-A, Boveroux P, Schnakers C, et al. Preserved feedforward but impaired top-down processes in the vegetative state. Science 2011;332:858–62. Bomba MD, Pang EW. Cortical auditory evoked potentials in autism: a review. Int J Psychophysiol 2004;53:161–9. Bonnel AC, Mottron L, Peretz I, Trudel M, Gallun E, Bonnel AM. Enhanced pitch sensitivity in individuals with autism: a signal detection analysis. J Cognit Neurosci 2003;15:1–10. Bonte ML, Mitterer H, Zellagui N, Poelmans H, Blomert L. Auditory cortical tuning to statistical regularities in phonology. Clin Neurophysiol 2005;116:2765–74. Bonte ML, Poelmans H, Blomert L. Deviant neurophysiological responses to phonological regularities in speech in dyslexic children. Neuropsychologia 2007;45:1427–37. Borghetti D, Pizzanelli C, Maritato P, Fabbrini M, Jensen S, Iudice A, et al. Mismatch negativity analysis in drug-resistant epileptic patients implanted with vagus nerve stimulator. Brain Res Bull 2007;73:81–5. Born J, Bothor R, Pietrowsky R, Fehm-Wolfsdorf G, Pauschinger P, Fehm HL. Influences of vasopressin and oxytocin on human event-related potentials in an attention task. J Psychophysiol 1987a;4:351–60.

446


Born J, Brüninger W, Fehm-Wolsdorf G, Pauschinger P, Fehm HL. Dose-dependent influences on electrophysiological signs of attention in humans after neuropeptide ACTH 4-10. Exp Brain Res 1987b;67:85–92. Born J, Fehm-Wolsdorf G, Lutzenberger W, Voigt KH, Fehm HL. Vasopressin and electrophysiological signs of attention in man. Peptides 1986;7:189–93. Born J, Pietrowsky R, Fehm HL. Neuropsychological effects on vasopressin in healthy humans. Prog Brain Res 1998;119:619–43. Böttcher-Gandor C, Ullsperger P. Mismatch negativity in event-related potentials of auditory stimuli as a function of varying interstimulus interval. Psychophysiology 1992;29:546–50. Bradlow AR, Kraus N, Nicol TG, McGee TJ, Cunningham J, Zecker SG. Effects of lengthened formant transition duration on discrimination and neural representation of synthetic syllables by normal and learning-disabled children. J Acoust Soc Am 1999;106:2086–96. Braff DL, Light GA. Preattentional and attentional cognitive deficits as targets for treating schizophrenia. Psychopharmacology 2004;174:75–85. Bramon E, Croft RJ, McDonald C, Virdi GK, Gruzelier JG, Baldeweg T, et al. Mismatch negativity in schizophrenia: a family study. Schizophr Res 2004;67:1–10. Brattico E, Kujala T, Tervaniemi M, Alku P, Ambrosi L, Monitillo V. Long-term exposure to occupational noise alters the cortical organization of sound processing. Clin Neurophysiol 2005;116:190–203. Brattico E, Tervaniemi M, Välimäki V, van Zuijen T, Peretz I. Cortical correlates of acquired deafness to dissonance. Ann NY Acad Sci 2003;999:158–60. Braun A, McArdie J, Jones J, Nechaev V, Zalewski C, Brewer C, et al. Tune deafness: processing melodic errors outside of conscious awareness as reflected by components of the auditory ERP. PloS ONE 2008;3:e2349. Brockhaus-Dumke A, Tendolkar I, Pukrop R, Schultze-Lutter F, Klosterkötter J, Ruhrmann S. Impaired mismatch negativity generation in prodromal subjects and patients with schizophrenia. Schizophr Res 2005;73:297–310. Brønnick KS, Nordby H, Larsen JP, Aarsland D. Disturbance of automatic auditory change detection in dementia associated with parkinson’s disease: a mismatch negativity study. Neurobiol Aging 2010;31:104–13. Bruder J, Leppänen PHT, Bartling J, Csépe V, Démonet J-F, Schulte-Körne G. Children with dyslexia reveal abnormal native language representations: evidence from a study of mismatch negativity. Psychophysiology 2011a;48:1107–18. Bruder J, Leppänen PHT, Bartling J, Csépe V, Démonet J-F, Schulte-Körne G. An investigation of prototypical and atypical within-category vowels and nonspeech analogues on cortical auditory evoked related potentials (AERPs) in 9 year old children. Int J Psychophysiol 2011b;79:106–17. Burger M, Hoppe U, Kummer P, Lohscheller J, Eysholdt U, Dollinger M. Waveletbased analysis of MMN responses in children. Biomed Tech 2007;52:111–6. Campbell K, Bell I, Bastien C. Evoked potential measures of information processing during natural sleep. In: Broughton RJ, Ogilvie RD, editors. Sleep arousal and performance. Cambridge, MA: Birkhauser, Boston; 1991. p. 88–116. Cansino S. Episodic memory decay along the adult lifespan: a review of behavioral and neurophysiological evidence. Int J Psychophysiol 2009;71:64–9. Carral V, Huotilainen M, Ruusuvirta T, Fellman V, Näätänen R, Escera C. A kind of auditory ‘primitive intelligence’ already present at birth. Eur J Neurosci 2005;21:3201–4. Catts SV, Shelley A-M, Ward PB, Liebert B, McConaghy N, Andrews S, et al. Brain potential evidence for an auditory sensory memory deficit in schizophrenia. Am J Psychiat 1995;152:213–9. Celsis P, Boulanouar K, Doyon B, Ranjeva JP, Berry I, Nespoulous JL, et al. Differential fMRI responses in the left posterior superior temporal gyrus and left supramarginal gyrus to habituation and change detection in syllables and tones. NeuroImage 1999;9:135–44. Ceponiene R, Haapanen M-L, Ranta R, Näätänen R, Hukki J. Auditory sensory impairment in children with oral clefts as indexed by event-related potentials: a review. J Craniofac Surg 2002;13:554–66. Ceponiene R, Hukki J, Cheour M, Haapanen M-L, Koskinen M, Alho K, et al. Dysfunction of the auditory cortex persists in infants with certain cleft types. Dev Med Child Neurol 2000;42:258–65. Ceponiene R, Hukki J, Cheour M, Haapanen M-L, Ranta R, Näätänen R. Cortical auditory dysfunction in children with oral clefts: relation with cleft type. Clin Neurophysiol 1999;110:1921–6. Ceponiene R, Lepistö T, Shestakova A, Vanhala R, Näätänen R, Yaguchi K. Speech sound-selective auditory impairment in infantile autism: can perceive but will not attend. P Natl Acad Sci USA 2003;100:5567–72. Chang Y, Xu J, Shi N, Zhang B, Zhao L. Dysfunction of processing task-irrelevant emotional faces in major depressive disorder patients revealed by expressionrelated visual MMN. Neurosci Lett 2010;472:33–7. Cheour M, Ceponiene R, Hukki J, Haapanen M-L, Näätänen R, Alho K. Brain dysfunction in neonates with cleft palate revealed by the mismatch negativity (MMN). Electroen Clin Neuro 1999;110:324–8. Cheour M, Ceponiene R, Lehtokoski A, Luuk A, Allik J, Alho K, et al. Development of language-specific phoneme representations in the infant brain. Nature Neurosci 1998b;1:351–3. Cheour M, Haapanen M-L, Ceponiene R, Hukki J, Ranta S, Näätänen R. Mismatch negativity (MMN) as an index of auditory sensory memory deficit in cleft-palate and catch-syndrome children. NeuroReport 1998a;9:2709–12. Cheour M, Haapanen M-L, Hukki J, Ceponiene R, Kurjenluoma S, Alho K, et al. The first neurophysiological evidence for cognitive brain dysfunctions in CATCH children. NeuroReport 1997;8:1785–7. Cheour M, Leppänen P, Kraus N. Mismatch negativity (MMN) as a tool for investigating auditory discrimination and sensory memory in infants and children. Clin Neurophysiol 2000;111:4–16.

Cheour M, Martynova O, Näätänen R, Erkkola R, Sillanpää M, Kero P, et al. Speech sounds learned by sleeping newborns. Nature 2002a;415:599–600. Cheour M, Ceponiene R, Leppänen P, Alho K, Kujala T, Renlund M, et al. Auditory sensory memory trace decays rapidly in newborns. Scand J Psychol 2002b;43:33–9. Cheour-Luhtanen M, Alho K, Sainio K, Rinne T, Reinikainen K, Pohjavuori M, et al. The ontogenetically earliest discriminative response of the human brain. Psychophysiol Special Rep 1996;33:478–81. Choudhury N, Benasich AA. Maturation of auditory evoked potentials from 6 to 48 months: prediction to 3 and 4 year language and cognitive abilities. Clin Neurophysiol 2011;122:320–38. Cong F, Kalyakin I, Huttunen-Scott T, Li H, Lyytinen H, Ristaniemi T. Single-trial based independent component analysis on mismatch negativity of children. Int J Neural Syst 2010;20:279–92. Cong F, Ristaniemi T, Lyytinen H. A potential real-time procedure to evaluate correlation of recordings among single trials (CoRaST) for mismatch negativity (MMN) with Fourier transformation. Clin Neurophysiol 2011;4:725–30. Cong F, Sipola T, Huttunen-Scott T, Xu X, Ristaniemi T, Lyytinen H. Hilbert-Huang versus Morlet wavelet transformation on mismatch negativity of children in uninterrupted sound paradigm. Nonlinear Biomed Phys 2009;3:1. Cooper RJ, Todd J, McGill K, Michie PT. Auditory sensory memory and the aging brain: a mismatch negativity study. Neurobiol Aging 2006;27:752–62. Corbera S, Corral M-J, Escera C, Idiazábal MA. Abnormal speech sound representation in persistent developmental stuttering. Neurology 2005;65: 1246–52. Corbera S, Escera C, Artigas J. Impaired duration mismatch negativity in developmental dyslexia. NeuroReport 2006;17:1051–5. Cornwell BR, Baas JMP, Johnson L, Holroyd T, Carver FW, Lissek S, et al. Neural responses to auditory stimulus deviance under threat of electric shock revealed by spatially-filtered magnetoencephalography. NeuroImage 2007;37:383–9. Coyle JT. Glutamate and schizophrenia: beyond the dopamine hypothesis. Cell Mol Neurobiol 2006;26:365–84. Csépe V, Dyslexia. Different Brain, Different behaviour. In: Csépe V, editor. Neuropsychology and cognition. New York: Kluwer Academic Publisher; 2002. p. 81–112. Csépe V, Karmos G, Molnár M. Evoked potential correlates of stimulus deviance during wakefulness and sleep in cat: Animal model of mismatch negativity. Electroencephalogr Clin Neurophysiol 1987;66:571–8. Csépe V, Karmos G, Molnár M. Subcortical evoked potential correlates of sensory mismatch process in cats. In: Bajic M, editor. Advances in biosciences. Oxford: Pergamon Press; 1988. p. 43–6. Csépe V, Karmos G, Molnár M, Winkler I. Cortical and intracerebral mismatch negativity - animal-model of stimulus comparison. Int J Psychophysiol 1989;7:166–8. Csépe V, Osman-Sági J, Molnár M, Gósy M. Impaired speech perception in aphasic patients: event-related potential and neurophysiological assessment. Neuropsychologia 2001;39:1194–208. Czamara D, Bruder J, Becker J, Bartling J, Hoffman P, Ludwig KU, et al. Association of a rare variant with mismatch negativity in a region between KIAA0319 and DCDC2 in dyslexia. Behav Genet 2011;41:110–9. Czigler I. Visual mismatch negativity: violation of nonattended environmental regularities. J Psychophysiol 2007;21:224–30. Czigler I, Csibra G. Event-related potentials in a visual discrimination task: negative waves related to detection and attention. Psychophysiology 1990;27:669–76. Czigler I, Csibra G. Event-related potentials and the identification of deviant visual stimuli. Psychophysiology 1992;29:471–84. Czigler I, Pató L. Unnoticed regularity violation elicits change-related brain activity. Biol Psychol 2009;80:339–47. Czigler I, Balázs L, Pató LG. Visual change detection: event-related potentials are dependent on stimulus location in humans. Neurosci Lett 2004;364:149–53. Czigler I, Balázs L, Winkler I. Memory-based detection of task-irrelevant visual changes. Psychophysiology 2002;39:869–73. Czigler I, Csibra G, Csontos A. Age and inter-stimulus interval effects on eventrelated potentials to frequent and infrequent auditory-stimuli. Biol Psychol 1992;33:195–206. Czigler I, Weisz J, Winkler I. ERPs and deviance detection: visual mismatch negativity to repeated visual stimuli. Neurosci Lett 2006a;401:178–82. Czigler I, Winkler I, Pató L, Várnagy A, Weisz J, Balázs L. Visual temporal window of integration as revealed by the mismatch negativity event-related potential to stimulus omission. Brain Res 2006b;1104:129–40. Dalkara T, Ayata C, Demirci M, Erdemli G, Onur R. Effects of cerebral ischemia on Nmethyl-D-aspartate and dihydropyridine-sensitive calcium currents: an electrophysiological study in the rat hippocampus in situ. Stroke 1996;27:127–33. Daltrozzo J, Wioland N, Mutschler V, Kotchoubey B. Predicting coma and other low responsive patients’ outcome using event-related potentials: a meta-analysis. Clin Neurophysiol 2007;118:606–14. Davalos DB, Kisley MA, Polk SD, Ross RG. Mismatch negativity in detection of interval duration deviation in schizophrenia. NeuroReport 2003;14:1283–6. Deacon D, Nousak JM, Pilotti M, Ritter W, Yang CM. Automatic change detection: does the auditory system use representations of individual stimulus features or gestalts? Psychophysiology 1998;35:413–9. Dehaene-Lambertz G. Electrophysiological correlates of categorical phoneme perception in adults. NeuroReport 1997;8:919–24. Dehaene-Lambertz G, Pena M, Christphe A, Landrieu P. Phoneme perception in a neonate with left sylvian infarct. Brain Lang 2004;88:26–38.

R. Näätänen et al. / Clinical Neurophysiology 123 (2012) 424–458 Deouell LY. The frontal generator of the mismatch negativity revisited. J Psychophysiol 2007;27:188–203. Deouell LY, Hämäläinen H, Bentin S. Unilateral neglect after right-hemisphere damage: contributions from event-related potentials. Audiol Neuro-Otol 2000a;5:225–34. Deouell LY, Bentin S, Soroker N. Electrophysiological evidence for an early (preattentive) information processing deficit in patients with right hemisphere damage and unilateral neglect. Brain 2000b;123:353–65. Desjardin RN, Trainor LJ, Hevenor S, Polak CP. Using mismatch negativity to measure auditory temporal resolution thresholds. NeuroReport 1999;10:2079–82. de Tommaso M, Guido M, Libro G, Losito L, Difruscolo O, Sardaro M, et al. Interictal lack of habituation of mismatch negativity in migraine. Cephalalgia 2004;24:663–8. Devrim-Ücok M, Keskin-Ergen HY, Ücok A. Mismatch negativity at acute and postacute phases of first-episode schizophrenia. Eur Arch Psy Clin N 2008;258:179–85. Dhawan J, Benveniste H, Nawrocky M, Smith SD, Biegon A. Transient focal ischemia results in persistent and widespread neuroinflammation and loss of glutamate NMDA receptors. NeuroImage 2010;51:599–605. Diaz F, Zurron M. Auditory evoked potentials in Down’s syndrome. Electroen Clin Neuro 1995;96:526–37. Dick BD, Connolly JF, McGrath PJ, Finley GA, Stroink G, Houlihan ME, et al. The disruptive effect of chronic pain on mismatch negativity. Clin Neurophysiol 2003;114:1497–506. Dittmann-Balcar A, Juptner M, Jentzen W, Schall U. Dorsolateral prefrontal cortex activation during automatic auditory duration mismatch processing in humans: a positron emission tomography study. Neurosci Lett 2001;308:119–212. Doeller CF, Opitz B, Mecklinger A, Krick C, Reith W, Schröger E. Prefrontal cortex involvement in preattentive auditory deviance detection: neuroimaging and electrophysiological evidence. NeuroImage 2003;20:1270–82. Dolan RJ, Bench CJ, Liddle PF, Friston KJ, Frith CD, Grasby M, et al. Dorsolateral prefrontal cortex dysfunction in the major psychoses – symptom or disease specificity. J Neurol Neurosur Ps 1993;56:1290–4. Draganova R, Eswaran H, Murphy P, Huotilainen M, Lowerey C, Preissl H. Sound frequency change detection in fetuses and newborns, a magnetoencephalographic study. NeuroImage 2005;28:354–61. Draganova R, Eswaran H, Murphy P, Lowery C, Preissl H. Serial magnetoencephalographic study of fetal and newborn auditory discriminative evoked responses. Early Hum Dev 2007;83:199–207. Dulude L, Labelle A, Knott VJ. Acute nicotine alteration of sensory memory impairment in smokers with schizophrenia. J Clin Psychopharmacol 2010;5:541–8. Duman O, Kizilay F, Fettahoglu C, Ozkaynak S, Haspolat S. Electrophysiologic and neuropsychologic evaluation of patients with centrotemporal spikes. Int J Neurosci 2008;118:118–22. Dunbar G, Boieijinga PH, Demazières A, Cisterni C, Kuchibhatla R, Wesnes K, et al. Effects of TC.1734 (AZD3480), a selective neuronal nicotinic receptor antagonist, on cognitive performance and the EEG of young healthy male volunteers. Psychopharmacology 2007;191:919–29. Duncan CC, Kaye WH. Effects of clonidine on event-related potential measures of information processing. Electroencephalogr Clin Neurophys 1987(Suppl. 40): 527–31. Duncan CC, Barry RJ, Connolly JF, Fischer C, Michie PT, Näätänen R, et al. Eventrelated potentials in clinical research: guidelines for eliciting, recording, and quantifying mismatch negativity, P300, and N400. Clin Neurophysiol 2009;120:1883–908. Dunn MA, Gomes H, Gravel J. Mismatch negativity in children with autism and typical development. J Autism Dev Disord 2008;38:52–71. Ehrlichman RS, Maxwell CR, Majumdar S, Siegel SJ. Deviance-elicited changes in event-related potentials are attenuated by ketamine in mice. J Cognit Neurosci 2008;20:1403–14. Ehrlichman R, Luminais S, White S, Rudnick ND, Ma N, Dow HC, et al. Neuregulin 1 transgenic mice display reduced mismatch negativity, contextual fear conditioning and social interactions. Brain Res 2009;1294:116–27. Engeland C, Mahoney C, Mohr E, Ilivitsky V, Knott VJ. Acute nicotine effects on auditory sensory memory in tacrine-treated and nontreated patients with Alzheimer’s disease. An event-related potential study. Pharmacol Biochem Be 2002;72:457–64. Escera C, Alho K, Schröger E, Winkler I. Involuntary attention and distractibility as evaluated with event-related brain potentials. Audiol Neuro-Otol 2000a;5:151–66. Escera C, Corral MJ. Role of mismatch negativity and novelty-P3 in involuntary auditory attention. J Psychophysiol 2007;21:251–64. Escera C, Corral MJ, Yago E. An electrophysiological and behavioral investigation of involuntary attention towards auditory frequency, duration and intensity changes. Cogn Brain Res 2002;14:325–32. Escera C, Grau C. Short-term replicability of the mismatch negativity. Electroen Clin Neuro 1996;100:549–54. Escera C, Yago E, Polo MD, Grau C. The individual replicability of mismatch negativity at short and long inter-stimulus intervals. Clin Neurophysiol 2000b;111:546–51. Fabiani M, Low KA, Wee E, Sable JJ, Gratton G. Reduced suppression or labile memory? Mechanisms of inefficient filtering of irrelevant information in older adults. J Cognit Neurosci 2006;18:637–50.

447

Fein G, Whitlow B, Finn P. Mismatch negativity: no difference between controls and abstinent alcoholics. Alcohol Clin Exp Res 2004;28:137–42. Fellman V, Huotilainen M. Cortical event-related potentials in newborn infants. Semin Fetal Neonat Med 2006;11:452–8. Fellman V, Kushnerenko E, Mikkola K, Ceponiene R, Leipälä J, Näätänen R. Atypical auditory event-related potentials in preterm infants – a possible sign of cognitive dysfunction? Pediatr Res 2004;56:291–7. Ferri R, Elia M, Agarwal N, Lanuzza B, Musumeci SA, Pennisi G. The mismatch negativity and the P3a components of the auditory event-related potentials in autistic low-functioning subjects. Clin Neurophysiol 2003;114:1671–80. Fischer C, Luauté J. Evoked potentials for the prediction of vegetative state in the acute stage of coma. Neuropsychol Rehab 2005;15:372–80. Fischer C, Dailler F, Morlet D. Novelty P3 elicited by the subject’s own name in comatose patients. Clin Neurophysiol 2008;19:2224–30. Fischer C, Luauté J, Adelaine P, Morlet D. Predictive value of sensory and cognitive evoked potentials for awakening from coma. Neurology 2004;63:669–73. Fischer C, Luauté J, Némoz C, Morlet D, Kirkorian G, Mauguière F. Improved prediction of awakening or nonawakening from severe anoxic coma using treebased classification analysis. Crit Care Med 2006a;34:1–5. Fischer C, Luauté J, Némoz C, Morlet D, Kirkorian G, Mauguière F. Editorial response: evoked potentials can be used as prognosis factor for awakening. Crit Care Med 2006b;34:2025. Fischer C, Morlet D, Bouchet P, Luaute J, Jourdan C, Salord F. Mismatch negativity and late auditory evoked potentials in comatose patients. Clin Neurophysiol 1999;110:1601–10. Fischer C, Morlet D, Giard M-H. Mismatch negativity and N100 in comatose patients. Audiol Neuro-Otol 2000;5:192–7. Fisher AE, Barnes GR, Hillebrand A, Holliday IE, Witton C, Richards IL. Abnormality of mismatch negativity in response to tone omission in dyslexic adults. Brain Res 2006;1077:90–8. Fisher DJ, Grant B, Smith DM, Borracci G, Labelle A, Knott VJ. Effects of auditory hallucinations on the mismatch negativity (MMN) in schizophrenia as measured by a modified ‘‘optimal’’ multi-feature paradigm. Int J Psychophysiol 2011;81:245–51. Fisher DJ, Labelle A, Knott VJ. Auditory hallucinations and the mismatch negativity: processing speech and non-speech sounds in schizophrenia. Int J Psychophysiol 2008;70:3–15. Fisher DJ, Labelle A, Knott VJ. The right profile: mismatch negativity in schizophrenia with and without auditory hallucinations as measured by a multi-feature paradigm. Clin Neurophysiol 2008;119:909–21. Fisher DJ, Lynne Scott T, Shah DK, Prise S, Thompson M, Knott VJ. Light up and see: enhancement of the visual mismatch negativity (vMMN) by nicotine. Brain Res 2010;1313:162–71. Fisher DJ, Grant B, Smith DM, Knott WJ. Effects of deviant probability on the ‘‘optimal’’ multi-feature mismatch negativity (MMN) paradigm. Int J Psychophysiol 2011;79:311–5. Franken IHA, Nijs I, Van Strien JW. Impulsivity affects mismatch negativity (MMN) measures. Biol Psychol 2005;70:161–7. Friedrich M, Weber C, Friederici AD. Electrophysiological evidence for delayed mismatch response in infants at-risk for specific language impairment. Psychophysiology 2004;41:772–82. Frodl-Bauch T, Kathmann N, Möller H-J, Hegerl U. Dipole localization and test– retest reliability of frequency and duration mismatch negativity generator processes. Brain Topogr 1997;10:3–8. Froyen D, van Atteveldt N, Blomert L. Exploring the role of low level visual processing in letter-speech sound integration: a visual MMN study. Front Integr Neurosci 2010;4:9. Froyen D, van Atteveldt N, Bonte M, Blomert L. Crossmodal enhancement of the MMN to speech sounds indicates early and automatic integration of letters and speech sounds. Neurosci Lett 2008;430:23–8. Froyen D, Bonte M, van Atteveldt N, Blomert L. The long road to automation: neurocognitive development of letter-speech sound processing. J Cognit Neurosci 2009;21:567–80. Froyen D, Willems G, Blomert L. Evidence for a specific cross-modal association deficit in dyslexia: an electrophysiological study of letter-speech sound processing. Dev Sci 2010;14:635–8. Fujioka T, Trainor LJ, Ross B, Kakigi R, Pantev C. Automatic encoding of polyphonic melodies in musicians and non-musicians. J Cognit Neurosci 2005;17:1578–92. Ge Y, Wu J, Sun X, Zhang K. Enhanced mismatch negativity in adolescents with posttraumatic stress disorder (PTSD). Int J Psychophysiol 2011;79:231–5. Gaeta H, Friedman D, Ritter W, Cheng J. An event-related potential study of agerelated changes in sensitivity to stimulus deviance. Neurobiol Aging 1998;19:447–59. Gaeta H, Friedman D, Ritter W, Cheng J. Changes in sensitivity to stimulus deviance in Alzheimer’s disease: an ERP perspective. NeuroReport 1999;10:281–7. Gaeta H, Friedman D, Ritter W, Cheng J. An event-related potential evaluation of involuntary attentional shifts in young and older adults. Psychol Aging 2001;16:55–68. Gaeta H, Friedman D, Ritter W, Hunt G. Age-related changes in neural trace generation of rule-based auditory features. Neurobiol Aging 2002;23:443–55. Ge Y, Wu J, Sun X, Zhang K. Enhanced mismatch negativity in adolescents with posttraumatic stress disorder (PTSD). Int J Psychophysiol 2011;79:231–5. Gene-Cos N, Pottinger R, Barrett G, Trimble M, Ring HA. A comparative study of mismatch negativity (MMN) in epilepsy and non-epilectic seizures. Epileptic Disord 2005;7:363–72.

448


Giard MH, Perrin F, Pernier J, Bouchet P. Brain generators implicated in processing of auditory stimulus deviance: a topographic event-related potential study. Psychophysiology 1990;27:627–40. Giese-Davis JE, Miller GA, Knight RA. Memory template comparison processes in anhedonia and dysthymia. Psychophysiology 1993;30:646–56. Gil R, Zai L, Neau JP, Jonveaux T, Agbo C, Rosolacc T, et al. Event-related auditory evoked potentials and multiple sclerosis. Electroen Clin Neuro 1993;88:182–7. Glass E, Sachse S, von Suchodoletz W. Auditory sensory memory in 2-year-old children: an event-related potential study. NeuroReport 2008a;19:569–73. Glass E, Sachse S, von Suchodoletz W. Development of auditory sensory memory from 2 to 6 years: an MMN study. J Neural Trans 2008b;115:1221–9. Gomes H, Molholm S, Ritter W, Kurtzberg D, Cowan N, Vaughan Jr HG. Mismatch negativity in children and adults, and effects of an attended task. Psychophysiology 2000;37:807–16. Gomes H, Sussman E, Ritter W, Kurtzberg D, Cowan N, Vaughan Jr HG. Electrophysiological evidence of developmental changes in the duration of auditory sensory memory. Dev Psychol 1999;35:294–302. Gomot M, Bruneau N, Laurent J-P, Barthélémy C, Saliba E. Left temporal impairment of auditory information processing in prematurely born 9-year-old children: an electrophysiological study. Int J Psychophysiol 2007;64:123–9. Gomot M, Giard M-H, Adrien J-L, Barthélémy C, Bruneau N. Hypersensitivity to acoustic change in children with autism: electrophysiological evidence of left frontal cortex dysfunctioning. Psychophysiology 2002;39:577–84. Gomot M, Giard M-H, Roux S, Barthélémy C, Bruneau N. Maturation of frontal and temporal components of mismatch negativity (MMN) in children. NeuroReport 2000;11:3109–12. Gosselin N, Mathieu A, Mazza S, Petit D, Malo J, Montplaisir J. Attentional deficits in patients with obstructive sleep apnea syndrome: an event-related potential study. Clin Neurophysiol 2006;117:2228–35. Gottesman II, Gould TD. The endophenotype concept in psychiatry: etymology and strategic intentions. Am J Psychiat 2003;160:636–45. Gottselig JM, Brandeis D, Hofer-Tinguely G, Borbély AA, Achermann P. Human central auditory plasticity associated with tone sequence learning. Learn Memory 2004;11:162–71. Grau C, Escera C, Yago E, Polo MD. Mismatch negativity and auditory sensory memory evaluation: a new faster paradigm. NeuroReport 1998;9:2451–6. Grau C, Polo MD, Yago E, Gual A, Escera C. Auditory sensory memory as indicated by mismatch negativity in chronic alcoholism. Clin Neurophysiol 2001;112:728–31. Grimm S, Schröger E, Bendixen A, Bäss P, Roye A, Deouell LY. Optimizing the auditory distraction paradigm: behavioural and event-related potential effects in a laterized multi-deviant approach. Clin Neurophysol 2008;119:934–47. Groenen P, Snik A, van der Broek P. On the clinical relevance of mismatch negativity: results from subjects with normal hearing and cochlear implant users. Audiol Neuro-Otology 1996;1:112–4. Grossheinrich N, Kademan S, Bruder J, Bartling J, von Suchodoletz W. Auditory sensory memory and language abilities in former late talkers: a mismatch negativity study. Psychophysiology 2010;47:822–30. Grzella I, Müller BW, Oades RD, Bender S, Schall U, Zerbin D, et al. Novelty elicited mismatch negativity in patients with schizophrenia on admission and discharge. J Psychiatr Neurosci 2001;26:235–46. Guérit J-M, Verougstraete D, de Tourtchaninoff M, Debatisse D, Witdoeckt C. ERPs obtained with the auditory oddball paradigm in coma and altered states of consciousness: clinical relationships, prognostic value, and origin of components. Clin Neurophysiol 1999;110:1260–9. Gumenyuk V, Korzyukov O, Alho K, Escera C, Näätänen R. Effects of auditory distraction on electrophysiological brain activity and performance in children aged 8–13 years. Psychophysiology 2004;41:30–6. Gumenyuk V, Korzyukov O, Escera C, Hämäläinen M, Huotilainen M, Häyrinen T, et al. Electrophysiological evidence of enhanced distractibility in ADHD children. Neurosci Lett 2005;374:212–7. Gumenyuk V, Roth T, Korzyukov O, Jefferson C, Kick A, Spear L, et al. Shift work sleep disorder is associated with an attenuated brain response of sensory memory and increased brain response to novelty: an ERP study. Sleep 2010;33:703–13. Gunter TC, Jackson JL, Mulder G. Focussing on aging: an electrophysiological exploration of spatial and attentional processing during reading. Biol Psychol 1996;43:103–45. Guttorm TK, Leppänen PHT, Poikkeus A-M, Eklund KM, Lyytinen P, Lyytinen H. Brain event-related potentials (ERPs) measured at birth predict later language development in children with and without familial risk for dyslexia. Cortex 2005;41:291–303. Guttorm TK, Leppänen PHT, Richardson U, Lyytinen H. Event-related potentials and consonant differentiation in newborns with familial risk for dyslexia. J Learn Disabil 2001;34:534–44. Halgren E, Baudena P, Clarke JM, Heit G, Liegeois C, Chauvel P, et al. Intracerebral potentials to rare target and distracter auditory and visual-stimuli .1. Superior temporal plane and parietal lobe. Electroencephalogr Clin Neurophysiol 1995a;94:191–220. Halgren E, Baudena P, Clarke JM, Heit G, Marinkovic K, Devaux B, et al. Intracerebral potentials to rare target and distracter auditory and visual-stimuli. 2. Medial, lateral and posterior temporal-lobe. Electroencephalogr Clin Neurophysiol 1995b;94:229–50. Halgren E, Marinkovic K, Chauvel P. Generators of the late cognitive potentials in auditory and visual oddball tasks. Electroencephalogr Clin Neurophysiol 1998;106:156–64.

Hall M-H, Schulze K, Rijsdijk F, Kalitindi S, McDonald C, Bramon E, et al. Are auditory P300 and duration MMN heritable and putative endophenotypes of psychotic bipolar disorder? A Maudsley bipolar twin and family study. Psychol Med 2009;39:1277–87. Hall M-H, Rijsdijk F, Kalitinidi S, Schulze K, Kravariti E, Kane F, et al. Genetic overlap between bipolar illness and event-related potentials. Psychol Med 2007;37:667–78. Hall MH, Schulze K, Rijsdijk F, Piccioni M, Ettinger U, Bramon E, et al. Heritability and reliability of P300, P50 and duration mismatch negativity. Behav Genet 2006;36:845–57. Hämäläinen H, Kujala T, Kekoni J, Hurskainen H, Pirilä J, Wikström H, et al. Effects of unilateral hippocampus – amygdala – partial temporal lobe resection on auditory EEG/MEG responses: a case study. Scand J Psychol 2007;48:367–73. Hämäläinen JA, Leppänen PHT, Guttorm TK, Lyyytinen H. Event-related potentials to pitch and rise time change in children with reading disabilities and typically reading children. Clin Neurophysiol 2008;119:100–15. Hämäläinen M, Hari R, Ilmoniemi RJ, Knuutila J, Lounasmaa OV. Magnetoencephalography – theory, instrumentation, and applications to noninvasive studies of the working human brain. Rev Mod Phys 1993;65:413–97. Hanagasi HA, Gurvit IH, Ermutlu N, Kaptanoglu G, Karamursel S, Idrisoglu HA, et al. Cognitive impairment in amyotropic lateral sclerosis: evidence from neuropsychological investigation and event-related potentials. Cognit Brain Res 2002;14:234–44. Hansenne M, Pinto E, Scantamburlo G, Couvreur A, Reggers J, Fuchs S, et al. Mismatch negativity is not correlated with neuroendocrine indicators of catecholaminergic activity in healthy subjects. Hum Psychopharm Clin 2003;18:201–5. Hari R, Hämäläinen M, Ilmoniemi R, Kaukoranta E, Reinikainen K, Salminen J, et al. Responses of the primary auditory cortex to pitch changes in a sequence of tone pips: neuromagnetic recordings in man. Neurosci Lett 1984;50:127–32. Harkrider AW, Hedrick MS. Acute effect of nicotine on auditory gating in smokers and non-smokers. Hearing Res 2005;202:114–28. Hawkins HL, Presson JC. Auditory information processing. In: Boff KR, Kaufman L, Thomas JP. (Eds.) Handbook of perception and human performance, vol 2. New York: Wiley; 1986. p. 261–4. He W, Chai H, Zheng L, Yu W, Chen W, Li J, et al. Mismatch negativity in treatmentresistant depression and borderline personality disorder. Prog Neuro-Psychoph 2010;34:366–71. Heaton P, Pring L, Hermelin B. Musical processing in high functioning children with autism. Ann NY Acad Sci 2001;930:443–4. Heekeren K, Daumann J, Neukirch A, Stock C, Kawohl W, Norra C, et al. Mismatch negativity generation in the human 5HT2A agonist and NMDA antagonist model of psychosis. Psychopharmacology 2008;199:77–88. Heim S, Eulitz C, Kaufmann J, Füchter I, Pantev C, Lamprecht-Dinnesen A, et al. Atypical organisation of the auditory cortex in dyslexia as revealed by MEG. Neuropsychologia 2000;38:1749–59. Heinke W, Kenntner R, Gunter TC, Sammler D, Olthoff D, Koelsch S. Sequential effects of increasing propofol sedation on frontal and temporal cortices as indexed by auditory event-related potentials. Anesthesiology 2004;100:617–25. Heinke W, Koelsch S. The effects of anesthetics on brain activity and cognitive function. Curr Opin Anaesthesiology 2005;18:625–31. Hermens DF, Ward PB, Redoblado Hodge MA, Kaur M, Naismith SL, Hickie IB. Impaired MMN/P3a complex in first-episode psychosis: cognitive and psychosocial associations. Prog Neuro-Psychoph 2010;34:822–9. Heslenfeld DJ. Visual mismatch negativity. in: Polich J. (Ed.). Detection of change: event-related potential and fMRI findings. Boston: Kluwer Academic Publishers; 2003. p. 41–60. Hirayasu Y, McCarley RW, Salisbury DF, Tanaka S, Kwon JS, Frumin M, et al. Planum temporale and Heschl gyrus volume reduction in schizophrenia: a magnetic resonance imaging study of first-episode patients. Arch Gen Psychiat 2000;57:692–9. Hirayasu Y, Potts GF, O’Donnell BF, Kwon JS, Arakaki H, Akdag SJ, et al. Auditory mismatch negativity in schizophrenia: topographic evaluation with a highdensity recording montage. Am J Psychiat 1998;155:1281–4. Hirayasu Y, Tanaka S, Shenton ME, Salisbury DF, DeSantis MA, Levitt JJ, et al. Prefrontal gray matter volume reduction in first episode schizophrenia. Cereb Cortex 2001;11:374–81. Hiruma T, Yabe H, Sato Y, Sutho T, Kaneko S. Differential effects of the hiba odor on CNV and MMN. Biol Psychol 2002;61:321–31. Hirvonen J, Jääskeläinen IP, Näätänen R, Sillanaukee P. Adenosine A1/A2a receptors mediate suppression of mismatch negativity by ethanol in humans. Neurosci Lett 2000;278:57–60. Holguin RS, Corral M, Cadaveira F. Mismatch negativity in young children of alcoholics from high-density families. Alcohol Clin Exp Res 1998;22:1363–8. Holopainen IE, Korpilahti P, Juottonen K, Lang H Sillanpää M. Attenuated auditory event-related potential (mismatch negativity) in children with developmental dysphasia. Neuropediatrics 1997;28:253–6. Holopainen IE, Korpilahti P, Juottonen K, Lang H, Sillanpää M. Abnormal frequency mismatch negativity in mentally retarded children and in children with developmental dysphasia. J Child Neurol 1998;13:178–83. Holst M, Eswaran H, Lowery C, Murphy P, Norton J, Preissl H. Development of auditory evoked fields in human fetuses and newborns: a longitudinal MEG study. Clin Neurophysiol 2005;116:1949–55.

R. Näätänen et al. / Clinical Neurophysiology 123 (2012) 424–458 Honbolygó F, Csépe V, Fekésházy A, Emri M, Márián T, Sárközy G, et al. Covering evidences on language impairment in Landau–Kleffner Syndrome revealed by behavioural and brain activity measures: a case study. Clin Neurophysiol 2006;117:295–305. Horimoto R, Inagaki M, Yano T, Sata Y, Kaga M. Mismatch negativity of the color modality during a selective attention task to auditory stimuli in children with mental retardation. Brain Dev JPN 2002;24:703–9. Horton J, Millar A, Labelle A, Knott VJ. MMN responsivity to manipulations of frequency and duration deviants in chronic, clozapine-treated schizophrenia patients. Schizophr Res 2011;126:202–11. Horváth J, Czigler I, Winkler I, Teder-Sälejärvi WA. The temporal window of integration in elderly and young adults. Neurobiol Aging 2007;28:964–75. ˇ izˇek J. Mismatch negativity in Hosák L, Kremlácˇek J, Kuba M, Libiger J, C methamphetamine dependence. A pilot study. Acta Neurobiol Exp 2008;68:7–102. Hosoi H, Imaizumi S, Sakaguchi T, Tonoike M, Murata K. Activation of the auditory cortex by ultrasound. Lancet 1998;351:496–7. Hugdahl K, Calhoun VD. An update on neurocognitive impairment in schizophrenia and depression. Front Hum Neurosci 2010;4:4. Huotilainen M, Kujala A, Hotakainen M, Parkkonen L, Taulu S, Simola J, et al. Shortterm memory functions of the human fetus recorded with magnetoencephalography. NeuroReport 2005;16:81–4. Huotilainen M, Lovio R, Kujala T, Tommiska V, Karma K, Fellman V. Could audiovisual training be used to improve cognition in extremely low birth weight children? Acta Paediatr 2011. doi: 10.1111/j.1651-2227.2011.02345.x. Huotilainen M, Shestakova A, Hukki J. Using magnetoencephalography in assessing auditory skills in infants and children. Int J Psychophysiol 2008;68:123–9. Huttunen T, Halonen A, Kaartinen J, Lyytinen H. Does mismatch negativity show differences in reading-disabled children compared to normal children and children with attention deficit? DevNeuropsychol 2007;31:453–70. Huttunen-Scott T, Kaartinen J, Tolvanen A, Lyytinen H. Mismatch negativity (MMN) elicited by duration deviations in children with reading disorder, attention deficit or both. Int J Psychophysiol 2008;69:69–77. Iijima, M., Osawa, M., Nageishi, Y., Ushijima, R., Iwata, M. Visual mismatch negativity (MMN) in aging. in: Ogura C, Koga Y, Shimokochi M. (Eds.), Recent Advances in Event-Related Brain Potentials Research. Amsterdam: Elsevier; 1996. p. 804–9. Ikeda K, Hayashi A, Hashimoto S, Kanno A. Distinctive MMN relative to sound types in adults with intellectual disability. NeuroReport 2004;15:1053–6. Ilvonen T-M, Kujala T, Kiesiläinen A, Salonen O, Kozou H, Pekkonen E, et al. Auditory discrimination after left hemisphere stroke: an MMN follow-up study. Stroke 2003;34:1746–53. Ilvonen T-M, Kujala T, Kozou H, Kiesiläinen A, Salonen O, Alku P, et al. The processing of speech and non-speech sounds in aphasic patients as reflected by the mismatch negativity (MMN). Neurosci Lett 2004;366:235–40. Ilvonen T-M, Kujala T, Tervaniemi M, Salonen O, Näätänen R, Pekkonen E. The processing of sound duration after left hemisphere stroke: event-related potential and behavioral evidence. Psychophysiology 2001;38:622–8. Inami R, Kirino E, Inoue R, Arai H. Transdermal nicotine administration enhances automatic auditory processing reflected by mismatch negativity. Pharmacol Biochem Be 2005;80:453–61. Inami R, Kirino E, Inoue E, Suzuki T, Arai H. Nicotine effects on mismatch negativity in nonsmoking schizophrenic patients. Neuropsychobiology 2007;56:64–72. Iv J, Zhao L, Gong J, Chen C, Miao D. Event-related potential based evidence of cognitive dysfunction in patients during the first episode of depression using a novelty oddball task. Psychiat Res-Neuroim 2010;182:58–66. Izquidero L. The role of NMDA receptors in memory. Trends Pharmacol Sci 1991;12:128–9. Jääskeläinen IP, Hirvonen J, Kujala T, Alho K, Eriksson CFP, Lehtokoski A, et al. Effects of naltrexone and ethanol on auditory event-related brain potentials. Alcohol 1998;15:105–11. Jääskeläinen IP, Lehtokoski A, Alho K, Kujala T, Pekkonen E, Sinclair JD, et al. Low dose of ethanol suppresses mismatch negativity of auditory event-related potentials. Alcohol Clin Exp Res 1995;19:607–10. Jääskeläinen IP, Näätänen R, Sillanaukee P. Effect of acute ethanol on auditory and visual event-related potentials: a review and reinterpretation. Biol Psychiat1996a;40:284–91. Jääskeläinen IP, Pekkonen E, Hirvonen J, Sillanaukee P, Näätänen R. Mismatch negativity subcomponents and ethyl alcohol. Biol Psychol 1996b;43:13–25. Jääskeläinen IP, Schröger E, Näätänen R. Electrophysiological indices of acute effects of ethanol on involuntary attention shifting. Psychopharmacology 1999b;141:16–21. Jääskeläinen IP, Varonen R, Näätänen R, Pekkonen E. Decay of cortical pre-attentive sound discrimination in middle-age. NeuroReport 1999a;10:123–6. Jacobs BJ, Schneider SL. Analysis of lexical-semantic processing and extensive neurological, electrophysiological, speech perception, and language evaluation following a unilateral left hemisphere lesion: pure word deafness? Aphasiology 2003;17:123–41. Jahshan C, Cadenhead KS, Rissling AJ, Kirihara K, Braff DL, Light GA. Automatic sensory information processing abnormalities across the illness course of schizophrenia. Psychol Med 2011. p. 1–13 [Epub ahead of print]. Jahshan C, Heaton RK, Golshan S, Cadenhead KS. Course of neurocognitive deficits in the prodrome and first episode of schizophrenia. Neuropsychology 2010;24:109–20. James L, Gordon E, Kraiuhin C, Meares R. Selective attention and auditory eventrelated potentials in somatisation disorder. Compr Psychiat 1989;30:84–9.

449

Jamieson GA, Dwivedi P, Gruzelier JH. Changes in mismatch negativity across prehypnosis, hypnosis and post-hypnosis conditions distinguish high from low hypnotic susceptibility groups. Brain Res Bull 2005;67:298–303. Jankowiak S, Berti S. Behavioral and event-related potential distraction effects with regularly occurring auditory deviants. Psychophysiology 2007;44:79–85. Jansson-Verkasalo E, Ceponiene R, Kielinen M, Suominen K, Linna S-L, Moilanen I, et al. Deficient auditory processing in children with Asperger syndrome, as indexed by event-related potentials. Neurosci Lett 2003a;338:197–200. Jansson-Verkasalo E, Ceponiene R, Valkama M, Vainionpää L, Laitakari K, Alku P, et al. Deficient speech-sound processing, as shown by the electrophysiologic brain mismatch negativity response, and naming ability in prematurely born children. Neurosci Lett 2003b;348:5–8. Jansson-Verkasalo E, Korpilahti P, Jäntti V, Valkama M, Vainionpää L, Alku P, et al. Neurophysiologic correlates of deficient phonological representations and object naming in prematurely born children. Clin Neurophysiol 2004;115:179–87. Jansson-Verkasalo E, Kujala T, Jussila K, Mattila ML, Moilanen I, Näätänen R, et al. Similarities in the phenotype of the auditory neural substrate in children with Asperger syndrome and their parents. Eur J Neurosci 2005;22:986–90. Jansson-Verkasalo E, Ruusuvirta T, Huotilainen M, Alku P, Kushnerenko E, Suominen K, et al. Atypical perceptual narrowing in prematurely born infants is associated with compromised language acquisition at 2 years of age. BMC Neurosci 2010;11:88. Järvelä LS, Hurme S, Holopainen IE, Leino M, Hatanpää A-M, Mikola H, et al. Auditory event related potentials as tools to reveal cognitive late effects in childhood cancer patients. Clin Neurophysiol 2011;122:62–72. Javitt DC. Neurophysiological approaches to analyzing brain dysfunction in schizophrenia. Biol Treatment Schizophr 1993;23:144–50. Javitt DC. Intracortical mechanisms of mismatch negativity dysfunction in schizophrenia. Audiol Neuro-Otol 2000;5:207–15. Javitt DC. When doors of perception close: bottom-up models of disrupted cognition in schizophrenia. Annu Rev Clin Psychol 2009a;5:249–75. Javitt DC. Glycine transport inhibitors for the treatment of schizophrenia: symptom and disease modification. Curr Opin Drug Discov Dev 2009b;12:468–78. Javitt DC, Shelley A, Ritter W. Associated deficits in mismatch negativity generation and tone matching in schizophrenia. Clin Neurophysiol 2000;111:1733–7. Javitt DC, Schroeder CE, Steinschneider M, Arezzo JC, Vaughan Jr HG. Electroen Clin Neuro 1992;83:87–90. Javitt DC, Spencer KM, Thaker GK, Winterer G, Hajós M. Neurophysiological biomarkers for drug development in schizophrenia. Nature Rev 2008;68:68–83. Javitt DC, Liederman E, Cienfuegos A, Shelley A-M. Panmodal processing imprecision as a basis for dysfunction of transient memory storage systems in schizophrenia. Schizophrenia Bull 1999;25:763–75. Javitt DC, Steinschneider M, Schroeder CE, Arezzo JC. Role of cortical N-methyl-Daspartate receptors in auditory sensory memory and mismatch negativity generation: implications for schizophrenia. P Natl Acad Sci USA 1996;93:11962–7. Javitt DC, Grochowski S, Shelley AM, Ritter W. Impaired mismatch negativity (MMN) generation in schizophrenia as a function of stimulus deviance, probability, and interstimulus/interdeviant interval. Electroen Clin Neuro 1998;108:143–53. Jessen F, Fries T, Kucharski C, Nishimura T, Hoenig K, Maier W, et al. Amplitude reduction of the mismatch negativity in first-degree relatives of patients with schizophrenia. Neurosci Lett 2001;309:185–8. Jung J, Morlet D, Mercier B, Confavreux C, Fischer C. Mismatch negativity (MMN) in multiple sclerosis: an event-related potentials study in 46 patients. Clin Neurophysiol 2006;117:85–93. Kaga M, Inagaki M, Uno A. Auditory verbal and non-verbal mismatch negativity (MMN) in patients with severe motor and intellectual disabilities. Electroen Clin Neuro 1999;49:194–8. Kähkönen S, Ahveninen J. Combination of magneto- and electroencephalography in studies of monoamine modulation on attention. Method Find Exp Clin 2002;24:27–34. Kähkönen S, Kesäniemi M, Nikouline VV, Karhu J, Ollikainen M, Holi M, et al. Ethanol modulates cortical activity: direct evidence with combined TMS and EEG. NeuroImage 2001;14:322–8. Kähkönen S, Mäkinen V, Jääskeläinen I, Pennanen S, Liesivuori J, Ahveninen J. Serotonergic modulation of mismatch negativity. Psychiat Res-Neuroim 2005a;138:61–74. Kähkönen S, Marttinen-Rossi E, Yamashita H. Alcohol impairs auditory processing of frequency changes and novel sounds: a combined MEG and EEG study. Psychopharmacology 2005b;177:366–72. Kähkönen S, Yamashita H, Rytsälä H, Suominen K, Ahveninen J, Isometsä E. Dysfunction in early auditory processing in major depressive disorder revealed by combined MEG and EEG. J Psychiat Neurosci 2007;32:316–22. Kaipio M-L, Alho K, Winkler I, Escera C, Surma-aho O, Näätänen R. Event-related brain potentials reveal covert distractibility in closed head injuries. NeuroReport 1999;10:2125–9. Kaipio M-L, Cheour M, Ceponiene R, Öhman J, Alku P, Näätänen R. Increased distractibility in closed head injury as revealed by event-related potentials. NeuroReport 2000;11:1463–8. Kaipio M-L, Novitski N, Tervaniemi M, Alho K, Öhman J, Salonen O, et al. Fast vigilance decrement in closed head injury patients as reflected by the mismatch negativity (MMN). NeuroReport 2001;12:1517–22. Kallio S, Revonsuo A, Lauerma H, Hämäläinen H, Lang H. The MMN amplitude increases in hypnosis: a case study. NeuroReport 1999;10:3579–82.

450


Kalyakin I, González N, Ivannikov A, Lyytinen H. Extraction of the mismatch negativity elicited by sound duration decrements: a comparison of three procedures. Data Knowl Eng 2009;68:1411–26. Kalyakin I, González N, Joutsensalo J, Huttunen T, Kaartinen J, Lyytinen H. Optimal digital filtering versus difference waves on the mismatch negativity in an uninterrupted sound paradigm. Dev Neuropsychol 2007;31:429–52. Kalyakin I, González N, Kärkkäinen T, Lyytinen H. Independent component analysis on the mismatch negativity in an uninterrupted sound paradigm. J Neurosci Meth 2008b;174:301–12. Kalyakin I, González N, Lyytinen H. Extraction of the mismatch negativity on two paradigms using independent component analysis. Proceedings of the CBMS 2008. In: Puuronen S, Pechenizkiy M, Tsymbal A, Lee DJ. (Eds.), 21st IEEE international symposium on computer-based medical systems, CBMS. Los Alamitos, CA: IEEE Computer Society Conference Publishing Services; 2008a. p. 59–64. Kane NM, Butler SR, Simpson T. Coma outcome prediction using event-related potentials: P3 and mismatch negativity. Audiol Neuro-Otol 2000;5:186–91. Kane NM, Curry SH, Butler SR, Cummings BH. Electrophysiological indicator of awakening from coma. Lancet 1993;341:688. Kane NM, Curry SH, Rowlands CA, Manara AR, Lewis T, Moss T, et al. Event-related potentials – neurophysiological tools for predicting emergence and early outcome from traumatic coma. Intens Care Med 1996;22:39–46. Karayanidis F, Andrews S, Ward PB, Michie PT. ERP indexes of auditory selective attention in aging and Parkinson’s disease. Psychophysiology 1995;32:335–50. Karma K. Auditory structuring in explaining dyslexia. In: McKevitt P, Nuallain SO, Mulvihill C. (Eds.), Advances in consciousness research, language, vision, and music, vol. 35. Amsterdam/Philadelphia: John Benjamins Publ. CO; 1999. p. 221–9. Kasai K, Hashimoto O, Kawakubo Y, Yumoto M, Kamio S, Itoh K, et al. Delayed automatic detection of change in speech sounds in adults with autism: a magnetoencephalographic study. Clin Neurophysiol 2005;116:1655–64. Kasai K, Nakagome K, Itoh K, Koshida I, Hata A, Iwanami A, et al. Impaired cortical network for preattentive detection of change in speech sounds in schizophrenia: a high-resolution event-related potential study. Am J Psychiatry 2002a;159:546–53. Kasai K, Shenton ME, Salisbury DF, Hirayasu Y, Lee C-U, Ciszewski AA, et al. Progressive decrease of left superior temporal gyrus gray matter volume in patients with first-episode schizophrenia. Am J Psychiat 2003b;160:156–64. Kasai K, Yamada H, Kamio S, Nakagome K, Iwanami A, Fukuda M, et al. Do high or low doses of anxiolytics and hypnotics affect mismatch negativity in schizophrenic subjects? An EEG and MEG study. Clin Neurophysiol 2002c;113:141–50. Kasai K, Shenton ME, Salisbury DF, Hirayasu Y, Onitsuka T, Spencer MH, et al. Progressive decrease of left Heschl gyrus and planum temporale gray matter volume in first-episode schizophrenia: a longitudinal magnetic resonance imaging study. Arch Gen Psychiat 2003a;60:766–75. Kasai K, Yamada H, Kamio S, Nakagome K, Iwanami A, Fukuda M, et al. Brain laterization for mismatch response to across- and within-category change of vowels. NeuroReport 2001;12:2467–71. Kasai K, Yamada H, Kamio S, Nakagome K, Iwanami A, Fukuda M, et al. Neuromagnetic correlates of impaired automatic categorical perception of speech sounds in schizophrenia. Schizophr Res 2002b;59:159–72. Katada E, Sato K, Ojika K, Ueda R. Cognitive event-related potentials: useful clinical information in Alzheimer’s disease. Curr Alzheimer Res 2004;1:63–9. Kathmann N, Wagner M, Rendtorff N, Engel RR. Delayed peak latency of the mismatch negativity in schizophrenics and alcoholics. Biol Psychiat 1995;37:754–7. Kaur M, Battisti RA, Ward PB, Ahmed A, Hickie IB, Hermens DF. MMN/P3a deficits in first episode psychosis: comparing schizophrenia-spectrum and affectivespectrum subgroups. Schizoph Res 2011;130:203–9. Kawakubo Y, Kamio S, Nose T, Iwanami A, Nakagome K, Fukuda M, et al. Phonetic mismatch negativity predicts social skills acquisition in schizophrenia. Psychiat Res 2007;152:261–5. Kawakubo Y, Kasai K, Kudo N, Rogers MA, Nakagome K, Itoh K, et al. Phonetic mismatch negativity predicts verbal memory deficit in schizophrenia. NeuroReport 2006;17:1043–6. Kazmerski VA, Friedman D, Ritter W. Mismatch negativity during attend and ignore conditions in Alzheimer’s disease. Biol Psychiat 1997;42:382–402. Kekoni J, Hämäläinen H, Saarinen M, Gröhn J, Reinikainen K, Lehtokoski A, et al. Rate effect and mismatch responses in the somatosensory system: ERP-recordings in humans. Biol Psychol 1997;46:125–42. Kelly AS, Purdy SC, Thorne PR. Electrophysiological and speech perception measures of auditory processing in experimental adult cochlear implant users. Clin Neurophysiol 2005;116:1235–46. Kemner C, Verbaten M, Cuperus J, Camfferman G, van Engeland H. Auditory eventrelated brain potentials in autistic children and three different control groups. Biol Psychiat 1995;38:150–65. Kemner C, Verbaten MN, Koelega HS, Buitelaar JK, van der Gaag RJ, Camfferman G, et al. Event-related potentials in children with attention-deficit and hyperactivity disorder: effects of stimulus deviancy and task relevance in the visual and auditory modality. Biol Psychiat 1996;40:522–34. Kenemans JL, Gren-’t jong T, Verbaten MN. Detection of visual change: mismatch or rareness? NeuroReport 2003;14:1239–42. Kenemans JL, Helby W, van den Heuvel EHM, Grent-’T-Jong T. Moderate alcohol disrupts a mechanism for detection of rare events in human visual cortex. J Psychopharmacol 2010;24:839–45.

Kiang M, Braff DL, Sprock J, Light GA. The relationship between preattentive sensory processing deficits and age in schizophrenia patients. Clin Neurophysiol 2009;120:1949–57. Kiang M, Light GA, Prugh J, Coulson S, Braff DL, Kutas M. Cognitive, neurophysiological, and functional correlates of proverb interpretation abnormalities in schizophrenia. J Int Neuropsych Soc 2007;13:653–63. Kida T, Nishihira Y, Hatta A, Fumuto M, Wasaka T. Automatic mismatch negativity detection in somatosensory modality and the effect of stimulus probability. Jpn Clin Neurophysiol (Tokyo) 2001;29:417–24 [in Japanese]. Kileny PR, Boerst A, Zwolan T. Cognitive evoked potentials to speech and tonal stimuli in children with implants. Otolaryng Head Neck 1997;117:161–9. Kilpeläinen R, Partanen J, Karhu J. Reduced mismatch negativity (MMN) suggests deficits in preattentive auditory processing in distractible children. NeuroReport 1999;10:3341–5. Kimura M, Katayama J, Ohira H, Schröger E. Visual mismatch negativity: new evidence from the equiprobable paradigm. Psychophysiology 2009;46:402–9. Kimura M, Schröger E, Czigler I. Visual mismatch negativity and its importance in visual cognitive sciences. NeuroReport 2011;22:669–73. Kircher TT, Rapp A, Grodd W, Buchkremer G, Weiskopf N, Lutzenberger W, et al. Mismatch negativity responses in schizophrenia: a combined fMRI and wholehead MEG study. Am J Psychiat 2004;161:294–304. Kisley MA, Davalos DB, Engleman LL, Guinther PM, Davis HP. Age-related change in neural processing of time-dependent stimulus features. Cognit Brain Res 2005;25:913–25. Kisley MA, Davalos DB, Layton HS, Pratt D, Ellis JK, Seger CA. Small changes in temporal deviance modulate mismatch negativity in humans. Neurosci Lett 2004a;358:197–200. Kisley MA, Noecker TL, Guinther PM. Comparison of sensory gating to mismatch negativity and self-reported perceptual phenomena in healthy adults. Psychophysiology 2004b;41:604–12. Kivisaari R, Lehtinen R, Autti T, Puuskari V, Jokela O, Ahveninen J, et al. Impaired pre-attentive auditory processing in opioid dependence with and without benzodiazepine co-dependence revealed by combined magnetoencephalography and electroencephalography. Prog Neuro-Psychoph 2007;31:1378–86. Knott V, Blais C, Scherling C, Camarda J, Millar A, Fisher D, et al. Neural effects of nicotine during auditory selective attention in smokers: an event-related potential study. Neuropsychobiology 2006;53:115–26. Knott VJ, Bolton K, Heenan A, Shah D, Fisher DJ, Villeneuve C. Effects of acute nicotine on event-related potential and performance indices of auditory distraction in nonsmokers. Nicotine Tobacco Res 2009;11:519–30. Koelsch S, Wittfoth M, Wolf A, Müller J, Hahne A. Music perception in cochlear implant users: an event-related potential study. Clin Neurophysiol 2004;115:966–72. Koelsch S, Heinke W, Sammler D, Olthoff D. Auditory processing during deep propofol sedation and recovery from unconsciousness. Clin Neurophysiol 2006;117:1746–59. Kohlmetz C, Altenmüller E, Schuppert M, Wieringa BM, Münte T. Deficit in automatic sound-change detection may underlie some music perception deficits after acute hemispheric stroke. Neuropsychologia 2001;39:1121–4. Kok A. Age-related changes in involuntary and voluntary attention as reflected in components of the event-related potential (ERP). Biol Psychol 2000;54:107–43. Korostenskaja M, Dapsys K, Siurkute A, Maciulis V, Ruksenas O, Kähkönen S. Effects of olanzapine on auditory P300 and mismatch negativity (MMN) in schizophrenia spectrum disorders. Prog Neuro-Psychoph 2005;29:543–8. Korostenskaja M, Nikulin VV, Kicic D, Nikulina AV, Kähkönen S. Effects of NMDA receptor antagonist memantine on mismatch negativity in healthy subjects. Brain Res Bull 2007;72:275–83. Korostenskaja M, Pardos M, Fujiwara H, Kujala TM, Horn P, Rose D, et al. Neuromagnetic evidence of impaired cortical auditory processing in pediatric intractable epilepsy. Epilepsy Res 2010a;92:63–73. Korostenskaja M, Pardos M, Kujala T, Rose DF, Xiang J, Horn P, et al. Impaired auditory information processing during acute migraine: a magnetoencephalography study. Int J Neurosci 2010b;121:355–65. Korpilahti P. Auditory discrimination and memory functions in SLI children: a comprehensive study with neurophysiological and behavioural methods. Scand J Logoped Phoniatr 1995;20:131–9. Korpilahti P, Lang HA. Auditory ERP components and mismatch negativity in dysphasic children. Electroen Clin Neuro 1994;91:256–64. Korpilahti P, Jansson-Verkasalo E, Mattila M-L, Kuusikko S, Suominen K, Rytky S, et al. Processing of affective speech prosody is impaired in Asperger syndrome. J Autism Dev Disord 2007;37:1539–49. Kotchoubey B. Event-related potentials predict the outcome of the vegetative state. Clin Neurophysiol 2007;118:477–9. Kotchoubey B, Lang S, Herb E, Maurer P, Schmalohr D, Bostanov V, et al. Stimulus complexity enhances auditory discrimination in patients with extremely severe brain injuries. Neurosci Lett 2003;352:129–32. Kotchoubey B, Lang S, Mezger G, Schmalohr D, Schneck M, Semmler A, et al. Information processing in severe disorders of consciousness: vegetative state and minimally conscious state. Clin Neurophysiol 2007;116:2441–53. Kozou H, Kujala T, Shtyrov Y, Toppila E, Stark J, Alku P, et al. The effect of different noise types on the speech and non-speech elicited mismatch negativity. Hearing Res 2005;199:31–9. Kramer AF, Trejo LJ, Humphrey D. Assessment of mental workload with taskirrelevant auditory probes. Biol Psychol 1995;40:83–100.

R. Näätänen et al. / Clinical Neurophysiology 123 (2012) 424–458 Krauel K, Schott P, Sojka B, Pause BM, Ferstl R. Is there a mismatch negativity analogue in the olfactory event-related potential? J Psychophysiol 1999;13:49–55. Kraus N, Koch D, McGee T, Nicol T, Cunningham J. Speech-sound discrimination in school-age children: psychophysical and neurophysiologic measures. J Speech Lang Hear Res 1999;42:1042–60. Kraus N, Cheour M. Speech-sound representation in the brain: studies using mismatch negativity. Audiol Neuro-Otol 2000;5:140–50. Kraus N, McGee T, Carrell TD, King C, Tremblay K, Nicol N. Central auditory plasticity associated with speech discrimination training. J Cognit Neurosci 1995;7:25–32. Kraus N, McGee TJ, Carrell TD, Zecker SG, Nicol TG, Koch DB. Auditory neurophysiologic responses and discrimination deficits in children with learning problems. Science 1996;273:971–3. Kraus N, McGee TJ, Littman T, Nicol TG, King C. Nonprimary auditory thalamic representation of acoustic change. J Neurophysiol 1994;72:1270–7. Kraus N, McGee T, Micco A, Sharma A, Carrell T, Nicol T. Mismatch negativity in school-age children to speech stimuli which are just perceptibly different. Electroen Clin Neuro 1993a;88:123–30. Kraus N, McGee T, Sharma A, Carrell T, Nicol T. Mismatch negativity event-related potential elicited by speech stimuli. Ear Hearing 1992;13:158–64. Kraus N, Micco A, Koch D, McGee T, Carrell T, Wiet R, et al. The mismatch negativity cortical evoked potential elicited by speech in cochlear-implant users. Hearing Res 1993b;65:118–24. Kreitschmann-Andermahr I, Rosburg T, Demme U, Gaser E, Nowak H, Sauer H. Effect of ketamine on the neuromagnetic mismatch field in healthy humans. Cognit Brain Res 2001;12:109–16. Kreitschmann-Andermahr I, Rosburg T, Meier T, Volz HP, Nowak H, Sauer H. Impaired sensory processing in male patients with schizophrenia: a magnetoencephalographic study of auditory mismatch detection. Schizophr Res 1999;35:121–9. Kremlácˇek J, Hosák L, Kuba M, Libiger J, Cˇizˇek J. Visual information processing in recently abstaining methamphetamine-dependent individuals: evoked potentials study. Doc Ophthalmol 2008;117:245–55. Kropotov JD, Alho K, Näätänen R, Ponomarev VA, Kropotova OV, Anichkov AD, et al. Human auditory-cortex mechanisms of preattentive sound discrimination. Neurosci Lett 2000;280:87–90. Kuhl P. Early language acquisition: cracking the speech code. Nature Rev 2004;5:831–43. Kuhl P, Coffey-Corina S, Padden D, Dawson G. Links between social and linguistic processing of speech in preschool children with autism: behavioral and electrophysiological measures. Dev Sci 2005;8:F1–F12. Kuhl PK, Williams KA, Lacerda F, Stevens KN, Lindblom B. Linguistic experience alters phonetic perception in infants by 6 months of age. Science 1991;225:606–8. Kujala A, Huotilainen M, Hotakainen M, Lennes M, Parkkonen L, Fellman V, et al. Speech-sound discrimination in neonates as measured with MEG. NeuroReport 2004;15:2089–92. Kujala A, Huotilainen M, Uther M, Shtyrov Y, Monto S, Ilmoniemi RJ, et al. Plastic cortical changes induced by learning to communicate with non-speech sounds. NeuroReport 2003;14:1683–7. Kujala T. The role of early discrimination deficits in language disorders. J Psychophysiol 2007;21:239–50. Kujala T, Brattico E. Detrimental noise effects on brain’s speech functions. Biol Psychol 2009;81:135–43. Kujala T, Näätänen R. The mismatch negativity in evaluating central auditory dysfunctions in dyslexia. Neurosci Biobehav Rev 2001;25:535–43. Kujala T, Näätänen R. The adaptive brain: a neurophysiological perspective. Progr Neurobiol 2010;91:55–67. Kujala T, Aho E, Lepistö T, Jansson-Verkasalo E, Nieminen-von Wendt T, von Wendt L, et al. Atypical pattern of discriminating sound features in adults with Asperger syndrome as reflected by the mismatch negativity. Biol Psychol 2007;75:109–14. Kujala T, Alho K, Huotilainen M, Ilmoniemi RJ, Lehtokoski A, Leinonen A, et al. Electrophysiological evidence for cross-modal plasticity in humans with earlyand late-onset blindness. Psychophysiology 1997;34:213–6. Kujala T, Alho K, Kekoni J, Hämäläinen H, Reinikainen K, Salonen O, et al. Auditory and somatosensory event-related brain potentials in early blind humans. Exp Brain Res 1995a;104:519–26. Kujala T, Alho K, Näätänen R. Cross-modal reorganization of human cortical functions. Trends Neurosci 2000b;3:115–20. Kujala T, Belitz S, Tervaniemi M, Näätänen R. Auditory sensory memory disorder in dyslexic adults as indexed by the mismatch negativity. Eur J Neurosci 2003;17:1323–7. Kujala T, Huotilainen M, Sinkkonen J, Ahonen AI, Alho K, Hämäläinen MS, et al. Visual cortex activation in blind humans during sound discrimination. Neurosci Lett 1995b;183:143–6. Kujala T, Karma K, Ceponiene R, Belitz S, Turkkila P, Tervaniemi M, et al. Plastic neural changes and reading improvement caused by audio-visual training in reading-impaired children. P Natl Acad Sci USA 2001;98:10509–14. Kujala T, Lepistö T, Nieminen-von Wendt T, Näätänen P, Näätänen R. Neurophysiologial evidence for cortical discrimination impairment of prosody in Asperger syndrome. Neurosci Lett 2005a;383:260–5. Kujala T, Lovio R, Lepistö T, Laasonen M, Näätänen R. Evaluation of multi-attribute auditory discrimination in dyslexia with the mismatch negativity. Clin Neurophysiol 2006;117:885–93.

451

Kujala T, Myllyviita K, Tervaniemi M, Alho K, Kallio J, Näätänen R. Basic auditory dysfunction in dyslexia as demonstrated by brain-activity measurements. Psychophysiol Special Rep 2000a;37:262–6. Kujala T, Palva JM, Salonen O, Alku P, Huotilainen M, Järvinen A, et al. The role of blind humans’ visual cortex in auditory processing. Neurosci Lett 2005b;379:127–31. Kujala T, Shtyrov Y, Winkler I, Saher M, Tervaniemi M, Sallinen M, et al. Detrimental effects of long-term noise exposure on the central auditory processing. Psychophysiology 2004;41:875–81. Kujala T, Alho K, Paavilainen P, Summala H, Näätänen R. Neural plasticity in processing of sound location by the early blind: an event-related potential study. Electroen Clin Neuro 1992;84:469–72. Kujala T, Kuuluvainen S, Saalasti S, Jansson-Verkasalo E, von Wendt L, Lepistö T. Speech-feature discrimination in children with Asperger syndrome as determined with the multi-feature mismatch negativity paradigm. Clin Neurophysol 2010;121:1410–9. Kurtzberg D, Vaughan Jr HG, Kreuzer JA, Fliegler KZ. Developmental studies and clinical application of mismatch negativity: problems and prospects. Ear Hearing 1995;16:105–17. Kushnerenko E, Ceponiene R, Balan P, Fellman V, Näätänen R. Maturation of the auditory change detection response in infants: a longitudinal ERP study. NeuroReport 2002;13:1843–8. Kushnerenko E, Winkler I, Horváth J, Näätänen R, Pavlov I, Fellman V, et al. Processing acoustic change and novelty in newborn infants. Eur J Neurosci 2007;26:265–74. Kwon M, Huotilainen M, Shestakova A, Kujala T, Näätänen R, Hämäläinen H. No effects of mobile phone use on cortical auditory change-detection in children: an ERP study. Bioelectromagnetics 2010;31:191–9. Kwon M, Kujala T, Huotilainen M, Shestakova A, Näätänen R, Hämäläinen H. Preattentive auditory information processing under exposure to the 902 MHz GSM mobile phone electromagnetic field: a mismatch negativity (MMN) study. Bioelectromagnetics 2009;30:241–8. Lachmann T, Berti S, Kujala T, Schröger E. Diagnostic subgroups of developmental dyslexia have different deficits in neural processing of tones and phonemes. Int J Psychophysiol 2005;56:105–20. Lähteenmäki P. Effects of childhood cancer on patients and their families – physical and physiological aspects. Annales Universitatis Turkuensis, Ser D Tom 338, Medica-Odontologia; 1999. Lalo E, Vercueil L, Bougerol T, Jouk P-S, Debû B. Late event-related potentials and movement complexity in young adults with Down syndrome. Neurophysiol Clin 2005;35:81–91. Lang H, Eerola O, Korpilahti P, Holopainen IE, Salo SK, Aaltonen O. Practical issues in the clinical application of mismatch negativity. Ear Hearing 1995;16:118–30. Lang HA, Nyrke T, Ek M, Aaltonen O, Raimo I, Näätänen R. Pitch discrimination performance and auditory event-related potentials. In. Brunia CHM, Gaillard AWK, Kok A, Mulder G, Verbaten MN. (Eds.), Psychophysiological brain research, vol. 1. Tilburg, The Netherlands: Tilburg University Press; 1990. p. 294–8. Laureys S, Perrin F, Schnakers C, Boly M, Majerus S. Residual cognitive function in comatose, vegetative and minimally conscious states. Curr Opin Neurol 2005;18:726–33. Lavoie S, Murray MM, Deppen P, Knyazeva MG, Berk M, Boulat O, et al. Glutathione precursor, N-acetyl-cysteine, improves mismatch negativity in schizophrenia patients. Neuropsychopharmacol 2007;33:2187–99. Leipälä JA, Partanen E, Kushnerenko E, Huotilainen M, Fellman V. Perinatal cerebral insults alter auditory event-related potentials. Early Hum Dev 2011;87:89–95. Leitman DI, Sehatpour P, Higgins BA, Foxe JJ, Silipo G, Javitt DC. Sensory deficits and distributed hierarchical dysfunction in schizophrenia. Am J Psychiat 2010;167:818–27. Lepistö T, Kajander M, Vanhala R, Alku P, Huotilainen M, Näätänen R. The perception of invariant speech features in children with autism. Biol Psychol 2008;77:25–31. Lepistö T, Kujala T, Vanhala R, Alku P, Huotilainen M, Näätänen R. The discrimination of and orienting to speech and non-speech sounds in children with autism. Brain Res 2005;1066:147–57. Lepistö T, Nieminen-von Wendt T, von Wendt L, Näätänen R, Kujala T. Auditory cortical change detection in adults with Asperger syndrome. Neurosci Lett 2007;414:136–40. Lepistö T, Silokallio S, Nieminen-von Wendt P, Alku T, Näätänen R, Kujala T. Auditory perception and attention as reflected by the brain event-related potentials in children with Asperger syndrome. Clin Neurophysiol 2006;117:2161–71. Lepistö T, Soininen M, Ceponiene R, Almqvist F, Näätänen R, Aronen E. Auditory event-related potential indices of increased distractibility in children with major depression. Clin Neurophysiol 2004;115:620–7. Leppänen PHT, Guttorm TK, Pihko E, Takkinen S, Eklund KE, Lyytinen H, et al. Maturational effects on newborn ERPs measured in the mismatch negativity paradigm. Exp Neurol 2004;190:S91–S101. Leppänen PHT, Lyytinen H. Auditory event-related potentials in the study of developmental language related disorders. Audiol Neuro-Otol 1997;2:308–40. Leppänen PHT, Eklund KM, Lyytinen H. Event-related brain potentials to change in rapidly presented acoustic stimuli in newborns. Dev Neuropsychol 1997;13:175–204. Leppänen PHT, Pihko E, Eklund KM, Lyytinen H. Cortical responses of infants with or without a genetic risk for dyslexia: II. Group effects. NeuroReport 1999;10:969–9673.

452


Leppänen PHT, Richardson U, Pihko E, Eklund KM, Guttorm TK, Aro M, et al. Brain responses to changes in speech sound durations differ between infants with and without familial risk for dyslexia. Dev Neuropsychol 2002;22:407–22. Leppänen PHT, Hämäläinen JA, Salminen HK, Eklund KM, Guttorm TK, Lohvansuu K, et al. Newborn brain event-related potentials revealing atypical processing of sound frequency and the subsequent association with later literacy skills in children with familial dyslexia. Cortex 2010;46:1362–76. Lessard N, Pare M, Lepore F, Lassonde M. Early-blind human subjects localize sound sources better than sighted subjects. Nature 1998;395:278–80. Leung S, Croft RJ, Baldeweg T, Nathan PJ. Acute dopamine D1 and D2 receptor stimulation does not modulate mismatch negativity (MMN) in healthy human subjects. Psychopharmacology 2007;194:443–51. Leung S, Croft RJ, O’Neill BV, Nathan PJ. Acute high-dose glycine attenuates mismatch negativity (MMN) in healthy human controls. Psychopharmacology 2008;196:451–60. Levänen S, Ahonen A, Hari R, McEvoy L, Sams M. Deviant auditory stimuli activate human left and right auditory cortex differently. Cerebr Cortex 1996;6:288–96. Levänen S, Hari R, McEvoy L, Sams M. Responses of the human auditory cortex to changes in one versus two stimulus features. Exp Brain Res 1993;97:177–83. Liasis A, Towell A, Alho K, Boyd S. Intracranial identification of an electric frontalcortex response to auditory stimulus change: a case study. Cognitive Brain Res 2001;11:227–33. Liasis A, Towell A, Boyd S. Intracranial auditory detection and discrimination potentials as substrates of echoic memory in children. Cognit Brain Res 1999;7:503–6. Liasis A, Towell A, Boyd S. Intracranial evidence for differential encoding of frequency and duration discrimination responses. Ear Hear 2000;21:252–6. Liasis A, Bamiou DE, Boyd S, Towell A. Evidence for a neurophysiologic auditory deficit in children with benign epilepsy with centro-temporal spikes. J Neural Trans 2006;113:939–49. Light GA, Braff DL. Mismatch negativity deficits are associated with poor functioning in schizophrenia patients. Arch Gen Psychiat 2005a;62:127–36. Light GA, Braff DL. Stability of mismatch negativity deficits and their relationship to functional impairment in chronic schizophrenia. Am J Psychiat 2005b;162:1741–3. Light GA, Swerdlow NR, Braff DL. Preattentive sensory processing as indexed by the MMN and P3a brain responses is associated with cognitive and psychosocial functioning in healthy adults. J Cognit Neurosci 2007;19:1624–32. Lin Y-Y, Hsiao F-J, Shih YH, Yiu C-H, Yen D-J, Kwan S-Y, et al. Plastic phase-locking and magnetic mismatch response to auditory deviants in temporal lobe epilepsy. Cereb Cortex 2007;17:2516–25. Lipton SA, Rosenberg PA. Excitatory amino acids as a final common pathway for neurologic disorders. New Engl J Med 1994;330:613–22. Liu T, Shi J, Zhang Q, Zhao D, Yang J. Neural mechanism of auditory sensory processing in children with high intelligence. NeuroReport 2007;18:1571–5. Lonka E, Lehtokoski A, Kujala T, Johansson R, Rimmanen S, Alho K, et al. The mismatch negativity (MMN) brain response as an index of speech perception recovery in cochlear-implant recipients. Audiol Neuro-otol 2004;9:160–2. Lorenzo-Lopez L, Amenedo E, Pazo-Alvarez P, Cadaveira F. Pre-attentive detection of motion direction changes in normal aging. NeuroReport 2004;15:2633–6. Lovio R, Näätänen R, Kujala T. Abnormal pattern of cortical speech feature discrimination in 6-year-old children at risk for dyslexia. Brain Res 2010;1335:53–62. Lovio R, Pakarinen S, Huotilainen M, Alku P, Silvennoinen S, Näätänen R. Auditory discrimination profiles of speech sound changes in 6-year-old children as determined with the multi-feature MMN paradigm. Clin Neurophysiol 2009;120:916–21. Luauté J, Fischer C, Adelaine P, Morlet D, Tell L, Boisson D. Late auditory eventrelated potentials can be useful to predict good functional outcome after coma. Arch Physic Med Rehab 2005;86:917–23. Luck SJ, Mathalon DH, O’Donnell BF, Hämäläinen MS, Spencer KM, Javitt DC, et al. A roadmap for the development and validation of event-related potential biomarkers in schizophrenia. Biol Psychiat 2011;70:28–34. Lyytinen H, Ahonen T, Eklund K, Guttorm TK, Laakso M-L, Leinonen S, et al. Developmental pathways of children with and without familial risk for dyslexia during the first years of life. Dev Neuropsychol 2001;20:535–54. Lyytinen H, Aro M, Eklund K, Erskinel J, Guttorm T, Laakso M-L, et al. The development of children at familial risk for dyslexia: birth to early school age. Ann Dyslexia 2004;54:184–220. Lyytinen H, Erskine J, Kujala J, Ojanen E, Richardson U. In search of a science-based application: a learning tool for reading acquisition. Scand J Psychol 2009;50:668–75. Lyytinen H, Erskine J, Tolvanen A, Torppa M. Trajectories of reading development: a follow-up from birth to school age of children with and without risk for dyslexia. Merrill-Palmer Quarterly 2006;52:514–46. Maekawa T, Goto Y, Kinukawa N, Taniwaki T, Kanba S, Tobimatsu S. Functional characterization of mismatch negativity to a visual stimulus. Clin Neurophysiol 2005;116:2392–402. Maekawa T, Tobimatsu S, Inada N, Oribe N, Onitsuka T, Kanba S, et al. Top-down and bottom-up visual information processing of non-social stimuli in highfunctioning autism spectrum disorder. Res Autism Spectr Disord 2011;5:201–9. Maekawa T, Tobimatsu S, Ogata K, Onitsuka T, Kanba S. Preattentive visual change detection as reflected by the mismatch negativity (MMN) – evidence for a memory-based process. Neurosci Res 2009;65:107–12. Mager R, Falkenstein M, Störmer R, Brand S, Müller-Spahn F, Bullinger AH. Auditory distraction in young and middle-aged adults: a behavioural and event-related potential study. J Neural Trans 2005;112:1165–76.

Magno E, Yeap S, Thakore JH, Garavan H, De Sanctis P, Foxe JJ. Are auditory-evoked frequency and duration mismatch negativity deficits endophenotypic for schizophrenia? High-density electrical mapping in clinically unaffected firstdegree relatives and first-episode and chronic schizophrenia. Biol Psychiat 2008;64:385–91. Magnusson KR, Brim BL, Das SR. Selective vulnerabilities of N-methyl-D-aspartate (NMDA) receptors during brain aging. Front Aging Neurosci 2010;2:11. Mäkelä JP, Salmelin R, Hokkanen L, Launes J, Hari R. Neuromagnetic sequelae of herpes simplex encephalitis. Electroen Clin Neuro 1998a;106:251–8. Mäkelä JP, Salmelin R, Kotila M, Salonen O, Laaksonen R, Hokkanen L, et al. Modification of neuromagnetic cortical signals by thalamic infarctions. Electroen Clin Neuro 1998b;106:433–43. Mäntysalo S, Salmi T. Effect of noise on the mismatch negativity of the event-related potential of the human brain. In: Bond NW, Siddle DAT. (Eds.) Psychobiology: issues and applications. North-Holland: Elsevier Science Publishers B.V.; 1989. p. 277–88. March L, Cienfuegos A, Goldbloom L, Ritter W, Cowan N, Javitt DC, et al. Normal time course of auditory recognition in schizophrenia, despite impaired precision of the auditory sensory (‘‘echoic’’) memory code. J Abnorm Psychol 1999;108:69–75. Marco-Pallares J, Grau C, Gual A, Escera C, Grau C. Mismatch negativity impairment associated with alcohol consumption in chronic alcoholics: a scalp current density study. Int J Psychophysiol 2007;1:51–7. Marco-Pallares J, Grau C, Ruffini G. Combined ICA-LORETA analysis of mismatch negativity. NeuroImage 2005;25:471–7. Marler JA, Chamolin CA, Gillam RB. Auditory memory for backward masking signals in children with language impairment. Psychophysiology 2002;39:767–80. Martin LF, Davalos DB, Kisley MA. Nicotine enhances automatic temporal processing as measured by the mismatch negativity waveform. Nicotine Tobacco Res 2009;11:698–706. Martynova O, Kirjavainen J, Cheour M. Mismatch negativity and late discriminative negativity in sleeping human newborns. Neurosci Lett 2003;340:75–8. Massaro DW. A comparison of forward versus backward recognition masking. J Exp Psychol 1973;100:434–6. Massaro DW. Backward recognition masking. J Acoust Soc Am 1975;58:1059–65. Matsubayashi J, Kawakubo Y, Suga M, Takei Y, Kumano S, Fukuda M, et al. The influence of gender and personality traits on individual difference in auditory mismatch: a magnetoencephalographic (MMNm) study. Brain Res 2008;1236:159–65. Matthews N, Todd J, Budd TW, Cooper G, Michie PT. Auditory lateralization in schizophrenia – mismatch negativity and behavioral evidence of a selective impairment in encoding interaural time cues. Clin Neurophysiol 2007;118:833–44. Maurer U, Bucher K, Brem S, Brandeis D. Altered responses to tone and phoneme mismatch in kindergartners at familial dyslexia risk. NeuroReport 2003;14:2245–50. Maurer U, Bucher K, Brem S, Benz R, Kranz F, Schulz E, et al. Neurophysiology in preschool improves behavioral prediction of reading ability throughout primary school. Biol Psychiat 2009;66:341–8. McGeer EG, McGeer PL. Neuroinflammation in Alzheimer’s disease and mild cognitive impairment: a field in its infancy. J Alzheimer’s Disease 2010;19:355–61. Mengler ED, Hogben JH, Michie PT, Bishop DVM. Poor frequency discrimination is related to oral language disorder in children: a psychoacoustic study. Dyslexia 2005;11:155–73. Menning H, Renz A, Seifert J, Maercker A. Reduced mismatch negativity in posttraumatic stress disorder: a compensatory mechanism for chronic hyperarousal? Int J Psychophysiol 2008;68:27–34. Menning H, Roberts LE, Pantev C, et al. Plastic changes in the auditory cortex induced by intensive frequency discrimination training. NeuroReport 2000;11:817–22. Mento G, Suppiej A, Altoè G, Bisiacchi PS. Functional hemispheric asymmetries in humans: electrophysiological evidence from preterm infants. Eur J Neurosci 2010;31:565–74. Mervaala E, Alhainen K, Helkala EL, Partanen J, Jousmäki V, Väyrynen M, et al. Electrophysiological and neuropsychological effects of a central alpha2antagonist atipamezole in healthy volunteers. Behav Brain Res 1993;55:85–91. Metz-Lutz M-N, Philippini M. Neuropsychological findings in rolandic epilepsy and Landau–Kleffner syndrome. Epilepsia 2006;47:S71–5. Michie PT. What has MMN revealed about the auditory system in schizophrenia? International J Psychophysiol 2001;42:177–94. Michie PT, Budd TW, Todd J, Rock D, Wichmann H, Box J, et al. Duration and frequency mismatch negativity in schizophrenia. Clin Neurophysiol 2000;111:1054–65. Michie PT, Innes-Brown H, Todd J, Jablensky AV. Duration mismatch negativity in biological relatives of patients with schizophrenia spectrum disorders. Biol Psychiat 2002;52:749–58. Mikkola K, Kushnerenko E, Partanen E, Serenius-Sirve S, Leipälä J, Huotilainen M, et al. Auditory event-related potentials and cognitive function of preterm children at five years of age. Clin Neurophysiol 2007;118:1494–502. Mikkola K, Wetzel N, Leipälä J, Serenius-Sirve S, Schröger E, Huotilainen M, et al. Behavioral and evoked potential measures of distraction in 5-year-old children born preterm. Int J Psychophysiol 2010;77:8–12. Minami Y, Kirino E. Schizophrenic patients are impaired in memory reinstatement underlying mismatch negativity system. Clin Neurophysiol 2005;116:120–8.

R. Näätänen et al. / Clinical Neurophysiology 123 (2012) 424–458 Missioner P, Ragot R, Derouesné C, Guez D, Renault B. Automatic attentional shifts induced by a noradrenergic drug in Alzheimer’s disease: evidence from evoked potentials. Int J Psychophysiol 1999;33:243–51. Miyajima M, Ohta K, Hara K, Iino H, Maehara T, Hara M, et al. Abnormal mismatch negativity for pure-tone sounds in temporal lobe epilepsy. Epilepsy Res 2011;94:149–57. Moberget T, Karns CM, Deouell LY, Lindgren M, Knight RT, Ivry RB. Detecting violations of sensory expectations following cerebellar degeneration: a mismatch negativity study. Neuropsychologia 2008;46:2569–79. Molholm S, Gomes H, Lobosco J, Deacon D, Ritter W. Feature versus gestalt representation of stimuli in the mismatch negativity system of 7- to 9-year-old children. Psychophysiology 2004;41:385–93. Molholm S, Martinez A, Ritter W, Javitt DC, Foxe JJ. The neural circuitry of preattentive auditory change-detection: an fMRI study of pitch and duration mismatch negativity generators. Cerebr Cortex 2005;15:545–51. Moreau P, Jolicoeur P, Peretz I. Automatic brain responses to pitch changes in congenital amusia. Ann NY Acad Sci 2009;1169:191–4. Morgan III CA, Grillon C. Abnormal mismatch negativity in women with sexual assault-related posttraumatic stress disorder. Biol Psychiat 1999;45:827–32. Morlet D, Bouchet P, Fischer C. Mismatch negativity and N100 monitoring: potential clinical value and methodological advances. Audiol Neuro-Otol 2000;5:198–206. Murakami T, Nakagome K, Kamio S, Kasai K, Iwanami A, Hiramatsu K-I, et al. The effects of benzodiazepines on event-related potential indices of automatic and controlled processing in schizophrenia. A preliminary report. Prog NeuroPsychoph 2002;26:651–61. Müller BW, Jüptner M, Jentzen W, Müller SP. Cortical activation to auditory mismatch elicited by frequency deviant and complex novel sounds: a PET study. NeuroImage 2002;17:231–9. Näätänen R. The role of attention in auditory information processing as revealed by event-related potentials and other brain measures of cognitive function. Behav Brain Sci 1990;13:201–88. Näätänen R. Attention and brain function. Hillsdale, NJ: Lawrence Erlbaum; 1992. Näätänen R. The perception of speech sounds by the human brain as reflected by the mismatch negativity (MMN) and its magnetic equivalent MMNm. Psychophysiology (Presidential Address, 1999) 2001;38:1–21. Näätänen R. Somatosensory mismatch negativity: a new clinical tool for developmental neurological research? Dev Med Child Neurol 2009;51:930–1. Näätänen R, Gaillard AWK. The orienting reflex and the N2 deflection of the eventrelated potential (ERP). In: Gaillard AWK, Ritter W. (Eds.), Tutorials in event related potential research: endogenous components. North Holland: Amsterdam; 1983. p. 119–41. Näätänen R, Kähkönen S. Central auditory dysfunction in schizophrenia as revealed by the mismatch negativity (MMN) and its magnetic equivalent MMNm – a review. Int J Neuropsychopharmacol 2009;12:125–35. Näätänen R, Kreegipuu K. The mismatch negativity (MMN) as an index of different forms of memory in audition. In: Bäckman L, Nyberg L, editors. Memory, aging, and brain. a festschrift in hounour of Lars-Göarn Nilsson. Psychology Press; 2011. p. 287–99. Näätänen R, Kujala T. The mismatch negativity and its magnetic equivalent: an index of language impairment or more general cognitive decline in autism? Biol Psychiat 2011;70:212–3. Näätänen R, Michie PT. Early selective attention effects on the evoked potential. A critical review and reinterpretation. Biol Psychol 1979;8:81–136. Näätänen R, Summala H. Road-user behavior and traffic accidents. North-Holland, New York: Amsterdam and American Elsevier; 1976. 270 p. Näätänen R, Winkler I. The concept of auditory stimulus representation in cognitive neuroscience. Psychol Bull 1999;6:826–59. Näätänen R, Gaillard AWK, Mäntysalo S. Early selective-attention effect on evoked potential reinterpreted. Acta Psychol 1978;42:313–29. Näätänen R, Kujala T, Kreegipuu K, Carlson S, Escera C, Baldeweg T, et al. The mismatch negativity: an index of cognitive decline in neuropsychiatric and neurological diseases and in aging. Brain 2011. doi:10.1093/brain/awr064. Näätänen R, Kujala T, Winkler I. Auditory processing that leads to conscious perception: a unique window to central auditory processing opened by the mismatch negativity and related responses. Psychophysiology 2011b;48:4–22. Näätänen R, Lehtokoski A, Lennes M, Cheour M, Huotilainen M, Iivonen A, et al. Language-specific phoneme representations revealed by electric and magnetic brain responses. Nature 1997;385:432–4. Näätänen R, Tervaniemi M, Sussman E, Paavilainen P, Winkler I. Primitive intelligence in the auditory cortex. Trends Neurosci 2001;24:283–8. Näätänen R, Paavilainen P, Rinne T, Alho K. The mismatch negativity (MMN) in basic research of central auditory processing: a review. Clin Neurophysiol 2007;118:2544–90. Näätänen R, Schröger E, Alho K. Electrophysiology of Attention. In Wixted J. (Ed.), Stevens’ handbook of experimental psychology, 3rd ed. John Wiley & Sons, Inc.; 2002. p. 601–53. Näätänen R, Schröger E, Karakas S, Tervaniemi M, Paavilainen P. Development of a memory trace for a complex sound in the human brain. NeuroReport 1993;4:503–6. Näätänen R, Pakarinen S, Rinne T, Takegata R. The mismatch negativity (MMN) – towards the optimal paradigm. Clin Neurophysiol 2004;115:140–4. Näätänen R, Simpson M, Loveless NE. Stimulus deviance and evoked potentials. Biol Psychol 1982;14:53–98. Naccache L, Puybasset L, Gaillard R, Serve E, Willer J. Auditory mismatch negativity is a good predictor of awakening in comatose patients: a fast and reliable procedure. Clin Neurophysiol 2005;116:988–9.

453

Nager W, Münte TF, Bohrer I, Lenarz T, Dengler R, Möbes J, et al. Automatic and attentive processing of sounds in cochlear implant patients – electrophysiological evidence. Restor Neurol Neurosci 2007;25:391–6. Nakagawa K, Shoji H, Katada A, Ozaki H. How regularities in stimulus series and in ISI affect on MMN in persons with intellectual disabilities. Int Congr Ser 2002;1232:363–6. Nakagome K, Ichikawa I, Kanno O, Akaho R, Suzuki M, Takazawa S, et al. Overnight effects of triazolam on cognitive function: an event-related potentials study. Neuropsychobiology 1998;38:232–40. Nashida T, Yabe H, Sato T, Sutoh T, Shinosaki N, Kaneko S. Automatic auditory processing in sleep. Sleep 2000;23:1–8. Naumann A, Bierbrauer J, Przuntek H, Daum I. Attentive and preattentive processing in narcolepsy as revealed by event-related potentials (ERPs). NeuroReport 2001;12:2807–11. Neumann N, Kotchoubey B. Assessment of cognitive functions in severely paralysed and severely brain-damaged patients: neuropsychological and electrophysiological methods. Brain Res Protoc 2004;14:25–36. Newcomer JW, Farber NB, Jevtovic-Todorovic V, Selke G, Melson AK, Hersey T, et al. Ketamine-induced NMDA-receptor hypofunction as a model of memory impairment and psychosis. Neuropsychopharmacol 1998;20:106–18. Nittono H, Momose D, Hori T. The vanishing point of the mismatch negativity at sleep onset. Clin Neurophysiol 2001;112:732–9. Niznikiewicz MA, Spencer KM, Dickey C, Volgmaier M, Seidman LJ, Shenton ME, et al. Abnormal pitch mismatch negativity in individuals with schizotypal personality disorder. Schizophr Res 2009;110:188–93. Nordby H, Brønnick KS, Hugdahl K. Processing of deviant visual events reflected by event-related brain potentials. In: Ogura C, Koga Y, Shimokochi M. Recent advances in event-related brain potential research. Amsterdam: Elsevier; 1996. p. 99–104. Novitski N, Huotilainen M, Tervaniemi M, Näätänen R, Fellman V. Neonatal frequency discrimination in 250–4000 Hz frequency range: electrophysiological evidence. Clin Neurophysiol 2007;118:417–9. Oades RD, Dittman-Balcar A, Schepker R, Eggers C, Zerbin D. Auditory event-related potentials (ERPs) and mismatch negativity (MMN) in healthy children and those with attention-deficit or Tourette/tic symptoms. Biol Psychol 1996;43:163–85. Oades RD, Zerbin DA, Dittmann-Balcar A, Eggers C. Auditory event-related potential (ERP) and difference-wave topography in schizophrenic patients with/without active hallucinations and delusions: a comparison with young obsessivecompulsive disorder (OCD) and healthy subjects. Int J Psychophysiol 1996;22:185–214. Oades RD, Wild-Wall N, Juran SA, Sachsse J, Oknina LB, Röpcke B. Auditory change detection in schizophrenia: sources of activity, related neuropsychological function and symptoms in patients with a first episode in adolescence, and patients 14 years after an adolescent illness-onset. BMC Psychiatry 2006;6:7. Oates PA, Kurtzberg D, Stapells DR. Effects of sensorineural hearing loss on cortical event-related potential and behavioural measures of speech-sound processing. Ear Hearing 2002;23:399–415. Ogura C, Nageishi Y, Fukao K, Shimoji Y, Hirano K, Hokama H, et al. Deviate N200 component of event-related potentials in Shuchaku–Seikaku, a premorbid personality of depression. Jpn J Psychiat Neurol 1991;45:641–51. Ogura C, Nageishi Y, Omura F, Fukao K, Ohta H, Kishimoto A, et al. N200 component of event-related potentials in depression. Biol Psychiat 1993;33:720–6. Oknina LB, Wild-Wall N, Oades RD, Juran SA, Röpcke B, Pfueller U, et al. Frontal and temporal sources of mismatch negativity in healthy controls, patients at onset of schizophrenia in adolescence and others at 15 years after onset. Scizophr Res 2005;76:25–41. Olney JW, Farber NB. Glutamate receptor dysfunction and schizophrenia. Arch Gen Psychiat 1995;52:998–1007. Opitz B, Rinne T, Mecklinger A, von Cramon DY, Schröger E. Differential contribution of frontal and temporal cortices to auditory change detection: fMRI and ERP results. NeuroImage 2002;15:165–74. Oram Cardy JE, Flagg EJ, Roberts W, Brian J, Roberts TPL. Magnetoencephalography identifies rapid temporal processing deficit in autism and language impairment. NeuroReport 2005a;16:329–32. Oram Cardy JE, Flagg EJ, Roberts W, Roberts TPL. Delayed mismatch field for speech and non-speech sounds in children with autism. NeuroReport 2005b;16:521–5. Oranje B, Jensen K, Wienberg M, Glenthøj BY. Divergent effects of increased serotonergic activity on psychophysiological parameters of human attention. Int J Neuropsychopharmacol 2008;11:453–63. Osawa M, Iijima M, Nageishi Y, Ushijima R, Iwata M. Automatic and controlled processing in normal aging and dementia. In: Ogura C, Koga Y, Shimokochi M, editors. Recent advances in event-related brain potential research 1996;Vol. 1099. p. 743–50. Paavilainen P, Alho K, Reinikainen K, Sams M, Näätänen R. Right-hemisphere dominance of different mismatch negativities. Electroencephalogr Clin Neurophysio 1991;78:466–79. Pakarinen S, Huotilainen M, Näätänen R. The mismatch negativity (MMN) with no standard stimulus. Clin Neurophysiol 2010;121:1043–50. Pakarinen S, Lovio R, Huotilainen M, Alku P, Näätänen R, Kujala T. Fast multi-feature paradigm for recording several mismatch negativities (MMNs) to phonetic and acoustic changes in speech sounds. Biol Psychol 2009;82:219–26. Pakarinen S, Takegata R, Rinne T, Huotilainen M, Näätänen R. Measurement of existensive auditory discrimination profiles using the mismatch negativity (MMN) of the auditory event-related potential (ERP). Clin Neurophysiol 2007;118:177–85.

454


Pang EW, Fowler B. Dissociation of the mismatch negativity and processing negativity attentional waveforms with nitrous oxide. Psychophysiology 1999;36:552–8. Pang EW, Edmonds GE, Desjardins R, Khan SC, Trainor LJ, Taylor MJ. Mismatch negativity to speech stimuli in 8-month-old infants and adults. Int J Psychophysiol 1998;29:227–36. Park H-J, Kwon JS, Youn T, Pae JS, Kim J-J, Kim M-S, et al. Statistical parametric mapping of LORETA using high density EEG and individual MRI: application to mismatch negativities in schizophrenia. Hum Brain Mapp 2002;17:168–78. Paul I, Bott C, Heim S, Eulitz C, Elbert T. Reduced hemispheric asymmetry of the auditory N260m in dyslexia. Neuropsychologia 2006a;44:785–94. Paul I, Bott C, Heim S, Wienbruch C, Elbert T. Phonological but not auditory discrimination is impaired in dyslexia. Eur J Neurosci 2006b;24:2945–53. Pause BM, Krauel K. Chemosensory event-related potentials (CSERP) as a key to the psychology of odors. Int J Psychophysiol 2000;36:105–22. Pazo-Alvarez P, Amenedo E, Cadaveira F. Automatic detection of motion direction changes in the human brain. Eur J Neurosci 2004;19:1978–86. Pazo-Alvarez P, Cadaveira F, Amenedo E. MMN in the visual modality: a review. Biol Psychol 2003;63:199–236. Peach RK, Newhoff M, Rubin SS. Attention in aphasia as revealed by event-related potentials: a preliminary investigation. In: Lemmer ML. (Ed.) Clinical aphasiology, vol. 21. Austin, TX: Pro-Ed; 1992. p. 323–33. Peach RK, Newhoff M, Rubin SS. Attention in aphasia as revealed by event-related potentials: a preliminary investigation. Clin Aphasiol 1993;21:323–33. Peach RK, Rubin SS, Newhoff M. A topographic event-related potential analysis of the attention deficit for auditory processing in Aphasia. Clin Aphasiol 1994;22:81–96. Pekkonen E. Mismatch negativity in aging and in Alzheimer’s and Parkinson’s diseases. Audiol Neuro-Otol 2000;5:216–24. Pekkonen E, Ahveninen J, Jääskeläinen IP, Seppä K, Näätänen R, Sillanaukee P. Selective acceleration of auditory processing in chronic alcoholics. Alcohol Clin Exp Res 1998;22:605–9. Pekkonen E, Hirvonen J, Ahveninen J, Kähkönen S, Kaakkola S, Huttunen J, et al. Memory-based comparison process not attenuated by haloperiodol: a combined MEG and EEG study. NeuroReport 2002;13:177–81. Pekkonen E, Hirvonen J, Jääskeläinen IP, Kaakkola S, Huttunen J. Auditory sensory memory and the cholinergic system: implication for Alzheimer’s disease. NeuroImage 2001a;14:376–82. Pekkonen E, Huotilainen M, Virtanen J, Näätänen R, Ilmoniemi RJ, Erkinjuntti T. Alzheimer’s disease affects parallel processing between the auditory cortices. NeuroReport 1996b;7:1363–8. Pekkonen E, Huotilainen M, Virtanen J, Sinkkonen J, Rinne T, Ilmoniemi R, et al. Agerelated functional differences between auditory cortices: a whole-head MEGstudy. NeuroReport 1995a;6:1803–6. Pekkonen E, Jääskeläinen IP, Erkinjuntti T, Hietanen M, Huotilainen M, Ilmoniemi RJ, et al. Preserved stimulus deviance detection in Alzheimer’s disease. NeuroReport 2001b;12:1649–52. Pekkonen E, Jääskeläinen IP, Hietanen M, Huotilainen M, Näätänen R, Ilmoniemi RJ, et al. Impaired preconscious auditory processing and cognitive function in Alzheimer’s disease. Clin Neurophysiol 1999;110:1942–7. Pekkonen E, Jääskeläinen IP, Kaakkola S, Ahveninen J. Cholinergic modulation of preattentive auditory processing in aging. NeuroImage 2005;27:387–92. Pekkonen E, Jousmäki V, Könönen M, Reinikainen K, Partanen J. Auditory sensory memory impairment in Alzheimer’s disease: an event-related potential study. NeuroReport 1994;5:2537–40. Pekkonen E, Jousmäki V, Reinikainen K, Partanen J. Automatic auditory discrimination is impaired in Parkinson’s disease. Electroen Clin Neuro 1995c;95:47–52. Pekkonen E, Osipova D, Laaksovirta H. Magnetoencephalographic evidence of abnormal auditory processing in amyotrophic lateral sclerosis with bulbar signs. Clin Neurophysiol 2004;115:309–15. Pekkonen E, Rinne T, Näätänen R. Variability and replicability of the mismatch negativity. Electroenceph Clin Neurophysiol 1995b;96:546–54. Pekkonen E, Rinne T, Reinikainen K, Kujala T, Alho K, Näätänen R. Aging effects on auditory processing: an event-related potential study. Exp Aging Res 1996a;22:171–84. Peretz I, Brattico E, Järvenpää M, Tervaniemi M. The amusic brain: in tune, out of key, and unaware. Brain 2009;132:1277–86. Pettigrew CM, Murdoch BE, Chenery HJ, Kei J. The relationship between the mismatch negativity (MMN) and psycholinguistic models of spoken word processing. Aphasiology 2004a;18:3–28. Pettigrew CM, Murdoch BE, Ponton CW, Finnigan S, Alku P, Sockalingam R, et al. Automatic auditory processing of English words as indexed by the mismatch negativity, using a multiple deviant paradigm. Ear Hearing 2004b;25:284–301. Pettigrew CM, Murdoch BE, Kei J, Ponton CW, Alku P, Chenery HJ. The mismatch negativity (MMN) response to complex tones and spoken words in individuals with aphasia. Aphasiology 2005;19:131–63. Pietrowsky R, Fehm HL, Born J. An analysis of the effects of corticotropin-releasing hormone (h-CRH), adenocorticotropin (ACTH) and b-endorphin on ERPs in humans. In: Brunia CHM, Gaillard AWK, Kok A. (Eds.), Psychol Brain Res 1990;2:106–10 [Tilbury University Press]. Pihko E, Kujala T, Mickos A, Antell H, Alku P, Byring R, et al. Magnetic fields evoked by speech sounds in pre-school children. Clin Neurophysiol 2005;116:112–9. Pihko E, Leppänen PHT, Eklund KM, Cheour M, Guttorm TK, Lyytinen H. Cortical responses of infants with and without a genetic risk for dyslexia: I. Age effects. NeuroReport 1999;10:901–5.

Pihko E, Kujala T, Mickos A, Alku P, Byring R, Korkman M. Language impairment is reflected in auditory evoked fields. Int J Psychophysiol 2008;68:161–9. Pihko E, Mickos A, Kujala T, Pihlgren A, Westman M, Alku P, et al. Group intervention changes brain activity in bilingual language-impaired children. Cereb Cortex 2007;17:849–58. Pincze Z, Lakatos P, Rajkai C, Ulbert I, Karmos G. Separation of mismatch negativity and the N1 wave in the auditory cortex of the cat: a topographic study. Clin Neurophysiol 2001;112:778–84. Pincze Z, Lakatos P, Rajkai C, Ulbert I, Karmos G. Effect of deviant probability and interstimulus/interdeviant interval on the auditory N1 and mismatch negativity in the cat auditory cortex. Brain Res Cognitive Brain Res 2002;13:249–53. Polo MD, Escera C, Gual A, Grau C. Mismatch negativity and auditory sensory memory in chronic alcoholics. Alcohol Clin Exp Res 1999;23:1744–50. Polo MD, Escera C, Yago E, Alho K, Gual A, Grau C. Electrophysiological evidence of abnormal activation of the cerebral network of involuntary attention in alcoholism. Clin Neurophysiol 2003;114:134–46. Polo MD, Newton P, Rogers D, Escera C, Butler S. ERPs and behavioural indices of long-term preattentive and attentive deficits after closed head injury. Neuropsychologia 2002;40:2350–9. Ponton CW, Don M. The mismatch negativity in cochlear implant users. Ear Hearing 1995;16:131–46. Ponton CW, Don M. Cortically-evoked activity recorded from cochlear implant users. Methods and Applications. In: Cullington H. (Ed.), Cochlear implants objective measures. London: Whurr Publishers Ltd; 2003. p. 187–230. Ponton CW, Eggermont JJ. Of kittens and kids: altered cortical maturation following profound deafness and cochlear implant use. Audiol Neuro-Otol 2001;6:363–3680. Ponton CW, Eggermont JJ. Electrophysiological measures of human auditory system maturation: Relationship with neuroanatomy and behavior. in: Burkhard RF, Don M, Eggermont JJ. (Eds.), Auditory evoked potentials: basic principles and clinical application. Philadelphia: Lippincott Williams & Wilkins; 2007. p. 358– 402. Ponton CW, Bernstein LE, Auer ET. Mismatch negativity with visual-only and audiovisual speech. Brain Topogr 2009;21:207–15. Ponton CW, Don M, Eggermont JJ, Kwong B. The integrated mismatch negativity (MMNi): a noise-free representation of evoked responses allowing single-point distribution-free statistical tests. Electroen Clin Neuro 1997;104:143–50. Ponton CW, Eggermont JJ, Don M, Waring MD, Kwong B, Cunningham J, et al. Maturation of the mismatch negativity: effects of profound deafness and cochlear implant use. Audiol Neuro-Otol 2000;5:167–85. Potts GF, Hirayasu Y, O’Donnell BF, Shenton ME, McCarley RW. High-density recording and topographic analysis of the auditory oddball event-related potential in patients with schizophrenia. Biol Psychiat 1998;44:982–9. Price GW, Michie PT, Johnston J, Innes-Brown H, Kent A, Clissa P, et al. A multivariate electrophysiological endophenotype, from a unitary cohort, shows greater research utility than any single feature in the Western Australian family study of schizophrenia. Biol Psychiat 2006;60:1–10. Pritchard W, Sokhadze E, Houliman M. Effects of nicotine and smoking on eventrelated potentials: a review. Nicotine Tobacco Res 2004;6:961–84. Pulvermuller F, Shtyrov Y, Kujala T, Naatanen R. Word-specific cortical activity as revealed by the mismatch negativity. Psychophysiol 2004;41:106–12. Qiu X, Yang X, Qiao Z, Wang L, Ning N, Shi J, et al. Impairment in processing visual information at the pre-attentive stage in patients with a major depressive disorder: a visual mismatch negativity study. Neurosci Lett 2011;491:53–7. Rabinowicz EF, Silipo GMA, Goldman R, Javitt DC. Auditory sensory dysfunction in schizophrenia: imprecision or distractibility. Arch Gen Psychiat 2000;57:1149–55. Ragazzoni A, Grippo A, Tozzi F, Zaccara G. Event-related potentials in patients with total locked-in state due to fulminant Guillain–Barré syndrome. Int J Psychophysiol 2000;37:99–109. Raggi A, Consonni M, Iannaccone S, Perani D, Zamboni M, Sferrazza B, et al. Auditory event-related potentials in non-demented patients with sporadic amyotrophic lateral sclerosis. Clin Neurophysiol 2008;119:342–50. Rahne T, von Specht H, Mühler R. Sorted averaging-application to auditory eventrelated responses. J Neurosci Meth 2008;172:74–8. Rasser PE, Schall U, Todd J, Michie PT, Ward PB, Johnston P, et al. Gray matter deficits, mismatch negativity, and outcomes in Schizophrenia. Schizophrenia Bull 2011;37:131–40. Raz A, Deouell LY, Bentin S. Is pre-attentive processing compromised by prolonged wakefulness? Effects of total sleep deprivation on the mismatch negativity. Psychophysiology 2001;38:787–95. Realmuto G, Begleiter H, Odencrantz J, Porjesz B. Event-related potential evidence of dysfunction in automatic processing in abstinent alcoholics. Bioll Psychiat 1993;33:594–601. Reinvang I, Nordby H, Nielsen CS. Information processing deficits in head injury assessed with ERPs reflecting early and late processing stages. Neuropsychologia 2000;38:995–1005. Reite M, Teale P, Rojas DC, Asherin R, Hernandez O. MEG auditory evoked fields suggest altered structural/functional asymmetry in primary but not secondary auditory cortex in bipolar disorder. Bipol Disord 2009;11:371–81. Renvall H, Hari R. Diminished auditory mismatch fields in dyslexic adults. Ann Neurol 2003;53:551–7. Restuccia D, Della Marca C, Valeriani M, Leggio MG, Molinari M. Cerebellar damage impairs detection of somatosensory input changes. A somatosensory mismatchnegativity study. Brain 2007;130:276–87.

R. Näätänen et al. / Clinical Neurophysiology 123 (2012) 424–458 Restuccia D, Zanini S, Cazzagon M, Del Piero I, Martucci L, Della Marca G. Somatosensory mismatch negativity in healthy children. Dev Med Child Neurol 2009;51:991–8. Richardson U, Leppänen PHT, Leiwo M, Lyytinen H. Speech perception of infants with high familial risk for dyslexia differs at the age of 6 months. Dev Neuropsychol 2003;23:387–97. Riekkinen Jr P, Pääkkönen A, Karhu J, Partanen J, Soininen H, Laakso M, et al. THA disrupts mismatch negativity in Alzheimer disease. Psychopharmacology 1997;133:203–6. Rinker T, Kohls G, Richter C, Maas V, Schulz E, Schecker M. Abnormal frequency discrimination in children with SLI as indexed by mismatch negativity (MMN). Neurosci Lett 2007;413:99–104. Rinne T, Alho K, Ilmoniemi RJ, Virtanen J, Näätänen R. Separate time behaviors of the temporal and frontal mismatch negativity sources. NeuroImage 2000;12:14–9. Rinne T, Degerman A, Alho K. Superior temporal and inferior frontal cortices are activated by infrequent sound duration decrements: an fMRI study. NeuroImage 2005;26:66–72. Rinne T, Gratton G, Fabiani M, Cowan N, Maclin E, Stinard A, et al. Scalp-recorded optical signals make sound processing in the auditory cortex visible. NeuroImage 1999;10:620–4. Rinne T, Särkkä A, Degerman A, Schröger E, Alho K. Two separate mechanisms underlie auditory change detection and involuntary control of attention. Brain Res 2006;1077:135–43. Rissling AJ, Makeig S, Braff DL, Light GA. Neurophysiologic markers of abnormal brain activity in schizophrenia. Curr Psychiat Reports 2010;12:572–8. Roberts TPL, Cannon KM, Tavabi K, Blaskey L, Khan SY, Monroe JF, et al. Auditory magnetic mismatch field latency: a biomarker for language impairment in autism. Biol Psychiat 2011;70:263–9. Roberts TPL, Schmidt GL, Egeth M, Blaskey L, Rey MM, Edgar C, et al. Electrophysiological signature: magnetoencephalographic studies of the neural correlates of language impairment in autism spectrum disorders. Int J Psychophysiol 2008;68:149–60. Röder B, Teder-Sälejärvi W, Sterr A, Rösler F, Hillyard SA, Neville HJ. Improved auditory spatial tuning in blind humans. Nature 1999;400:162–6. Rodriguez HS, Corral M, Cadaveira F. Mismatch negativity in young children of alcoholics from high-density families. Alcohol Clin Exp Res 1998;22:1363–8. Roeske D, Ludwig KU, Neuhoff N, Becker J, Bartling J, Bruder J, et al. First-genomewide association scan on neurophysiological endophenotypes points to transregulation effects on SLC2A3 in dyslexic children. Mol Psychiatr 2011;16:97–107. Roger C, Hasbroucq T, Rabat A, Vidal F. Neurophysics of temporal discrimination in the rat: a mismatch negativity study. Psychophysiol 2009;46:1028–32. Roman S, Canévet G, Marquis P, Triglia J-M, Liégeois-Chauvel C. Relationship between auditory perception skills and mismatch negativity recorded in free field in cochlear-implant users. Hearing Res 2005;201:10–20. Rosburg T. Left hemispheric dipole locations of the neuromagnetic mismatch negativity to frequency, intensity and duration deviants. Cogn Brain Res 2003;16:83–90. Rosburg T, Marinou V, Haueisen J, Smesny S, Sauer H. Effects of lorazepam on the neuromagnetic mismatch negativity (MMNm) and auditory evoked field component N100m. Neuropsychopharmacol 2004;29:1723–33. Rosburg T, Trautner P, Dietl T, Korzyukov OA, Boutros NN, Schaller C, et al. Subdural recordings of the mismatch negativity (MMN) in patients with focal epilepsy. Brain 2005;128:819–28. Rosburg T, Trautner P, Ludowig E, Schaller C, Kurthen M, Elger CE, et al. Hippocampal event-related potentials to tone duration deviance in a passive oddball paradigm in humans. NeuroImage 2007;37:274–81. Rothenberger, A. Electrical brain activity in children with hyperkinetic syndrome: evidence of frontal cortical dysfunction. In: Sergeant J. (Ed.), European approaches to hyperkinetic disorder. Zürich: Trümpi; 1995. p. 255–270. Rothenberger A, Banaschewski T, Heinrich H, Moll GH, Schmidt MH, van’t Klooster B. Comorbidity in ADHD-children: effects of coexisting conduct disorder or tic disorder on event-related brain potentials in an auditory selective-attention task. Eur Arch Psychiat Clin Neurosci 2000;250:101–10. Rowland LP, Shneider NA. Medical progress: amyotrophic lateral sclerosis. New Engl J Med 2001;344:1688–700. Ruby P, Caclin A, Boulet S, Delpuech C, Morlet D. Odd sound processing in the sleeping brain. J Cognitive Neurosci 2008;20:296–311. Rudner M, Foo C, Sundewall-Thorén E, Lunner T, Rönnberg J. Phonological mismatch and explicit cognitive processing in a sample of 102 hearing-aid users. Int J Audiol 2008;47:S163–70. Ruusuvirta T, Huotilainen M, Fellman V, Näätänen R. Numerical discrimination in newborn infants as revealed by event-related potentials to tone sequences. Eur J Neurosci 2009;30:620–4. Ruusuvirta T, Koivisto K, Wikgren J, Astikainen P. Processing of melodic contours in urethane-anaesthetized rats. Eur J Neurosci 2007;26:701–3. Ruusuvirta T, Penttonen M, Korhonen T. Auditory cortical event-related potentials to pitch deviances in rats. Neurosci Lett 1998;248:45–8. Salisbury DF, Kuroki N, Kasai K, Shenton ME, McCarley RW. Progressive and interrelated functional and structural evidence of post-onset brain reduction in schizophrenia. Arch Gen Psychiat 2007;64:521–9. Salisbury DF, Shenton ME, Griggs CB, Bonner-Jackson A, McCarley RW. Mismatch negativity in chronic schizophrenia and first-episode schizophrenia. Arch Gen Psychiat 2002;59:686–94.

455

Sallinen M, Kaartinen J, Lyytinen H. Is the appearance of mismatch negativity during stage 2 sleep related to the elicitation of K-complex. Electroen Clin Neuro 1994;91:140–8. Sallinen M, Kaartinen J, Lyytinen H. Processing of auditory stimuli during tonic and phasic periods of REM sleep as revealed by event-related brain potentials. J Sleep Res 1996;5:220–8. Sallinen M, Lyytinen H. Mismatch negativity during objective and subjective sleepiness. Psychophysiology 1997;34:694–702. Salmi J, Huotilainen M, Pakarinen S, Siren T, Alho K, Aronen ET. Does sleep qualify affect involuntary attention switching system? Neurosci Lett 2005;390:150–5. Salo S, Peltola MS, Aaltonen O, Johansson R, Lang AH, Laurikainen E. Stability of memory traces for speech sounds in cochlear implant patients. Logoped Phoniatr Vocol 2002;27:132–8. Sams M, Hämäläinen M, Antervo A, Kaukoranta E, Reinikainen K, Hari R. Cerebral neuromagnetic responses evoked by short auditory stimuli. Electroen Clin Neuro 1985b;61:254–66. Sams M, Paavilainen P, Alho K, Näätänen R. Auditory frequency discrimination and event-related potentials. Electroen Clin Neuro 1985a;62:437–48. Sams M, Hari R, Rif J, Knuuttila J. The human auditory sensory memory trace persists about 10 s: neuromagnetic evidence. J Cognitive Neurosci 1993;5:363–70. Sandmann P, Kegel A, Eichele T, Dillier N, Lai W, Bendixen A, et al. Neurophysiological evidence of impaired musical sound perception in cochlear-implant users. Clin Neurophysiol 2010;121:2070–82. Santos MAR, Munhoz MSL, Peixoto MAL, Haase VG, Rodrigues JL, Resende LM. Mismatch negativity contribution in multiple sclerosis patients. Revi Bras Otorrinolaringol 2006;72:800–7. Särkämö T, Pihko E, Laitinen S, Forsblom A, Soinila S, Mikkonen M, et al. Music and speech listening enhance the recovery of early sensory processing after stroke. J Cognitive Neurosci 2010a;22:2716–27. Särkämö T, Tervaniemi M, Laitinen S, Forsblom A, Soinila S, Mikkonen M, et al. Music listening enhances cognitive recovery and mood after middle cerebral artery stroke. Brain 2008;131:866–76. Särkämö T, Tervaniemi M, Soinila S, Autti T, Silvennoinen HM, Laine M, et al. Cognitive deficits associated with acquired amusia after stroke: a neuropsychological follow-up study. Neuropsychologia 2009;47:2642–51. Särkämö T, Tervaniemi M, Soinila S, Autti T, Silvennoinen HM, Laine M, et al. Auditory and cognitive deficits associated with acquired amusia in stroke: a magnetoencephalography and neuropsychological follow-up study. PLoS ONE 2010b;5:e15157. Sasaki T, Campbell KB, Bazana PG, Stelmack RM. Individual differences in mismatch negativity measures of involuntary attention shift. Clin Neurophysiolo 2000;111:1553–60. Sato Y, Yabe H, Todd J, Michie P, Shinozaki N, Sutoh T, et al. Impairment in activation of a frontal attention-switch mechanism in schizophrenic patients. Biol Psychol 2002;62:49–63. Sato Y, Yabe H, Hiruma T, Sutoh T, Shinozaki N, Nashida T, et al. Do changes in probability on the MMN have a different effect in schizophrenic patients. In: Hashimoto I, Kakigi R. (Eds.), Recent advances in human neurophysiology. Amsterdam: Elsevier, 1998. p. 803–8. Satterfield JH, Schell AM, Nicholas T, Backs RW. Topographic study of auditory event-related potentials in normal boys and boys with attention deficit disorder with hyperactivity. Psychophysiology 1988;25:591–606. Sauer H, Volz HP. Functional magnetic resonance imaging and magnetic resonance spectroscopy in schizophrenia. Curr Opin Psychiat 2000;13:21–6. Sawada M, Iida J, Ota T, Negoro H, Tanaka S, Sadamatsu M, Kishimoto T. Effects of osmotic-release methylphenidate in attention-deficit/hyperactivity disorder as measured by event-related potentials. Psychiat Clin Neuros 2010;64:491–8. Schall U, Catts SV, Chaturvedi S, Liebert B, Redenbach J, Karayanidis F, et al. The effect of clozapine therapy on frontal lobe dysfunction in schizophrenia: neuropsychology and event-related potential measures. Int J Neuropsychopharmacol 1998;1:19–29. Schall U, Catts SV, Karayanidis F, Ward PB. Auditory event-related potential indices of fronto-temporal information processing in schizophrenia syndromes: valid outcome prediction of clozapine therapy in a three-year follow-up. Int J Neuropsychopharmacol 1999;2:83–93. Schall U, Johnston P, Todd J, Ward PB, Michie PT. Functional neuroanatomy of auditory mismatch processing: an event-related fMRI study of duration-deviant oddballs. NeuroImage 2003;20:729–36. Schiff S, Valenti P, Andrea P, Lot M, Bisiacchi P, Gatta A, et al. The effect of aging on auditory components of event-related brain potentials. Clin Neurophysiol 2008;119:1795–802. Schreiber H, Stolz-Born G, Kornhuber H, Born J. Event-related potential correlates of impaired selective attention in children at high risk for schizophrenia. Biol Psychiat 1992;32:634–51. Schreiber H, Stolz-Born G, Pietrowsky R, Kornhuber HH, Fehm HL, Born J. Improved event-related potential signs of selective attention after the administration of the cholecystokinin analog ceruletide in healthy persons. Biol Psychiat 1995;37:702–12. Schroeder MM, Ritter W, Vaughan Jr HG. The mismatch negativity to novel stimuli reflects cognitive decline. Ann NY Acad Sci 1995;769:399–401. Schroeder MM, Handelsman L, Torres L, Dorfman D, Rinaldi P, Jacobsen J, et al. Early and late cognitive event-related potentials mark stages of HIV-1 infection in the drug-user risk group. Biol Psychiat 1994;35:54–69.

456


Schröger E. On the detection of auditory deviants: a pre-attentive activation model. Psychophysiol 1997;34:245–2457. Schröger E, Tervaniemi M, Wolff C, Näätänen R. Preattentive periodicity detection in auditory patterns as governed by time and intensity information. Cognit Brain Res 1996;4:145–8. Schulte-Körne G, Bruder J. Clinical neurophysiology of visual and auditory processing in dyslexia: a review. Clinl Neurophysiol 2010;121:1794–809. Schulte-Körne G, Deimel W, Bartling J, Remschmidt H. Auditory processing and dyslexia: evidence for a specific speech processing deficit. NeuroReport 1998;9:337–40. Schulte-Körne G, Deimel W, Bartling J, Remschmidt H. Pre-attentive processing of auditory patterns in dyslexic human subjects. Neurosci Lett 1999;276:41–4. Schulte-Körne G, Deimel W, Bartling J, Remschmidt H. Speech perception deficit in dyslexic adults as measured by mismatch negativity (MMN). Int J Psychophysiol 2001;40:77–87. Sculthorpe LD, Ouellet DR, Campbell KB. MMN elicitation during natural sleep to violations of an auditory pattern. Brain Res 2009;1290:52–62. Schwieler L, Linderholm KR, Nilsson-Todd LK, Erhardt S, Engberg G. Clozapine interacts with the glycine site of the NMDA receptor: electrophysiological studies of dopamine neurons in the rat ventral tegmental area. Life Sci 2008;83:170–5. Sebastian C, Yasin I. Speech versus tone processing in compensated dyslexia: discrimination and lateralization with a dichotic mismatch negativity (MMN) paradigm. Int J Psychophysiol 2008;70:115–26. Seri S, Cerquiglini A, Pisani F, Curatolo P. Autism in tuberous sclerosis: evoked potential evidence for a deficit in auditory sensory processing. Clin Neurophysiol 1999;110:1825–30. Seri S, Pisani F, Thai JN, Cerquiglini A. Pre-attentive sensory processing in autistic spectrum disorder. Are electromagnetic measurements telling us a coherent story. Int J Psychophysiol 2007;63:159–63. Serra JM, Escera C, Sánchez-Turet M, Sánchez-Sastre J, Grau C. The H1-receptor antagonist chlorpheniramine decreases the ending phase of the mismatch negativity of the human auditory event-related potentials. Neurosci Lett 1996;203:77–80. Shafer VL, Morr ML, Datta H, Kurzberg D, Schwartz RG. Neurophysiological indexes of speech processing deficits in children with specific language impairment. J Cognitive Neurosci 2005;17:1168–80. Shafer VL, Ponton C, Datta H, Morr ML, Schwartz RG. Neurophysiological indices of attention to speech in children with specific language impairment. Clin Neurophysiol 2007;118:1230–43. Shankarnarayan VC, Maruthy S. Mismatch negativity in children with dyslexia speaking Indian languages. Behav Brain Funct 2007;3:36. Sharma M, Purdy SC, Newall P, Wheldall K, Beaman R, Dillon H. Electrophysiological and behavioral evidence of auditory processing deficits in children with reading disorder. Clin Neurophysiol 2005;117:1130–44. Sharma M, Purdy SC, Newall P, Wheldall K, Beaman R. Refractory effects on auditory-evoked responses in children with reading disorders. NeuroReport 2007;18:133–6. Sharma A, Purdy SC, Newall P, Wheldall K, Beaman R, Dillon H. Electrophysiological and behavioral evidence of auditory processing deficits in children with reading disorder. Clin Neurophysiol 2006;117:1130–44. Sharma M, Purdy AS, Kelly SC. Comorbidity of auditory processing, language, and reading disorders. J Speech Lang Hear R 2009;52:706–22. Shelley AM, Ward PB, Catts SV, Michie PT, Andrews S, McConaghy N. Mismatch negativity: an index of a preattentive processing deficit in schizophrenia. Biol Psychiat 1991;203:77–80. Shestakova A, Brattico E, Huotilainen M, Galunov V, Soloviev A, Sams M, et al. Abstract phoneme representations in the left temporal cortex: magnetic mismatch negativity study. NeuroReport 2002;13:1813–6. Shestakova A, Huotilainen M, Ceponiene R, Cheour M. Event-related potentials associated with second language learning in children. Clin Neurophysiol 2003;114:1507–12. Shin KS, Kim JS, Kang DH, Koh Y, Choi JS, O’Donnell BF, et al. Pre-attentive auditory processing in ultra-high-risk for schizophrenia with magnetoencephalography. Biol Psychiat 2009;65:1071–8. Shinozaki N, Yabe H, Sato Y, Hiruma T, Sutoh T, Nashida T, et al. The difference in mismatch negativity between the acute and post-acute phase of schizophrenia. Biol Psychol 2002;59:105–19. Shinozaki N, Yabe H, Sutoh T, Hiruma T, Kaneko S. Somatosensory automatic responses to deviant stimuli. Cognit Brain Res 1998;7:165–71. Shtyrov Y, Pulvermüller F. Language in the mismatch negativity design: motivations, benefits, and prospects. J Psychophysiol 2007;21:176–87. Shtyrov Y, Kujala T, Ahveninen J, Tervaniemi M, Alku P, Ilmoniemi RJ, et al. Background acoustic noise and the hemispheric lateralization of speech processing in the human brain: magnetic mismatch negativity study. Neurosci Lett 1998;251:141–4. Shtyrov Y, Kujala T, Ilmoniemi RJ, Näätänen R. Noise affects speech-signal processing differently in the cerebral hemispheres. NeuroReport 1999;10:2189–92. Siegal M, Blades M. Language and auditory processing in autism. Trends Cogn Sci 2003;7:378–80. Simoens VL, Istók E, Hyttinen S, Hirvonen A, Näätänen R, Tervaniemi M. Psychosocial stress attenuates general sound processing and duration change detection. Psychophysiology 2007;44:30–8. Simpson TP, Manara AR, Kane NM, Barton RL, Rowlands CA, Butler SR. Effect of propofol anaesthesia on the event-related potential mismatch negativity and the auditory-evoked potential N1. Britt J Anaesthesia 2002;89:382–8.

Smolnik R, Molle M, Fehm HL, Born J. Brain potentials and attention after acute and subchronic intranasal administration of ACTH 4-10 and desacetyl-alpha-MSH in humans. Neuroendocrinology 1999;70:63–72. Smolnik R, Pietrowsky R, Fehm HL, Born J. Enhanced selective attention after lowdose administration of the benzodiazepine antagonist flumazenil. J Clin Psychopharm 1998;18:241–7. Sorokin A, Alku P, Kujala T. Change and novelty detection in speech and non-speech sound streams. Brain Res 2010;1327:77–90. Spackman LA, Towell A, Boyd SG. Somatosensory discrimination: an intracranial event-related potential study of children with refractory epilepsy. Brain Res 2010;1310:68–76. Spackman LA, Boyd SG, Towell A. Effects of stimulus frequency and duration on somatosensory discrimination responses. Exp Brain Res 2007;117:21–30. Squires KC, Squires NK, Hillyard SA. Decision-related cortical potentials during an auditory signal detection task with cued observation intervals. J Exp Psychol Human 1975;1:268–79. Srinivasan N, Baijal S. Concentrative meditation enhances preattentive processing: a mismatch negativity study. NeuroReport 2007;18:1709–12. Stagg C, Hindley P, Tales A, Butler S. Visual mismatch negativity: the detection of stimulus change. NeuroReport 2004;15:659–63. Stapells DR. Cortical event related potentials to auditory stimuli. In: Katz J. (Ed.), Handbook of clinical audiology, 5th ed. Baltimore, MD: Lippincott & Wilkins; 2002. p. 378–406. Stefanics G, Kimura M, Czigler I. Visual mismatch negativity reveals automatic detection of sequential regularity violation. Front Hum Neurosci 2011;5:46. Stix G. How to build a better learner. Sci Am 2011;305:50–7. Stone JM, Bramon E, Pauls A, Sumich A, McGuire PK. Thalamic neurochemical abnormalities in individuals with prodromal symptoms of schizophrenia – relationship to auditory event-related potentials. Psychiat Res-Neuroim 2010;183:174–6. Stoodley CJ, Hill R, Stein JF, Bishop DVM. Auditory event-related potentials differ in dyslexic even when auditory psychophysical performance is normal. Brain Res 2006;1121:190–9. Sullivan EV, Shear PK, Zipursky RB, Sagar HJ, Pfefferbaum A. A deficit profile of executive, memory, and motor functions in schizophrenia. Biol Psychiat 1995;36:641–53. Sysoeva OV, Maluchenko NV, Smirnov KS, Shleptsova VA, Ivanitsky AM, Tonevitsky AG. Pecularities of brain information processing in persons with different serotonin transporter gene variants. B Exp Biol Med 2009;148:731–4. Takei Y, Kumano S, Hattori S, Uehara T, Kawakubo Y, Kasai K, et al. Preattentive dysfunction in major depression: a magnetoencephalography study using auditory mismatch negativity. Psychophysiology 2009;46:52–61. Takei Y, Kumano S, Maki Y, Hattori S, Kawakubo Y, Kasai K, et al. Preattentive dysfunction in bipolar disorder: a MEG study using mismatch negativity. Prog Neuro-Psychoph 2010;34:903–12. Tales A, Butler S. Visual mismatch negativity highlights abnormal preattentive visual processing in Alzheimer’s disease. NeuroReport 2006;17:887–90. Tales A, Haworth J, Wilcock G, Newton P, Butler S. Visual mismatch negativity highlights abnormal pre-attentive visual processing in mild cognitive impairment and Alzheimer’s disease. Neuropsychologia 2008;46:1224–32. Tales A, Muir J L, Bayer A, Jones R, Snowden RJ. Phasic visual alertness in Alzheimer’s disease and ageing. NeuroReport 2002a;13:2557–60. Tales A, Newton P, Troscianko T, Butler S. Mismatch negativity in the visual modality. NeuroReport 1999;110:3363–7. Tales A, Troscianko T, Wilcock GK, Newton P, Butler SR. Age-related changes in the preattentional detection of visual change. NeuroReport 2002b;13:969–72. Tanaka M, Okubo O, Fuchigami T, Harada K. A study of mismatch negativity in newborns. Pediatr Int 2001;43:281–6. Tarkka IM, Luukainen-Markkula R, Pitkänen K, Hämäläinen H. Alterations in visual and auditory processing in hemispatial neglect: an evoked potential follow-up study. Int J Psychophysiol 2011;79:272–9. Taylor MJ, Baldeweg T. Application of EEG, ERP and intracranial recordings to the investigation of cognitive functions in children. Dev Sci 2002;5:318–34. Tervaniemi M, Winkler I, Näätänen R. Pre-attentive categorization of sounds by timbre as revealed by event-related potentials. NeuroReport 1997;8:2571–4. Tervaniemi M, Kujala A, Alho K, Virtanen J, Ilmoniemi RJ, Näätänen R. Functional specialization of the human auditory cortex in processing phonetic and musical sounds: a magnetoencephalographic (MEG) study. NeuroImage 1999; 9:330–6. Tervaniemi M, Medvedev SV, Alho K, Pakhomov SV, Roudas MS, van Zuijen TL, et al. Lateralized automatic auditory processing of phonetic versus musical information: a PET study. Hum Brain Mapp 2000;10:74–9. Thönnesen H, Zvyagintsev M, Harke KC, Boers F, Dammers J, Norra C, et al. Optimized mismatch negativity paradigm reflects deficits in schizophrenia patients. A combined EEG and MEG study. Biol Psychol 2008;77:205–16. Tikhonravov D, Neuvonen T, Pertovaara A, Savioja K, Ruusuvirta T, Näätänen R, et al. Effects of an NMDA receptor antagonist MK-801 on an MMN-like response recorded in anesthetized rats. Brain Res 2008;1203:97–102. Tikhonravov D, Neuvonen T, Pertovaara A, Savioja K, Ruusuvirta T, Näätänen R, et al. Dose-related effects of memantine on a mismatch negativity-like response in anesthetized rats. Neuroscience 2010;167:1175–82. Todd J, Michie PT, Jablensky AV. Association between reduced duration mismatch negativity (MMN) and raised temporal discrimination thresholds in schizophrenia. Clin Neurophysiol 2003;114:2061–70. Todd J, Michie PT, Schall U, Karayanidis F, Yabe H, Näätänen R. Deviant matters: duration, frequency, and intensity deviants reveal different patterns of

R. Näätänen et al. / Clinical Neurophysiology 123 (2012) 424–458 mismatch negativity reduction in early and late schizophrenia. Biol Psychiat 2008;63:58–64. Todd, J, Michie PT, Schall U, Ward P, Catts S. Mismatch negativity (MMN) reduction in schizophrenia -impaired prediction-error generation, estimation or salience. Int J Psychophysiol, in press. Toiviainen P, Tervaniemi M, Louhivuori J, Saher M, Huotilainen M, Näätänen R. Timbre similarity: convergence of neural, behavioral, and computational approaches. Music Percept 1998;16:223–41. Towey JP, Tenke CE, Bruder GE, Leite P, Friedman D, Liebowitz M, et al. Brain eventrelated potential correlates of overfocused attention in obsessive-compulsive disorder. Psychophysiology 1994;31:535–43. Toyomaki A, Kusumi I, Matsuyama T, Kako Y, Ito K, Koyama T. Tone duration mismatch negativity deficits predict impairment of executive function in schizophrenia. Prog Neuro-Psychoph 2008;32:95–9. Trainor L, McFadden M, Hodgson L, Darragh L, Barlow J, Matsos L, et al. Changes in auditory cortex and the development of mismatch negativity between 2 and 6 months of age. Int J Psychophysiol 2003;51:5–15. Trainor L, Samuel SS, Desjardins RN, Sonnadara RR. Measuring temporal resolution in infants using mismatch negativity. NeuroReport 2001;12:2443–8. Trautwein PG, Ponton CW, Kwong B, Waring MD. Neuropsysiological and psychophysical measures of duration discrimination in normal-hearing adults and adults with cochlear implants. In: Proceedings 16th international congress on acoustics and 135th meeting Acoustic Society of America, 1998. p. 877-8. Tremblay K, Kraus N, Carrel TD, McGee T. Central auditory system plasticity: Generalization to novel stimuli following listening training. J Acoust Soc Am 1997;102:3762–73. Tremblay K, Kraus N, McGee T. The time course of auditory perceptual learning: neurophysiological changes during speech-sound training. NeuroReport 1998;9:3557–60. Troche SJ, Houlihan ME, Stelmack RM, Rammsayer TH. Mental ability and the discrimination of auditory frequency and duration change without focused attention: an analysis of mismatch negativity. Pers Individ Differ 2010;49:228–33. Troche SJ, Houlihan ME, Stelmack RM, Rammsayer TH. Mental ability, P300, and mismatch negativity: analysis of frequency and duration discrimination. Intelligence 2009;37:365–73. Tse C-Y, Penney TB. On the functional role of temporal and frontal cortex activation in passive detection of auditory deviance. NeuroImage 2008;41:1462–70. Turetsky BI, Calkins ME, Light GA, Olincy A, Radant AD, Swerdlow NR. Neurophysiological endophenotypes of schizophrenia: the viability of selected candidate measures. Schizophrenia Bull 2007;33:69–94. Turetsky BI, Bilker WE, Siegel SJ, Kohler CG, Gur RE. Profile of auditory informationprocessing deficits in schizophrenia. Psychiat Res 2009;165:27–37. Umbricht D, Krljes S. Mismatch negativity in schizophrenia: a meta-analysis. Schizophr Res 2005;76:1–23. Umbricht DS, Bates JA, Lieberman JA, Kane JM, Javitt DC. Electrophysiological indices of automatic and controlled auditory information processing in first-episode, recent-onset and chronic schizophrenia. Biol Psychiat 2006;59:762–72. Umbricht D, Javitt D, Novak G, Bates J, Pollack S, Lieberman J, et al. Effects of clozapine on auditory event-related potentials in schizophrenia. Biol Psychiat 1998;44:716–25. Umbricht D, Javitt D, Novak G, Bates J, Pollack S, Lieberman J, et al. Effects of risperidone on auditory event-related potentials in schizophrenia. Int J Neuropsychopharmacol 1999;2:299–304. Umbricht D, Koller R, Schmid L, Skrabo A, Grübel C, Huber T, et al. How specific are deficits in mismatch negativity generation to schizophrenia. Biol Psychiat 2003;53:1120–31. Umbricht D, Koller R, Vollenweider FX, Schmid L. Mismatch negativity predicts psychotic experiences induced by NMDA receptor antagonist in healthy volunteers. Biol Psychiat 2002;51:400–6. Umbricht D, Schmid L, Koller R, Vollenweider FX, Hell D, Javitt DC. Ketamineinduced deficits in auditory and visual context-dependent processing in healthy volunteers: implications for models of cognitive deficits in schizophrenia. Arch Gen Psychiat 2000;57:1139–47. Umbricht D, Vyssotki D, Latanov A, Nitsch R, Lipp HP. Deviant-related electrophysiological activity in mice: is there mismatch negativity in mice. Clin Neurophysiol 2005;116:353–63. Urban A, Kremlácek J, Masopust J, Libiger J. Visual mismatch negativity among patients with schizophrenia. Schizophr Res 2008;102:320–8. Uwer R, Albrecht R, von Suchodoletz W. Automatic processing of tones and speech stimuli in children with specific language impairment. Dev Med Child Neurol 2002;44:527–32. Uwer R, von Suchodoletz W. Stability of mismatch negativities in children. Clin Neurophysiol 2000;111:45–52. Valeriani M, Galli F, Tarantino S, Graceffa D, Pignata E, Miliucci R, et al. Correlation between normal brain excitability and emotional symptomatology in paediatric migraine. Cephalalgia 2008;29:204–13. van der Stelt O, Belger A. Application of electroencephalography to the study of cognitive and brain functions in schizophrenia. Schizophr Bull 2007;33:955–70. van der Stelt O, van Boxtel GJM. Auditory P300 and mismatch negativity in comatose states. Clin Neurophysiol 2008;119:2172–4. van Hooff JC, de Beer NAM, Brunia CHM, Cluitmans PJM, Kortsen HHM. Eventrelated potential measures of information processing during general anesthesia. Electroen Clin Neuro 1997;103:268–81.

457

van Hooff JC, de Beer NAM, Brunia CHM, Cluitmans PJM, Kortsen HHM, Tavilla G, et al. Information processing during cardiac surgery: an event related potential study. Electroen Clin Neuro 1995;96:433–52. Vanhanen M, Karhu J, Koivisto K, Pääkkönen A, Partanen J, Laakso M, et al. ERPs reveal deficits in automatic cerebral stimulus processing in patients with NIDDM. NeuroReport 1996;7:2767–71. Vanhaudenhuyse A, Laureys S, Perrin F. Cognitive event-related potentials in comatose and post-comatose states. Neurocrit Care 2008;8:262–70. van Leeuwen T, Been P, Kuijpers C, Zwarts F, Maassen B, van der Leij A. Mismatch response is absent in 2-month-old infants at risk for dyslexia. NeuroReport 2006;17:351–5. van Woerkom TC, Fortgens C, Rompel-Martens CM, van de Wetering BJ. Auditory event-related potentials in adult patients with Gilles de la Tourette’s syndrome in the oddball paradigm. Electroen Clin Neuro 1988;71:443–9. van Woerkom TCAM, Roos RAC, van Dijk JG. Altered attentional processing of background stimuli in Gilles de la Tourette syndrome: a study in auditory event-related potentials evoked in an oddball paradigm. Acta Neurol Scand 1994;90:116–23. Vaz Pato M, Jones SJ, Perez N, Sprague LC. Mismatch negativity to single and multiple pitch-deviant tones in regular and pseudo-random complex tone sequences. Neurophysiology 2002;113:519–27. Verbaten MN, van Engeland H. (Neuro) physiologic similarities between childhood developmental disorders and schizophrenia. In: Den Boer JA, Westenberg HGM, Praag HM. (Eds.), Advances in the neurobiology of schizophrenia. John Wiley & Sons Ltd; 1995. p. 369–400. Verbaten MN, Overtoom CCE, Koelega HS, Swaab-Barneveld H, van der Gaag RJ, Buitelaar J, et al. Methylphenidate influences on both early and late ERP waves of ADHD children in a continuous performance test. J Abnorm Child Psychol 1994;22:561–78. Verleger R, Neukäter W, Kömpf D, Viereggem P. On the reasons for the delay of P3 latency in healthy elderly subjects. Electroen Clin Neuro 1991;79:488–502. Vieregger P, Verleger R, Wascher E, Stüven F, Kömpf D. Auditory selective attention is impaired in Parkinson’s disease – event-related evidence from EEG potentials. Cognit Brain Res 1994;2:117–29. Vuust P, Brattico E, Glerean E, Seppänen M, Pakarinen S, Tervaniemi M, et al. New fast mismatch negativity paradigm for determining the neural prerequisites for musical ability. Cortex 2011;47:1091–9. Wable J, van der Abbeele T, Gallégo S, Frachet B. Mismatch negativity: a tool for the assessment of stimuli discrimination in cochlear implant subjects. Clin Neurophysiol 2000;111:743–51. Wang W, Zhu SZ, Pan LC, Hu AH, Wang YH. Mismatch negativity and personality traits in chronic primary insomniacs. Funct Neurol 2001;16:3–10. Weber C, Hahne A, Friedrich M, Friederici AD. Reduced stress pattern discrimination in 5-month-olds as a marker of risk for later language impairment: neurophysiological evidence. Cognit Brain Res 2005;25:180–7. Wei J-H, Chan T-C, Luo Y-J. A modified oddball paradigm ‘‘cross-modal delayed response’’ and the research on mismatch negativity. Brain Res Bull 2002;57:221–30. Wertz RT, Auther LL, Burch-Sims GP, Abou-Khalil R, Kirshner HS, Duncan GW. A comparison of the mismatch negativity (MMN) event-related potential to tone and speech stimuli in normal and aphasic adults. Aphasiology 1998;12:499–507. Wible CG, Kubicki M, Yoo S-S, Kacher DF, Salisbury DF, Anderson MC, et al. A functional magnetic resonance imaging study of auditory mismatch in schizophrenia. Am J Psychiat 2001;158:938–43. Wienberg M, Glenthoj BY, Jensen KS, Oranje B. A single high dose of escitalopram increases mismatch negativity without affecting processing negativity or P300 amplitude in healthy volunteers. J Psychopharmacol 2010;24:1183–92. Wijnen VJM, van Boxtel GJM, Eilander HJ, de Gelder B. Mismatch negativity predicts recovery from the vegetative state. Clin Neurophysiol 2007;118:597–605. Wild-Wall N, Oades RD, Juran SA. Maturation processes in automatic change detection as revealed by event-related brain potentials and dipole source localization: significance for adult AD/HD. Int J Psychophysiol 2005;58: 34–46. Winkler I. Interpreting the mismatch negativity. J Psychophysiol 2007;21:147–63. Winkler I, Näätänen R. The effects of auditory backward masking on event-related brain potentials. Electroen Clin Neuro 1994;44:185–9. Winkler I, Reinikainen K, Näätänen R. Event-related brain potentials reflect echoic memory in humans. Percept Psychophys 1993;53:443–9. Winkler I, Kujala T, Tiitinen H, Sivonen P, Alku P, Lehtokoski A, et al. Brain responses reveal the learning of foreign language phonemes. Psychophysiology 1999c;36:638–42. Winsberg BG, Javitt DC, Silippo GS. Electrophysiological indices of information processing in methylphenidate responders. Biol Psychiat 1997;42:434–45. Winsberg BG, Javitt DC, Silippo GS, Doneshka P. Mismatch negativity in hyperactive children: effects of methylphenidate. Psychopharmacol Bull 1993;29:229–33. Woods DL. Auditory selective attention in middle-aged and elderly subjects: an event-related brain potential study. Electroen Clin Neuro 1992;84:456–68. Woods DL, Clayworth CC. Age-related changes in human middle latency auditory evoked potentials. Electroen Clin Neuro 1986;65:297–303. Woods DL, Knight RT. Electrophysiologic evidence of increased distractibility after dorsolateral prefrontal lesions. Neurology 1986;36:212–6. Woods DL, Alho K, Algazi A. Intermodal selective attention I: effects on eventrelated potentials to lateralized auditory and visual stimuli. Electroen Clin Neuro 1992;82:341–55.

458


Wu JC, Maguire G, Riley G, Lee A, Keator D, Tang C, et al. Increased dopamine activity associated with stuttering. NeuroReport 1997;8:767–70. Wynn JK, Sugar C, Horan WP, Kern R, Green MF. Mismatch negativity, social cognition, and functioning in schizophrenia patients. Biol Psychiat 2010;67:940–7. Yamasue H, Yamada H, Yumoto M, Kamio S, Kudo N, Uetsuki M, et al. Abnormal association between reduced magnetic mismatch field to speech sounds and smaller left planum temporale volume in schizophrenia. NeuroImage 2004;22:720–7. Yokoyama Y, Nakashima K, Shimoyama R, Urakami K, Takahashi K. Distribution of event-related potentials in patients with dementia. Electroen Clin Neuro 1995;35:431–7. Youn T, Park H-J, Kim J-J, Kim MS, Kwon JS. Altered hemispheric asymmetry and positive symptoms in schizophrenia: equivalent current dipole of auditory mismatch negativity. Schizophr Res 2003;59:253–60.

Yppärilä H, Karhu J, Westerén-Punnonen S, Musialowicz T, Partanen J. Evidence of auditory processing during postoperative propofol sedation. Clini Neurophysiol 2002;113:1357–64. Zarza-Lucianez A, Arce-Arce S, Bhathal H, Sanjuan-Martin F. Mismatch negativity and conscience level in severe traumatic brain injury. Rev Neurologia 2007;44:465–8. Zerouali Y, Jemel B, Godbout R. The effects of early and late night partial sleep deprivation on automatic and selective attention: an ERP study. Brain Res 2010;1308:87–99. Zhang XL, Cohen HL, Porjesz B, Begleiter H. Mismatch negativity in subjects at high risk for alcoholism. Alcohol Clin Exp Res 2001;25:330–7. Zurrón M, Díaz F. Auditory event-related potentials in mentally retarded subjects during active and passive oddball experiments. Biol Psychiat 1997;41:201–8.