Invited ReviewThe mismatch negativity (MMN) – A unique window to disturbed central auditory processing in ageing and different clinical conditions
Highlights
► 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.
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-detection (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, Pekkonen et al., 1995b, 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, Ilvonen et al., 2004) and in comatose (Kane et al., 1993, Kane et al., 1996, Fischer et al., 1999, Fischer and Luauté, 2005) and persistent-vegetative-state (PVS) patients (Wijnen et al., 2007).
The auditory MMN response is mainly generated by a change-detection 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, Näätänen et al., 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, Rinne et al., 2006), a right frontal-cortex process which, in turn, initiates further cerebral processes which may lead to conscious change detection (Näätänen, 1990, Näätänen, 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, Halgren et al., 1995b, Halgren et al., 1998, Baudena et al., 1995; Kropotov et al., 1995, 2000; Liasis et al., 1999, 2000a,b; Rosburg et al., 2005, Rosburg et al., 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, Frodl-Bauch et al., 1997, Escera et al., 2002), MEG (Levänen et al., 1993, Levänen et al., 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, Tales et al., 2002a, Tales et al., 2002b, Tales et al., 2008, Tales and Butler, 2006, Maekawa et al., 2005, Maekawa et al., 2009, Berti and Schröger, 2004, Berti and Schröger, 2006, Stagg et al., 2004, Stefanics et al., 2011, Heslenfeld, 2003; Pazo-Alvarez et al., 2003, Pazo-Alvarez et al., 2004, Froyen et al., 2010, Iijima et al., 1996, Kenemans et al., 2003, Kimura et al., 2009, Czigler, 2007, Czigler and Csibra, 1990, Czigler and Csibra, 1992, Czigler et al., 2002, Czigler et al., 2004, Czigler et al., 2006a, Czigler et al., 2006b, 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, Spackman et al., 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, Csépe et al., 1988, Csépe et al., 1989, Pincze et al., 2001, Pincze et al., 2002); rabbit (Astikainen et al., 2001); rat (Astikainen et al., 2006, Ruusuvirta et al., 1998, Ruusuvirta et al., 2007, Roger et al., 2009, Tikhonravov et al., 2008, Tikhonravov et al., 2010); guinea pig (Kraus et al., 1994); and mouse (Umbricht et al., 2005, Ehrlichman et al., 2008, Ehrlichman et al., 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, Näätänen et al., 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, Kujala et al., 2006, Kujala et al., 2007, Kujala et al., 2010, Pakarinen et al., 2007, Pakarinen et al., 2009, Pakarinen et al., 2010). In addition, these MMN-based objective tests can be extended to all aspects of short-term auditory sensory memory, too, such as its 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 Pulvermuller, 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, Tales et al., 2002b, Kenemans et al., 2010, Tales and Butler, 2006, Tales et al., 2002a, Tales et al., 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, Kremláček 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, Akatsuka et al., 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.
Section snippets
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
The MMN as an index of shortened sensory-memory duration (Table 2)
The MMN elicitation depends on the presence of the sensory-memory 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
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
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
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 mastoid-recorded MMN (with nose reference) is unaffected in
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
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, Ahveninen et al., 2000b). In addition, in patients with persistent developmental stuttering, the MMN to phonetic contrasts was
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
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, Kane et al., 1996, Fischer et al., 1999, Fischer et al., 2004, Fischer et al., 2006a, Fischer et al., 2006b; Luauté et al., 2005, Morlet et al., 2000, Fischer and Luauté, 2005, Daltrozzo et al., 2007, Vanhaudenhuyse
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, Salisbury et al., 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
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, Kane et al., 1996, Fischer et al., 2000, Fischer et al., 2006a, Fischer et al., 2006b; 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
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,
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, Tremblay et al., 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
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
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.
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