Cross‐diagnostic comparison of duration mismatch negativity and P3a in bipolar disorder and schizophrenia

Abstract

Objectives Bipolar disorder and schizophrenia share common pathophysiological processes and may have similar perceptual abnormalities. Mismatch negativity (MMN) and P3a—event-related potentials associated with auditory preattentional processing—have been extensively studied in schizophrenia, but rarely in bipolar disorder. Furthermore, MMN and P3a have not been examined between diagnostic subgroups of patients with bipolar disorder. We evaluated MMN and P3a in patients with bipolar disorder compared to patients with schizophrenia and healthy controls. Methods MMN and P3a were assessed in 52 bipolar disorder patients, 30 schizophrenia patients, and 27 healthy control subjects during a duration-deviant auditory oddball paradigm. Results Significant MMN and P3a amplitude reductions were present in patients with bipolar disorder and schizophrenia relative to controls. The MMN reduction was more prominent in patients with schizophrenia than bipolar disorder, at a trend level. P3a did not differ significantly between patient groups. There were no MMN or P3a differences between patients with bipolar I (n = 34) and bipolar II (n = 18) disorder. Patients with bipolar I disorder failed to show lateralized MMN, in contrast to the other groups. No MMN or P3a differences were found between patients with bipolar disorder taking (n = 12) and not taking (n = 40) lithium, as well as between those taking (n = 30) and not taking (n = 22) antipsychotic medications. Conclusions Patients with bipolar disorder showed deficits in preattentive auditory processing, including MMN deficits that are less severe and P3a deficits that are slightly more pronounced, than those seen in schizophrenia.

Nonhuman primate model of schizophrenia using a noninvasive EEG method

“…Consistent with this behavioral deficit, the amplitudes of both the MMN (7) and the P3 (8) have been found to be reduced in schizophrenia patients, leading to the proposals that reduced MMN is a marker of progressive pathology (7) and that reductions in both MMN and P3a are markers of vulnerability for this disorder (8,9).…”

“…Other prior studies reveal associations between physiological measures and behavioral deficits: (i) both humans (34) and monkeys exhibit schizophrenia-like deficits on task-switching (19) when treated with ketamine; and (ii) the amplitude reduction of MMN has been correlated with behavioral deficits present in schizophrenia patients (1,7), and the reduction of both MMN and P3 has been associated with vulnerability for schizophrenia (8,9). Here, to further explore these relationships and the suitability of the rhesus macaque as an animal model for schizophrenia, we studied the amplitude of MMN and P3a ERP responses in NHPs in relation to the administration of ketamine.…”

Auditory-prosodic processing in bipolar disorder; from sensory perception to emotion

“…There is however, some indirect psychophysiological data to suggest reduced auditory receptiveness to changes in duration (elicited in mismatch negativity paradigms; Andersson et al, 2008;Jahshan et al, 2012;Takei et al, 2010) and amplitude (elicited in loudness dependence auditory evoked potential and prepulse inhibition paradigms; Gogos et al, 2009;Lee et al, 2012;Park et al, 2010) in patients with the disorder. Impairments in the bottom up processing of these acoustic cues may critically impact prosodic emotion perception in patients with BD; however this remains to be seen.…”

Dissociable auditory mismatch response and connectivity patterns in adolescents with schizophrenia and adolescents with bipolar disorder with psychosis: A magnetoencephalography study

“…This may cast light upon the trajectory of shared and non-shared pathophysiology. Unfortunately, it is not easy to fully discuss these observations in the light of the previous literature, as there have been many contradictory EEG and MEG findings indicating both similarities (Kaur et al, 2011) and differences (Jahshan et al, 2012b) between schizophrenia and bipolar disorder, for the most part conducted in adults, and those with chronic illnesses. Our data suggest that early-latency cortical responses are altered in ABP patients, however, this does not appear to be the case here in adolescent schizophrenia, where the modulation of the N100-like response appears normal (both latency and topography in the early peak observed here matches the N100 features).…”