Auditory recovery cycle dysfunction in schizophrenia: a study using event-related potentials.
ABSTRACT Previous event-related potential (ERP) studies reported evidence of impaired auditory information processing in patients with schizophrenia. The recovery cycle of the auditory N1 ERP component was measured in 17 patients with schizophrenia and 17 age- and sex-matched healthy volunteers. Subjects performed a visual distraction task while listening to 80-dB SPL, 1000-Hz tone pairs, presented with intra-pair intervals of 1, 3, 5 or 7 s, with inter-pair intervals of 9-13 s. Patients with schizophrenia had significantly reduced N1 amplitudes for S1 stimuli compared with healthy volunteers. For N1 amplitudes elicited by S2 stimuli, there was a significant group effect whilst the main effect of intra-pair interval was not significant. These results provide additional evidence of inhibitory auditory processing deficits in schizophrenia.
SourceAvailable from: Hannu Tiitinen[Show abstract] [Hide abstract]
ABSTRACT: The current review constitutes the first comprehensive look at the possibility that the mismatch negativity (MMN, the deflection of the auditory ERP/ERF elicited by stimulus change) might be generated by so-called fresh-afferent neuronal activity. This possibility has been repeatedly ruled out for the past 30 years, with the prevailing theoretical accounts relying on a memory-based explanation instead. We propose that the MMN is, in essence, a latency- and amplitude-modulated expression of the auditory N1 response, generated by fresh-afferent activity of cortical neurons that are under nonuniform levels of adaptation.Psychophysiology 08/2009; 47(1):66-122. DOI:10.1111/j.1469-8986.2009.00856.x · 3.18 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: Examining visual word recognition memory (WRM) with nose-referenced EEGs, we reported a preserved ERP 'old-new effect' (enhanced parietal positivity 300-800 ms to correctly-recognized repeated items) in schizophrenia ([Kayser, J., Bruder, G.E., Friedman, D., Tenke, C.E., Amador, X.F., Clark, S.C., Malaspina, D., Gorman, J.M., 1999. Brain event-related potentials (ERPs) in schizophrenia during a word recognition memory task. Int. J. Psychophysiol. 34(3), 249-265.]). However, patients showed reduced early negative potentials (N1, N2) and poorer WRM. Because group differences in neuronal generator patterns (i.e., sink-source orientation) may be masked by choice of EEG recording reference, the current study combined surface Laplacians and principal components analysis (PCA) to clarify ERP component topography and polarity and to disentangle stimulus- and response-related contributions. To investigate the impact of stimulus modality, 31-channel ERPs were recorded from 20 schizophrenic patients (15 male) and 20 age-, gender-, and handedness-matched healthy adults during parallel visual and auditory continuous WRM tasks. Stimulus- and response-locked reference-free current source densities (spherical splines) were submitted to unrestricted Varimax-PCA to identify and measure neuronal generator patterns underlying ERPs. Poorer (78.2+/-18.7% vs. 87.8+/-11.3% correct) and slower (958+/-226 vs. 773+/-206 ms) performance in patients was accompanied by reduced stimulus-related left-parietal P3 sources (150 ms pre-response) and vertex N2 sinks (both overall and old/new effects) but modality-specific N1 sinks were not significantly reduced. A distinct mid-frontal sink 50-ms post-response was markedly attenuated in patients. Reductions were more robust for auditory stimuli. However, patients showed increased lateral-frontotemporal sinks (T7 maximum) concurrent with auditory P3 sources. Electrophysiologic correlates of WRM deficits in schizophrenia suggest functional impairments of posterior cortex (stimulus representation) and anterior cingulate (stimulus categorization, response monitoring), primarily affecting memory for spoken words.International journal of psychophysiology: official journal of the International Organization of Psychophysiology 04/2009; 73(3):186-206. DOI:10.1016/j.ijpsycho.2009.02.003 · 2.65 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: The N1 component of the auditory evoked potential (AEP) is a robust and easily recorded metric of auditory sensory-perceptual processing. In patients with schizophrenia, a diminution in the amplitude of this component is a near-ubiquitous finding. A pair of recent studies has also shown this N1 deficit in first-degree relatives of schizophrenia probands, suggesting that the deficit may be linked to the underlying genetic risk of the disease rather than to the disease state itself. However, in both these studies, a significant proportion of the relatives had other psychiatric conditions. As such, although the N1 deficit represents an intriguing candidate endophenotype for schizophrenia, it remains to be shown whether it is present in a group of clinically unaffected first-degree relatives. In addition to testing first-degree relatives, we also sought to replicate the N1 deficit in a group of first-episode patients and in a group of chronic schizophrenia probands. Subject groups consisted of 35 patients with schizophrenia, 30 unaffected first-degree relatives, 13 first-episode patients, and 22 healthy controls. Subjects sat in a dimly lit room and listened to a series of simple 1,000-Hz tones, indicating with a button press whenever they heard a deviant tone (1,500 Hz; 17% probability), while the AEP was recorded from 72 scalp electrodes. Both chronic and first-episode patients showed clear N1 amplitude decrements relative to healthy control subjects. Crucially, unaffected first-degree relatives also showed a clear N1 deficit. This study provides further support for the proposal that the auditory N1 deficit in schizophrenia is linked to the underlying genetic risk of developing this disorder. In light of recent studies, these results point to the N1 deficit as an endophenotypic marker for schizophrenia. The potential future utility of this metric as one element of a multivariate endophenotype is discussed.European Archives of Psychiatry and Clinical Neuroscience 12/2010; 261(5):331-9. DOI:10.1007/s00406-010-0176-0 · 3.36 Impact Factor