453 Auditory oddball responses in first episode schizophrenic patients

453 Auditory oddball responses in first episode schizophrenic patients

174 Abstracts /International Journal In recent neuropsychiatric research, mismatch negativity (MMN) as an early component of the auditory evoked e...

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174

Abstracts

/International

Journal

In recent neuropsychiatric research, mismatch negativity (MMN) as an early component of the auditory evoked event related potentials has become an important tool to assess deficits of early attention processes in schizophrenic patients. MMN probably constitutes the earliest marker of cognitive function and has been related to a modality-specific sensory working memory. This study assessed the neuromagnetic mismatch reaction of 15 male schizophrenic inpatients on stable neuroleptic medication in comparison to 16 healthy controls. Neuropsychological tests of all participants and the psychopathological assessment of schizophrenics by means of rating scales formed part of the investigation. Magnetoencephalographic measurement of MMN was performed over both contralateral temporal lobes with a 31-channel biomagnctometer first order gradiometer centered on T3 (lo/20 system). The used oddball paradigm consisted of 50 ms computer-generated tone pips with 5 ms rise and fall times at 90 dB. The 1000 Hz tone represented the standard while 1050 Hz and 5000 Hz tones and tone omission were selected as deviants. Each type of deviant occurred with a 10% pseudorandom probability within the same trial block. The 1000 Hj: and 5000 Hz standard tones were also recorded separately. & raw data were digitally bandpass liltered and data processing included the application of a regression-based algorithm for the correction of eye artifacts. The sensory field of the standard tone was then subtracted per channel from the field of deviant tones and root mean squared in order to obtain the mean global field power (MGFP) of the mismatch reaction. This reaction was normalized by the t&poral average of the standard tone MGFP. Paired t-values were calculated for these power values. At the day of the measurements all patients were assessed psychopathologically by an experienced psychiatrist using the Scale for the Assessment of Positive Symptoms (SAPS), the Scale for the Assessment of Negative Symptoms (SANS) and the Brief Psychiatric Rating Scale (BPRS). Furthermore, a neuropsychological test battery was applied to patients as well as probands. Mismatch generation in schizophrenics proved to be significantly impaired for all three conditions with an emphasis over the left hemisphere. Our study therefore extends previous reports of a reduced mismatch reaction in schizophrenic patients to the field of magnetoencephalography, using different qualities of mismatch in the same paradigm. The data confirm the theory of impaired auditory information processing in schizophrenics already at the level of the primary auditory cortex. Deficient generation of MMN probably represents an impaired generation and/or faster decay of the sensory memory trace on the basis of left-hemispherically pronounced disturbed sensory processing in male patients with schizophrenia. The magnetoencephalographic results and their relationship to neuropsychological and psychopathological aspects are discussed with respect to methodological considerations.

453 AUDITORY ODDBALL RESPONSES EPISODE SCHIZOPHRENIC PATIENTS

IN FIRST

of Psychophysiology

30 (1998)

95-271

U. Isoglu-Alkac’, M. Devrim’, A. Ucok’, A. Tecer’, E. Kiziltan2, N. Ermutlu’, I. Yucesir’ and T. Demiralp’* ‘Electra-Neuro-Physiology Research and Application Center Department of Physiology and ’ Department of Psychiatry, Istanbul University, Istanbul Medical Faculty, Fizyoloji AD, Capa-Istanbul, 34390 Turkey Studies on P3 in schizophrenia reported homogenously widespread amplitude decrease of P3 but contradictory results on the P3 latency. In the present study, N2 and P3 components of the auditory oddball responses recorded from Fz, Cz, Pz, P3 and P4 scalp regions were investigated in twelve lirstepisode schizophrenics and twelve normal control subjects. The patients were diagnosed as having schizophrenia by DSM.II1.R after SCID.1 (Structured Clinical Interview for DSM-III-R, patient form). The stimuli were tones of 80 dB intensity and 50 ms duration. Two types of auditory stimuli, low frequency (1000 Hz) and high frequency (2000 Hz) tones, were applied with regular interstimulus intervals of 1 s. The amplitudes and latencies of the N2 and P3 peaks were tested by a repeated measures ANOVA design. The first-episode schizophrenic patients showed an overall prolongation of N2 (270.86 ms vs. 197.41 ms; F(22,l) = 17.35; p < 0.0004) and P3 latencies (392.39 ms vs. 312.49 ms; F(22,l) = 16.49; p < 0.001) and a decrease of frontal P3 amplitudes compared to controls (F@8,4) = 2.42; p = 0.05, Fz: t = 1.95432 p < 0.06). The N2 amplitude did not differ between groups. In contrast to a widespread P3 amplitude decrease reported in chronic schizophrenics, only frontally localized decrease of P3 amplitude suggests that frontal areas are primarily affected at the onset of the first-schizophrenic episode. Additionally, the prolongations of the P3 and N2 latencies are in line with consistently reported prolonged reaction times in schizophrenia, and suggest slowing of stimulus classification process even in early stages of schizophrenia.

454 PREFRONTAL

AROUSAL

IN ACUTE PSYCHOSIS

M. Valkonen-Korhonen’* , H. Ypplrila2, J. Lehtonen’, J. Partanen2, and J. Karhu2 ‘Department of Psychiatry, University of Kuopio, Post box 1777, 70211 Kuopia, Finland 2Department of Clinical Neurophysiology, University of Kuopio, Finland Novel stimuli activate a distributed network involving prefrontal and posterior association cortex as well as temporal and hippocampal structures. Frontal areas modulate and integrate a variety of cortical functions. Schizophrenia is associated with a reduction in pyramidal and intemeuronal cell populations, and neuropil alterations in the frontal and cingulate corteces have been reported. These abnormalities may alter sensory gating and habituation i.e. the automatic capacity for information processing, and thus induce changes in cognitive function and behaviour.