Altered auditory processing in acutely psychotic never-medicated first-episode patients

Abstract

Individuals with psychosis fail to differentiate external impulses and suffer from distortions of reality testing. Schizophrenia group illnesses are also associated with deficits in working memory and perception. We examined the manifestations of a very early phase of psychotic illness to automatic auditory deviance detection to clarify the basic mechanisms underlying misinterpretations of perception. Methods: Twenty-five never-medicated patients admitted for hospital evaluation of acute psychosis were studied. Fifty-eight EEG channels were recorded during an auditory oddball paradigm. Event-related potentials (ERPs) time-locked to non-attended deviant auditory stimuli were studied in patients and compared with healthy controls. Auditory processing was examined both at the level of the measured biosignals (standard and deviant responses) and with subtraction waveforms. Topographical differences were characterized using global field power (GFP) and minimum norm estimates. Results: The maximum GFP amplitudes and mean amplitudes of the 58 channels within the time windows corresponding to the previously known ‘N2b’, ‘P3a’ and ‘P3b’ components were clearly reduced in patients when compared to healthy controls. However, the groups did not differ during attention-independent automatic processing corresponding to the ‘N1’ and ‘MMN’ components, or with respect to the peak latencies of the GFP maxima. Conclusions: Impairment of the processing of a deviance in simple auditory input in acutely ill drug-naive first-episode psychotic patients only appears in attention-dependent processing after about 250 ms. The alterations in auditory processing differed between stimulus types, suggesting at least two mechanisms underlying the auditory discrimination impairments in acute psychosis. After 250 ms there was a linear and gradually increasing difference in magnitude between the groups in their responses to deviant stimuli, probably related to arousal. In addition, however, there was a striking difference between the groups in the processing of standard stimuli. The early processing was similar in patients and controls, but the striking difference appeared in later processing. The sensory memory deficits associated with psychosis may be explained by an abnormality in sensory model formation rather than by impaired deviant detection.