Article

Sensory Gating in Schizophrenia: P50 and N100 Gating in Antipsychotic-Free Subjects at Risk, First-Episode, and Chronic Patients

Department of Psychiatry and Psychotherapy, University of Cologne, Cologne, Germany.
Biological psychiatry (Impact Factor: 9.47). 05/2008; 64(5):376-84. DOI: 10.1016/j.biopsych.2008.02.006
Source: PubMed

ABSTRACT Abnormal sensory gating in schizophrenia has frequently been reported; however, only limited data on unmedicated patients and patients at risk to develop a psychosis have, as yet, been available.
P50 and N100 suppression were assessed with an auditory double-click paradigm in five groups: 18 at-risk subjects who did not develop a full psychosis within the follow-up period of 2 years, 21 truly prodromal subjects who developed frank psychosis within the follow-up period, 46 antipsychotic-naïve subjects with first-episode schizophrenia, 20 antipsychotic-free subjects with chronic schizophrenia, and 46 healthy control subjects.
P50 and N100 suppression indices differed significantly between groups and were lowest in chronic schizophrenia patients. Compared with healthy control subjects, P50 suppression was significantly impaired in at-risk subjects, truly prodromal and first-episode patients (stimulus 2 [S2]/stimulus 1 [S1] P50 amplitude ratio), and chronic schizophrenia patients (difference and ratio), and N100 suppression was significantly reduced in truly prodromal and first-episode patients (S1-S2 difference) and in chronic schizophrenia patients (difference and ratio) but not at-risk subjects. At-risk subjects with and without conversion to psychosis did not significantly differ on any test parameter.
Sensory gating is already impaired in early stages of schizophrenia, though this is most prominent in chronic stages. Future studies will have to clarify the type and impact of variables modifying sensory gating disturbances, such as illness progression and genetic load. Furthermore, the meaning and nature of differences between P50 and N100 suppression need further elucidation.

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    • "e l s e v i e r . c o m / l o c a t e / s c h r e s exhibit abnormalities in several characteristics of the AEP sensorial gating (For review see Patterson et al., 2008; Brockhaus-Dumke et al., 2008; Myles-Worsley et al., 2004). These alterations in sensory gating in schizophrenics are similar to those reported in rats with NVHL (Vohs et al., 2009; Swerdlow et al., 2012). "
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    • "exhibit abnormalities in several characteristics of the AEP sensorial gating (For review see Patterson et al., 2008; Brockhaus-Dumke et al., 2008; Myles-Worsley et al., 2004). These alterations in sensory gating in schizophrenics are similar to those reported in rats with NVHL (Vohs et al., 2009; Swerdlow et al., 2012). "
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    ABSTRACT: The neonatal ventral hippocampal lesion (NVHL) is an established neurodevelopmental ratmodel of schizophrenia. Rats with NVHL exhibit several behavioral, molecular and physiological abnormalities that are similar to those found in schizophrenics. Schizophrenia is a severe psychiatric illness characterized by profound disturbances of mental functions including neurophysiological deficits in brain information processing. These déficits can be assessed by auditory evoked potentials (AEPs), where schizophrenics exhibit abnormalities in amplitude, duration and latency of such AEPs. The aim of the present study was to compare the density of cells in the temporal cerebral cortex and the N40-AEP of adult NVHL rats versus adult sham rats.We found that rats with NVHL exhibit significant lower amplitude of the N40-AEP and a significant lower number of cells in bilateral regions of the temporal cerebral cortex compared to sham rats. Because the AEP recordings were obtained from anesthetized rats, we suggest that NVHL leads to inappropriate innervation in thalamic-cortical pathways in the adult rat, leading to altered function of cortical networks involved in processing of primary auditory information
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    • "According to recent findings, sensory gating abnormalities represent early clinical symptoms of schizophrenia, typically characterized as a decreased ability of the brain to inhibit various responses to insignificant stimuli.1,5,7,13–18 Typical symptoms manifest as hypervigilance and difficulty in focusing attention, most likely due to disturbances of inhibitory neuronal activity in the hippocampus related to deficits of nicotinic cholinergic modulation.7,17,19,20 "
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    ABSTRACT: Sensory gating disturbances in schizophrenia are often described as an inability to filter redundant sensory stimuli that typically manifest as inability to gate neuronal responses related to the P50 wave, characterizing a decreased ability of the brain to inhibit various responses to insignificant stimuli. It implicates various deficits of perceptual and attentional functions, and this inability to inhibit, or "gate", irrelevant sensory inputs leads to sensory and information overload that also may result in neuronal hyperexcitability related to disturbances of habituation mechanisms. These findings seem to be particularly important in the context of modern electrophysiological and neuroimaging data suggesting that the filtering deficits in schizophrenia are likely related to deficits in the integrity of connections between various brain areas. As a consequence, this brain disintegration produces disconnection of information, disrupted binding, and disintegration of consciousness that in terms of modern neuroscience could connect original Bleuler's concept of "split mind" with research of neural information integration.
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