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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Auditory evoked potentials were recorded using a paired click, conditioning-testing paradigm in 10 schizophrenics and in 10 normal subjects with no family history of psychotic disorder. The paradigm is used to demonstrate central nervous system gating of responsiveness to auditory stimuli by examining the extent to which the response to the conditioning stimulus diminishes the response to a test stimulus occurring a short time later. Recordings were made at conditioning-testing intervals of 500 msec, 150 msec, and 75 msec to determine subjects' gating of responsiveness to stimuli repeated at various intervals. The schizophrenics had conditioning-testing ratios indicative of poor gating of the auditory P50 wave at the 500-msec and 150-msec intervals, but most patients had good sensory gating at the 75-msec interval. Normal subjects showed good sensory gating at all three intervals. Results suggest that although sensory gating mechanisms responsible for changes in neuronal response at longer intervals are chronically defective in schizophrenics, other gating mechanisms functioning at shorter intervals appear to be intact and function well in most patients. The results may lead to increased specification of the neurobiological basis of sensory abnormalities in schizophrenia.
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PMID:Sensory gating in schizophrenics and normal controls: effects of changing stimulation interval. 292 Jan 90

Gating of auditory sensory responsiveness was examined in 75 psychiatric inpatients using a conditioning-testing paradigm with the P50 wave of the auditory evoked response, in which pairs of stimuli are presented to the subject. In previous studies, most schizophrenics did not decrement the second response to the extent seen in normals. Acutely ill patients, who were representative of patients admitted to a public university teaching service and a proprietary hospital, were used to examine the extent to which diminished sensory gating is found in diagnoses other than schizophrenia. About half of these patients showed diminished sensory gating that correlated with measures of severity of illness. The data, taken together with that from other studies using this paradigm, suggest that diminished sensory gating, like several other psychophysiological abnormalities, is a trait deficit in schizophrenia, but a state deficit in many other mental illnesses.
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PMID:Neurophysiological assessment of sensory gating in psychiatric inpatients: comparison between schizophrenia and other diagnoses. 358 Apr 35

A deficit in inhibitory gating of auditory evoked responses was examined in 15 schizophrenic patients, their first-degree relatives, and normal subjects, using a conditioning-testing paradigm with the P50 wave of the auditory evoked response. This paradigm demonstrates inhibition by presenting paired stimuli to the subject; the P50 wave evoked by the second stimulus is reduced because of inhibitory mechanisms activated during the response to the first stimulus. In normal subjects, the mean amplitude of the second P50 response was reduced to less than 20%. In the schizophrenics, the mean amplitude of the second response was more than 85% of the first, a result that replicates our previous finding of a deficit in inhibition in schizophrenia. Approximately half the first-degree relatives, generally including at least one parent, had a similar deficit. Presence of this deficit in the parents was associated with a family history of schizophrenia. Family members with this deficit also had significantly higher scores on several scales of the Minnesota Multiphasic Personality Inventory than did family members without the deficit. Despite the deficit in inhibition, other characteristics of the P50 wave were normal in the relatives, in contrast to unmedicated schizophrenics, who showed additional abnormalities in wave latency and amplitude.
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PMID:Deficits in sensory gating in schizophrenic patients and their relatives. Evidence obtained with auditory evoked responses. 673 21

Diminished suppression of the P50 response to repeated auditory stimuli is one example of a deficit in elementary sensory processing in schizophrenia. Normal subjects suppress the response to the second of two paired auditory stimuli. Although normal suppression is occasionally observed in schizophrenic patients, it generally disappears with subsequent testing. We have previously reported that slow wave sleep (SWS) transiently normalized suppression in schizophrenic patients and that the degree of suppression was positively correlated with the depth of SWS attained. We hypothesized that schizophrenic patients may have a defect that causes a neuronal mechanism to fail after brief use and that its activity can be restored by a transient period of inactivity. The present study examined whether this effect of sleep in schizophrenic patients is specific to SWS or is due to nonspecific factors involved in any period of unconsciousness. After baseline recordings, 10 schizophrenic subjects were allowed a period of sleep until they attained rapid-eye-movement (REM) sleep. They were awakened at the end of the REM period, and postsleep recordings were obtained. REM-stage sleep failed to normalize suppression in any of the schizophrenic subjects. P50 suppression was subsequently assessed after a period of non-REM (NREM) sleep. Subjects who reached stage-2 sleep did demonstrate a transient correction in auditory gating. These results replicate our previous findings and suggest that the sleep effect is specific to NREM sleep. A desensitized nicotinic receptor that is resensitized during cholinergic inactivity in NREM sleep is one possible mechanism for this effect.
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PMID:Normalization of the auditory P50 gating deficit of schizophrenic patients after non-REM but not REM sleep. 756 49

To replicate the findings of a sensory gating deficit in schizophrenia, and to determine if normals and schizophrenics are equally affected by cognitively mediated task-relevant factors, 10 healthy and 10 schizophrenic young adults were tested in two experimental conditions. In the first condition a pair of identical auditory clicks (conditioning stimulus and testing stimulus) was administered at an inter-stimulus interval fixed at 500 msec. In the second condition, the second stimulus could have one of two possible frequencies, and subjects were required to count the presentations of one and ignore the other. Subjects also completed two matched blocks of single stimulus (i.e. testing only) presentations to provide a baseline for assessing the effect of the warning stimulus on the evoked response. We found, in disagreement with previous results, that in schizophrenics, passive exposure to the paired stimuli produced a suppression of P50 amplitude to the second stimulus, that did not differ from that found in normals. However, under paired presentation conditions, testing P50 amplitude in normals, but not in schizophrenics, was enhanced by the count/no-count task introduction. We suggest that both groups are equally susceptible to the task independent (possibly "hard-wired") suppressing effect of a conditioning stimulus presentation. However, only normals seem to exhibit a task-dependent effect, whose action at the P50 range demands the presence of a warning (conditioning) stimulus. Inspection of the full epoch data showed an apparently lesser task-related, warning dependent modulation of early ERP activity in schizophrenics, and a normal (or even supernormal) modulation of late activity. We consider this to support a notion of an early processing deficit in schizophrenia.
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PMID:Sensory gating deviance in schizophrenia in the context of task related effects. 787 34

Concept of defective filtering mechanisms, resulting in sensory overload, is one of many hypotheses of pathogenesis of schizophrenia. Clinical observation finds confirmation in laboratory tests, measuring the blocking of response to a stimulus received immediately after a preceding stimulus. In schizophrenia, sensorimotor gating (suppression of efferent component of startle reflex) and gating of evoked response P50 AEP are shown to be deficient. The independence of this defect from the clinical phase of the illness and the examination of the relatives, imply a genetically conditioned predisposition. Searching for responsible structures gave rise to the hippocampal model of schizophrenia. Investigations of neurotransmitter systems disturbances have not given any explicit results yet. Results imply a necessity for the verification and extension of former studies.
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PMID:[Sensory overload and schizophrenia: sensory gating as a measure of dysfunction of stimuli filtration]. 791 84

Alterations in dopamine neurotransmission have been strongly implicated in the pathogenesis of schizophrenia for nearly 2 decades. Recently, the genes for five dopamine receptors have been cloned and characterized, and genetic and physical map information has become available. Using these five loci as candidate genes, we have tested for genetic linkage to schizophrenia in nine multigenerational families which include multiple affected individuals. In addition to testing conservative disease models, we have used a neurophysiological indicator variable, the P50 auditory evoked response. Deficits in gating of the P50 response have been shown to segregate with schizophrenia in this sample and may identify carriers of gene(s) predisposing for schizophrenia. Linkage results were consistently negative, indicating that a defect at any of the actual receptor sites is unlikely to be a major contributor to schizophrenia in the nine families studied.
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PMID:Linkage analysis of schizophrenia with five dopamine receptor genes in nine pedigrees. 809 67

Diminished suppression of the P50 component of the evoked potential following repeated auditory stimuli is one example of a deficit in elementary sensory processing in schizophrenia. Normal subjects suppress the P50 evoked potential to the second of two paired auditory stimuli. Although normal P50 suppression is occasionally observed in schizophrenic patients, it generally disappears with subsequent testing. The object of this experiment was to determine conditions for the reproducible normalization of P50 suppression in schizophrenic patients. After baseline recordings, 12 schizophrenic subjects were allowed to sleep for 10 minutes. The depth of sleep obtained was assessed by electroencephalography (EEG). Normalization of P50 suppression was observed for approximately 3 minutes in all subjects who entered slow wave sleep, but not in those whose EEG records remained desynchronized. Some change was even observed in subjects who had only persistent alpha waves. The amount of normalization was correlated with the deepest stage of sleep reached. Normal control subjects did not show this phenomenon but instead had a transient decrease in sensory gating after waking from sleep. The results suggest that schizophrenic patients may have a defect that causes a neuronal mechanism critical to sensory gating to fail after brief use, although its activity can be transiently restored by a short period of inactivity. A rapidly desensitized neurotransmitter receptor is one possible mechanism of such an effect.
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PMID:Normalization of auditory sensory gating in schizophrenic patients after a brief period for sleep. 814 Jan 80

Decreased amplitude of the P50 component of the averaged evoked potential has been reported in schizophrenic patients. In an attempt to determine the relationship of this decrease to subtype diagnosis, we compared P50 amplitudes in 24 neuroleptic-free schizophrenic patients with paranoid (n = 13) versus nonparanoid (n = 11) subtype diagnoses. Eleven normal subjects and 11 cocaine users served as control groups. The schizophrenic patients were studied again after they had been treated with neuroleptics for 2 weeks. The control groups were studied again at least 2 weeks later. At baseline, the nonparanoid patients had significantly lower P50 amplitudes than did the normal subjects. The paranoid patients did not differ from the normal control subjects. The cocaine users had significantly decreased P50 amplitudes as compared with the normal control subjects. Neuroleptic treatment had no effect on P50 amplitudes in the paranoid patients but normalized amplitudes in the nonparanoid patients. The data suggest that P50 measurements may be useful in identifying subtypes of schizophrenia.
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PMID:The P50 component of the auditory evoked potential and subtypes of schizophrenia. 837 62

Diminished gating of the auditory evoked response to repeated stimuli is a psychophysiological defect associated with schizophrenia and several other psychiatric illnesses. The P50 wave of the auditory evoked response to the second of paired stimuli is decreased in most normal subjects, whereas many psychotic subjects show significantly less decrement. The aim of this experiment was to test whether the cold-pressor test, which causes transient distress and pain accompanied by increased sympathetic activity, also causes a transient impairment in P50 auditory sensory gating in normal control subjects. Ten normal control subjects with normal gating of the P50 response immersed their hands in an ice water bath for 2 min. This cold-pressor test diminished P50 auditory gating in nine of these subjects, although the degree of impairment was highly variable among subjects. The impairment in gating was transient, with partial resolution by 30 min. The cold-pressor test was subjectively viewed as painful and also caused blood pressure to increase. Thus, a transient stressor can impair P50 auditory gating in some subjects.
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PMID:Transient impairment in P50 auditory sensory gating induced by a cold-pressor test. 838 6


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