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

In this study we performed quantitative EEG analyses in 12 drug-naive patients who fulfilled DSM-IIIR criteria for schizophrenia and in a group of 12 healthy subjects. The schizophrenic patients were found to have slower activity (delta and theta) than the controls. These differences were most marked in the frontal region for delta band and in the occipital region for theta band. The schizophrenic patients also had more beta 1 activity, particularly in the occipital leads. Conversely, they had less alpha 2 activity over all regions examined. Our findings indicate cerebral dysfunction in schizophrenia and are in line with the hypothesis of hypofrontality in this disorder.
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PMID:[Quantitative analysis of EEG background activity in drug-naive schizophrenic patients]. 806 45

Neuroleptic-induced tardive dyskinesia (TD) continues to be a serious problem in the psychopharmacology of schizophrenia. The overall mean prevalence of TD among chronically neuroleptic-treated patients is approximately 24 percent. The annual incidence in younger adults is 4 to 5 percent. Aging is a major risk factor for TD. Our ongoing prospective study suggests that the annual incidence in patients over age 45 is over 30 percent. Other likely risk factors include female gender, mood disorders, "organic" brain dysfunction or damage, diabetes mellitus, and early extrapyramidal side effects. Metoclopramide, a D2-receptor blocker commonly used in non-psychiatric medical patients, can also produce persistent TD. TD can best be assessed for research purposes by a combination of subjective and objective methods. In recent years, several instrumental procedures have been developed to objectively quantify various abnormal movements. The advantages and limitations of the traditional rating scales and the newer instrumental approaches are discussed. The course of TD is variable but often not progressive. The early theory that striatal dopamine receptor supersensitivity causes TD has now given way to the hypothesis of multiple neurotransmitter system involvement. Several animal studies have reported striatal neuronal damage with prolonged neuroleptic treatment, although its relevance to TD remains unclear. Treatments for TD, other than neuroleptic withdrawal, are still experimental.
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PMID:Tardive dyskinesia. 810 Jun 43

We examined the frequency characteristics of the electroencephalogram (EEG) in 102 schizophrenic patients (44 first-episode and 58 chronic patients) and 102 normal comparison subjects. EEGs of schizophrenic patients had more delta (1-3 Hz) and theta (3.125-8 Hz) activity and less alpha (8.125-13 Hz) activity than normal comparison subjects. There were no significant differences in the EEG frequency composition of first-episode and chronic patients. Because first-episode and chronic patients were characterized by different disorder durations and treatment histories, the similarity of their EEGs suggests that EEG abnormalities are stable characteristics of schizophrenia and are not treatment-related epiphenomena. A principal components analysis of EEG power bands identified an augmented low frequency-diminished alpha component and a beta component. Schizophrenic patients had significantly higher scores on the augmented low frequency-diminished alpha component than did normal comparison subjects, and there was no significant group difference in scores on the beta component. The findings of this investigation suggest that EEG abnormalities in schizophrenia reflect aspects of brain dysfunction.
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PMID:Resting EEG in first-episode and chronic schizophrenia. 814 53

Impaired attention is commonly observed among schizophrenia patients and those at genetic risk for the disease. This article reviews over 40 studies that used various versions of the Continuous Performance Test (CPT) as the primary measure of attention. These studies of normal subjects, affected patients, and various at-risk populations demonstrate that the CPT is a psychometrically sound procedure that consistently discriminates affected patients from controls. Sufficiently difficult versions of this task have also demonstrated that impaired attention is (1) evident in schizophrenia patients regardless of clinical state, (2) detectable before illness onset, (3) apparently heritable, (4) specific--in terms of distinct profile patterns--to schizophrenia, and (5) predictive of later behavioral disturbances in susceptible individuals. Selected studies are also discussed that examine the role of attentional deficit in the pathophysiology of schizophrenia and its potential consequences for personality development. With respect to pathophysiology, preliminary data suggest that subcortical brain dysfunction has an important role in the attentional deficits tapped by the CPT. With respect to personality, an association between chronically impaired attention and deficient social skills has been found. It is concluded that the CPT is a cost-effective measure of the attentional deficit commonly found in affected schizophrenia subjects and those at risk for the disorder, and is therefore a potentially valuable screening device for preventive intervention programs.
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PMID:Impaired attention, genetics, and the pathophysiology of schizophrenia. 819 20

Psychotic symptoms are prominent in schizophrenia and a frequent neuropsychiatric manifestation of Alzheimer's disease (AD), occurring in approximately 50% of patients affected. The shared psychiatric symptoms suggest common cerebral pathophysiologies. Radiologic and pathologic findings indicate a predilection toward limbic involvement, with structural and atrophic changes of the medical temporal region predominating in both disorders. Neurochemical alterations affecting the dopaminergic/cholinergic axis appear to be central to both schizophrenia and AD. The basic pathologies of the two disorders are different, but they have similarities in the pattern of regional brain dysfunction, biochemical dysfunction, and symptomatology. We represent a selective review of these similarities. Insights drawn from these observations enrich the understanding of each disorder.
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PMID:Schizophrenia and Alzheimer's disease: clinical and pathophysiologic analogies. 873 86

This study compared patients across 5 psychiatric diagnostic groups: Depression, Mania, Schizophrenia, Schizoaffective Disorder, and Psychosis NOS, all of whom are psychotic. Differences in overall cognitive profiles and in dysfunctional memory mechanisms, as well as the effect of psychosis on cognitive functioning were explored using the Neurobehavioral Cognitive Status Examination (NCSE), a brief screening instrument. Results indicated pronounced deficit in memory and abstract reasoning associated with schizophrenic illness, which is not secondary to psychosis and points to localized brain dysfunction. Both encoding and postencoding memory mechanisms were affected. Results support a hypothesis of progressive dysfunction associated with the severity and chronicity of the illness. Implications of findings in aiding diagnostic determination, patient management and rehabilitation are discussed.
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PMID:A comparison of cognitive profiles in schizophrenia and other psychiatric disorders. 877 46

In large families with affective illness, identification of a biological variable is needed that reflects brain dysfunction at an earlier point than symptom development. Eye movement disorder, a possible vulnerability marker in schizophrenia, is less clearly associated with affective illness, although a subgroup of affective disorders shows smooth-pursuit eye movement disorder. The auditory P300 event-related potential may be a useful marker for risk to schizophrenia, but a role in bipolar illness is less certain. The distribution of these two biological variables and their association with symptoms in two multiply affected bipolar families is described. In a single, five-generation family identified for linkage studies through two bipolar I (BPI) probands, 128 members (including 20 spouses) were interviewed. The 108 related individuals had diagnoses of BPI (7), bipolar II (2), cyclothymia (3), or major depressive disorder (19). Eight others had generalised anxiety (1), minor depression (5), intermittent depression (1), or alcoholism (1). Sixty-nine subjects had no psychiatric diagnosis. P300 latency (81) and eye tracking (71) were recorded from a subgroup of relatives within the pedigree. Eye tracking was abnormal in 11 of 71 relatives (15.5%) and was bimodally distributed. In these 11 relatives, clinical diagnoses included minor depression (1), alcoholism (1) and generalised anxiety disorder (1). P300 latency was normally distributed and did not differ from controls. In a second family in which five of seven siblings have BPI illness, P300 latency and eye movement disorder were found in affected relatives and in some unaffected offspring. In these large families, clinical diagnoses of general anxiety, alcoholism and minor depression, when associated with eye tracking abnormality, may be considered alternative clinical manifestations of the same trait that in other relatives is expressed as bipolar illness.
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PMID:Implications of comorbidity for genetic studies of bipolar disorder: P300 and eye tracking as biological markers for illness. 886 53

In vivo imaging and post-mortem neuropathology studies have detected a variety of abnormalities in brain function and structure in patients with schizophrenia. Current models of the neural mechanisms involved focus primarily on frontal and medial temporal lobe structures and their interconnections, because deficits in these systems are relatively prominent against a background of generalized cerebral dysfunction, and because individuals with acquired lesions in these areas show many of the symptoms characteristic of schizophrenia. Family and twin studies have demonstrated similar abnormalities in some of the unaffected biological relatives of schizophrenics, indicating that some of these neuropathological changes are mediated in part by genetic predisposition to the disorder. Further, obstetric complications are associated with an increased risk for phenotypic schizophrenia and with greater severity of its neuropathological features in individuals at elevated genetic risk. These latter findings, combined with evidence of heterotopic displacement of neurones in temporolimbic and frontal regions and evidence that cognitive dysfunction during childhood precedes schizophrenia, imply that at least some of these brain abnormalities are neuro-developmental in origin. The view emerging from this work is that schizophrenia is a brain disease the neuropathological features of which result at least in part from the unique and interacting influences of genetic factors and adverse obstetric events in utero.
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PMID:Abnormalities of brain structure and function in schizophrenia: implications for aetiology and pathophysiology. 901 12

In order to examine the neuropsychological profile of schizotypal personality disorder (SPD), we studied a wide array of cognitive functions in 10 right-handed men who met DSM-III-R criteria for SPD and 10 matched normal controls. Cognitive functions included abstraction, verbal and spatial intelligence, memory and learning, language, attention, and motor skills. Neuropsychological profiles were constructed by standardizing test scores based on the means and standard deviations of the normal control group. SPD subjects showed significant decrements in performance on the California Verbal Learning Test, a word-list learning measure which requires semantic clustering for more efficient performance, and on the Wisconsin Card Sort Test, a measure requiring concept formation, abstraction, and mental flexibility. These results suggest possible areas of specific neuropsychological dysfunction in SPD, and are consistent with current hypotheses of left-temporal and prefrontal brain dysfunction in schizophrenia.
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PMID:Neuropsychological dysfunction in schizotypal personality disorder: a profile analysis. 904 85

Hallucinations in schizophrenia represent an important clinical problem, an interesting neuropsychological enigma, and a significant challenge for neuroscientific research. Functional neuroimaging techniques allow the in vivo, systems-level study of brain dysfunction underlying this debilitating symptom. Clinical and scientific vantage points that can inform the design and interpretation of functional neuroimaging studies of schizophrenic hallucinations are outlined. These include considerations of the phenomenology of hallucinations, the relationship of hallucinations to other symptoms of schizophrenia, and the neuropsychological functions that are thought to be disrupted in hallucinations. They also include the anatomical and chemical brain systems in which abnormalities are implicated in schizophrenia, the neurologic conditions in which hallucinations may occur, the neurochemical contexts that are associated with hallucinations, and the methodologic details of the functional neuroimaging techniques employed. Bottom-up and top-down functional neuroimaging strategies for the investigation of schizophrenic hallucinations with positron emission tomography (PET), single photon emission computed tomography (SPECT) and functional magnetic resonance imaging (fMRI) are reviewed. Bottom-up approaches start with or measure the biology associated with hallucinations. Top-down approaches start from the specific neuropsychological dysfunctions thought to be associated with hallucinations. The distributed brain regions, systems and functions implicated in schizophrenic hallucination formation are then discussed in the context of an integration of bottom-up and top-down approaches. Focus is placed upon abnormalities in the functions of, and interactions among, auditory-linguistic association cortices, caudal and rostral limbic/paralimbic systems, prefrontal cortices, ventral striatum and (non-specific projection and associative) thalamic nuclei, as well as upon the glutamatergic, GABAergic and ventral tegmental dopaminergic modulation of these systems.
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PMID:Functional neuroimaging of hallucinations in schizophrenia: toward an integration of bottom-up and top-down approaches. 915 29


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