Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In human beings, amphetamine can induce both schizophreniform psychosis and oral-facial dyskinesia resembling tardive dyskinesia, while neuroleptic agents reduce the manifestations of both conditions. This suggests that such psychosis and movement disorder may occur by the same or very similar mechanisms. It is thought that tardive dyskinesia may result from neuroleptic-induced denervation hypersensitivity to dopamine. The author cites evidence suggesting that amphetamine may act on dopaminergic pathways in the CNS to produce a denervation hypersensitivity like that caused by neuroleptic agents. Clinical evidence compatible with a denervation hypersensitivity hypothesis of schizophrenia is then discussed.
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PMID:Schizophrenia and tardive dyskinesia: is schizophrenia also a "denervation hypersensitivity"? 90 2

Investigations aimed at identifying the clinical characteristics that discriminate tardive dyskinesia (TD) from non-TD patients have yielded disparate findings. We have suggested, based on pharmacological and neuroradiological studies, that TD in schizophrenia may be a covariate of positive symptoms while drug-induced parkinsonism (DIP) may relate to negative symptoms. To investigate this hypothesis, we examined in 47 institutionalized schizophrenic patients the relationship of TD and DIP with psychopathology clusters rated on the Positive and Negative Syndrome Scale. We found that involuntary movements of TD were significantly associated with the activation cluster (p < .01), whereas DIP was significantly associated with the anergia cluster (p < .01). These findings thus support the position that TD is a specific facet of the positive syndrome in schizophrenia, while DIP is a specific feature of the negative syndrome. Clinically, the data suggest that schizophrenic patients with predominant positive symptoms may be at increased risk for TD, while those with prominent negative features could be at increased risk for DIP. In analogy with the positive/negative dichotomy, we propose that TD could be regarded as a "positive," while DIP as a "negative" movement disorder.
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PMID:"Positive" and "negative" movement disorders in schizophrenia. 130 14

Free radicals are reactive chemical species with an unpaired electron that are produced through a variety of physiologic and pathologic processes. Free radicals have been implicated in a variety of neuropsychiatric conditions, many of which are marked by the gradual development of psychopathologic symptoms and movement disorder. There is evidence that radical-induced damage may be important in Parkinson's disease, tardive dyskinesia, metal intoxication syndromes, and Down's syndrome, and possibly also in schizophrenia, Huntington's disease, and Alzheimer's disease. Although some of this evidence is highly speculative, it may offer an avenue for further understanding and treatment of these conditions.
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PMID:Oxygen radicals and neuropsychiatric illness. Some speculations. 184 28

Investigations aimed at identifying the clinical characteristics that discriminate Tardive dyskinesia (TD) from non-TD patients have yielded disparate findings. A number of studies have suggested that TD may be a feature of negative schizophrenia. In particular, the association of TD with high prevalence of "soft" neurological signs, cognitive deficits, and abnormal brain morphology on CT scan in some patients, have led several investigators to propose that negative schizophrenia may be a risk factor for TD. The neurochemical profile of TD, however, is not consistent with this hypothesis. In the following communication, we present our studies which suggest that TD is specific to and an intergral part of positive schizophrenia. The data suggest that schizophrenic patients with predominant positive symptoms may be at increased risk for the development of TD. In addition, we present evidence linking TD with left cerebral hemispheric dysfunction. By comparison, we provide evidence that negative schizophrenia is related to diencephalic damage, and discuss its relevance to negative schizophrenia and to Parkinsonism. We also provide evidence that negative schizophrenia may be a risk factor for acute drug-induced dystonia. Thus, these findings are consistent with our model that negative schizophrenia is a risk factor for Parkinsonism, whereas positive schizophrenia is related to TD. In analogy with the positive/negative dichotomy of schizophrenia, we propose that TD could be considered a "positive," where Parkinsonism a "negative" movement disorder.
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PMID:The relationship of tardive dyskinesia to positive schizophrenia. 193 27

Clinical analyses of 19th century psychiatric practice have been limited by the paucity of available records. Using the richly detailed casebooks of Ticehurst House Asylum, it was possible to study over 600 admissions and assess them using the Research Diagnostic Criteria. Over 80% of cases conformed to recognizable psychiatric illness, mainly schizophrenia and manic-depressive psychosis. Movement disorder, often equivalent to tardive dyskinesia, was noted in nearly one-third of schizophrenics. Violence, masturbation and severe psychopathology were also common features. The implications of these findings in terms of treatment, diagnosis and the rise of the asylum are discussed.
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PMID:Rich and mad in Victorian England. 265 31

A range of cerebral structures was assessed in a series of 172 CT scans of groups of psychiatric patients (including 101 in-patients with chronic schizophrenia) and related to assessments of clinical state and psychological function. Ventricular indices were increased in patients with schizophrenia by comparison with patients with other psychiatric disorders: brain area, which is modestly positively correlated with ventricular indices, was significantly (P less than 0.01) reduced in patients with schizophrenia. Among in-patients with chronic schizophrenia, measures of increased ventricular size were significantly associated with impaired social behaviour and with movement disorder. Memory for famous names in the distant past (a test of remote memory) was the only psychological test which showed significant associations with indices of ventricular size; this suggests that ventricular enlargement and its psychological sequelae occur relatively early in the disease process. Dichotomization of the sample of schizophrenic patients around the mean age of onset revealed that a range of clinical and psychological functions are significantly more abnormal in those with an early age of onset than in those in whom the onset was later. Early onset cases also perform less well academically and occupationally before illness onset. Within the early onset group some significant correlations between cognitive function and brain area were seen. The findings suggest that: (i) some at least of the structural changes in schizophrenia arise at a time when the brain is still developing; and (ii) age of onset is an important determinant of social and intellectual impairment and is relevant to the relationship between brain structure and cognitive deficits.
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PMID:The spectrum of structural brain changes in schizophrenia: age of onset as a predictor of cognitive and clinical impairments and their cerebral correlates. 272 13

Neurochemical indices of dopaminergic function were assessed in basal ganglia of post-mortem brains of control subjects and schizophrenic patients who had been rated in life for the presence of movement disorder and neuroleptic intake. In schizophrenics who had been treated chronically with doses of neuroleptics, concentrations of dopamine D2 receptors were significantly increased above controls, whereas dopamine D1 receptors and dopamine metabolism were unchanged. Increased D2 receptors were also observed in basal ganglia of drug-free patients. Concentrations of dopamine D1 and D2 receptors in schizophrenics with movement disorder. Moreover, no relationship was found between dopamine receptor levels and the severity of movement disorder. Concentrations of the dopamine metabolite homovanillic acid were increased in the putamen and nucleus accumbens in a small number of patients with movement disorder compared with controls or patients without movement disorder. No changes were observed in markers of cholinergic and GABA-containing neurones. The present findings are not consistent with a "dopamine receptor hypersensitivity" concept of movement disorder in schizophrenia.
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PMID:Chemical and structural changes in the brain in patients with movement disorder. 286 Jun 53

The role of neuroleptics in causing the tardive dyskinesia syndrome is controversial. To properly assess the contribution of drugs as the etiology of dyskinesias, the effects of aging, the natural history of psychosis, and characteristics of spontaneous dyskinesias must be considered. Though the buccolinguo-masticatory triad is seen more often in tardive than in spontaneous dyskinesias, these two disorders have many symptoms in common. Other dyskinesias, such as idiopathic and tardive dystonia or tardive Tourette's syndrome and dyskinesias in untreated schizophrenia, are poorly understood. Chronic neuroleptic treatment may only precipitate TD in those already predisposed to develop such movement disorders. Tardive dyskinesia is not a unique movement disorder, but rather spans several clinical and epidemiological phenomena which must be considered in a balanced evaluation of how much of the permanent dyskinesias should be attributed to neuroleptic drugs.
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PMID:Is tardive dyskinesia a unique disorder? 286 Jun 61

The prevalence and distribution of involuntary movements in age-matched chronic schizophrenics treated and not treated with neuroleptics were compared. While exposure to neuroleptic drugs in the past was important, high rates of movement disorder were associated with the severe, untreated illness. Ventricular enlargement correlated with severe movement disorder but not with past neuroleptic exposure. It is suggested that in the context of Schizophrenia neuroleptic drugs may act to promote what are features of the illness for some, and that in the search for predisposing factors illness, as well as treatment variables, is worthy of consideration.
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PMID:Involuntary disorders of movement in chronic schizophrenia--the role of the illness and its treatment. 286 Jun 63

Sydenham's chorea is a movement disorder seen in rheumatic fever with basal ganglia pathology. This disorder has been associated with an increased frequency of psychopathology in both the acute choreiform stage and later in life. We conducted a prospective study of 29 subjects with Sydenham's chorea and 29 age- and sex-matched controls. The total number of psychiatric symptoms 10 years after the initial contact was much greater in the study group than in controls (p less than 0.001). Similarly, schizophrenia was more common in the study group compared to controls (p less than 0.01). Possible neuropathological associations and treatment are discussed.
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PMID:Sydenham's chorea and psychopathology. 318 98


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