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

We have performed an epidemiological study concerning tardive dyskinesia on a sample of 332 chronic schizophrenic patients (142 males and 190 females, mean age 48.6 years, mean duration of neuroleptic treatment 14.5 years). We could conclude that the age of patients at the time of assessment procedures is the most important variable. The prevalence of tardive dyskinesia was significantly higher in the older population. The significance of an insidious beginning of the illness might be only secondary to the highly significant role of the age. Other factors, such as sex, type of schizophrenia, initial syndrome, present psychic state, organic syndromes and neuroleptic-induced extrapyramidal syndrome, do not seen to play a role in the prevalence of tardive dyskinesia.
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PMID:Epidemiology of tardive dyskinesia Part I. 0 94

Tardive dyskinesia has been regarded as a long-term complication of neuroleptic administration to patients with the diagnosis of schizophrenia. However, nine of the first fourteen patients evaluated for an investigation of tardive dyskinesia met diagnostic criteria for depression. Neuroleptics produce blockade of post-synaptic dopaminergic receptors. Tardive dyskinesia occurs when neuroleptics are discontinued, and is regarded as a manifestation of super-sensitive post-synaptic dopaminergic receptors. Tardive dyskinesia occurs when neuroleptics are discontinued, and is regarded as a manifestation of super-sensitive post-synaptic dopaminergic receptors. Chronically decreased neurotransmission in the synapse of a patient with depression may contribute to the development of a super-sensitive receptor and could explain the high proportion of patients with depression seen in this sample of patients with tardive dyskinesia.
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PMID:Tardive dyskinesia and depressive illness. 1 Jun 3

Side effects of high and low potency neuroleptics are contrasted. Low potency drugs are more likely to cause central, autonomic and peripheral side effects of all types with the exception of extrapyramidal symptoms. The tendency to produce tardive dyskinesia cannot be compared as relevant data do not currently exist. Greater affinity for the dopamine receptor and twenty to seventy-fold greater milligram and molar potency are advanced as arguments for greater specificity of high potency drugs in the treatment of psychoses. It is proposed that the high potency neuroleptics might be considered the drugs of choice in the treatment of schizophrenia and schizophreniform psychoses.
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PMID:A pharmacological and theoretical comparison of high and low potency neuroleptics. 2 19

Research on psychoactive drugs: antianxiety, antidepressant, and antipsychotic was reviewed. The drug families and their usual side effects were described. Proliferation of drug use, polypharmacy, and tardive dyskinesia were seen as areas of concern; advances in biological explanations of schizophrenia and manic-depressive disorders, and increasing knowledge about the brain's neurotransmitters brightened the investigative efforts.
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PMID:Psychologists and psychoactive drugs. 3 17

Oculomotor signs were evaluated in 172 psychiatric patients. Schizophrenic patients demonstrated a significantly higher incidence of staring, pursuit breaks, and lateral glances than did controls or other psychiatric patients. Oculomotor signs may help to differentiate schizophrenia from affective and nonpsychotic disorders. Patients with tardive dyskinesia and patients treated with tricyclic antidepressants demonstrated a significant elevation in mean blink rate. Elevated blink rates may be on early indicator of tardive dyskinesia.
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PMID:Oculomotor signs in a psychiatric population: a preliminary report. 3 48

It has been proposed that the etiologies of tardive dyskinesia and Huntington's chorea and of some forms of schizophrenia and the affective disorders involve a cholinergic imbalance with respect to a second neurotransmitter. This relative over- or underactivity of the cholinergic system could result from altered synthesis, storage, release, degradation, or reuptake or from a variety of receptor interactions. Under these hypotheses, clinical symptoms would reflect both the brain region in which the imbalance occurs and the neurotransmitter with which acetylcholine is interacting. Effective treatments could involve the correction of this hypothetical imbalance by changing the relative availability of either one or both of the neurotransmitters. Both precursor loading with choline or dimethylaminoethanol and cholinesterase inhibition may be useful in evaluating the effects of increased cholinergic activity in these disease states; the relative merits of these strategies are discussed.
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PMID:Cholinergic imbalance hypotheses of psychoses and movement disorders: strategies for evaluation. 13 84

The hypotheses of relative cholinergic underactivity in Huntington's disease, tardive dyskinesia, mania, and schizophrenia were pharmacologically investigated, using physostigmine and choline chloride. Intravenous physostigmine improved the involuntary movements of all of four patients with tardive dyskinesia and three of six patients with Huntington's disease. Physostigmine infusion also decreased manic symptoms in six of nine patients with mania, but had no beneficial effects in three patients with schizophrenia. Precursorloading with choline chloride may increase brain acetylcholine levels and central cholinergic activity. In patients with movement disorders a transient improvement during physostigmine infusion predicted a positive response to a trial of oral choline chloride. One manic patient may have been improved by choline chloride, however choline chloride did not improve symptoms in four of six schizophrenix patients. Chronic treatment with oral choline chloride increases plasma levels of choline during administration and for approximately 48 hr after discontinuation of treatment. A single 5-g dose of choline chloride also transiently raises plasma choline levels. These results with physostigmine support the hypotheses of cholinergic underactivity in Huntington's disease, tardive dyskinesia, and mania. Agents which might chronically increase cholinergic activity such as choline chloride should be further tested in these disorders.
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PMID:Pharmacological investigations of the cholinergic imbalance hypotheses of movement disorders and psychosis. 14 24

Following 6 years of continuous chlorpromazine therapy for schizophrenia, a young woman developed multifocal tics and vocalizations characteristic of Tourette syndrome. The symptoms first appeared when chlorpromazine was withdrawn. They were permanent, although partially ameliorated by chronic haloperidol therapy. Because of her age and past history, these symptoms were attributed to chronic neuroleptic therapy analogous to neuroleptic-induced tardive dyskinesia, rather than to Tourette syndrome per se. These symptoms suggest that chronic receptor-site blockade can result in hypersensitivity of dopamine receptor sites, and that this may play a role in the pathophysiology of Gilles de la Tourette syndrome. This is the first evidence that hypersensitivity of dopamine receptors is involved in the pathophysiology of Tourette syndrome.
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PMID:Gilles de la Tourette syndrome after long-term chlorpromazine therapy. 28 1

Although many scales to measure tardive dyskinesia have been developed, none has been widely accepted. The authors used the Abnormal Involuntary Movement Scale (AIMS) to evaluate a group of 293 inpatients who had been given a primary or secondary diagnosis of schizophrenia. They found a tardive dyskinesia prevalence of 30% using a criterion rating of 3 (moderate symptoms) or more on the AIMS. The prevalence figure declined as the criterion became more severe. They also found that women had a much higher prevalence of the disorder only when more severe symptoms were used as the criterion. They conclude that the AIMS is a reliable instrument for assessing tardive dyskinesia.
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PMID:A systematic investigation of tardive dyskinesia in inpatients. 45 54

Apomorphine, a direct-acting dopamine agonist, stimulates release of growth hormone (hGH) and suppresses release of prolactin (PRL) from the anterior pituitary. Previous studies comparing the magnitude of these responses in schizophrenics and controls suggest that many acute (and some chronic) schizophrenics have exaggerated hGH responses; many chronic schizophrenics (and patients with tardive dyskinesia) have blunted hGH responses to apomorphine, and possibly blunted PRL responses. The present studies extend and confirm these findings in chronic schizophrenics; in addition, several studies were undertaken to further characterize these apomorphine-induced endocrine responses. Studies in which apomorphine was given on 2 or 3 separate occasions to each of five subjects indicate that the hGH response is a highly reproducible individual index, but PRL suppression is a less satisfactory measure. hGH responses to apomorphine were consistently antagonized by pretreatment with haloperidol, supporting the concept that the hGH-releasing effect of apomorphine is mediated by its action on dopamine receptors. Cyproheptadine pretreatment was associated with erratic increases or decreases in the hGH response to apomorphine, but did not alter PRL levels or apomorphine-induced PRL suppression. The relationship of these findings to biological hypotheses of schizophrenia and to neuroleptic-induced receptor changes is discussed.
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PMID:Neuroendocrine effects of apomorphine: characterization of response patterns and application to schizophrenia research. 54 Feb 9


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