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)

Two hundred and thirty-two psychiatric Outpatients on depot fluphenazine decanoate for more than six months were examined for Tardive Dyskinesia (TD), using the AIMS rating scale, and the prevalence rates of TD at different criteria of severity were assessed. The prevalence rates ranged from 7% for patients with severe TD to 45% for patients with any degree of TD. The sex distribution of patients with TD showed no bias but the female patients were significantly older than the male patients. Increases in prevalence rates of TD were associated with the combination of an anticholinergic anti-Parkinsonian drug with the depot neuroleptic, and with the concomitant use of an oral neuroleptic with the depot preparation. Implications of these findings for the long-term management of schizophrenia are discussed.
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PMID:Tardive dyskinesia in outpatients on depot phenothiazine. 257 66

The demography, course of illness, cognitive dysfunction and neurological consequences of long term treatment of 11 family pairs with long history of chronic schizophrenic illness were studied. There was concordance for the presence of tardive dyskinesia in 6 pairs; each of 2 brother-brother pairs; 3 brother-sister pairs and one of mother-daughter pair. There was concordance for the absence of tardive dyskinesia in 5 pairs, each of 3 father-son pairs and 2 brother-sister pairs. In schizophrenic patients the presence or absence of tardive dyskinesia in one member of the family is a risk factor for the development of the syndrome in another member with the same psychotic illness. Those pairs with tardive dyskinesia were characterized by negative symptoms of schizophrenia and evidence of intellectual deterioration.
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PMID:Familial psychosis and vulnerability to tardive dyskinesia. 260 29

Smooth pursuit eye movements (SPEMs) have been consistently found to be abnormal in the majority of schizophrenic patients. The traditional SPEM measurement technique, however, fails to inform us about the underlying oculomotor deficit in these patients, since it remains a non-specific and a global oculomotor measure. A number of diverse clinical features such as tardive dyskinesia (TD) or negative symptoms correlate with the SPEM abnormality. Other eye movement abnormalities such as fixation difficulties, increased "volitional" saccadic latency and saccadic distractibility in anti-saccade paradigm have also been noted in schizophrenic patients. Still, it remains unclear how these different eye movement measures relate with each other and with the traditional SPEM measure, the presence of which is so widely described in schizophrenia. The advantage of some newer oculomotor paradigms is their functional specificity and the degree to which their biology is known. To further address these issues and to search for clinical correlates of various eye movement abnormalities found in schizophrenia, we have developed a battery of oculomotor measures to be administered to a large number of clinically well described schizophrenic patients and normal controls. The results from a preliminary analysis of a relatively small number of subjects are presented here, thus limiting the scope of possible conclusions. But, these results do indicate that this technique of studying multiple paradigms for oculomotor control in schizophrenia may prove to be fruitful.
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PMID:Oculomotor abnormalities and their clinical correlates in schizophrenia. 262 22

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

1. The paper presents arguments derived from both, clinical work and animal experiments, for or against the traditional hypothesis suggesting that tardive dyskinesia (TD) is caused by supersensitivity to dopamine. The main aim of this study was to answer the question posed in the title - whether the supersensitivity to dopamine evoked in rodents by neuroleptics can be regarded as an adequate pharmacological model of TD. 2. The data presented here prove that chronic administration of neuroleptics to schizophrenic patients cannot be the only factor inducing TD; furthermore, symptoms similar or identical to those of TD are also observed in the course of other disorders, not connected with neuroleptics, e.g. aging or schizophrenia itself. 3. Clinical data offer no clear evidence for the existence of a direct cause-effect relationship between super-sensitivity to dopamine and occurrence of TD. 4. The role of brain degeneration, caused by different factors but in particular by the process of aging, in the pathogenesis of dyskinetic disorders, including TD, has been stressed. 5. Pharmacological and biochemical data show that chronic administration of classic neuroleptics to animals induces an increase in the density of dopamine D-2 receptors (Bmax). It seems that this receptor-mediated supersensitivity may concern both the postsynaptic and the presynaptic D-2 dopamine receptors. On the other hand, it is not clear enough whether a dopamine D-1 receptor-mediated supersensitivity might also be a causal factor of TD. 6. The analysis in animals, of biochemical and pharmacological effects of neuroleptics which do not induce TD showed that in some situations these drugs may also evoke the receptor-mediated supersensitivity concerning dopamine D-2 receptors. 7. The method of a prolonged (approx. 1 year) oral administration of neuroleptics seems to differentiate those which induce TD from those which do not, at least regarding the induction of an increase of Bmax for butyrophenone neuroleptics and an increase of apomorphine-induced stereotypy, however, some exceptions are noted. 8. The above analysis of clinical and experimental data suggests that the supersensitivity to dopamine in rats treated chronically with neuroleptics cannot be accepted as a model which reflects the etiopathogenesis of TD. Neither a positive nor a negative result obtained in this test is reliable enough, and either depends on the tested parameters (apomorphine stereotypy and [3H]spiperon binding seem to be the most reliable), route of neuroleptic administration, duration of treatment and, probably, a number of other, still unknown factors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Can the supersensitivity of rodents to dopamine be regarded as a model of tardive dyskinesia? 268 86

Medical charts of 387 in-patients (schizophrenia n = 284, tardive dyskinesia, TD, n = 48), were analyzed to evaluate efficacy and adverse effects of clozapine. These patients were previously treated with between two and four other neuroleptics and were either therapy resistant or had severe side effects. Schizophrenic patients were treated with clozapine for 48 +/- 35 (TD 49 +/- 40) days, dosage was 189 +/- 119 (TD 220 +/- 176) mg. Four per cent showed worsening, 13% no change, 38% slight improvement, 42% marked improvement and 3% nearly total reduction of symptoms. In TD, 44% showed marked improvement, but only in 17% the drug was superior to previous neuroleptics. Adverse effects occurred in 56% of patients. Most frequent were sedation (17%), EEG alterations (16%), increase of liver enzymes (8%), hypotension (7%), hypersalivation (5%), fever (5%), ECG alterations (4%), tachycardia (3%), gastro-intestinal (3%) and delirious states (2%). A gradual increase in dosage seems to considerably reduce the incidence of some side effects. Clozapine treatment had to be discontinued because of severe side effects in 5.9%. In none of these patients did serious complications such as agranulocytosis occur. Only EEG alterations were significantly related to clozapine dosage (P less than 0.0005). At dismissal, most patients continued to receive clozapine; only in 22% (TD 20%) was it replaced by another neuroleptic. Thus, the ratio benefit/risk of clozapine treatment seems to be satisfactory in most of the negatively selected patients. Nevertheless, a gradual increase in dosage and careful control of hematological and other variables is highly recommended.
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PMID:Efficacy and adverse effects of clozapine in the treatment of schizophrenia and tardive dyskinesia--a retrospective study of 387 patients. 281 68

Free radicals are highly toxic compounds which can react with a number of molecules such as glycoproteins or amino acids. These reactions can lead to the denaturation of proteins, destabilization of cellular membrane and eventually, cell death. Free radicals have been recently implicated in the pathogenesis and clinical course of a number of neuropsychiatric disorders including aging of the central nervous system (CNS), schizophrenia, and the development of tardive dyskinesia during chronic use of neuroleptics. This paper provides an overview of the nature of free radicals and discusses briefly their participation in the toxicity associated with catecholamines in the CNS.
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PMID:Free radical mechanisms in the central nervous system: an overview. 284 Apr 5

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 long-term prognosis of tardive dyskinesia (TD) has been insufficiently studied. Symptoms are reversible in many patients, but an irreversible course is widely believed to be the expected outcome. This pessimistic view has led to the assumption that neuroleptics should not be used in patients with TD because these drugs will produce an inevitable aggravation of TD. To clarify this issue, 27 patients were serially evaluated over 5 years for changes in neuroleptic treatment, TD, and mental status. Ten patients were able to discontinue medications; 15 required continued low-dose neuroleptic therapy [average 223 mg/day chlorpromazine (CPZ) equivalents], and two needed high doses (1000-2000 mg/day CPZ equivalents) to control psychosis. The majority of patients improved by more than 50% in both treated and untreated groups. In 8 of 27 patients (29.6%) TD resolved; in 1 patient TD increased by 25%. Younger patients improved the most. Prognosis was most favorable if neuroleptics were discontinued, but improvement was still possible with low to moderate doses (less than 600 mg/day CPZ equivalents). The large majority of patients with schizophrenia or schizoaffective illness relapsed, and required continued drug treatment. TD must be evaluated over several years to monitor the resolving/persisting course. Control of psychosis and improvement of TD during low-dose neuroleptic treatment suggest the antipsychotic and neurological effects of neuroleptics may involve different thresholds or mechanisms of action.
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PMID:Tardive dyskinesia: reversible and irreversible. 286 Jun 64

Movement abnormalities in neuroleptic-treated, psychiatric patients are classified as (a) initial syndromes, including dystonia, parkinsonism, and hyperkinetic abnormalities such as initial dyskinesia (ID) and akathisia, all of which are related to the neuroleptic dose and can be considered as overdose phenomena; (b) tardive syndromes, mainly the classic tardive dyskinesia (TD) syndrome, more seldom tardive akathisia and tardive dystonia, which may all develop or aggravate after withdrawal of neuroleptic treatment; and (c) age-related, spontaneous dyskinesia, akathisia, and dystonia, and schizophrenia-related, hyperkinetic, often stereotyped, movements and restlessness. ID and TD can occur simultaneously, and may depend, at least partially, on identical mechanisms. The pathophysiology of TD is still not clear, and the traditional dopamine (DA) hypersensitivity model seems inadequate. Animal experiments suggest that blockade of some DA receptors in the brain (e.g., in ventromedian striatum) may counteract hyperkinesia and produce parkinsonism, while a concomitant blockade of other similar receptors in other brain regions (e.g., in anterodorsal striatum) may aggravate movements. This offers an explanation for the concomitant occurrence of parkinsonism and hyperkinetic movement abnormalities (ID and akathisia) relatively early in a neuroleptic treatment, and may also contribute to the understanding of the pathophysiology of TD. It is concluded that pathophysiologically TD is a heterogeneous syndrome depending on a subtle balance between several neurotransmitters in the brain, including DA receptor blockade and hypersensitivity of DA and GABA receptors.
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PMID:Pathophysiological mechanisms underlying tardive dyskinesia. 286 Jun 66


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