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Biomedical subjects

S R Kay

Publications and source records attributed to S R Kay.

119 records · Page 7Linked to original sources
PubMedDate not supplied

L-dopa in the treatment of negative schizophrenic symptoms: a single-subject experimental study.

Adjunctive Sinemet (L-DOPA plus carbidopa) therapy was assessed for a neuroleptic nonresponsive schizophrenic with a longstanding negative syndrome. A twenty-seven week double-blind placebo-controlled reversal design found significant improvement specifically for negative symptoms while treated with combined haloperidol-Sinemet as compared against haloperidol-placebo. The eight-week adjunctive treatment reversed a worsening trend in attention, abstract thinking, passive withdrawal, psychomotor retardation, and a cluster of seven negative parameters, while positive symptoms were unaffected. This seemed to represent more than simple reversal of drug-induced akinesia and underscores the importance of distinguishing between positive and negative syndromes in psychopharmacological research.

Antipsychotic Agents↗
PubMedDate not supplied

The relationship of tardive dyskinesia to positive schizophrenia.

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.

Adult↗
PubMedDate not supplied

The role of melatonin in the antipsychotic and motor-side effects of neuroleptics: a hypothesis.

Three phenomena concerning the antipsychotic action of classic neuroleptic drugs have not been adequately explained by the dopamine hypothesis: (1) administration of neuroleptic drugs is commonly associated with an initial period of 3-6 weeks prior to demonstration of antipsychotic effects; (2) similarly, neuroleptic-induced Parkinsonism commonly emerges only after several weeks of neuroleptic therapy; (3) moreover, Parkinsonism may disappear despite continuous neuroleptic treatment. An understanding of these phenomena might shed new light into the nature of the antipsychotic actions of these agents, and hence the pathophysiology of schizophrenia. We propose that the increase in melatonin secretion, which occurs with the initiation of neuroleptic therapy, may be responsible for the delay in the antipsychotic effects of neuroleptics and may also account for the lag in the development of drug-induced Parkinsonism as well as its disappearance. The implications of this hypothesis for the treatment of schizophrenia and the prophylaxis of drug-induced Parkinsonism are discussed.

Antipsychotic Agents↗
PubMedDate not supplied

Subjective awareness of abnormal involuntary movements in schizophrenia.

A wide majority of schizophrenic patients with Tardive dyskinesia, a neurological disorder produced by chronic neuroleptic therapy, lack awareness of their involuntary movements. This by contrast to patients with Parkinsonism who usually are aware of their abnormal movements. In the following communication we present a series of studies which are aimed at providing further insight into the issue of awareness of involuntary movements in schizophrenic patients with tardive dyskinesia. In addition, we investigated whether edentulosness, which may be a risk factor for orofacial dyskinesias in the elderly, is also a risk factor for neuroleptic-induced orofacial dyskinesias. We found that: (a) one's awareness of involuntary movements is related to some but not all muscle groups, (b) tardive dyskinesia may be associated with a significant distress, (c) lack of awareness may be a feature of frontal lobe dysfunction in schizophrenia, (d) patients who lack awareness of their involuntary movements have a higher prevalence of pineal calcification, and (e) edentulosness, which is related to deficits in the orofacial sensorimotor system, increases the risk for neuroleptic-induced orofacial dyskinesias.

Adult↗
PubMedDate not supplied

Drug-induced parkinsonism: relationship to age at onset of schizophrenia.

On the basis of the association of negative schizophrenia with parkinsonism and early age of onset, we predicted that the latter two would covary, as reflecting a similar pathological process. To test this prediction, we studied in 40 neuroleptic-treated female schizophrenic patients with drug-induced movement disorders the association of age at onset with drug-induced parkinsonism and, for comparison, also with persistent tardive dyskinesia (TD) and acute drug-induced dystonia. We found that onset of schizophrenia during adolescence, significantly predicted the presence of parkinsonism but, by contrast, was unrelated to TD and acute drug-induced dystonia. Our findings suggest a specific association between early age at onset of schizophrenia and parkinsonism, implying that the former may be a risk factor for parkinsonism. The significance of these findings to the pathophysiology of negative schizophrenia and parkinsonism are discussed.

Adult↗
PubMedDate not supplied

Melatonin secretion and the pathophysiology of Meige's disease (idiopathic orofacial dystonia): a hypothesis.

Meige's disease is a form of focal dystonia characterized by symmetric dystonic spasms of facial muscles, sometimes associated with dystonic movements of other midline muscle groups. The etiology and pathophysiology of the disease have not been established. There is evidence that Meige's disease may result from striatal dopaminergic preponderance coupled with cholinergic overactivity. Several authors have noted a high prevalence of depression in patients with Meige's disease, suggesting a common neurochemical abnormality. Depression, in turn, is associated with decreased pineal melatonin secretion. We propose, based on studies demonstrating that melatonin regulates dopaminergic, cholinergic and GABA-ergic functions, that alterations in melatonin functions may enhance the development of the disease. This hypothesis may open new avenues toward understanding the pathophysiology of the disease and developing newer therapeutic strategies.

Bipolar Disorder↗
PubMedDate not supplied

Edentulousness and neuroleptic-induced neck and trunk dyskinesia.

Edentulousness, by disrupting trigeminal propioceptive input from the oral cavity to the basal ganglia, may increase the risk for neuroleptic-induced orofacial dyskinesia. Since lesions of the globus pallidus alter trigeminal sensory-induced reflexive neck muscle activity in rats and the putamen-caudate complex regulates vestibular and propioceptive mechanisms, edentulousness could facilitate also the expression of neuroleptic-induced neck and trunk dyskinesias. In a sample of 131 neuroleptic-treated chronic schizophrenic patients, we found that edentulous patients exhibited significantly more neck and trunk dyskinesias as compared to nonedentulous patients (p less than 005). By contrast, dyskinesias of the face, tongue, and extremities did not differ between the two cohorts of patients. Our findings imply that edentulousness may increase the risk of neck and trunk dyskinesias and highlight the importance of the dental status in tardive dyskinesia.

Adolescent↗