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Tardive dyskinesia and impaired glucose tolerance
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AbstractThe authors examined the role of impaired glucose metabolism in the pathophysiology of tardive dyskinesia in schizophrenic patients with and without persistent TD. Glucose tolerance and insulin levels were determined in 86 patients with persistent tardive dyskinesia and in 108 patients without tardive dyskinesia. Dyskinesias were assessed by the abnormal involuntary movement scale (AIMS) and extrapyramidal symptoms by the Simpson—Angus rating scale (SARS). Fasting blood glucose levels were significantly lower while the first and second hour glucose levels did not reveal any differences in patients with tardive dyskinesia compared with those without tardive dyskinesia. Insulin levels did not differ in these two groups. Our cross‐sectional epidemiological study does not suggest hyperglycemia to be a risk factor for tardive dyskinesia. However, prospective long‐term studies with multiple assessment points are needed to clarify the role of glucose metabolism in the development of tardive dyskinesia. Copyright © 2002 John Wiley & Sons, Ltd.
Title: Tardive dyskinesia and impaired glucose tolerance
Description:
AbstractThe authors examined the role of impaired glucose metabolism in the pathophysiology of tardive dyskinesia in schizophrenic patients with and without persistent TD.
Glucose tolerance and insulin levels were determined in 86 patients with persistent tardive dyskinesia and in 108 patients without tardive dyskinesia.
Dyskinesias were assessed by the abnormal involuntary movement scale (AIMS) and extrapyramidal symptoms by the Simpson—Angus rating scale (SARS).
Fasting blood glucose levels were significantly lower while the first and second hour glucose levels did not reveal any differences in patients with tardive dyskinesia compared with those without tardive dyskinesia.
Insulin levels did not differ in these two groups.
Our cross‐sectional epidemiological study does not suggest hyperglycemia to be a risk factor for tardive dyskinesia.
However, prospective long‐term studies with multiple assessment points are needed to clarify the role of glucose metabolism in the development of tardive dyskinesia.
Copyright © 2002 John Wiley & Sons, Ltd.
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