Chong Siow-Ann, Lum Alvin, Huak Chan Yiong, Kane John
Woodbridge Hospital/ Institute of Mental Health, Singapore.
Hum Psychopharmacol. 2002 Aug;17(6):305-7. doi: 10.1002/hup.413.
The 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.
作者研究了葡萄糖代谢受损在伴有和不伴有持续性迟发性运动障碍的精神分裂症患者迟发性运动障碍病理生理学中的作用。测定了86例持续性迟发性运动障碍患者和108例无迟发性运动障碍患者的糖耐量和胰岛素水平。通过异常不自主运动量表(AIMS)评估运动障碍,通过辛普森-安格斯评定量表(SARS)评估锥体外系症状。与无迟发性运动障碍的患者相比,迟发性运动障碍患者的空腹血糖水平显著降低,而第一小时和第二小时的血糖水平没有差异。两组的胰岛素水平没有差异。我们的横断面流行病学研究并不表明高血糖是迟发性运动障碍的危险因素。然而,需要进行具有多个评估点的前瞻性长期研究,以阐明葡萄糖代谢在迟发性运动障碍发生中的作用。