Hsu Jung Lung, Wang Han-Cheng, Hsu Wei-Chih
Department of Neurology, Shin Kong Wu Ho-Su Memorial Hospital, 95 Wen Chang Road, Shih Lin District, Taipei, Taiwan.
J Neurol. 2004 Dec;251(12):1486-90. doi: 10.1007/s00415-004-0571-4.
Hyperglycemia-induced unilateral basal ganglion lesions occur mostly in Asian patients. A signal abnormality in the basal ganglion region is evident on these patients' neuroimaging. Despite characteristic imaging findings and clinical manifestations, the underlying mechanism is still unclear. To clarify the underlying pathophysiology of unilateral basal ganglion lesions, we examined the [18F]-fluorodeoxyglucose (FDG) positron emission tomography (PET) findings in 3 patients with hyperglycemia. The PET studies were performed at 3 weeks, 5 weeks, and 7 months after clinical onset. The markedly reduced rates of cerebral glucose metabolism in the corresponding lesions on T1-weighted magnetic resonance images provided direct evidence of regional metabolic failure. We suggest that the metabolic derangements associated with hyperglycemia and vascular insufficiency contribute to regional metabolic failure in patients with poorly controlled diabetes mellitus.
高血糖诱导的单侧基底节病变多见于亚洲患者。这些患者的神经影像学检查显示基底节区有明显的信号异常。尽管有特征性的影像学表现和临床表现，但其潜在机制仍不清楚。为了阐明单侧基底节病变的潜在病理生理学，我们检查了3例高血糖患者的[18F] - 氟脱氧葡萄糖（FDG）正电子发射断层扫描（PET）结果。PET研究在临床发病后3周、5周和7个月进行。T1加权磁共振图像上相应病变处脑葡萄糖代谢率明显降低，为区域代谢衰竭提供了直接证据。我们认为，与高血糖和血管功能不全相关的代谢紊乱导致了糖尿病控制不佳患者的区域代谢衰竭。
