Otsuka M, Ichiya Y, Shima F, Kuwabara Y, Sasaki M, Fukumura T, Kato M, Masuda K, Goto I
Department of Radiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
J Neurol Sci. 1992 Sep;111(2):195-9. doi: 10.1016/0022-510x(92)90068-v.
Striatal 18F-Dopa uptake and glucose metabolism were studied by positron emission tomography with 6-L-[18F]fluorodopa and [18F]fluorodeoxyglucose, respectively, in 8 patients with idiopathic dystonia. Patients with abnormal findings on the brain CT and MRI were excluded from this study. The clinical diagnosis consisted of torsion dystonia in 3 patients, focal dystonia limited in the arm in 3 and cervical dystonia (spasmodic torticollis) in 2. The 18F-Dopa uptake, corrected by nonspecific retention in the cerebellum, at 120 min post-administration was evaluated, and increased 18F-Dopa uptake in the putamen and in the caudate head was observed in the patients with idiopathic dystonia compared to the normal controls. The striatal glucose metabolism in the patients with idiopathic dystonia showed no difference with the normal controls. These findings suggest that pathogenetic mechanism of idiopathic dystonia involves increased presynaptic activity of the dopaminergic system in the striatum.
分别采用正电子发射断层扫描技术,使用6-L-[18F]氟多巴和[18F]氟脱氧葡萄糖,对8例特发性肌张力障碍患者的纹状体18F-多巴摄取和葡萄糖代谢进行了研究。脑CT和MRI检查结果异常的患者被排除在本研究之外。临床诊断包括3例扭转性肌张力障碍患者、3例局限于手臂的局灶性肌张力障碍患者和2例颈部肌张力障碍(痉挛性斜颈)患者。评估了给药后120分钟时经小脑非特异性滞留校正后的18F-多巴摄取情况,结果显示,与正常对照组相比,特发性肌张力障碍患者壳核和尾状核头部的18F-多巴摄取增加。特发性肌张力障碍患者的纹状体葡萄糖代谢与正常对照组无差异。这些发现提示,特发性肌张力障碍的发病机制涉及纹状体中多巴胺能系统突触前活性增加。