Bartenstein P, Weindl A, Spiegel S, Boecker H, Wenzel R, Ceballos-Baumann A O, Minoshima S, Conrad B
Department of Nuclear Medicine, Technische Universität München, Germany.
Brain. 1997 Sep;120 ( Pt 9):1553-67. doi: 10.1093/brain/120.9.1553.
Repeated PET cerebral blood flow measurements using H2(15)O were performed in 13 patients with confirmed Huntington's disease and nine age-matched controls. The activation paradigm consisted of an externally triggered finger opposition task (1.5 Hz) with the dominant hand, the control condition being the auditory input. In the patients with Huntington's disease, impaired activity of the striatum and its frontal motor projection areas (rostral supplementary motor area, anterior cingulate and premotor cortex) could be demonstrated along with enhanced activity mainly in parietal areas during movement. The results suggest that the pathology of Huntington's disease causes impairment of the output part of the basal ganglia-thalamo-cortical motor circuit and may induce a compensatory recruitment of additional accessory motor pathways involving the parietal cortex.
使用H2(15)O对13例确诊为亨廷顿舞蹈症的患者及9名年龄匹配的对照者进行了多次PET脑血流量测量。激活模式包括由外部触发的优势手对指任务(1.5赫兹),对照条件为听觉输入。在亨廷顿舞蹈症患者中,可证明纹状体及其额叶运动投射区(嘴侧辅助运动区、前扣带回和运动前皮质)活动受损,同时在运动期间主要在顶叶区域活动增强。结果表明,亨廷顿舞蹈症的病理改变导致基底神经节-丘脑-皮质运动回路输出部分受损,并可能诱导涉及顶叶皮质的额外辅助运动通路的代偿性募集。