Bucher S F, Seelos K C, Dodel R C, Paulus W, Reiser M, Oertel W H
Department of Neurology, Klinikum Grosshadern, Ludwig-Maximilians-University, Munich, Germany.
Arch Neurol. 1996 Jul;53(7):682-6. doi: 10.1001/archneur.1996.00550070124020.
To study noninvasively the functional anatomy and pathophysiologic characteristics of the globus pallidus external (GPe) and internal (GPi) divisions.
Structural and functional neuroimaging using high-resolution magnetic resonance imaging.
University medical center research facility. SUBJECTS. Seven patients with pallidal lesions, 4 with an akinetic-rigid syndrome and 3 with a dystonic syndrome, and 15 age-matched volunteers.
T2-weighted anatomical magnetic resonance imaging and number of activated voxels in the GP during rapid supination and pronation of the hand.
T2-weighted images showed hyperintense bilateral lesions in the GP of all patients. Patients with dystonic syndromes had isolated lesions in the GPi. Patients with signs of akinetic-rigid syndromes showed abnormalities in the GPe or in central portions of the GP (GPc). Patients with lesions in both parts of the GP had akinetic-rigid or dystonic syndromes. All patients showed activation in the areas of the lesions. The number of activated voxels in the GP was significantly smaller (P < .005, Wilcoxon signed rank test) in patients than in control subjects. Activation of the GP was predominantly contralateral to the moving hand.
Lesions in the GPi result in a loss of inhibitory pallidal projections to the thalamus, which may explain the hyperkinetic signs. Lesions in the GPe lead to an increased inhibition of the thalamus, which may explain the hypokinetic signs. Neuronal activation in lesion sites suggests the presence of remaining functionally vital tissue.
无创性研究苍白球外侧部(GPe)和内侧部(GPi)的功能解剖及病理生理特征。
采用高分辨率磁共振成像进行结构和功能神经影像学研究。
大学医学中心研究机构。
7例苍白球病变患者,其中4例患有运动不能-强直综合征,3例患有肌张力障碍综合征,以及15名年龄匹配的志愿者。
T2加权解剖磁共振成像以及手部快速旋前和旋后时苍白球内激活体素的数量。
T2加权图像显示所有患者苍白球均有双侧高信号病变。肌张力障碍综合征患者的病变仅位于苍白球内侧部。有运动不能-强直综合征体征的患者苍白球外侧部或苍白球中央部(GPc)出现异常。苍白球两部分均有病变的患者患有运动不能-强直或肌张力障碍综合征。所有患者病变区域均有激活。患者苍白球内激活体素的数量显著少于对照组(P < 0.005,Wilcoxon符号秩检验)。苍白球的激活主要位于与运动手对侧。
苍白球内侧部病变导致苍白球向丘脑的抑制性投射丧失,这可能解释了运动亢进体征。苍白球外侧部病变导致对丘脑的抑制增加,这可能解释了运动减退体征。病变部位的神经元激活提示存在功能上仍至关重要的组织。