Marsden C D, Obeso J A, Zarranz J J, Lang A E
Brain. 1985 Jun;108 ( Pt 2):463-83. doi: 10.1093/brain/108.2.463.
Twenty-eight patients with focal (arm or leg) or hemidystonia due to tumour, arteriovenous malformation, infarction, haemorrhage or hemiatrophy are described. All had typical dystonic movements and/or postures, identical to those seen in idiopathic (primary) torsion dystonia. The site(s) of the lesion responsible, as defined by CT (computerized tomography) scan or pathological examination, was in the contralateral caudate nucleus, lentiform nucleus (particularly the putamen) or thalamus, or in a combination of these structures. Review of 13 other patients in the literature with hemidystonia and lesions defined by CT scan, and of 7 other patients with pathologically discrete lesions associated with hemidystonia, also indicated involvement of these structures. Dystonia may be due to abnormal input from thalamus to premotor cortex, due to lesions either of the thalamus itself, or of the striatum projecting by way of the globus pallidus to the thalamus.
本文描述了28例因肿瘤、动静脉畸形、梗死、出血或半侧萎缩导致局灶性(手臂或腿部)或半身肌张力障碍的患者。所有患者均有典型的肌张力障碍运动和/或姿势,与特发性(原发性)扭转性肌张力障碍所见相同。经计算机断层扫描(CT)或病理检查确定,责任病变部位位于对侧尾状核、豆状核(尤其是壳核)或丘脑,或这些结构的组合。对文献中另外13例有半身肌张力障碍且经CT扫描确定有病变的患者,以及另外7例有与半身肌张力障碍相关的病理上离散病变的患者的回顾,也表明这些结构受累。肌张力障碍可能是由于丘脑本身或通过苍白球投射到丘脑的纹状体病变,导致丘脑向运动前皮质的输入异常所致。