Takahashi H, Snow B J, Nygaard T G, Calne D B
Neurodegenerative Disorder Centre, University of British Columbia, University Hospital-UBC Site, Vancouver, Canada.
Adv Neurol. 1993;60:586-90.
Parkinsonism without dystonia has been reported in several older members of families with DRD. This raises the question whether such patients represent a variant in the clinical picture of DRD, or a separate disease, IP. We employed 6-FD PET to study the nigrostriatal dopaminergic function in a woman with typical DRD and two of her relatives with late-onset parkinsonism. These two had an excellent and prolonged therapeutic response to small doses of L-DOPA, without complications. We found that the dystonic patient and the women with "benign" parkinsonism had normal striatal 6-FD uptake. In conjunction with other clinical evidence, our PET study indicates that the biochemical lesion in these members may be "proximal" to dopa decarboxylase, as is suggested in DRD patients. We conclude that the adult-onset parkinsonism in DRD families is due to the same pathophysiological mechanism as the childhood-onset dystonia in the disease. DRD may display substantial clinical heterogeneity depending on the age of onset.
在患有多巴胺反应性肌张力障碍(DRD)的家族中,已有数名老年成员被报道出现无肌张力障碍的帕金森综合征。这就引发了一个问题,即这类患者是代表了DRD临床症状的一种变异,还是一种独立的疾病——特发性帕金森病(IP)。我们使用6-氟多巴(6-FD)正电子发射断层扫描(PET)来研究一名典型DRD女性患者及其两名患有迟发性帕金森综合征的亲属的黑质纹状体多巴胺能功能。这两人对小剂量左旋多巴(L-DOPA)有良好且持久的治疗反应,且无并发症。我们发现,肌张力障碍患者以及患有“良性”帕金森综合征的女性纹状体6-FD摄取正常。结合其他临床证据,我们的PET研究表明,这些家族成员中的生化病变可能与DRD患者一样,发生在多巴脱羧酶“近端”。我们得出结论,DRD家族中的成年发病帕金森综合征与该疾病中儿童期发病的肌张力障碍具有相同的病理生理机制。根据发病年龄,DRD可能表现出显著的临床异质性。