Cardoso F, Jankovic J
Department of Neurology, Baylor College of Medicine, Houston, Tex.
Arch Neurol. 1995 Mar;52(3):263-70. doi: 10.1001/archneur.1995.00540270055019.
Trauma to the peripheral nervous system is a well-recognized cause of dystonia and tremor, but peripherally induced parkinsonism has not previously been documented. We seek to characterize peripherally induced tremor and parkinsonism and propose possible mechanisms for this phenomenon.
Review of records of patients evaluated in the Movement Disorders Clinic between 1977 and 1993. In addition to demographic and clinical information, the records were screened for any potential predisposing factors.
Twenty-eight patients in whom the onset of tremor, parkinsonism, or both was anatomically and temporally related to local injury.
The type and site of injury were verified by history and examination of records whenever possible. Severity of tremor and parkinsonism was assessed by clinical rating scales. Three patients with tremor and parkinsonism had their striatal [18F]-fluorodopa uptake and raclopride binding measured with positron emission tomography.
Response to conventional antitremor and antiparkinsonian medication was assessed by a clinical rating scale.
Severe local injury preceded the onset of movement disorder by 47.5 +/- 74.7 days (mean +/- SD). The mean age at onset of movement disorder was 46.5 +/- 14.1 years. Tremor was present in all 28 patients, 11 of whom exhibited additional parkinsonian features. In 20 patients, the movement disorder spread beyond the original site. Possible predisposing factors were identified in 13 patients; nine had essential tremor or a family history of essential tremor. In addition to tremor, dystonia and myoclonus were evident in 13 and three patients, respectively. Reflex sympathetic dystrophy was present in six patients. Tremor did not improve with medications, and only seven patients with parkinsonism responded to therapy with levodopa.
Central reorganization in response to peripheral injury may give rise to a motor disturbance, including tremor and parkinsonism.
外周神经系统创伤是肌张力障碍和震颤的一个公认病因，但此前尚未有外周诱导性帕金森病的记录。我们旨在对外周诱导性震颤和帕金森病进行特征描述，并提出这一现象的可能机制。
回顾1977年至1993年间在运动障碍诊所接受评估的患者记录。除人口统计学和临床信息外，还对记录进行筛查以寻找任何潜在的诱发因素。
28例患者，其震颤、帕金森病或两者的发作在解剖学和时间上与局部损伤相关。
尽可能通过病史和记录检查来核实损伤的类型和部位。通过临床评分量表评估震颤和帕金森病的严重程度。3例有震颤和帕金森病的患者通过正电子发射断层扫描测量其纹状体[18F] - 氟多巴摄取和雷氯必利结合情况。
通过临床评分量表评估对传统抗震颤和抗帕金森药物的反应。
严重局部损伤在运动障碍发作前47.5±74.7天（平均±标准差）出现。运动障碍发作时的平均年龄为46.5±14.1岁。28例患者均有震颤，其中11例还表现出其他帕金森病特征。20例患者的运动障碍扩散至原部位以外。13例患者中发现了可能的诱发因素；9例有特发性震颤或特发性震颤家族史。除震颤外，13例和3例患者分别出现了肌张力障碍和肌阵挛。6例患者存在反射性交感神经营养不良。震颤未因药物治疗而改善，仅7例帕金森病患者对左旋多巴治疗有反应。
对外周损伤的中枢重组可能导致运动障碍，包括震颤和帕金森病。
