Tolosa E, Montserrat L, Bayes A
Neurology Service, Hospital Clinic i Provincial de Barcelona, Faculty of Medicine, Barcelona, Spain.
Mov Disord. 1988;3(1):61-9. doi: 10.1002/mds.870030108.
We have studied the orbicularis oculi reflex to paired stimuli in patients with various forms of focal dystonia and in normal controls. In normals, the conditioning stimulus (CS) facilitated the test stimulus (TS) early response (R1), but markedly inhibited the TS polysynaptic late response (R2). In all types of dystonias studied the CS facilitated the TSR1 as in normals. However, in patients with blepharospasm (alone or associated with oromandibular dystonia), spasmodic torticollis, or spasmodic dysphonia, it inhibited the TSR2 significantly less than that of the controls, with marked enhancement of the recovery curve of the late response. The TSR2 recovery curve of patients with focal arm dystonia was normal. These results are indicative of increased brainstem interneuron excitability in the various dystonias mediated by the cranial nerves, but not in focal arm dystonias such as dystonic writer's cramp. This abnormality might be caused by an abnormal input possibly from the basal ganglia upon these brainstem cells. Our results also suggest that a similar pathophysiology underlies the various focal dystonias of the head and neck.
我们研究了各种类型局灶性肌张力障碍患者和正常对照者对成对刺激的眼轮匝肌反射。在正常人中,条件刺激(CS)促进了测试刺激(TS)的早期反应(R1),但显著抑制了TS的多突触晚期反应(R2)。在所有研究的肌张力障碍类型中,CS如同在正常人中一样促进了TSR1。然而,在眼睑痉挛(单独或合并口下颌肌张力障碍)、痉挛性斜颈或痉挛性发声障碍患者中,它对TSR2的抑制明显少于对照组,晚期反应的恢复曲线明显增强。局灶性手臂肌张力障碍患者的TSR2恢复曲线正常。这些结果表明,在由颅神经介导的各种肌张力障碍中,脑干中间神经元兴奋性增加,但在局灶性手臂肌张力障碍如肌张力障碍性书写痉挛中并非如此。这种异常可能是由基底神经节对这些脑干细胞的异常输入引起的。我们的结果还表明,类似的病理生理学是头颈部各种局灶性肌张力障碍的基础。