Paroxysmal kinesigenic dyskinesia (PKD), the most common type of paroxysmal movement disorder, is characterized by sudden and brief attacks of choreoathetosis or dystonia triggered by sudden voluntary movements. PKD is mainly caused by mutations in the PRRT2 or TMEM151A gene. The exact pathophysiological mechanisms of PKD remain unclear, although the function of PRRT2 protein has been well characterized in the last decade. Based on abnormal ion channels and disturbed synaptic transmission in the absence of PRRT2, PKD may be channelopathy or synaptopathy, or both. In addition, the cerebellum is regarded as the key pathogenic area. Spreading depolarization in the cerebellum is tightly associated with dyskinetic episodes. Whereas, in PKD, other than the cerebellum, the role of the cerebrum including the cortex and thalamus needs to be further investigated.

阵发性运动诱发性运动障碍 (PKD) 是阵发性运动障碍的最常见类型，其特征是由突然的随意运动引发的突然而短暂的舞蹈手足徐动症或肌张力障碍发作。PKD 主要由PRRT2或TMEM151A基因突变引起。尽管 PRRT2 蛋白的功能在过去十年中已得到很好的表征，但 PKD 的确切病理生理机制仍不清楚。基于在 PRRT2 缺失的情况下离子通道异常和突触传递紊乱，PKD 可能是离子通道病变或突触病变，或两者兼而有之。此外，小脑被认为是关键致病部位。小脑广泛的去极化与运动障碍发作密切相关。而在多囊肾中，除了小脑之外，大脑皮层和丘脑的作用还需要进一步研究。