Bathien N, Rondot P, Koutlidis R M
J Physiol (Paris). 1981 Apr;77(1):131-41.
Electrophysiological and pharmacological analysis of L-Dopa-induced dyskinesia and tardive dyskinesia (L.DD) due to neuroleptics was performed on 12 patients with Parkinson's disease and on 12 others with psychotic diseases. This analysis included the examination of spinal reflexes, monosynaptic H reflex, polysynaptic cutaneous reflex of the lower limb, muscular responses to passive movement [stretch reflex and shortening reaction (SR)] and the study of the motor response to a dopaminergic stimulus (I.V. injection of Piribedil (PBD), a dopamine agonist). There was no difference in EMG activity between L.DD and TD. Three EMG patterns can be distinguished: anarchic discharge pattern (ADA), tonic grouping discharge pattern (AST) and rhythmic burst pattern (ABR). PBD effects indicate a possible relationship between the EMG patterns and the sensitivity level of the motor dopamine receptors. During L-Dopa dyskinesia and tardive dyskinesia, the same changes in spinal reflexes were observed. Muscle tone tested by muscular responses to passive movement (shortening and myotatic reaction) was normal. Monosynaptic excitability explored by H/M ratio was within the normal range. In contrast, the polysynaptic nociceptive reflex was increased in every case. In Parkinsonian patients with L-Dopa dyskinesia, this pattern of the spinal reflexes was significantly different in comparison to the rigid phase. Intravenous infusion of PBD suppressed tremor and provoked the occurrence of dyskinetic activity in Parkinsonian patients with L-Dopa dyskinesia during the rigid phase. During the dyskinetic phase, as in tardive dyskinesia, PBD increases these phenomena and changes EMG activity in rhythmic pattern. It is suggested that L-Dopa dyskinesia and tardive dyskinesia can be determined by testing EMG activity, spinal reflexes and dopaminergic reactivity. There is evidence to suggest that the various types of involuntary abnormal movement represent a single entity, and that dopamine receptor supersensitivity may be involved.
对12例帕金森病患者和12例精神病患者进行了左旋多巴诱发的异动症和抗精神病药物所致迟发性运动障碍(L.DD)的电生理和药理学分析。该分析包括检查脊髓反射、单突触H反射、下肢多突触皮肤反射、肌肉对被动运动的反应[牵张反射和缩短反应(SR)]以及对多巴胺能刺激(静脉注射多巴胺激动剂匹莫齐特(PBD))的运动反应研究。L.DD和TD之间的肌电图活动没有差异。可以区分出三种肌电图模式:无规律放电模式(ADA)、强直性分组放电模式(AST)和节律性爆发模式(ABR)。PBD效应表明肌电图模式与运动多巴胺受体的敏感性水平之间可能存在关系。在左旋多巴异动症和迟发性运动障碍期间,观察到脊髓反射有相同的变化。通过肌肉对被动运动的反应(缩短和肌伸张反应)测试的肌张力正常。通过H/M比值探索的单突触兴奋性在正常范围内。相比之下,多突触伤害性反射在每种情况下均增加。在患有左旋多巴异动症的帕金森病患者中,这种脊髓反射模式与僵直期相比有显著差异。静脉输注PBD可抑制震颤,并在僵直期诱发患有左旋多巴异动症的帕金森病患者出现异动症活动。在异动症期,与迟发性运动障碍一样,PBD会加剧这些现象并使肌电图活动改变为节律性模式。有人提出,左旋多巴异动症和迟发性运动障碍可以通过测试肌电图活动、脊髓反射和多巴胺能反应性来确定。有证据表明,各种类型的不自主异常运动代表一个单一实体,并且可能涉及多巴胺受体超敏反应。