Meara R J, Cody F W
Department of Neurology, Manchester Royal Infirmary, UK.
Electroencephalogr Clin Neurophysiol. 1993 Aug;89(4):261-8. doi: 10.1016/0168-5597(93)90105-x.
Stretch reflexes were elicited in flexor carpi radialis (FCR) of healthy subjects and patients with Parkinson's disease by forcible ramp and hold extensions of the wrist joint. Individual patients were studied off treatment when rigidity was detected clinically at the joint and throughout the clinical response to anti-parkinsonian medication that abolished or reduced their rigidity. In this way the possible effects of inter-subject variability upon the relationship between reflex behaviour and rigidity were eliminated. The long-latency (M2) stretch reflexes of the patient group were increased on average compared to those of healthy subjects. However, in the large majority of individual patients there were no significant correlations between the amplitudes of their M2 or total (short-latency (M1) + M2) reflex activities, recorded off and on treatment, and the accompanying changes in clinically assessed rigidity. These results suggest that parkinsonian rigidity cannot be uniquely attributed to the increased reflex responsiveness measured by the present laboratory techniques. However, the techniques used to test reflex function in our study differed in several respects (e.g., background activity, stretching wave form) from those employed during clinical assessment of rigidity so that the balance of reflex mechanisms may have varied in the two situations. Therefore, these results cannot be taken as definitive evidence against a reflex origin of rigidity.
通过对腕关节进行强制斜坡式伸展并保持，在健康受试者和帕金森病患者的桡侧腕屈肌（FCR）中引出牵张反射。当在临床上检测到关节僵硬时以及在整个抗帕金森药物治疗过程中，对个体患者进行停药研究，该治疗消除或减轻了他们的僵硬症状。通过这种方式，消除了个体间差异对反射行为与僵硬之间关系的可能影响。与健康受试者相比，患者组的长潜伏期（M2）牵张反射平均增加。然而，在绝大多数个体患者中，停药和服药时记录的M2或总（短潜伏期（M1）+M2）反射活动的幅度与临床评估的僵硬程度的伴随变化之间没有显著相关性。这些结果表明，帕金森病性僵硬不能唯一归因于通过目前实验室技术测量的反射反应性增加。然而，我们研究中用于测试反射功能的技术在几个方面（例如，背景活动、拉伸波形）与临床评估僵硬时所采用的技术不同，因此在这两种情况下反射机制的平衡可能有所不同。因此，这些结果不能被视为反对僵硬反射起源的确凿证据。
