Prince of Wales Clinical School and Neuroscience Research Australia, University of New South Wales, Randwick, Sydney, NSW, 2052, Australia.
Prince of Wales Hospital, Institute of Neurological Sciences, Randwick, Sydney, NSW, 2031, Australia.
Exp Brain Res. 2019 Jul;237(7):1853-1867. doi: 10.1007/s00221-019-05553-8. Epub 2019 May 13.
We studied 12 patients with Parkinson's disease (PD): 6 with postural instability (Hoehn and Yahr Stage 3) and 6 without (Stage 2 or 2.5), using a quantitative test based on the clinical pull test. Their findings were compared with those for 12 healthy controls. The patients on their usual medications were pulled either forwards or backwards at the level of the shoulders and asked not to take a step in a series of five trials. Acceleration was monitored for the upper trunk, sacrum, and both tibias. EMG was measured in soleus and tibialis anterior (TA) muscles in all and for thigh and truncal muscles in a subgroup. A target of 0.2 g trunk acceleration was used, but smaller perturbations were used in very unstable patients. All the Stage 3 patients lost balance in at least one trial for the posterior perturbations but none for the anterior ones. None of the Stage 2 patients lost balance. There was increased tonic EMG and agonist activity but no difference in EMG onset or initial force production compared to healthy controls. For posterior perturbations, there were two related disorders that separated the PD patients from controls. There was a significantly higher ratio of sacral-to-applied acceleration and both PD groups showed reduced knee acceleration and shortened latency, more so for the Stage 3 group. The increased sacral-to-C7 acceleration ratio was correlated with the tonic level of activation of the hamstrings (HS), quadriceps, and lumbar paraspinal muscles (PS), while the tibial acceleration latency was also correlated with the level of tonic PS activation. We also found that the size of balance responses, 0-200 ms post-perturbation, correlated significantly with the level of tonic activation in nearly all the muscles studied. We confirmed that PD patients show greater instability posteriorly than anteriorly to applied perturbations. Our findings support increasing axial and limb rigidity as the cause of the impaired pull test rather than postural bradykinesia and suggest that tonic truncal and thigh muscle activation may be an important underlying cause.
我们研究了 12 例帕金森病（PD）患者：6 例姿势不稳定（Hoehn 和 Yahr 分期 3 期），6 例无（分期 2 期或 2.5 期），使用基于临床拉力测试的定量测试。将他们的发现与 12 名健康对照者进行比较。患者在服用常规药物的情况下，在肩部水平向前或向后拉动，并要求在连续五次试验中不迈出一步。监测上躯干、骶骨和胫骨的加速度。所有患者均测量比目鱼肌和胫骨前肌（TA）的肌电图，部分患者还测量大腿和躯干肌肉的肌电图。使用 0.2g 躯干加速度作为目标，但在非常不稳定的患者中使用较小的干扰。所有 3 期患者在后向干扰的至少一次试验中失去平衡，但在前向干扰中没有。没有 2 期患者失去平衡。与健康对照组相比，PD 患者的张力性肌电图和激动剂活动增加，但肌电图起始和初始力产生无差异。对于后向干扰，有两个相关的障碍将 PD 患者与对照组分开。骶骨与施加加速度的比值显著升高，PD 两组的膝关节加速度降低，潜伏期缩短，3 期组更为明显。增加的骶骨与 C7 加速度比值与腘绳肌（HS）、股四头肌和腰椎旁脊柱肌肉（PS）的紧张水平激活相关，而胫骨加速度潜伏期也与 PS 紧张激活水平相关。我们还发现，平衡反应的大小（扰动后 0-200ms）与几乎所有研究肌肉的紧张激活水平显著相关。我们证实 PD 患者对施加的干扰向后比向前更不稳定。我们的发现支持轴向和肢体僵硬增加是拉力测试受损的原因，而不是姿势性运动迟缓，并表明紧张性躯干和大腿肌肉激活可能是一个重要的潜在原因。
