EMG responses to free fall in elderly subjects and akinetic rigid patients
EMG responses to free fall in elderly subjects and akinetic rigid patients
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老年受试者和不能运动的僵硬患者对自由落体的肌电图反应
DOI：
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发表时间：
1999
影响因子：
11
通讯作者：
A. Young
中科院分区：
文献类型：
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作者：
A. Bisdorff;A. Bronstein;C. Wolsley;M. Gresty;A. Davies;A. Young
研究了年轻和老年正常受试者、前庭功能缺失患者和运动不能-僵硬综合征患者对自由落体的EMG惊吓反应。其目的是在有跌倒倾向的患者群体中检测“着陆反应”的早期阶段的任何紊乱。在正常受试者的自愿肌肉收缩（tibilais前）的特点也进行了比较时，诱发的非惊人的声音和自由落体惊吓。方法受试者仰卧在沙发上，意外释放成自由落体。测量了由头戴式线性加速度计检测的自由落体开始时的多个表面EMG记录的延迟。结果和结论：（1）年轻正常人的肌电图反应发生在：胸锁乳突肌54 ms，腹肌69 ms，四头肌78 ms，三角肌80 ms，胫骨前肌85 ms。这种模式的肌肉激活，这不是一个简单的rostrocaudal进展，可能是时间/空间组织在惊吓脑干中心。(2)自发性胫骨肌肌电图激活是更早和更强的反应，一个惊人的刺激（下降）比一个非惊人的刺激（声音）。这表明，惊吓反应可以被视为一种网状机制，提高运动反应性。(3)老年受试者表现出类似的激活序列，但延迟约20毫秒。这种延迟超过可以解释为中枢和外周运动传导减慢，因此表明年龄依赖性延迟中枢处理。(4)前庭性患者的潜伏期正常，表明自由落体惊吓可由非前庭输入引起。(5)特发性帕金森病患者的Lavenin反应正常，而多系统萎缩（MSA）患者的反应较早，Steele-Richardson-Olszewski（SRO）综合征患者的反应延迟或不存在。该患者组的研究结果表明：（1）缺乏多巴胺能对惊吓反应时间的影响，（2）MSA并发小脑受累可能导致惊吓抑制解除，（3）SRO中广泛的网状结构损伤严重干扰了对自由落体的反应。
OBJECTIVES The EMG startle response to free fall was studied in young and old normal subjects, patients with absent vestibular function, and patients with akinetic-rigid syndromes. The aim was to detect any derangement in this early phase of the “landing response” in patient groups with a tendency to fall. In normal subjects the characteristics of a voluntary muscle contraction (tibilais anterior) was also compared when evoked by a non-startling sound and by the free fall startle. METHODS Subjects lay supine on a couch which was unexpectedly released into free fall. Latencies of multiple surface EMG recordings to the onset of free fall, detected by a head mounted linear accelerometer, were measured. Results and conclusions—(1) EMG responses in younger normal subjects occurred at: sternomastoid 54 ms, abdominals 69 ms, quadriceps 78 ms, deltoid 80 ms, and tibialis anterior 85 ms. This pattern of muscle activation, which is not a simple rostrocaudal progression, may be temporally/spatially organised in the startle brainstem centres. (2) Voluntary tibialis EMG activation was earlier and stronger in response to a startling stimulus (fall) than in response to a non- startling stimulus (sound). This suggests that the startle response can be regarded as a reticular mechanism enhancing motor responsiveness. (3) Elderly subjects showed similar activation sequences but delayed by about 20 ms. This delay is more than can be accounted for by slowing of central and peripheral motor conduction, therefore suggesting age dependent delay in central processing. (4) Avestibular patients had normal latencies indicating that the free fall startle can be elicited by non-vestibular inputs. (5) Latencies in patients with idiopathic Parkinson’s disease were normal whereas responses were earlier in patients with multiple system atrophy (MSA) and delayed or absent in patients with Steele-Richardson-Olszewski (SRO) syndrome. The findings in this patient group suggest: (1) lack of dopaminergic influence on the timing of the startle response, (2) concurrent cerebellar involvement in MSA may cause startle disinhibition, and (3) extensive reticular damage in SRO severely interferes with the response to free fall.