Bisdorff A R, Bronstein A M, Wolsley C, Gresty M A, Davies A, Young A
Hôpital de la Ville, Esch-sur-Alzette, Luxembourg.
J Neurol Neurosurg Psychiatry. 1999 Apr;66(4):447-55. doi: 10.1136/jnnp.66.4.447.
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 (tibialis anterior) was also compared when evoked by a non-startling sound and by the free fall startle.
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.
(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.
对年轻和老年正常受试者、前庭功能缺失患者以及运动不能-强直综合征患者进行肌电图(EMG)对自由落体的惊吓反应研究。目的是检测有跌倒倾向的患者组在“着地反应”这一早期阶段是否存在任何紊乱。在正常受试者中,还比较了由非惊吓声音和自由落体惊吓诱发的随意肌收缩(胫前肌)的特征。
受试者仰卧在一张沙发上,沙发意外地被释放使其自由落体。通过头戴式线性加速度计检测自由落体开始时多个表面肌电图记录的潜伏期。
(1)年轻正常受试者的肌电图反应出现在:胸锁乳突肌54毫秒、腹部肌肉69毫秒、股四头肌78毫秒、三角肌80毫秒、胫前肌85毫秒。这种肌肉激活模式并非简单的从头到尾的进展,可能在惊吓脑干中枢中按时间/空间进行组织。(2)对惊吓刺激(跌倒)的反应中,胫前肌的随意肌电图激活比非惊吓刺激(声音)更早且更强。这表明惊吓反应可被视为一种增强运动反应性的网状机制。(3)老年受试者表现出相似的激活顺序,但延迟约20毫秒。这种延迟超过了中枢和外周运动传导减慢所能解释的范围,因此提示中枢处理存在年龄依赖性延迟。(4)无前庭功能的患者潜伏期正常,表明自由落体惊吓可由非前庭输入诱发。(5)特发性帕金森病患者的潜伏期正常,而多系统萎缩(MSA)患者的反应更早,斯蒂尔-理查森-奥尔谢夫斯基(SRO)综合征患者的反应延迟或缺失。该患者组的研究结果提示:(1)多巴胺能对惊吓反应的时间没有影响,(2)MSA中同时存在的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。