Djajadikarta Zoë J, Dongés Siobhan C, Brooks Jack, Kennedy David S, Gandevia Simon C, Taylor Janet L
Neuroscience Research Australia, Sydney, NSW, Australia.
Neuroscience Research Australia, Sydney, NSW, Australia.
Mult Scler Relat Disord. 2020 Nov;46:102584. doi: 10.1016/j.msard.2020.102584. Epub 2020 Oct 14.
A common and disruptive symptom of multiple sclerosis is difficulty in walking. Deficits in ankle proprioception and in plantarflexor muscle function may contribute to these mobility issues. In this study, ankle proprioceptive ability and plantarflexor performance of people with multiple sclerosis (PwMS) were compared to healthy controls to determine whether multiple sclerosis causes impairments in these systems.
PwMS (n = 30, median EDSS 4.0, IQR 2) were compared to age- and sex-matched healthy controls (n = 30) across tests of ankle proprioception and plantarflexor muscle performance. Proprioceptive tests: detection of passive movement, reaction time and ankle joint position sense. Plantarflexor performance: strength, fatigue, recovery and voluntary activation (level of neural drive) of the plantarflexor muscles, assessed through brief and sustained fatiguing (2 min) isometric maximal voluntary contractions with nerve stimulation to evoke superimposed and resting muscle twitches.
PwMS had unimpaired movement detection and joint position sense but had a slower reaction time to respond with plantarflexion to an imposed ankle movement (between group difference = 0.11 [95% CI; 0.05 to 0.17] s). During brief, maximal contractions PwMS produced lower torque (difference = -25.1 [-42.0 to -8.2] Nm) with reduced voluntary activation (difference = -14.6 [-25.1 to -4.1]%) but no impairment of the muscle itself (resting twitch torque difference = 0.3 [-2.8 to 2.2] Nm). At the end of the fatiguing contraction, neural drive decreased for PwMS (-19.5 [-27.1 to -11.9]%, p <0.0001) but not for controls (-2.5 [-6.9 to 1.8]%, p = 0.242). Fatigue did not affect the resting twitch size for controls (-1.3 [-2.7 to -0.03] Nm, p = 0.134) or PwMS (-0.1 [-1.1 to 1.0] Nm, p = 0.90).
PwMS showed no deficit in their ability to sense ankle position or imposed movements but were slow when a motor response was required. Their plantarflexor muscles produced similar torque with electrical stimulation but voluntary strength was impaired. Both groups experienced overall fatigue following the 2-minute maximal voluntary contraction but PwMS also had significantly reduced neural drive indicating central fatigue. PwMS showed mainly central deficits in motor output at the ankle with little impairment of proprioceptive acuity.
行走困难是多发性硬化症常见且具有破坏性的症状。踝关节本体感觉和跖屈肌功能缺陷可能导致这些行动能力问题。在本研究中,将多发性硬化症患者(PwMS)的踝关节本体感觉能力和跖屈肌表现与健康对照者进行比较,以确定多发性硬化症是否会导致这些系统受损。
在踝关节本体感觉和跖屈肌性能测试中,将PwMS患者(n = 30,中位扩展残疾状态量表[EDSS]为4.0,四分位间距[IQR]为2)与年龄和性别匹配的健康对照者(n = 30)进行比较。本体感觉测试:被动运动检测、反应时间和踝关节位置觉。跖屈肌表现:通过短暂和持续疲劳(2分钟)的等长最大自主收缩并进行神经刺激以诱发叠加和静息肌肉抽搐,评估跖屈肌的力量、疲劳、恢复和自主激活(神经驱动水平)。
PwMS患者的运动检测和关节位置觉未受损,但对施加的踝关节运动做出跖屈反应的反应时间较慢(组间差异 = 0.11 [95%置信区间;0.05至0.17]秒)。在短暂的最大收缩过程中,PwMS患者产生的扭矩较低(差异 = -25.1 [-42.0至-8.2]牛米),自主激活降低(差异 = -14.6 [-25.1至-4.1]%),但肌肉本身未受损(静息抽搐扭矩差异 = 0.3 [-2.8至2.2]牛米)。在疲劳收缩结束时,PwMS患者的神经驱动下降(-19.5 [-27.1至-11.9]%,p <0.0001),而对照组未下降(-2.5 [-6.9至1.8]%,p = 0.242)。疲劳对对照组(-1.3 [-2.7至-0.03]牛米,p = 0.134)或PwMS患者(-0.1 [-1.1至1.0]牛米,p = 0.90)的静息抽搐大小无影响。
PwMS患者在感知踝关节位置或施加运动的能力方面没有缺陷,但在需要运动反应时速度较慢。他们的跖屈肌在电刺激下产生类似的扭矩,但自主力量受损。两组在进行2分钟最大自主收缩后均出现总体疲劳,但PwMS患者的神经驱动也显著降低,表明存在中枢性疲劳。PwMS患者主要在踝关节运动输出方面存在中枢性缺陷,本体感觉敏锐度受损较小。