Thomas C K, Zaidner E Y, Calancie B, Broton J G, Bigland-Ritchie B R
Department of Neurological Surgery, University of Miami School of Medicine, Miami, Florida 33136, USA.
Exp Neurol. 1997 Dec;148(2):414-23. doi: 10.1006/exnr.1997.6690.
Muscle weakness and failure of central motor drive were assessed in triceps brachii muscles of individuals with chronic cervical spinal cord injury (SCI) and able-bodied controls. Electrical stimuli were applied to the radial nerve during rest and during triceps submaximal and maximal voluntary contractions (MVCs). The mean forces and integrated EMGs generated by SCI subjects during MVCs were significantly less than those produced by controls (P < 0.01), with 74 and 71% of muscles generating <10% control force and EMG, respectively. There was an inverse linear relationship between the evoked and voluntary forces (n = 32 muscles of SCI subjects) which, when extrapolated to zero evoked force, also showed significant whole muscle weakness for SCI compared to control subjects (P < 0. 01). Severe muscle atrophy was revealed which might reflect disuse and/or muscle denervation subsequent to motoneuron loss. Many triceps muscles of SCI subjects showed no force occlusion (n = 41) or were impossible to stimulate selectively (n = 61). Force was always evoked when the radial nerve was stimulated during MVCs of SCI subjects. The force elicited by single magnetic shocks applied to the motor cortex at Cz' during voluntary contractions of SCI subjects was also inversely related to the voluntary triceps force exerted (n = 18), but usually no force could be elicited during MVCs. Thus central motor drive was probably maximal to these muscles, and the force evoked during MVCs by below-lesion stimulation must come from activation of paralyzed muscle. SCI subjects also had significantly longer mean central nervous system (CNS) conduction times to triceps (P < 0.01) suggesting that the measured deficits reflect CNS rather than peripheral nervous system factors. Thus, the weak voluntary strength of these partially paralyzed muscles is not due to submaximal excitation of higher CNS centers, but results mainly from reduction of this input to triceps motoneurons.
在慢性颈脊髓损伤(SCI)患者和健全对照者的肱三头肌中评估肌肉无力和中枢运动驱动功能。在休息时以及肱三头肌次最大和最大自主收缩(MVC)期间,对桡神经施加电刺激。SCI受试者在MVC期间产生的平均力量和积分肌电图明显低于对照组(P < 0.01),分别有74%和71%的肌肉产生的力量和肌电图小于对照组的10%。诱发力和自主力之间存在反向线性关系(n = SCI受试者的32块肌肉),当外推到零诱发力时,与对照受试者相比,SCI患者的全肌肉无力也很明显(P < 0.01)。显示出严重的肌肉萎缩,这可能反映了运动神经元丧失后的废用和/或肌肉去神经支配。许多SCI受试者的肱三头肌没有力量封闭(n = 41)或无法选择性刺激(n = 61)。在SCI受试者的MVC期间刺激桡神经时总是能诱发出力量。在SCI受试者自主收缩期间,在Cz'处对运动皮层施加单次磁刺激所诱发的力量也与所施加的肱三头肌自主力量呈负相关(n = 18),但在MVC期间通常无法诱发出力量。因此,中枢运动驱动可能对这些肌肉是最大的,并且在MVC期间由损伤以下刺激诱发的力量一定来自瘫痪肌肉的激活。SCI受试者到肱三头肌的平均中枢神经系统(CNS)传导时间也明显更长(P < 0.01),这表明所测量的缺陷反映的是中枢神经系统而非外周神经系统因素。因此,这些部分瘫痪肌肉的自主力量较弱不是由于高级中枢神经系统中心的次最大兴奋,而是主要由于对肱三头肌运动神经元的这种输入减少。