Muscle Weakness, Paralysis, and Atrophy after Human Cervical Spinal Cord Injury

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 cont...

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Bibliographic Details
Published in:	Experimental neurology Vol. 148; no. 2; pp. 414 - 423
Main Authors:	Thomas, C.K., Zaidner, E.Y., Calancie, B., Broton, J.G., Bigland-Ritchie, B.R.
Format:	Journal Article
Language:	English
Published:	Amsterdam Elsevier Inc 01-12-1997 Elsevier
Subjects:	Adult Atrophy Biological and medical sciences Electric Stimulation Electromyography Female Humans Injuries of the nervous system and the skull. Diseases due to physical agents Male Medical sciences motor evoked potential Motor Neurons - physiology muscle compound action potential Muscle Contraction muscle denervation muscle strength Muscle Weakness - etiology Muscle, Skeletal - innervation Muscle, Skeletal - pathology Muscle, Skeletal - physiopathology nerve stimulation Neural Conduction Paralysis - etiology Radial Nerve - physiology Radial Nerve - physiopathology Reaction Time Reference Values Spinal Cord Injuries - complications Spinal Cord Injuries - physiopathology Time Factors Traumas. Diseases due to physical agents twitch occlusion voluntary muscle activation muscle strength voluntary muscle activation twitch occlusion motor evoked potential nerve stimulation muscle compound action potential muscle denervation Human Nervous system diseases Spinal cord Motor system disorder Triceps muscle Trauma Atrophy Striated muscle disease Central nervous system disease Complication Paralysis Spinal cord disease Cervical spine
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Summary:	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.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0014-4886 1090-2430
DOI:	10.1006/exnr.1997.6690