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

Thomas, Christine K.; Zaidner, E.Y.; Calancie, Blair; Broton, James G.; Bigland-Ritchie, B.

doi:10.1006/exnr.1997.6690

Cited by 146 publications

(147 citation statements)

References 18 publications

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“…70% on average in triceps brachii and vastus lateralis). 11,12 Survival of thoracic motoneurons is just as important, despite the low proportion of motoneurons at these cord levels because thoracic motoneurons support respiration and trunk control. 34,35 Reduced numbers of large diameter motor axons in ventral roots occurred after spinal contusion due to a sports or motor vehicle accident, and after a laceration injury induced by gunshot ( Fig.…”

Section: Motoneuron Death Occurs Irrespective Of the Level Or Cause Omentioning

confidence: 99%

“…12 Even though models of spinal cord injury often show only a peripheral rim of spared white matter at the lesion epicenter, the extent varying with lesion severity, 48 most repair strategies focus on repair of long fiber pathways or remyelination 49,50 without consideration of how the requirements for axon regeneration or sprouting may have to change to accommodate death of spinal neurons. Motoneuron death must induce reorganization of spinal circuitry because motoneurons act as the central hub to coordinate output to muscle.…”

Section: Grumbles and Thomasmentioning

confidence: 99%

“…The contributions of chronic muscle denervation (due to motoneuron death and/or ventral root avulsion) and alterations in muscle use to the striking muscle weakness and atrophy seen after human spinal cord injury also remain unclear. [9][10][11][12][13] Motoneuron death after human spinal cord injury has largely been inferred from physiological signs of muscle denervation, not from morphological analysis. For example, various muscles innervated from the lesion epicenter have been unresponsive to electrical stimulation of their peripheral nerves, consistent with complete muscle denervation.…”

Section: Introductionmentioning

confidence: 99%

“…[14][15][16][17][18] Other studies have shown signs of partial denervation (low motor unit counts, positive sharp waves, small amplitude compound muscle action potentials, muscle weakness that exceeds that expected from disuse atrophy, atrophied and angular muscle fibers), including indications of intramuscular motor axon sprouting, an important compensatory mechanism for recovery of muscle innervation after death of some motoneurons in a motor pool (large polyphasic motor unit potentials, stronger than usual motor unit forces, increased motor unit fiber density, increased jitter in re-innervated muscle fibers). 12,[19][20][21][22][23] In this study, we address an important and often overlooked aspect of SCI-the effect of injury on the lesioned spinal cord segment and denervation of skeletal muscle as a contributor to muscular weakness. Our aim was to estimate the extent of motoneuron death from the number of large diameter myelinated axons in ventral roots taken post-mortem from individuals who had sustained a spinal cord injury at least 6 months earlier.…”

Section: Introductionmentioning

confidence: 99%

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Motoneuron Death after Human Spinal Cord Injury

Grumbles

Thomas

2017

Journal of Neurotrauma

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The severe muscle weakness and atrophy measured after human spinal cord injury (SCI) may relate to chronic muscle denervation due to motoneuron death and/or altered muscle use. The aim of this study was to estimate motoneuron death after traumatic human SCI. The diameter and number of myelinated axons were measured in ventral roots post-mortem because ventral roots contain large diameter (> 7 lm) myelinated axons that typically arise from motoneurons and innervate skeletal muscle. In four cases (SCI levels C7, C8, T4, and L1) involving contusion (n = 3) or laceration (n = 1), there was a significant reduction in the number of large diameter myelinated axons at the lesion epicenter (mean -standard error [SE]: 45 -11% Uninjured), one level above (51 -14%), and one (27 -12%), two (45 -40%), and three (54 -23%) levels below the epicenter. Reductions in motoneuron numbers varied by side and case. These deficits result from motoneuron death because the gray matter was destroyed at and near the lesion epicenter. Muscle denervation must ensue. In seven cases, ventral roots at or below the epicenter had large diameter myelinated axons with unusually thin myelin, a sign of incomplete remyelination. The mean -SE g ratio (axon diameter/fiber diameter) was 0.60 -0.01 for axons of all diameters in five above-lesion ventral roots, but increased significantly for large diameter fibers ( ‡ 12 lm) in three roots at the lesion epicenter. Motoneuron death after human SCI will coarsen muscle force gradation and control, while extensive muscle denervation will stifle activity-based treatments.

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Section: Motoneuron Death Occurs Irrespective Of the Level Or Cause Omentioning

confidence: 99%

Section: Grumbles and Thomasmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Motoneuron Death after Human Spinal Cord Injury

Grumbles

Thomas

2017

Journal of Neurotrauma

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“…This is particularly critical for interpreting motor recovery that occurs over time or after intervention, if spurious conclusions are to be avoided. The ability of SCI subjects to maximally activate their muscles by voluntary effort can be assessed by comparing the maximum voluntary force to that elicited by cortical stimulation [16]. If voluntary drive is maximal, no additional force should be evoked in the test muscle or muscle group in response to magnetic stimulation of the appropriate motor cortical area.…”

Section: Voluntary Contractionsmentioning

confidence: 99%

Physiological methods to measure motor function in humans and animals with spinal cord injury

Thomas

Noga

2003

JRRD

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Abstract-This article compares some physiological methods commonly used to measure the functional capability of the motor system in humans and animals after spinal cord injury. Some of the differences between animal and human experimentation are considered first. Then we discuss how to measure the effectiveness of conduction through the motor system. We describe ways to assess the integration of different inputs at the spinal cord and to measure the responsiveness of the neuromuscular system. We conclude that comparisons across species are invaluable to understand the control of movement, both before and after injury.

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Chronic muscle recordings reveal recovery of forelimb function in spinal injured female rats after cortical epidural stimulation combined with rehabilitation and chondroitinase ABC

Sinopoulou

Spejo

Roopnarine

et al. 2022

J of Neuroscience Research

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Cervical level spinal cord injury (SCI) can severely impact upper limb muscle function, which is typically assessed in the clinic using electromyography (EMG). Here, we established novel preclinical methodology for EMG assessments of muscle function after SCI in awake freely moving animals. Adult female rats were implanted with EMG recording electrodes in bicep muscles and received bilateral cervical (C7) contusion injuries. Forelimb muscle activity was assessed by recording maximum voluntary contractions during a grip strength task and cortical motor evoked potentials in the biceps. We demonstrate that longitudinal recordings of muscle activity in the same animal are feasible over a chronic post-injury time course and provide a sensitive method for revealing post-injury changes in muscle activity. This methodology was utilized to investigate recovery of muscle function after a novel combination therapy. Cervical contused animals received intraspinal injections of a neuroplasticitypromoting agent (lentiviral-chondroitinase ABC) plus 11 weeks of cortical epidural electrical stimulation (3 h daily, 5 days/week) and behavioral rehabilitation (15 min daily, 5 days/week). Longitudinal monitoring of voluntary and evoked muscle activity revealed significantly increased muscle activity and upper limb dexterity with the combination treatment, compared to a single treatment or no treatment. Retrograde mapping of motor neurons innervating the biceps showed a predominant distribution across spinal segments C5-C8, indicating that treatment effects were likely due to neuroplastic changes in a mixture of intact and injured motor neurons. Thus, longitudinal assessments of muscle function after SCI correlate with skilled reach and grasp performance and reveal functional benefits of a novel combination therapy.

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

Cited by 146 publications

References 18 publications

Motoneuron Death after Human Spinal Cord Injury

Motoneuron Death after Human Spinal Cord Injury

Physiological methods to measure motor function in humans and animals with spinal cord injury

Chronic muscle recordings reveal recovery of forelimb function in spinal injured female rats after cortical epidural stimulation combined with rehabilitation and chondroitinase ABC

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