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Lower Motor Neuron Abnormality in Chronic Cervical Spinal Cord Injury: Implications for Nerve Transfer Surgery
Emily M Krauss, MD MSc FRCSC, University of British Columbia, Victoria, BC, Canada and Michael James Berger, MD, PhD, FRCPC, CSCN Diplomate (EMG), University of British Columbia, Division of Physical Medicine and Rehabilitation, Vancouver, BC, Canada

Introduction:Nerve transfers (NT) are a surgical option for restoring some upper limb functions in cervical spinal cord injuries (SCI), even in patients who are years after initial injury (i.e. chronic SCI). Success of NT is predicated on the health of the lower motor neuron (LMN) below the level of injury. We hypothesize that conventional electrodiagnostic techniques can demonstrate concomitant LMN injury at the level of SCI (i.e. metameric injury), potentially influencing the response to NT in the recipient muscle.

Materials & Methods: Six patients (n=11 limbs) with chronic SCI (neurological level C4-C6, AIS A-C; duration from injury=13±9.6 years) were prospectively evaluated using nerve conduction studies and needle electromyography (EMG), with standardized evaluation of potential recipient groups. Representative recipient muscles included long head of triceps (radial nerve), flexor pollicis longus (FPL; anterior interosseous nerve) and either extensor indicis proprius or extensor digitorum communis (EIP or EDC; posterior interosseous nerve). Distal amplitudes of compound muscle action potentials (CMAP) were described as normal, abnormal or absent, compared to established laboratory norms (FPL and EIP only). Evidence of muscle fibrosis (reduced insertional activity) and active denervation (e.g. fibrillations, positive sharp waves) were used as indicators of LMN involvement.

Results: Based on clinical indication, the electrodiagnostic feasibility of 22 potential NTs were evaluated. All 11 limbs demonstrated evidence of active denervation below the neurological level of injury. In 24/28 muscle groups, there was either evidence of active denervation, muscle fibrosis or absent/reduced CMAP. All limbs demonstrated evidence of denervation in either EIP, FPL, or both, indicating that the LMN abnormality extended several segments below the level of injury, below the metamere. In 8/11 muscles that demonstrated a CMAP, there was also evidence of denervation, indicative of a partial LMN injury.

Conclusions: All limbs in this study demonstrated evidence of LMN abnormality, extending several levels below the neurological level of injury. This data suggests that patients with chronic SCI should undergo comprehensive electrodiagnostic assessments, with careful evaluation of each potential recipient muscle group, in order to determine LMN integrity. The high prevalence of LMN abnormality suggests that screening should take place earlier in the natural history of SCI, in order to avoid irreversible neuromuscular mal-adapations (e.g. muscle fibrosis, end plate degradation, Wallerian degeneration). It is unclear whether a muscle with preserved CMAP, but with LMN abnormality on EMG, would still be a candidate recipient muscle.
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