Impact of disuse muscular atrophy on the compound muscle action potential.

BACKGROUND: Disuse atrophy from immobilization is the result of decreased neural activity and muscle unloading. METHODS: We studied the impact of disuse on hand intrinsic compound muscle action potentials (CMAPs) in a cohort of 39 patients with unilateral 6-week immobilization of the hand in a cast, after distal radius fracture. We excluded patients with nerve injury. We compared side-to-side CMAP characteristics at the time of cast removal and at a subsequent follow-up visit, after a mean interval of 7.8 weeks. RESULTS: Statistically significant reductions in CMAP amplitude were noted for the abductor pollicis brevis (29.2%), abductor digiti minimi (19.0%), and first dorsal interosseus (24.9%). There was partial repair of the relative CMAP reduction at the follow-up visit (20.1%, 10.7%, and 8.7%, respectively). There was no significant change in CMAP duration. CONCLUSIONS: These results provide a framework for quantifying the degree of hand intrinsic CMAP amplitude reduction attributed to disuse.

Correction: Systematic prospective electrophysiological studies of the median nerve after simple distal radius fracture.

[This corrects the article DOI: 10.1371/journal.pone.0231502.].

Systematic prospective electrophysiological studies of the median nerve after simple distal radius fracture.

PURPOSE: To assess whether there is a measurable impairment of median nerve conduction study parameters with uncomplicated distal radius fracture. METHODS: Patients were assessed prospectively at the time of cast removal (visit 1) after a standard 6-8 week immobilization for uncomplicated distal radius fracture. Patients with prior entrapment neuropathy or polyneuropathy were excluded. Patients were asked to report sensory symptoms. Median and ulnar motor and sensory conduction studies were performed bilaterally, as well as transcarpal stimulation. All electrophysiologic studies were repeated at a follow-up visit 2, on average 7.8 weeks later. RESULTS: 39 patients were assessed at visit 1 and 30 (77%) were available for follow-up visit 2. Paresthesia in the median territory on the fractured side were reported in 20% at visit 1 and 26% at visit 2. Electrophysiological evidence of only mild carpal tunnel syndrome was found on the fractured side in 4/39 at visit 1 and 6/30 at visit 2. There were only 2 cases of moderate-marked median neuropathy, both asymptomatic and on the unfractured side. Median motor and sensory latencies and amplitudes did not show statistically significant differences between fractured and unfractured sides with the single exception of median distal motor latency at visit 1. CONCLUSIONS: Median territory paresthesia at the time of cast removal following distal radius fracture are often not associated with electrophysiologic evidence of median neuropathy. Most median nerve electrophysiologic parameters do not significantly differ between the fractured and uninjured sides. Significant traumatic median neuropathy is not likely to be a frequent manifestation of uncomplicated distal radius fracture. LEVEL OF EVIDENCE: Diagnostic analysis, Level III.

Distal Cervical Spondylotic Amyotrophy: Case Reports Demonstrating Clinical/Imaging Segmental Discrepancy.

Monomelic pure motor amyotrophy may seem to be an ominous syndrome as it leads to consideration of motor neuron disease. We present a series of 3 very similar cases where unilateral pure distal lower motor neuron paresis and atrophy was limited to the C8-T1 myotomes, without long-tract signs. Electrodiagnostic studies were in keeping with a restricted anterior horn cell disorder. Neuroimaging showed very focal spinal cord compression at the C6-7 level. Two patients underwent surgical decompression. All 3 patients were improved or stable at follow-up. Distal spondylotic amyotrophy is characterized by equal involvement of thenar and hypothenar muscles, in contrast to amyotrophic lateral sclerosis or Hirayama disease. We discuss the striking 2-level discrepancy between imaging and clinical localization. Proposed explanations are arterial or venous compromise caudal to the site of compression. Anatomical variation such as a prefixed brachial plexus is unlikely. A similar imaging/clinical discrepancy has been documented in Hirayama disease and spondylotic myelopathy.