Late Denervation in Patients with Antecedent Paralytic Poliomyelitis

TLDR

New weakness, fatigue, and pain can emerge decades after acute paralytic poliomyelitis, constituting a recognized syndrome. The study compared clinical, electromyographic, and muscle‑biopsy findings in 18 post‑polio patients—13 with new weakness and 5 asymptomatic controls—to investigate late denervation. Late denervation was detected in all patients, with active denervation present in both symptomatic and asymptomatic groups, and the degree of past reinnervation correlated with ongoing motor‑unit instability. However, ongoing denervation does not distinguish patients with new weakness from those without, indicating that extensive reinnervation may be followed by late denervation of previously reinnervated fibers.

Abstract

The development of new weakness, fatigue, and pain decades after acute paralytic poliomyelitis is a recognized syndrome. We conducted a controlled study of this syndrome by analyzing clinical, electromyographic, and muscle-biopsy features in 18 patients with a history of poliomyelitis--13 reporting 1 to 20 years of new weakness and 5 without new symptoms. The patients with new weakness also reported new muscle atrophy (9 of 13) and fatigue (10 of 13), symptoms not reported by the controls. The age at the time of acute poliomyelitis, severity of poliomyelitis, residual disability, number of years since acute poliomyelitis, and age at the time of study were comparable in the weakening and control groups. Evidence of remote denervation consistent with antecedent poliomyelitis was demonstrated in all patients by electromyography or muscle biopsy or both. In addition, active denervation (as evidenced by spontaneous activity on conventional electromyography, increased jitter on single-fiber electromyography, or atrophic myofibers) was found in 12 patients in the weakening group and in all 5 controls. Immunohistochemical detection of myofibers expressing the neural-cell adhesion molecule corroborated ongoing denervation in both patient groups. When muscle data from both groups were pooled, correlations were observed between the extent of past reinnervation and the degree of ongoing motor-unit instability. We conclude that the extensive reinnervation of denervated muscle that occurs in paralytic poliomyelitis may be followed by late denervation of the previously reinnervated muscle fibers. Electromyographic and muscle-biopsy evidence of ongoing denervation does not distinguish between stable patients with prior paralytic poliomyelitis and those with new weakness.