Late Progression of Poliomyelitis Paralysis: Discussion of Pathogenesis

Progression of weakness and muscle atrophy may be seen years after paralytic polio-myelitis. This paralysis probably results from physiologic and aging changes rather than from persistent infection. Nevertheless, persistent neural infection with polioviruses can occur in animals and humans. A recrudescence of paralysis and muscle wasting has been repeatedly observed years after paralytic poliomyelitis. This phenomenon raises questions regarding the possible pathogenesis of late sequel-ae without persistent infection and the possibility of chronic infection of neural cells with polio-viruses. Late Sequelae Without Persistent Infection Morphologic studies quantitating motor neurons at different ages [1] and physiologic studies esti-mating the size of motor units with aging [2] both indicate that in humans after the sixth decade of life an attrition of anterior horn cells begins. This appears to be of little clinical significance in normal individuals. However, if the population of anterior horn cells has been depleted by prior poliovirus infection, this attrition might cause appreciable weakness [3]. Furthermore, the re-maining anterior horn cells may be overloaded because of sprouting and widening of their fields of innervation, which might accelerate this cell loss. These phenomena of normal aging have been proposed as an explanation of the late accentua-tion of paralysis after paralytic poliomyelitis [4], and this mode of pathogenesis of late sequelae requires no speculation that there is viral persistence. Persistence of Polioviruses in Neural Systems of Animals Persistent infection with polioviruses seems highly unlikely, in view of the very rapid cytolytic nature of infection in cell cultures. Nevertheless, polio-viruses can persist in animals. Theiler's murine Please address requests for reprints to Dr. Richard T