Polioencephalitis, stress, and the etiology of post-polio sequelae.
Post-mortem neurohistopathologies that document polio virus-induced lesions in reticular formation and hypothalamic, thalamic, peptidergic, and monoaminergic neurons in the brain are reviewed from 158 individuals who contracted polio before 1950. This polioencephalitis was found to occur in every case of poliomyelitis, even those without evidence of damage to spinal motor neurons. These findings, in combination with data from the 1990 National Post-Polio Survey and new magnetic resonance imaging studies documenting post-encephalitis-like lesions in the brains of polio survivors, are used to present two hypotheses: 1) polioencephalitic damage to aging reticular activating system and monoaminergic neurons is responsible for post-polio fatigue, and 2) polioencephalitic damage to enkephalin-producing neurons is responsible for hypersensitivity to pain in polio survivors. In addition, the antimetabolic action of glucocorticoids on polio-damaged, metabolically vulnerable neurons may be responsible for the fatigue and muscle weakness reported by polio survivors during emotional stress.
Bruno
R L
RL
Post-Polio Rehabilitation and Research Service, Kessler Institute for Rehabilitation, East Orange, NJ 07018.
Frick
N M
NM
Cohen
J
J
D001921:Brain / Q000473:pathology*; D005221:Fatigue / Q000378:metabolism; D005938:Glucocorticoids / Q000378:metabolism; D006801:Humans; D008279:Magnetic Resonance Imaging; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D010146:Pain / Q000503:physiopathology; D011051:Poliomyelitis / Q000473:pathology*; D016262:Postpoliomyelitis Syndrome / Q000473:pathology*; D012154:Reticular Formation / Q000473:pathology; D013312:Stress, Physiological / Q000503:physiopathology
D005938:Glucocorticoids