In developed countries the viral transmission is oral to oral, whereas in developing countries where the sanitation is poor the transmission is fecal to oral. Acutely, the polio enterovirus enters the body via the gastrointestinal tract and reproduces in the gastrointestinal lymphoid tissue, termed gut-associated lymphoid tissue (GALT). Oral secretion of the virus takes place for several days and stool excretion for several weeks.

At a critical concentration, the virus spreads to the large motor nuclei of the spinal cord, the brainstem, and the reticular formation. The vestibular and brainstem motor nuclei, hypothalamus, thalamus, cerebellum, and the precentral motor cerebral cortex also can be infected by the poliovirus. The infected neurons, because of Nissl granule dissolution, are phagocytosed by inflammatory cells, causing neuronal loss and gliosis. Most affected neurons have an altered morphology, and half are destroyed during the first week of acute paralysis. Neuron loss then causes a cycle of muscle denervation and reinnervation, resulting in muscle loss of function.

The pathology of the postpolio syndrome remains unclear. It is suggested that postpolio fatigue is similar to that seen in chronic fatigue syndrome, both of which may cause fatigue by causing a relative depletion of central dopamine.24 This theory is supported by preliminary data that suggest a decrease in postpolio symptoms with the use of bromocriptine, the same drug used for relief of PD symptoms.25

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