Abstract
The theory that poliomyelitis is primarily a general systemic infection, with secondary invasion of the central nervous system, is shown to be untenable. Experimentally, the virus is strictly neurotropic, reproducing the disease in monkeys regularly and easily only when introduced into nervous tissue or into the nose. The latter is also a nervous route, since the olfactory nerves end peripherally in processes exposed on the mucosal surface and centrally in the brain itself. From the olfactory bulb, connecting nerve tracts lead through the brain stem to the spinal cord. This series of nerve tracts and centers corresponds with the distribution of lesions in man and with localizations of virus in monkeys after intranasal instillation. In man, the only important extranervous lesions consist of general lymphoid hyper plasia without corresponding distribution of virus, and they are probably incidental to the lymphocytic reaction in the central nervous system. The early symptoms in man are predominantly nervous. The order of their development agrees with the route of invasion through the interbrain, midbrain, medulla, posterior spinal horns and ganglia, and anterior spinal horns, suggested by experimental and pathological data. The tendency of human poliomyelitis to interrupted progression ("halting phenomenon") is emphasized in relation to the dromedary, abortive and other types of case, and also to the potential value of treatment. Large doses of immune serum may prevent the passage of virus from one neuron to another.

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