The early lesions of poliomyelitis after intranasal inoculation: With comments on their relationship to the early clinical manifestations and to the nonparalytic cases

Abstract

Summary 1.Intravital staining with trypan blue of monkeys intransally inoculated with poliomyelitis virus gives selective staining in the central nervous system of areas of gray matter corresponding with those in which virus has previously been found to be present—particularly in the olfactory bulb and olfactory areas of the cortex and of the corpus striatum, in the brain stem, and spinal cord.The localizations of the dye are due largely to capillary dilatation of the capillary bed and partly to staining of tissue cells (endothelium of capillaries) and, in the medulla and cord, to staining of the nerve cells themselves. It is assumed that the capillary hyperemia is the first response to invasion of nerve cells with virus after the latter has reached the critical concentration necessary to affect the cellular metabolism. 2.By sacrificing animals, intravitally stained, on various days of the preparalytic period, the order of appearance and the descending progress of the lesions can be followed. 3.The first stage consists of lesions limited to the olfactory bulb and is accompanied by fever. 4.The second dtage consists of a marked and extensive reaction in the brain stem down to the medulla, with implication of the secondary olfactory centers (amygdaloid nucleus, uncinate gyrus). 5.The third stage consists of an increased involvement of the medulla and beginning implication of the spinal cord. 6.Later stages show localization in restricted areas in the cord itself, sometimes unilateral, with beginning subsidence of the reactions in the brain stem. 7.No significant variations were found in theorder of development of the lesions, but conspicuous variations occurred in theirspeed of evolution, their extent, and severity and in their localizations in the cord. 8.The present experiments suggest that, since the host cells for poliomyelitis virus are in all probability nerve cells, and since nerve cell degeneration in most of the areas manifestly invaded above the level of the medulla was conspicuously slight or absent, these cells must in many instances be invaded by virus without undergoing destruction and are therefore capable of full recovery. This principle is probably true even in the highly susceptible anterior horns of the cord and may account not only for the nonparalytic cases but also for the recovery, partial or complete, of the many patients with paralysis. 9.Reasons are discussed for believing that the present experiments can fairly be applied to human poliomyelitis; that inflammatory reactions in the brain stem occur in the brain stem in nonparalytic cases and in the preparalytic stage of paralytic cases, and that they are responsible for the initial and other early symptoms which are constant in recognizable cases of the disease. 10.It is not necessary or correct to postulate a preliminary period of systemic, general, or extranervous infection. The concept of poliomyelitis as a primary disease of the central nervous system is reaffirmed.