Page:Acute Poliomyelitis.djvu/41



Charcot and Joffroy, who were among the first to investigate the pathology of the disease, taught that acute poliomyelitis was a parenchymatous process; that the ganglion cells attacked by the virus were destroyed; and that an inflammatory reaction followed. This teaching was based upon observation of a case in which several years after the initial attack the principal lesion discovered was destruction of the ganglion cells. This conception of acute poliomyelitis as a systemic disease corresponds completely with the clinical picture. In Charcot's day, as only cases of long standing were examined, the opinion prevailed that the disease produced a purely motor paralysis. Hence, little attention was paid to the observations of Roger and Damaschino, who laid special stress upon the interstitial nature of the changes, but who left open the question why the changes were limited to the anterior horns.

Rissler and v. Kahlden strongly advocated Charcot's theory. Rissler supported his advocacy by citing one special case in which the infiltration of the vessel and of the interstitial tissue was less marked than the degeneration of the ganglion cells. I should like to emphasize that he was the first to record and depict these interstitial changes. Further, he did not blindly adhere to Charcot's tenets, but admitted the possibility that the disease virus might simultaneously implicate the ganglion cells and the vessel walls. As von Kahlden relied solely upon observation of chronic cases, his horizon was limited.

All recent observers agree that Charcot's doctrine is untenable. The changes beyond the motor region, for example, in the posterior columns and in the pia, are not explicable as secondary to degeneration of ganglion cells; nor is there, at least in many areas, a primary affection of the ganglion cells. Thus, in the bulb, in distinctly infiltrated areas, even with our modern delicate staining methods, the ganglion cells appear normal. At first sight, such a condition as is depicted in Plate I, Fig. I, where neurophages occur in the midst of a densely infiltrated tissue, seems to support Char-