mained almost unappreciated until the accumulated evidence from the recent epidemics emphasized its enormous value.
The first of these great epidemics appeared in 1905 almost simultaneously in Norway and Sweden. Wickman fully reported the Swedish epidemic. He distinguished several new types,—a meningitic, an abortive, and a form resembling Landry's paralysis. The basis of Landry's paralysis he found sometimes to be an acute poliomyelitis; but he further noted—what until then had not been recognized—that most fatal cases run a course closely resembling that of a Landry's paralysis. His observations showed that the disease was a general infection with specific localization in the nervous system. Wickman's work was followed by that of Leegaard (1909), upon the Norwegian epidemic of 1905; by that of Zappert and others (1909), upon the Austrian epidemic of 1908; by the report of the American School (1910), upon the New York epidemic of 1907; and by a particularly valuable contribution from Ed. Müller (1910), upon the Hesse-Nassau epidemic of 1909.
Although Prévost and Vulpian, in 1865, had described atrophy of the anterior horn and of the motor ganglion cells in a case of infantile paralysis in which the acute stage of the disease was long passed; and Roger and Damaschino. in 1871, had reported the changes in the stage of recovery; Rissler, in 1885, was the first to give a comprehensive description of the pathologic-anatomical processes of the acute stage. He demonstrated the inflammatory reaction in the blood vessels and also the degeneration in the ganglion cells. Later, isolated cases were reported by Dauber, Goldscheider, Siemerling, Redlich, and others. Wickman, in 1905, published the first work comprising a large series of recent cases. By his, and by the subsequent investigations of Forssner, Sjovall, Harbitz and Scheel, Marburg, Beneke, Strauss and others, the pathological anatomy of the acute stage was conclusively demonstrated to be an acute meningoencephalopoliomyelitis.
Thanks, not only to the researches above mentioned, but also to those of Charcot and Joffroy, Roth, Fr. Schultze, and others, the changes in the chronic stage, however, had then long been known.
The first attempt to explain the morbid process was made by Charcot. He conceived it to be a primary degeneration of the ganglion cells with secondary involvement of the vessels. This was a simple and apparently adequate conception and it conformed
