Polioencephalitis

First of all, in order to distinguish this from two other lesions which have been termed polioencephalitis inferior (progressive bulbar paralysis) and polioencephalitis superior (nuclear ophthalmoplegia), let us speak of this as polioencephalitis corticalis. What proof have we that there is such a condition? Anatomical proof, none; we are willing to concede, however, that some of the many cases of atrophy and sclerosis may have been due to this polioencephalitis, but it is unfortunate for Strümpell's theory that all of the autopsies made soon after the onset of the disease have shown other conditions, and not a polioencephalitis.

Before dismissing the subject of acute polioencephalitis it is necessary to devote a few paragraphs to the mention of a similar inflammatory process in other parts of the central nervous system.

The restriction of the inflammatory process to the gray matter in the polioencephalitis group was explained by the presumption that viruses are present mainly in the cell bodies of neurons, as they have an affinity for the nerve cells themselves: gangliocytotropism or neurocytotropism (Környey 1933)

Encephalitic processes are further subdivided into three main types: □ Polioencephalitis (Greek: polios, grey) is grey-matter predominant. □ Leukoencephalitis (Greek: leukos, white) is white-matter predominant. □ Panencephalitis (Greek: pan-, all) affects both grey and white matter.