The CNS in Guillain-Barre Syndrome

Oculomotor abnormalities found in cases of Fisher's syndrome can be explained by a central mechanism at least as well as by a peripheral one, and the two mechanisms are not mutually exclusive.

Abstract

To the Editor. —We read with interest the article on eye movement disorders in Fisher's syndrome by Meienberg and Ryffel 1 and the editorial on the CNS in Guillain-Barre syndrome by Ropper. 2 We agree with the conclusions expressed by the former authors that the oculomotor abnormalities found in cases of Fisher's syndrome can be explained by a central mechanism at least as well as by a peripheral one, and that the two mechanisms are not mutually exclusive. Ropper's view that the peripheral hypothesis provides the answer in all cases is extreme and misinterprets available evidence. Few could take issue with his statement that there is an absence of primary pathologic change in the brain stems of persons with Guillain-Barre syndrome, but this cannot be instantly extrapolated to include Fisher's syndrome. In our own series of patient with brain-stem encephalitis, 3 all 18 patients had ophthalmoplegia and ataxia, and ten