Radiation Therapy of the Guillain-Barré Syndrome

Abstract

Encephalomyeloradiculitis is an obscure clinical entity which has been the subject of considerable investigation, but its etiology remains unknown and therapy has been of a palliative nature only. This report deals with the clinical features of the disease and records the results of roentgen therapy in two cases, one the chronic type of involvement, and the other acute in character. In 1892, Osler (1) gave a clinical description of the syndrome, which he called “infectious polyneuritis.” The cerebrospinal fluid was not examined. Guillain and Barré (3), in 1916, reported a carefully studied series of cases and called attention for the first time to the fact that a normal cerebrospinal fluid cell count, associated with a high protein level, was the distinguishing characteristic of the syndrome. Several writers (2, 4, 5) have confirmed this observation. A number of names have been applied to the condition. Bradford, Bashford, and Wilson (4) reported 30 cases and stressed the importance of albuminocytologic dissociation as the distinctive feature. They coined the term, “acute infective polyneuritis.” The nomenclature of this syndrome also includes “acute ascending paralysis” (5) and “infectious neuronitis” (2). The authors cited above described an acute disease of the central nervous system characterized by a sudden onset and afebrile course, a flaccid paralysis involving cranial as well as peripheral nerves, radiculitis, and muscular soreness, with little or no involvement of the sensory tracts. There was an antecedent acute infection in most cases. The course was of several weeks duration, ending in recovery. More recently, McIntyre (7) and De Jong (8) have recorded a large series of cases and showed that the syndrome includes not only the acute cases ending in recovery, but also a second group running a protracted course, frequently with the development of permanent paralysis, and a third group terminating fatally, usually from bulbar paralysis. The clinical manifestations were similar in all groups, and albuminocytologic dissociation as described by Guillain and Barre was present in all cases. Most workers believe that some filtrable virus is responsible for the Guillain-Barré syndrome, although no specific virus has been proved to be the sole causative agent. Many authors have emphasized the frequency of antecedent upper respiratory infection. Others have reported diphtheria, thermal burns, and measles preceding the onset of the syndrome. It may well be that multiple neurotoxins are capable of producing the pathological changes found in these cases. The process is usually widespread, involving the brain, spinal cord, and peripheral nerves. Most of the changes are degenerative in type. Beading and fragmentation of the axis cylinders and myelin sheaths, proliferation of Schwarm cells, and, to a lesser degree, phagocytic and lymphocytic infiltration are characteristic.