[Guillain-Barré syndrome and acute disseminated encephalomyelitis (ADEM)].

ABSTRACT

I would like to report the results of our immunological study on Guillain-Barré syndrome (GBS) and to consider the relationship between GBS and acute disseminated encephalomyelitis (ADEM). First of all, I referred to the historical view of the diagnostic criteria of GBS. Immunological study on GBS started after the report of experimental allergic neuritis (EAN) by Waksman and Adams (1995). We made EAN rabbits by immunization with peripheral myelin and observed the process of motor paralysis. In EAN, humoral and cellular immune responses to P2 protein and its synthetic peptides were obtained in accordance with the motor weakness. In patients with GBS we also investigated the humoral and cellular immune responses to P2 protein. Anti-P2 protein antibody and sensitized lymphocytes against P2 protein and its synthetic peptides were detected in GBS as well as in EAN. We also detected antineural antibodies such as anti-P0, anti-galactocerebroside and anti-GM1 ganglioside antibodies in GBS. And also anti-GQ1b antibody was detected in patients with Fisher syndrome and GBS with ophthalmoplegia. More than 50 years ago, Baker (1943) described 5 forms of GBS including 1) abortive or mononeuritic 2) polyneuritic 3) spinal, 4) bulbar and 5) cerebral forms. Guillain (1953) didn't deny the bulbar and cerebral forms, although he apparently denied the spinal form of GBS with Babinski's sign. According to "Merritt's Textbook of Neurology", lesions of ADEM (postinfectious and postvaccinal encephalomyelitis) involved not only the brain and the spinal cord but also the peripheral nerve. Guillain (1953) objected against "Landry-Guillain-Barré syndrome" proposed by Haymaker and Kernohan (1949). Guillain (1953) described that Landry's ascending paralysis was different from GBS and Landry's paralysis must belong to category of ADEM, as van Bogaert also commented. In our recent study for T cell subsets in GBS and ADEM, significant increase in activated CD4 and helper inducer cells were observed in both GBS and ADEM, which suggested the presence of a common pathogenic mechanism in these diseases. After considering the classification of immunological nervous diseases, we would propose a clinical entity "acute immuno-logical nervous diseases" including GBS, Fisher syndrome and ADEM.