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November 1970

Immunosuppression and the Guillain-Barré Syndrome

Author Affiliations

From the Department of Neurology (Dr. Drachman); the Section of Infectious Diseases—Hypersensitivity, Department of Medicine (Dr. Paterson); Northwestern University Clinical Virology Laboratory, departments of medicine and pathology (Dr. Berlin); and the Renal Section, Department of Medicine (Dr. Roguska); Northwestern University McGaw Medical Center, Chicago.

Arch Neurol. 1970;23(5):385-393. doi:10.1001/archneur.1970.00480290005001

ALTHOUGH idiopathic polyneuritis, or the "Landry-Guillain-Barré (LGB) syndrome" has been known for more than 100 years,1 its nosologic limits, etiology, and treatment remain a matter of controversy.2-23 Current opinion favors an autoallergic pathogenesis, and many authors have drawn attention to experimental allergic neuritis (EAN) first described by Waksman and Adams24 as the appropriate experimental model of this clinical condition.12,14-17 As a natural outgrowth of this concept, immunosuppressive treatment has been suggested as specific therapy for the LGB syndrome. Experimentally, steroids have been shown to prevent EAN,25 and both steroids and immunosuppressive drugs will prevent the closely related experimental allergic encephalomyelitis (EAE) consistently in animals.26-30 With but one exception,31 the drugs are effective only if given before the onset of clinical evidence of paralysis. The use of steroids and adrenocorticotropic hormone in humans with idiopathic polyneuritis has been less successful, however.5,7,10,12,-17,21-23,32

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