ALTHOUGH idiopathic polyneuritis, or the "Landry-Guillain-Barré (LGB) syndrome" has been known for more than 100 years,¹its nosologic limits, etiology, and treatment remain a matter of controversy.²⁻²³Current opinion favors an autoallergic pathogenesis, and many authors have drawn attention to experimental allergic neuritis (EAN) first described by Waksman and Adams²⁴as the appropriate experimental model of this clinical condition.¹²,¹⁴⁻¹⁷As 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,²⁵and both steroids and immunosuppressive drugs will prevent the closely related experimental allergic encephalomyelitis (EAE) consistently in animals.²⁶⁻³⁰With but one exception,³¹the 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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Drachman et al. (1970) studied this question.
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