Guillain-Barré syndrome, or infective neuronitis, is a neurological entity characterized by inflammation of multiple nerves with facial diplegia and albuminocytological dissociation of the cerebrospinal fluid. The pathogenesis is not well understood. Attempts to isolate a responsible micro-organism have proved unsuccessful.1 In many instances the disease appears a few days after administration of a sulfonamide, after an infection of the upper respiratory tract, or after any of a wide variety of illnesses.2 In 1950 Reitman and Rothschild3 discussed an illuminating case in which the Guillain-Barré syndrome developed nine days after injection of tetanus antitoxin. Several similar cases had been previously reported.4 The initial pathological response of the nervous system consists in pronounced swelling of the nerve fibers in the spinal roots, spinal cord tracts, and the cranial and peripheral nerves.5
Such observations suggested to us that the disease might be, in some instances at least, a
Blood A, Locke W, Carabasi R. GUILLAIN-BARRÉ SYNDROME TREATED WITH CORTICOTROPIN (ACTH): REPORT OF A CASE. JAMA. 1953;152(2):139–140. doi:10.1001/jama.1953.63690020013004g
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