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Guillain-Barré Syndrome
Michel Bonduelle, MD
Arch Neurol. 1998;55:1483-1484.
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INTRODUCTION
In 1859, Landry1 described the clinical features of acute ascending weakness without amyotrophy. Other 19th-century clinical descriptions followed, but the full extent of the motor polyradiculoneuritis and the characteristic albuminocytologic dissociation in the cerebrospinal fluid was only described in 1916 by Guillain, Barré, and Strohl.2 Guillain (1876-1961), who eventually held Charcot's Professorial Chair at the Salpiêtrière in Paris, France, encountered the syndrome in soldiers while he was chief staff physician for the Sixth Army Neurological Center at the North front in France. Over the subsequent 20 years, more than 30 such cases were documented in the international medical literature to which Guillain3 himself added 10 cases in his follow-up article of 1936. The condition became known internationally under the rubric Guillain-Barré syndrome (GBS). Although the condition was originally suspected to be infectious in nature, the distinctive pathological features led to hypotheses of immunological origin. This article cites . . . [Full Text of this Article]
EARLY REFERENCES
FULL CLINICAL DESCRIPTION
ADDITIONAL FEATURES AND CLINICAL VARIANTS
Ataxia Cranial Nerve Involvement Autonomic Involvement Natural History and Prognosis Cytoalbuminic Dissociation Etiologic and Pathological Features and Pathogenesis
Paris VI University, Paris, France
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Hand weakness onset Guillain-Barre syndrome
Mori et al.
J. Neurol. Neurosurg. Psychiatry 2004;75:169-170.
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