Abstract
The Guillain-Barré Syndrome (GBS) is the most common cause of acute neuromuscular paralysis in developed countries, affecting 1–2 people per 100,000 annually. The mortality is about 10%, and approximately 20% of patients are left with significant motor disability. Our understanding of GBS has evolved since Landry’s description of the clinical features of “acute ascending paralysis” in the late 1800s and Guillain and Barré’s recognition of the albuminocytological dissociation in the cerebrospinal fluid in the early 1900s. It is classically regarded an acute demyelinating polyradiculoneuropathy, characterized clinically by the acute onset of symmetric weakness and arreflexia with relatively minor sensory impairment. Cerebrospinal fluid (CSF) analysis characteristically yields an elevated protein concentration but little or no pleocytosis, and the electrophysiology reveals evidence of demyelination. Over the years, however, unusual variants of this syndrome have been recognized, including an axonal form. Plasmapheresis and intravenous immunoglobulin (IVIg) have become the mainstay of therapy and steroids are thought not to be beneficial.
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© 2006 Humana Press Inc., Totowa, NJ
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Benatar, M. (2006). Guillain-Barré Syndrome. In: Benatar, M. (eds) Neuromuscular Disease. Humana Press. https://doi.org/10.1007/978-1-59745-106-2_11
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DOI: https://doi.org/10.1007/978-1-59745-106-2_11
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