Guillain-Barre Syndrome


Last Updated : 3/25/2016
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Shawn Aylward
Guillain-Barre syndrome is an acute immune-mediated process resulting in injury to the peripheral nerves. It has a slight male predominance and a bimodal age distribution. Symptoms typically develop 3-6 weeks after an infection, often viral upper respiratory infections. Patients will complain of weakness that begins in the feet and ascends over time. If left untreated, it can cause weakness of the respiratory muscles and thus respiratory failure. Early diagnosis and treatment is paramount in reducing morbidity and mortality.

Guillain-Barre syndrome (GBS) is an immune-mediated process also referred to as acute inflammatory demyelinating polyneuropathy (AIDP). French neurologists Guillain, Barré and Strohl have been given credit for its description in a pair of WWI soldiers who developed acute areflexic paralysis with spontaneous recovery in 1916. The neuropathy usually affects the motor, sensory, and autonomic nerves in the extremities though it may also involve the ocular motor nerves, respiratory, facial, and bulbar muscles.

There is a broad differential in those presenting with acute weakness that can include stroke, encephalitis, acute poliomyelitis, acute myelopathy, myasthenia gravis, toxins, metabolic derangements (hypokalaemia, hypophosphataemia), myopathy, and disorders of periodic paralysis. Careful history and exam is able to localize the issue to the peripheral nerves, thus excluding cerebral, brain stem, spinal cord, cauda equina, muscle or neuromuscular junction causes. The differential for peripheral neuropathy includes AIDP, botulism, tick paralysis, post-rabies vaccine neuropathy, heavy metal/drugs, porphyria, diphtheria, and critical illness neuropathy.


Contributor Information and Disclosures Shawn Aylward
Assistant professor, Nationwide Children’s Hospital,
The Ohio State University. Columbus, OH. USA

First Created : 3/6/2001
Last Updated : 3/25/2016
Contributor Information and Disclosures

Last Updated : 3/25/2016
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