Guillain-Barrè syndrome (GBS) is a subacute immune-mediated demyelinating neuropathy that may cause profound weakness and respiratory failure. Although the disease affects motor fibers preferentially, paresthesias and pain are common sensory manifestations. Autonomic dysfunction in GBS can affect the sympathetic and parasympathetic nervous systems. Autonomic manifestations comprise a combination of autonomic failure and autonomic overreactivity, the latter most commonly being manifested as sinus tachycardia and systemic hypertension. The core features of GBS are the acute onset of an ascending, predominantly motor polyradiculoneuropathy associated with areflexia and increased cerebrospinal fluid protein. Septic and autonomic complications are the major causes of death in GBS because respiratory failure is usually successfully managed with mechanical ventilation. The mainstay of treatment is supportive for the management of orthostatic hypotension (OH) and bowel and bladder symptoms. Because there is suggestive evidence of an immune-mediated process, treatment with intravenous (IV) immunoglobulin or plasma exchange should be undertaken in patients who have moderate to severe weakness, respiratory compromise, or who continue to worsen.
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