Guillain-Barre Syndrome

Scuba Diving Concerns:

This condition has skeletal muscle weakness which can involve extremity, truncal or bulbar groups and typically evolves over a matter of several hours to a few days can affect diving and boat crew abilities creating safety in the water as well as buddy rescue concerns. In the C. Miller-Fisher variant, ataxia as well as ophthalmoplegia (internal and external) accompany the obligatory findings of areflexia. Dysautonomia may also be present, posing an additional concern regarding tolerance of water pressure and immersion changes, blood pressure and cardiac rhythm disturbances that may be especially life-threatening in the underwater environment.

Return to diving:

Can be considered after full recovery of strength and autonomic nervous system function. Tendon-stretch reflexes may never return but would not prohibit return to diving.

Data needed to decide return to diving:

Neurology or PM&R (physical medicine and rehabilitation) consultation with quantified strength testing of all motor groups and assessment of autonomic nervous system function (orthostatic BP measurements, treadmill testing and, if appropriate, thermal stress testing). Consider performing gear management, entrance and water exit testing and buddy rescue.


Plasmapheresis and/or intravenous immunoglobulin (IVIG) therapy is warranted in those cases which involve weakness progressing to the point of impairing walking or respiratory abilities. Adrenocorticosteroid therapy is not beneficial and may actually worsen the outcome.

Disease notes:

Antecedent flu-like illness within two weeks prior to the onset of neurological symptoms occurs in approximately 65% of cases. This syndrome often occurs in clusters of small epidemic proportions and may have broad spectral presentations ranging from minor (e.g. Bell’s palsy) to severe (complete paralysis of all skeletal muscle groups with respiratory and cardiovascular support dependency).

Obviously, diving should not be considered and cannot occur under these conditions.

Some of these patients may experience relapses and progress to chronic inflammatory demyelinating polyneuropathy (CIDP). HIV victims may present with AIDP. Lyme disease may mimic AIDP. The presence of pleocytosis in the CSF is incompatible with AIDP and suggest alternative diagnoses (e.g. sarcoidosis, leptomeningeal lymphomatosis).


Ernest S. Campbell, M.D., FACS

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