Key result
Diving beyond 100 m triggers high-pressure neurological syndrome potentially mediated by serotonin.
Why the study?
High-pressure neurological syndrome occurs in divers beyond 100 m depth with unclear pathogenesis and limited prevention strategies.
This review highlights the pathogenesis of high-pressure neurological syndrome in deep diving and suggests serotonin as a key mediator and potential therapeutic target.
High-pressure neurological syndrome (HPNS) is a condition encountered in diving beyond a depth of 100 m. Manifestations include headache, tremor, myoclonus, neuropsychiatric disturbances and EEG changes. Convulsions are seen only in experimental animals. Most of the changes are reversible on surfacing but some such as memory disturbances may linger on for long periods. Excessive atmospheric pressure is the most important factor in the pathogenesis of HPNS. Neurotransmitter changes occur of which serotonin appears to be a more likely mediator because of the resemblance of HPNS to serotonin syndrome. Anesthetics and anticonvulsants have been used in experimental animals but are unsuitable for use in human divers. Breathing gas mixtures such as heliox have enabled the extension of depth of diving without HPNS. Use of 5-HT1A receptor antagonists may provide an interesting approach to prevention of HPNS.
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K. K. Jain (2009) conducted a review in High-pressure neurological syndrome (HPNS). High-pressure neurological syndrome is a condition encountered in diving beyond 100 m, characterized by neurological disturbances, where serotonin may be a key mediator.
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