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Human brainstem auditory-evoked potentials in deep experimental diving to pressures up to 62.5 bar
J Lorenz1, G Athanassenas, P Hampe
1Underwater Medicine Department, DLR-Institute for Aerospace Medicine, Linder Höhe, Cologne, Germany.
Summary
High pressure neurologic syndrome (HPNS) effects on divers were studied using brainstem auditory-evoked potentials (BAEP). Slower compression and longer acclimation reduced HPNS symptoms and BAEP changes, indicating pressure affects neural transmission.
Area of Science:
- Neuroscience
- Diving Physiology
- High-Pressure Biology
Background:
- High Pressure Neurologic Syndrome (HPNS) limits human diving capabilities.
- The precise neural mechanisms of HPNS remain incompletely understood.
- Brainstem Auditory-Evoked Potentials (BAEP) offer a method to investigate neural function under pressure.
Purpose of the Study:
- To elucidate the neural underpinnings of HPNS.
- To assess the impact of compression rates and acclimation on HPNS.
- To investigate changes in auditory pathway function during deep dives.
Main Methods:
- Recorded BAEP in divers during two experimental chamber dives (Titan VIII and Titan XI) to depths up to 615 msw.
- Monitored for clinical HPNS symptoms, including vestibular disturbances and tremor.
- Analyzed latency and amplitude changes in BAEP components, particularly the IV/V complex.
Main Results:
- Prolongation of the IV/V complex in BAEP was observed at 525 msw during rapid compression (Titan VIII).
- Clinical signs and IV/V delay diminished with extended acclimation at depth (Titan XI) and slower compression.
- Absence of significant changes in Wave I and Wave III latency suggests suppression of pontomesencephalic transmission.
Conclusions:
- HPNS symptoms and BAEP alterations are influenced by compression rates and acclimation time.
- Pressure appears to suppress synaptic transmission or enhance inhibitory modulation within the auditory pathway.
- No persistent BAEP changes were noted post-dive, indicating reversible effects.