BRAIN-STEM AUDITORY-EVOKED POTENTIALS DURING A HELIUM-OXYGEN SATURATION DIVE TO 450 METERS OF SEAWATER

Citation
J. Lorenz et al., BRAIN-STEM AUDITORY-EVOKED POTENTIALS DURING A HELIUM-OXYGEN SATURATION DIVE TO 450 METERS OF SEAWATER, Undersea & hyperbaric medicine, 22(3), 1995, pp. 229-240
Citations number
26
Categorie Soggetti
Medicine Miscellaneus","Marine & Freshwater Biology
ISSN journal
10662936
Volume
22
Issue
3
Year of publication
1995
Pages
229 - 240
Database
ISI
SICI code
1066-2936(1995)22:3<229:BAPDAH>2.0.ZU;2-N
Abstract
When divers are exposed to extreme atmospheric pressures they may exhi bit symptoms of the high pressure nervous syndrome (HPNS). Although cl inical HPNS symptoms are well described, little is known about the und erlying pathophysiologic mechanisms. Special HPNS signs like vertigo a nd tremor suggested sensory-motor hyperexcitability resulting from bra instem dysfunction. We therefore studied brainstem auditory evoked pot entials (BAEP) repeatedly in four divers during an experimental deep h elium-oxygen saturation dive to 450 meters of seawater (msw). Wave I ( auditory nerve response) latency decreased whereas interpeak latencies (IPLs) I-III and I-V, which indicate respective cochieo-pontine and c ochleo-mesencephalic transmission time, prolonged during the dive. IPL s III-V also prolonged the dive, but with greater variability among di vers. Two divers showed a marked reversal of the normal attenuation ef fect of increased stimulus presentation rates on IV and V amplitudes d uring compression, an effect that subsided during the stay at bottom d epth. This finding might indicate a relative enhancement of synaptic e xcitability and is presumed to be a feature of HPNS. Wave I latency re duction might at least partly be caused by accelerated sound conductio n in dense helium. Additionally, an upward shift of middle ear resonan ce frequencies in helium can induce a basal shift of the main cochlear portion responding to the wide band clicks. This effect may reduce wa ve I latency due to greater relative input from the basal high frequen cy-short latency-cochlear neurons. Pressure-induced decrease of nerve conduction velocity, delay of synaptic transmission, and inhibitory mo dulation of midbrain auditory afferents possibly contributed to observ ed interpeak latency prolongations. Clinical HPNS signs, such as tired ness, dizziness, postural and intentional hand tremor, ataxia, and ops oclonus, were noted in three divers after reaching 300 msw and continu ed throughout the 37-h stay at bottom depth.