Lorenz J, Brooke S T, Petersen R, Török Z, Wenzel J
DLR-Institute of Aerospace Medicine, Cologne, Germany.
Undersea Hyperb Med. 1995 Sep;22(3):229-40.
When divers are exposed to extreme atmospheric pressures they may exhibit symptoms of the high pressure nervous syndrome (HPNS). Although clinical HPNS symptoms are well described, little is known about the underlying pathophysiologic mechanisms. Special HPNS signs like vertigo and tremor suggested sensory-motor hyperexcitability resulting from brainstem dysfunction. We therefore studied brainstem auditory evoked potential (BAEP) repeatedly in four divers during an experimental deep helium-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 cochleo-pontine and cochleo-mesencephalic transmission time, prolonged during the dive. IPLs III-V also prolonged the dive, but with greater variability among divers. Two divers showed a marked reversal of the normal attenuation effect of increased stimulus presentation rates on IV and V amplitudes during compression, an effect that subsided during the stay at bottom depth. This finding might indicate a relative enhancement of synaptic excitability and is presumed to be a feature of HPNS. Wave I latency reduction might at least partly be caused by accelerated sound conduction in dense helium. Additionally, an upward shift of middle ear resonance frequencies in helium can induce a basal shift of the main cochlear portion responding to the wide band clicks. This effect may reduce wave I latency due to greater relative input from the basal high frequency-short latency-cochlear neurons. Pressure-induced decrease of nerve conduction velocity, delay of synaptic transmission, and inhibitory modulation of midbrain auditory afferents possibly contributed to observed interpeak latency prolongations. Clinical HPNS signs, such as tiredness, dizziness, postural and intentional hand tremor, ataxia, and opsoclonus, were noted in three divers after reaching 300 msw and continued throughout the 37-h stay at bottom depth.
当潜水员暴露于极端大气压力时，他们可能会出现高压神经综合征（HPNS）的症状。尽管临床HPNS症状已有详细描述，但对其潜在的病理生理机制却知之甚少。诸如眩晕和震颤等特殊的HPNS体征提示脑干功能障碍导致感觉运动性过度兴奋。因此，我们在一次实验性的深氦氧饱和潜水至450米海水深度（msw）的过程中，对四名潜水员反复进行了脑干听觉诱发电位（BAEP）研究。在潜水过程中，波I（听神经反应）潜伏期缩短，而峰间潜伏期（IPL）I-III和I-V（分别指示蜗神经核到脑桥和蜗神经核到中脑的传导时间）延长。IPL III-V在潜水过程中也延长，但潜水员之间的变异性更大。两名潜水员在加压过程中，刺激呈现率增加对波IV和波V振幅的正常衰减效应出现明显逆转，这种效应在停留于底部深度期间消退。这一发现可能表明突触兴奋性相对增强，并且被认为是HPNS的一个特征。波I潜伏期缩短可能至少部分是由于在高密度氦气中声音传导加速所致。此外，氦气中中耳共振频率的上移可导致对宽带点击做出反应的主要耳蜗部分发生基底移位。由于来自基底高频-短潜伏期-耳蜗神经元的相对输入增加，这种效应可能会缩短波I潜伏期。压力引起的神经传导速度降低、突触传递延迟以及中脑听觉传入神经的抑制性调制可能导致了观察到的峰间潜伏期延长。三名潜水员在达到300 msw后出现了临床HPNS体征，如疲劳、头晕、姿势性和意向性手部震颤、共济失调和眼球阵挛，并且在整个37小时的底部停留期间持续存在。
