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Human Brainstem Auditory-Evoked Potentials in Deep Experimental Diving to Pressures up to 62,5 bar
Abstract
The neural mechanisms underlying the high pressure neurologic syndrome (HPNS), which limit man's safe advance to extreme diving depths, are still unclear. This work was aimed at a better understanding of HPNS through study of brainstem auditory-evoked potentials (BAEP). BAEP were repeatedly recorded within 2 experimental chamber dives, Titan VIII (2 divers, maximum depth of 560 msw, compression time to bottom 109 h) and Titan XI (3 divers, maximum depth of 615 msw, compression time to bottom 240 h). Prolongation of the IV/V-complex occurred in 2 divers upon reaching 525 msw during Titan VIII compression and was accompanied by vestibular disturbances and amplitude increases of finger tremor. Both categories of changes--clinical signs and IV/V delay--gradually diminished during a 4-day stay at 545 msw, suggesting that they depended on excessive compression rates and insufficient acclimation time. Longer holding times at intermittent depths during Titan XI clearly reduced both HPNS symptoms and magnitude of prolongation of IV/V latencies. Wave I and wave III latency did not significantly change, pointing to a suppression of pontomesencephalic transmission. We infer that pressure suppresses synaptic transmission or triggers an increase of cortical or subcortical efferent inhibitory modulation of upper pontine and midbrain auditory afferents. Postdive controls revealed no persistent changes of BAEP measures in either the Titan VIII or XI divers.
... However, it has been known that there is remarkable individual variation of susceptibility to hyperbaric pressure [4,5]. It has been found that for both human and animal [6][7][8][9] the brainstem auditory-evoked potential (BAEP) changes in latency, interpeak latency (IPl) and amplitude of waves under increasing pressure. BAEP had previously been used to quantitatively assess the effect of high pressure on synaptic events [6,9]. ...
... It has been found that for both human and animal [6][7][8][9] the brainstem auditory-evoked potential (BAEP) changes in latency, interpeak latency (IPl) and amplitude of waves under increasing pressure. BAEP had previously been used to quantitatively assess the effect of high pressure on synaptic events [6,9]. one of the mechanisms of HPNS is related to changes of cell membrane fluidity [13]. ...
... As a result, the hyperbaric helium environment would cause IPl1-4 to lengthen _____________________________________________________________________________ _____________________________________________________________________________ and the amplitude to reduce. As proved by lorenz, BAEP latency began to prolong at a pressure greater than 2.3 MPa [6]. This cytological evidence constitutes one of the mechanisms of HPNS. ...
It is suggested that one of the mechanisms for high pressure nervous syndrome (HPNS) is related to nervous cell membranous fluidity. Both pressure and fatty acid components of cell membranes would influence membrane fluidity. The present research probed into the relationship between different fatty acid components of brain cell membrane and individuals' degree of HPNS.
Four groups of mice were compressed to 4.1 MPa with an He-O2 mixture over a period of two hours. These animals had been fed with different diets for a period of months prior to the procedure. We recorded interpeak latency of Wave 1 to Wave 4 (IPL1-4) of brainstem auditory-evoked potential (BAEP) at different stages of compression. Animals were sacrificed immediately after surfacing. Both polyunsaturated fatty acids (PUFAs) and saturated fatty acids (SFAs) of brain cell membranes were analyzed by HPLC.
Upon arriving at 4 MPa, the IPL1-4 readings of the four groups were prolonged 0.294 +/- 0.400 milliseconds (ms), 0.156 +/- 0.200 ms, 0.009 +/- 0.182 ms and 0.025 +/- 0.137 ms separately; each corresponded to its own PUFA-percent constitution of 16.2 +/- 4.5%, 24.8 +/- 4.3%, 33.5 +/- 8.8% and 32.3 +/- 2.9% respectively on the basis of total fatty acids.
Varying fractions of PUFAs, implying different membrane fluidity, interfered with disturbance of synaptic transmission during hyperbaric exposure. In other words, the higher the ratio of PUFAs/SFAs to the brain cell membrane, the stronger the ability for animals to antagonize the pressure effect.
... El SNAP se compone de síntomas y signos clínicos, y comprende trastornos psicológicos (y neuropsiquiátricos), signos neurológicos [12] y cambios neurofisiológicos clínicos [13,14]. Si bien el SNAP se ha caracterizado primariamente en humanos, se ha observado también en animales de experimentación expuestos a condiciones hiperbáricas [15][16][17]. Desde un punto de vista neurológico, el SNAP comprende componentes motores, sensoriales, vegetativos y cognitivos (Tabla I). ...
... HPNS entails clinical symptoms and signs, which involve psychological and neuropsychiatric disturbances, neurological signs [12], and changes in clinical neurophysiology recordings [13,14]. Though HPNS has been characterized in humans, it has also been observed in experimental animals exposed to hyperbaric conditions [15][16][17]. From a neurological point of view, HPNS entails motor, sensory, and vegetative components ( Table I). The earliest signs of HP-NS begin to occur at pressure of 1.3 MPa (120 m), displaying mild manifestations such as dizziness, nausea, tremor at distal extremities, and moderate alteration of cognitive function [18]. ...
Pressure is a thermodynamic variable that, like temperature, affects the states of matter. High pressure is an environmental characteristic of the deep sea. Immersion to depth brings about an increase in pressure of 0.1 MPa (1 atm) for each 10 m of seawater. Humans exposed to high pressure, mostly professional divers, suffer effects that are proportional to their exposure.
The nervous system is one of the most sensitive targets of high pressure. The high pressure neurological syndrome (HPNS) begins to show signs at about 1.3 MPa (120 m) and its effects intensify at greater depths. HPNS starts with tremor at the distal extremities, nausea, or moderate psychomotor and cognitive disturbances. More severe consequences are proximal tremor, vomit, hyperreflexia, sleepiness, and psychomotor or cognitive compromise. Fasciculations and myoclonia may occur during severe HPNS. Extreme cases may show psychosis bouts, and focalized or generalized convulsive seizures. Electrophysiological studies during HPNS display an EEG characterized by reduction of high frequency activity (alpha and beta waves) and increased slow activity, modification of evoked potentials of various modalities (auditory, visual, somatosensory), reduced nerve conduction velocity and changes in latency. Studies using experimental animals have shown that these signs and symptoms are progressive and directly dependent on the pressure. HPNS features at neuronal and network levels are depression of synaptic transmission and paradoxical hyperexcitability.
HPNS is associated with exposure to high pressure and its related technological means. Experimental findings suggest etiological hypotheses, prevention and therapeutic approaches for this syndrome.
Kot J: Medical equipment for multiplace hyperbaric chambers. Part I: Devices for monitoring and cardiac support. Europ J Underwater Hyperbaric Med 2005, 6(4): 115-120. All medical devices introduced into the hyperbaric chamber should be of an appropriate design and fit for use in the hyperbaric environment and they should be certified by the manufacturer for hyperbaric conditions. However, until now only several medical devices are CE marked for usage in hyperbaric chambers. Therefore users often need to perform themselves checking of the medical equipment needed for continuation of intensive care during hyperbaric treatment. To make this task easier, this paper presents review of reports of usage of medical devices under increased pressure. Part 1 is concerning devices for monitoring and cardiac support. Part 2 will describe mechanical ventilators and Part 3 will be devoted to infusion pumps and syringes. INTRODUCTION Hyperbaric chamber is an active medical device, which is potentially hazardous taking into accounts its application, and exposure of people inside to increased ambient pressure and increased partial pressure of oxygen. Therefore all hyperbaric systems have to be in accordance with the Council Directive 93/42/EEC of 14 June 1993 concerning medical devices (1). Moreover, according to this Directive all equipment which is introduced into the hyperbaric chamber should be should be certified by manufacturer for hyperbaric conditions and CE marked accordingly covering the hyperbaric environment conditions. Unfortunately, nowadays only several medical devices, which are needed, for continuation of intensive care inside the hyperbaric chamber are marked by manufacturers as compatible with hyperbaric conditions. Therefore users are still forced to perform some checking of devices before putting it into the chamber and usually this is done on the responsibility of the users. Equipment that does not belong to the internal equipment of the chamber and which is not a medical device, should be of an appropriate design and fit for use in the hyperbaric environment up to the maximum working pressure of the chamber it is used within (2). The general recommendations for medical devices used in hyperbaric chamber systems are presented in the Annex B of the pr14931 "Pressure vessels for human occupancy (PVHO) – Multi-place pressure chamber systems for hyperbaric therapy – Performance, safety requirements and testing" (3), which describes the potential hazards which certain medical devices represent, the risks induced by medical devices likely to be used within hyperbaric chamber systems intended for hyperbaric oxygen therapy and the recommendations for manufacturers of medical devices and users of hyperbaric chamber systems, in order to achieve the highest possible level of safety of the patient and the attendants. In cases when the medical devices need to be introduced into the hyperbaric environment and it is not certified by the manufacturer for the use in such conditions, the user (personnel of hyperbaric centres) has to check it before installing. The structure of the device is checked from a point of view of raised pressure, of oxygen enriched atmosphere and of electrical supply. Furthermore, the function of the device is checked under hyperbaric conditions to verify the controls, the performances of the device's probes, the operating of the device's built-in electronics, the device's display and the flow rates, pressures and frequencies with which the device dispenses the medical products to the patients. In case of any doubt, the installation of this medical device in hyperbaric chamber should be abandoned. To guide medical users, the review of literature is presented here to report medical devices, which have been used under hyperbaric conditions. This is divided into three parts: the part 1 is concerning devices for monitoring and cardiac support, the part 2 will describe mechanical ventilators and the last part 3 will be devoted to infusion pumps and syringes.
To investigate the effect of regular scuba diving on central processing sequences of sport divers who have no history of noise exposure or ear-related accidents using a comprehensive topographic examination of the central hearing system.
Cross-sectional controlled comparison study.
General sports diving community.
81 sport divers with a mean of 300 dives each were compared with a control group of 81 non-divers.
The participants were classified into three age groups. Hearing test results were combined for both ears. Examination included brainstem evoked response audiometry (BERA), cortical evoked response audiometry (CERA) and dichotic listening tests to screen for retrocochlear and central hearing disorders. Testing of brainstem latencies was performed in a gender-dependent manner.
BERA showed a pathological extension of the I-V-latency in one diver. Magnetic tomographic imaging ruled out brainstem lesions. No reason for the measured latency could be detected. All other latencies (I-III, III-V and I-V) in both gender groups were within normal limits. No statistically significant differences between divers and non-divers could be detected. Dichotic listening showed no clinical abnormalities in any of the participants, but in the age group 18-29 years divers performed significantly better than non-divers (p = 0.01). CERA revealed no significant differences between divers and non-divers in the age group 18-29 years and 30-39 years, whereas divers in the age group 41-50 demonstrated significantly better test results (p = 0.045) (difference of the means: 4.18 dB).
Dichotic listening and CERA did not reveal a significant reduction of central hearing performance in divers. Persistent on-shore BERA wave latency prolongations that were present in one study could not be confirmed in our study group. This first comprehensive topographic examination of the central hearing system of divers showed no abnormalities.
High pressure nervous syndrome (HPNS) is an instinctive response of mammalian high-class nervous functions to increased hydrostatic pressure. Electrophysiological activity of mammalian central nervous system (CNS), including brainstem auditory-evoked potential (BAEP), has characteristic changes under pressure. Here we recorded BAEP of 63 mice exposed to 0-4.0 MPa. The results showed that interpeak latencies between wave I and wave IV (IPL1-4) and their changes under pressures (deltaIPL1-4) responded to increasing pressure in a biphase pattern, shortened under pressure from 0 to 0.7MPa, then prolonged later. There were significantly negative correlations between base IPL1-4s and deltaIPL1-4s (p < 0.01). Individual IPL1-4s were supposed to respond to increasing pressure in a relative steady pattern in accordance with its base IPL1-4s. Those with shorter-base IPL1-4 presented direct increases in IPL1-4. However, those with longer-base IPL1-4 had a decreased IPL1-4 under small to moderate pressure then rebounded later. Our results suggested that mammalian CNS functions were susceptible to small to moderate pressure, as well as a higher pressure than 1.0MPa. Mice, as a statistical mass, had an "optimum" pressure about 0.7MPa, rather than atmospheric pressure, referred as shortest IPL1-4s. An individual's response to high pressure might be relied on his base biological condition. Our results highlighted a new approach to investigate a practical strategy to medical selecting barotolerant candidates for deep divers. Diversity of individual susceptibility to hydrostatic pressure was under discussed. Underlying mechanisms of the "optimum" pressure for CNS function and its significance to neurophysiology remain open to further exploration.
Four divers were chosen as subjects to conduct the 1,100 kPa He-O2 simulated saturation dive. Brainstem auditory evoked potentials of the divers were monitored during different stages of the exposure. At 1,100 kPa, with both 10 and 50 Hz clicks, interpeak latencies I-V were prolonged by 0.242 and 0.360 ms, respectively, indicating impedance of synaptic transmission. Results showed that interpeak latencies I-V were prolonged by 0.242 and 0.360 ms, respectively, indicating impedance of synaptic transmission. However, the latency of wave I was shortened by 0.11 ms, which was presumed to be due to different mechanical sound transmission velocity at hyperbaric helium environment. Interestingly, the latency of wave I prolonged gradually during hyperbaric exposure to 1,100 kPa. This might be used for the measurement of effects of hydrostatic pressure and He on the central nervous system (CNS). These changes coupled with easy perspiration and fatigue of the divers suggest that the pressure of the present experiment had certain effects of the CNS on the divers, although they were moderate and temporary.
Direct pressure applied on the inner ear cannot induce hearing loss.
Three possible causes have been described in the literature for inner ear permanent lesions during scuba diving: pressure imbalance between the middle ear and the external ear, appearance of microbubbles in the internal ear, and direct effect of pressure on the inner ear. We seek to determine whether this last factor can be involved.
We submitted two groups of guinea pigs previously implanted with an electrode in the round window to a protocol of air diving in a hyperbaric chamber. Eardrums of animals in one of the two groups had been perforated beforehand. Twenty dives were practiced over 4 weeks. We chose dive parameters consistent with common sport diving: maximal pressure of 4 atmosphere absolute and duration of 30 minutes. Auditory threshold and cochlear spontaneous activity were recorded at regular intervals. Furthermore, we recorded spontaneous cochlear activity in Heliox 400-m and 600-m dives to determine whether our conclusions hold for "extreme" diving.
In the group with perforated eardrums, no variation of those parameters were recorded, even in extreme diving. Important variations were noticed in the other group.
Pressure applied directly on the inner ear during diving does not disturb cochlear activity.
Brain auditory evoked potential (BAEP) in mice exposed to hyperbaric H2O2 pressure was monitored to reveal the correlation between altered synaptic transmission and hydrogen narcosis or isobaric HPNS. Inter peak latencies and wave amplitudes were selected as indices of assessment. The animals were exposed either to He-O2 or H2-O2 at 2.1 MPa and 4.1 MPa. Results showed that synaptic transmission was inhibited to various extents. The inhibition was partly due to the narcotic effect of hydrogen, which was added to the effect caused by hydrostatic pressure. On the other hand, asymmetrical reaction of each segment in the neuro-network might be responsible for the occurrence of HPNS.
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