Search

Diving fisheries are an important source of income and protein for many coastal communities around the world. However, these fisheries are also the cause of both fatal and non-fatal injuries. The aim of this study is to estimate the costs of decompression sickness (DCS) in the diving small-scale fisheries that target benthic resources in the Yucatan, Mexico. The DCS cases that occurred during three fishing seasons for sea cucumber (Isostichopus badionotus) and one for spiny lobster (Panulirus argus) were used to calculate the direct medical costs. The catch data during the same fishing seasons were used to calculate the potential losses caused by disability as indirect costs. In the three years (from 2013 to 2016) the total number of fishermen treated in the region numbered 282; 116 during lobster fishing and 166 during sea cucumber season. The direct medical costs were estimated to be USD $120,269; the temporary loss of income in USD $724,377; and the permanent loss of income was USD $737,053. Considering the direct and indirect costs, the social costs of diving in both small-scale fisheries was USD $1,614,121. This is a first approach to estimate the cost of the use of diving in fisheries for the health services but for the fishing communities as well. Furthermore, this is an important first step on the road to a full economic evaluation of the benthic fisheries in order to improve their management., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

The venous bubble load in the body after diving may be used to infer risk of decompression sickness (DCS). Retrospective analysis of post-dive bubbling and DCS was made on seven studies. Each of these investigated interventions, using an 18 meters of sea water (msw) air dive profile from Royal Navy Table 11 (Mod Air Table), equivalent to the Norwegian Air tables. A recent neurological DCS case suggested this table was not safe as thought. Two-hundred and twenty (220) man-dives were completed on this profile. Bubble measurements were made following 219 man-dives, using Doppler or 2D ultrasound measurements made on the Kisman-Masurel and Eftedal-Brubakk scales, respectively. The overall median grade was KM/EB 0.5 and the overall median maximum grade was KM/EB 2. Two cases of transient shoulder discomfort ("niggles") were observed (0.9% (95% CL 0.1% - 3.3%)) and were treated with surface oxygen. One dive, for which no bubble measurements were made, resulted in a neurological DCS treated with hyperbaric oxygen. The DCS risk of this profile is below that predicted by models, and comparison of the cumulative incidence of DCS of these data to the large dataset compiled by DCIEM [1, 2] show that the incidence is lower than might be expected., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Introduction: Neurological symptoms after breathhold (BH) diving are often referred to as "Taravana" and considered a form of decompression sickness. However, the presence of "high" gas embolism after BH diving has never been clearly shown. This study showed high bubble formation after BH diving., Materials and Methods: We performed transthoracic echocardiography on a 53-year-old male spearfishing diver (180 cm; 80 kg; BMI 24.7) 15 minutes before diving and at 15-minute intervals for 90 minutes after diving in a 42-meter-deep pool. Number of dives, bottom time and surface intervals were freely determined by the diver. Dive profiles were digitally recorded for depth, time and surface interval, using a freediving computer. Relative surface interval (surface interval/diving time) and gradient factor were calculated., Reults: High bubble grades were found in all the recorded echocardiograms. From the first to third recording (45 minutes), Grade 4 Eftedal-Brubakk (EB) bubbles were observed. The 60-, 75- and 90-minute recordings showed a reduction to Grades 3, 2 and 1 EB. Mean calculated GF for every BH dive was 0.22; maximum GF after the last dive was 0.33., Conclusions: High bubble grades can occur in BH diving, as confirmed by echocardiographic investigation. Ordinary methods to predict inert gas supersaturation may not able to predict Taravana cases., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission.

Purpose: The frequent ascents made during yo-yo diving may contribute to gas bubble clearance but paradoxically may also increase the risk of central nervous system decompression illness (DCI). We evaluated the risk of DCI due to yo-yo dives with very short surface intervals, using a controlled animal model., Methods: Dives were conducted on air to a depth of 90 meters (10 atmospheres absolute) for 32 minutes of bottom time, at a descent/ascent rate of 10 meters/ minute. Sprague-Dawley rats weighing ~ 300 grams were divided randomly into three groups. Group A performed a square dive protocol without any surface intervals, Group B conducted a protocol that included two surface intervals during the dive, and Group C performed a protocol with three surface intervals. Ascent/descent rate for surface intervals, each lasting one minute, was also 10 meters/minute., Results: Manifestations of DCI were observed in 13 of 16 animals in Group A (81.3%), six of 12 in Group B (58.3%), and two of 12 in Group C (16.7%). Mortality rates were similar in all groups., Conclusions: Surface intervals during dives breathing air significantly reduced DCI risk in the rat. Further studies are required using a larger animal model to reinforce the results of the present investigation., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission.

The diver's nervous system is extremely sensitive to high ambient pressure, which is the sum of atmospheric and hydrostatic pressure. Neurological complications associated with diving are a difficult diagnostic and therapeutic challenge. They occur in both commercial and recreational diving and are connected with increasing interest in the sport of diving. Hence it is very important to know the possible complications associated with this kind of sport. Complications of the nervous system may result from decompression sickness, pulmonary barotrauma associated with cerebral arterial air embolism (AGE), otic and sinus barotrauma, high pressure neurological syndrome (HPNS) and undesirable effect of gases used for breathing. The purpose of this review is to discuss the range of neurological symptoms that can occur during diving accidents and also the role of patent foramen ovale (PFO) and internal carotid artery (ICA) dissection in pathogenesis of stroke in divers., (Copyright © 2014 Polish Neurological Society. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.)

Aims: The main objectives of the present study was to establish an animal model of decompression sickness (DCS) after heliox saturation diving, and to use this model to evaluate possible morphological changes in the CNS induced by DCS using structural MRI., Methods: Two groups of rats were pressurized with heliox to 5 bar (pO2 = 50 kPa). The saturation time was three hours; decompression rate was 1 bar/10 seconds or 1 bar/20 seconds. A 7.0 Tesla small animal MRI scanner was used for detection of possible morphological changes in the brain and spinal cord, two hours and one week after the dive, compared to one week prior to the dive., Results: Neurological symptoms of DCS were observed in seven out of 10 animals. MRI of the brain and spinal cord did not reveal any morphological CNS injuries., Conclusion: This diving procedure was successful in causing DCS in a large proportion of the animals. However, despite massive neurological signs of DCS, no visible CNS injuries were observed in the MRI scans.

The United Kingdom Ministry of Defence commissioned work to define the relationship between the internal pressure of a distressed submarine (DISSUB), the depth from which escape is made and the risk of decompression illness (DCI). The program of work used an animal model (goat) to define these risks and this paper reports the incidence and type of DCI observed. A total of 748 pressure exposures comprising saturation only, escape only or saturation followed by escape were conducted in the submarine escape simulator between 1993 and 2006. The DCI following saturation exposures was predominantly limb pain, whereas following escape exposures the DCI predominantly involved the central nervous system and was fast in onset. There was no strong relationship between the risk of DCI and the range of escape depths investigated. The risk of DCI incurred from escape following saturation was greater than that obtained by combining the risks for the independent saturation only, and escape only, exposures. The output from this program of work has led to improved advice on the safety of submarine escape.

The Royal Navy requires reliable advice on the safe limits of escape from a distressed submarine (DISSUB). Flooding in a DISSUB may cause a rise in ambient pressure, increasing the risk of decompression sickness (DCS) and decreasing the maximum depth from which it is safe to escape. The aim of this study was to investigate the pressure/depth limits to escape following saturation at raised ambient pressure. Exposure to saturation pressures up to 1.6 bar (a) (160 kPa) (n = 38); escapes from depths down to 120 meters of sea water (msw) (n = 254) and a combination of saturation followed by escape (n = 90) was carried out in the QinetiQ Submarine Escape Simulator, Alverstoke, United Kingdom. Doppler ultrasound monitoring was used to judge the severity of decompression stress. The trials confirmed the previously untested advice, in the Guardbook, that if a DISSUB was lying at a depth of 90 msw, then it was safe to escape when the pressure in the DISSUB was 1.5 bar (a), but also indicated that this advice may be overly conservative. This study demonstrated that the upper DISSUB saturation pressure limit to safe escape from 90 msw was 1.6 bar (a), resulting in two cases of DCS.

Lidocaine is the most extensively studied substance for adjuvant therapy in neurological decompression illness (DCI), but results have been conflicting. In this retrospective cohort study, we compared 14 patients who received adjuvant intravenous lidocaine for neurological decompression sickness and cerebral arterial gas embolism between 2001 and 2011 against 21 patients who were treated between 1996 and 2001 and did not receive lidocaine. All patients were treated with hyperbaric oxygen (HBO2) therapy according to accepted guidelines. Groups were comparable for all investigated confounding factors, except that significantly more control patients had made an unsafe dive (62% vs. 14%, p = 0.007). Groups had comparable injury severity as measured by Dick and Massey score (lidocaine 2.7 +/- 1.7, control 2.0 +/- 1.6), an adapted version of the Dick and Massey score, and the Blatteau score. Number of HBO2 sessions given was comparable in both groups (lidocaine 2.7 +/- 2.3, control 2.0 +/- 1.0). There was neither a positive nor a negative effect of lidocaine on outcome (relative risk for objective neurological signs at follow-up in the lidocaine group was 1.8, 95% CI 0.2-16). This is the first retrospective cohort study of lidocaine in neurological DCI. Since our study is under-powered to draw definitive conclusions, a prospective multicenter study remains the only way to reliably determine the effect of lidocaine in neurological decompression illness.

Technical divers perform deep, mixed-gas 'bounce' dives, which are inherently inefficient because even a short duration at the target depth results in lengthy decompression. Technical divers use decompression schedules generated from modified versions of decompression algorithms originally developed for other types of diving. Many modifications ostensibly produce shorter and/or safer decompression, but have generally been driven by anecdote. Scientific evidence relevant to many of these modifications exists, but is often difficult to locate. This review assembles and examines scientific evidence relevant to technical diving decompression practice. There is a widespread belief that bubble algorithms, which redistribute decompression in favour of deeper decompression stops, are more efficient than traditional, shallow-stop, gas-content algorithms, but recent laboratory data support the opposite view. It seems unlikely that switches from helium- to nitrogen-based breathing gases during ascent will accelerate decompression from typical technical bounce dives. However, there is evidence for a higher prevalence of neurological decompression sickness (DCS) after dives conducted breathing only helium-oxygen than those with nitrogen-oxygen. There is also weak evidence suggesting less neurological DCS occurs if helium-oxygen breathing gas is switched to air during decompression than if no switch is made. On the other hand, helium-to-nitrogen breathing gas switches are implicated in the development of inner-ear DCS arising during decompression. Inner-ear DCS is difficult to predict, but strategies to minimize the risk include adequate initial decompression, delaying helium-to-nitrogen switches until relatively shallow, and the use of the maximum safe fraction of inspired oxygen during decompression.

Divers and patients lacking glucose-6-phosphate dehydrogenase (G6PD) may face a serious threat of central nervous system oxygen toxicity (CNS-OT) during exposure to hyperbaric oxygen (HBO), due to the important part played by G6PD in cellular redox balance. Our objective was to investigate G6PD deficiency as a risk factor for CNS-OT. We exposed G6PD-deficient (G6PDdef) and wild type (WT) mice to HBO at 405 kPa. Latency to CNS-OT was measured by observing the animal and monitoring the time to appearance of convulsions. Changes in glutathione peroxidase (GPx) and catalase activity were measured in red blood cells, and levels of endothelial and neuronal nitric oxide synthase (eNOS and nNOS) and 3-nitrotyrosine (NT) were measured in extracts of whole brain tissue by Western blot analysis. Unexpectedly, latency to CNS-OT was more than twice as long in G6PDdef mice compared with WT (36.9 ± 15.4 and 15.6 ± 13.2 min, respectively, P < 0.005). No significant differences were found in GPx and catalase activity or in protein levels of eNOS. However, nNOS and NT levels were lower in G6PDdef mice compared with WT (50.6%, P < 0.01 and 52.8%, P < 0.05, respectively). Our results suggest that the enhanced resistance of G6PDdef mice to HBO is due in part to a reduction in nNOS and NT levels in the brain. We conclude that G6PD deficiency at the level of the animals in the present study may not be a risk factor for developing CSN-OT, but this remains to be verified for human subjects.

Known and unpublished data regarding hyperbaric pressure (HP) effects on voltage dependent-Ca2+ channels (VDCCs) were reviewed in an attempt to elucidate their role in the development of high-pressure neurological syndrome (HPNS). Most postulated effects from studies performed in the last two decades (e.g., depressed maximal current) rely on indirect findings, derived from extracellular [Ca2+] manipulation or by observing Ca(2+)-dependent processes. More recent experiments have tried to directly measure Ca2+ currents under high pressure conditions, some of which are potentially challenging previous indirect findings on one hand, but support findings from work done on neuronal behavior on the other. Additional support for some of the recent findings is provided by computer simulation of pressure effects on a spinal motor neuron activity. HP effect on different types of VDCCs seems to be selective - i.e., HP may suppress, facilitate or not change their activity. Thus, the specific distribution of the various types of the channels in each synaptic terminal or throughout the neuron will determine their function and will influence the neuronal network behavior under HP. Further research is needed in order to fully understand the HPNS etiology.

The U.S. Navy recommends submarine escape for depths down to 600 fsw, with deeper escapes entailing the risks of decompression sickness, nitrogen (N2) narcosis and CNS oxygen (O2) toxicity. However, the escape equipment, including the submarine escape and immersion equipment and the escape trunk, could probably function even at 1,000 fsw. Here we report a theoretical analysis of the risks of both N2 narcosis and CNS O2 toxicity for different escape profiles from 600 to 1,000 fsw. The effect of N2 narcosis, calculated as a function of N2 pressure in the brain using Gas Man software, was expressed as equivalent narcosis depth (END), corresponding to the depth at which the same pressure of N2 would be produced in the brain after five minutes of scuba diving with air. The risk of O2-induced convulsions was estimated using the model developed by Arieli et al. Different dwell times (DTs) at maximal pressure in the escape trunk (from 0 to 60 s) and lungs-to-brain circulation times (10 to 30 s) were included in our analysis. When DT in the escape trunk is very short (e.g., 10 s), the risk of either incapacitating N2 narcosis and/or O2-induced convulsions occurring in the trunk is low, even during escapes from 1,000 fsw.

Pressure above 1.1 MPa induces in mammals and humans the high pressure neurological syndrome (HPNS). HPNS is characterized by cognitive and motor decrements associated with sleep disorders, EEG changes, tremor, and convulsions that ultimately may lead to death. Previous theories proposed that augmented response of the glutamatergic N-methyl-D-aspartate receptor (NMDAR) or reduced GABAergic inhibition may be involved. Recently, we have reported that isolated NMDAR response was augmented at high pressure. We now test whether this augmentation induces neuronal hyperexcitability. We studied high pressure effects on pharmacologically isolated NMDAR field excitatory postsynaptic potentials (fEPSPs) and on their efficacy in generating population spikes (PSs). Sprague-Dawley male rats were used. Hippocampal coronal brain slices were prepared, constantly superfused with physiological solutions, gas-saturated at normobaric pressure, and compressed up to 10.1 MPa with helium. fEPSPs and PSs were recorded from the dendritic and the somatic layers of CA1 pyramidal neurons in response to Schaefer collaterals stimulation with trains of five stimuli at 25 Hz. Pressure caused PSs to appear earlier in the train. However, PS delay, rise time and decay time were increased and PS amplitude, frequency, and number were decreased in the last responses in the train. The decrease in late fEPSPs was associated with a reduction of the total number of PSs in the train, apparently without a change in the synaptic efficacy. These results may partially explain the neuronal hyperexcitability observed at pressure. Therefore, it is postulated that significant hyperexcitability is attained at pressure only when the normal fast fEPSP is intact.

Introduction: There is evidence that increased ambient pressure causes an increase in postural sway. This article documents postural sway at pressures not previously studied and discusses possible mechanisms., Methods: Eight subjects participated in a dry chamber dive to 240 msw (2.5 MPa) saturation pressure. Two subjects were excluded due to unilateral caloric weakness before the dive. Postural sway was measured on a force platform. The path length described by the center of pressure while standing quietly for 60 seconds was used as test variable. Tests were repeated 38 times in four conditions: with eyes open or closed, while standing on bare platform or on a foam rubber mat., Results: Upon reaching 240 msw, one subject reported vertigo, disequilibrium and nausea, and in all subjects, mean postural sway increased 26% on bare platform with eyes open (p < 0.05) compared to predive values. There was no significant improvement in postural sway during the bottom phase, but a trend was seen toward improvement when the subjects were standing with eyes closed on foam rubber (p = 0.1). Postural sway returned to predive values during the decompression phase., Discussion: Postural imbalance during deep diving has been explained previously as HPNS possibly including a specific effect on the vestibulo-ocular reflex. Although vertigo and imbalance are known to be related to compression rate, this study shows that there remains a measurable increase in postural sway throughout the bottom phase at 240 msw, which seems to be related to absolute pressure.

CNS O2 toxicity is manifested most profoundly by generalized motor convulsions. The hypothesis was tested that HBO2 triggers seizures by an excitatory to inhibitory neurotransmitter imbalance produced by neuronal nitric oxide (NO) activity. Anesthetized rats were exposed to 5 ATA HBO2 for 75 min with or without prior inhibition of nNOS. Interstitial NO and amino acids: aspartate (Asp), glutamate (Glu) and gamma-aminobutyric acid (GABA) were determined in the striatum by microdialysis coupled with HPLC. Blood flow and EEG in the same striatal region were measured simultaneously. Rats treated with 7-NI showed no EEG spikes of O2 toxicity, while seizure latency for untreated rats was 63 +/- 7 min. Significant increases in NO metabolites and blood flow were observed in control rats before seizures. HBO2 did not change Glu significantly and increased Asp slightly whereas GABA decreased progressively by 37 +/- 7%. Pretreatment with 7-NI led to a significantly smaller decline in GABA. Overall, the simplified excitotoxicity index Glu/GABA increased significantly after 60 min of HBO2 in control but fell in rats treated with 7-NI. We conclude that HBO2-stimulated neuronal NO production promotes an imbalance between glutamatergic and GABAergic synaptic function implicated in the genesis of oxygen-induced seizures.

Exposure to high pressures (HP) has been associated with the development of the high pressure neurological syndrome (HPNS) in deep-divers and experimental animals. In contrast, many diving mammals are naturally able to withstand very high pressures. Although at a certain pressure range humans are also able to perform to some extent, the severe signs of HPNS at higher pressures motivated the research on the pathophysiology underlying this syndrome rather than on possible adaptive mechanisms. Thermodynamically, high pressure resembles cooling. Both conditions usually involve reduction in the entropy and slowing down of kinetic rates. We have observed in rat corticohippocampal brain slices that high pressure slows and reduces excitatory synaptic activity. However, this was associated with increased gain of the system, allowing the depressed inputs to elicit regular firing in their target cells. This increased gain was partially mediated by elevated excitability of their dendrites and reduction in the background inhibition. This compensation is efficient at low-medium frequencies. However, it induces abnormal spike reverberation at the high frequency band (> 50 Hz). Synaptic depression that requires less vesicles/transmitter turn over may serve as an energy-saving mechanism when enzymes and membrane pumps activity are slowed down at pressure. It is even more efficient if a similar reduction is induced in inhibitory synaptic activity. Unfortunately, the frequency response characteristics at this mode of operation may make the system vulnerable to external signals (noise, auditory, visual, etc) at frequencies that elicit 'resonance' responses. Therefore, it is expected that humans exposed to pressures above 1.5 MPa display lethargy and fatigue, certain reduction in cognitive and memory functions when the system is working in an 'economic' mode. The more serious signs of HPNS such as nausea, vomiting, severe tremor, disturbance of motor coordination, and seizures, may be the consequence of an interaction between the 'economic' mode of operation and resonance-inducing environmental disturbances.

Compressed air or a nitrogen-oxygen mixture produces from 0.3 MPa nitrogen narcosis. The traditional view was that anaesthesia or narcosis occurs when the volume of a hydrophobic site is caused to expand beyond a critical amount by the absorption of molecules of a narcotic gas. The observation of the pressure reversal effect on general anaesthesia has for a long time supported the lipid theory. However, recently, protein theories are in increasing consideration since results have been interpreted as evidence for a direct anaesthetic-protein interaction. The question is to know whether inert gases act by binding processes on proteins of neurotransmitter receptors. Compression with breathing mixtures where nitrogen is replaced by helium which has a low narcotic potency induces from 1 MPa, the high pressure nervous syndrome which is related to neurochemical disturbances including changes of the amino-acid and monoamine neurotransmissions. The use of narcotic gas (nitrogen or hydrogen) added to a helium-oxygen mixture, reduced some symptoms of the HPNS but also had some effects due to an additional effect of the narcotic potency of the gas. The researches performed at the level of basal ganglia of the rat brain and particularly the nigro-striatal pathway involved in the control of the motor, locomotor and cognitive functions, disrupted by narcosis or pressure, have indicated that GABAergic neurotransmission is implicated via GABAa receptors.

The studies of Paul Bert, presented in his book "La Pression Barométrique" in 1878, were at the origin of the modern hyperbaric physiology. Indeed his research demonstrated the effects of oxygen at high pressure, that compression effects must be dissociated from decompression effects, and that neurological troubles and death of divers during or after decompression were due to the fast rate of decompression. However, it is only in 1935 that the work of Behnke et al. attributed the complaints reported at 3 bars and above in compressed air or nitrogen-oxygen mixture to the increase in partial pressure of nitrogen which induces nitrogen narcosis. Little is known about the origins and mechanisms of this narcosis. The traditional view was that anaesthesia or narcosis occurred when the volume of a hydrophobic membrane site was caused to expand beyond a critical amount by the absorption of molecules of a narcotic gas. The observation of the pressure reversal effect during general anaesthesia has long supported this lipid theory. However, recently, protein theories have met with increasing recognition since results with gaseous anaesthetics have been interpreted as evidence for a direct gas-protein interaction. The question is to know whether inert gases, that disrupt dopamine and GABA neurotransmissions and probably glutamatergic neurotransmission, act by binding to neurotransmitter protein receptors.

Repetitive breath-hold (BH) diving can lead to accumulation of nitrogen (N2) in blood and tissues, which may give rise to decompression illness (DCI). An unusual condition is "Taravana", the diving syndrome reported by Cross in the 1960s. That report generated wide discussion as to whether BH diving can cause DCI. Paulev was the first person to suggest the link between DCI and BH diving. He, a submarine medical officer developed symptoms of DCI after a series of BH dives, having proceeded the dives by spending time in a hyperbaric chamber at 20 meters for 8 minutes. Recently four professional Japanese BH divers (Ama) with histories of diving accidents were reported. Magnetic resonance imaging of these divers detected cerebral infarcts localized in the watershed areas of the brain. A survey conducted on their island revealed that many Ama divers had experienced stroke-like events. A clinical feature of DCI in BH diving is that the damage is limited to the brain. Although the mechanisms of brain damage in BH diving are unclear, N2 bubbles passing through the lungs or the heart so as to become arterialized are most likely to be the etiological factor.

Raised internal pressure in a distressed submarine rapidly increases the risk of decompression sickness (DCS) following submarine escape. The hypothesis that breathing a hyperoxic gas during escape may reduce the risk of DCS was tested using goats. Shallow air saturation and simulated submarine escape dives were carried out either singularly or in combination (saturation, escape, or saturation followed by escape) using air or 60% / 40% oxygen (O2) / nitrogen (N2) mixture as breathing gas during the escapes. Post-surfacing, animals were observed for signs of DCI and O2 toxicity. Precordial Doppler ultrasound was used to score venous gas emboli (VGE) using the Kisman Masurel (KM) scale. Following escape from 2.5 MPa, the rate at which VGE disappeared in the hyperoxic group (n = 8) was significantly faster(p < 0.05) than the air group (n = 7). One case of pulmonary barotrauma with arterial gas embolism occurred in the air group, but no cases of DCS were observed. After saturation at 0.18 MPa followed by escape from 2.5 MPa, DCS occurred in four of 15 animals in the air group and in two of 16 animals in the hyperoxic group. The rate of disappearance of VGE was significantly faster (p < 0.01) in the hyperoxic group. O2 toxicity was not discernible in any of the animals.

The high pressure neurological syndrome (HPNS), a neurological condition during elevated pressure especially in deep diving, has been simulated with experimental animals. Rats were subjected to 61 bars with slow pressure increase and one or two hours constant high pressure; subsequently the pressure was released to sea level within 20 seconds--leading to immediate oxygen depletion and death of animals--or with slow decompression rates allowing survival. In all animals, brains and partly other organs were investigated morphologically. In animals sacrificed immediately, subtle changes in different brain regions were found: symmetrical occurrence of dark neurons in the hippocampus formation, cortex and brain stem, reduced expression of tyrosin hydroxylase in the substantia nigra and enhanced expression of Bax protein in some of these regions. The dark neurons were only observed after aldehyde fixation, otherwise the brains were unaltered despite ultrarapid decrease of highly elevated pressure. In animals that were allowed to survive for different time periods, some of these subtle changes were equally noted by light and electron microscopy. Furthermore, the ventricles were enlarged, the astrocytic reaction in the hippocampus increased and some signs of the destruction of the adrenal gland were visible. We conclude, that HPNS leads to minimal changes within the nervous system. The behaviour of animals during pressure was slightly altered, the weights after the experiments reduced, but no lasting sequelae were noted. Since both in human and experimental deep diving conditions signs of psychosis were reported, this HPNS model must be considered as a tentative animal model of human psychosis.

The United States Naval Special Warfare Community uses oxygen tolerance testing to screen Navy combat swimmer candidates for sensitivity to the toxic effects of hyperbaric oxygen (HBO2). Between 1976 and 1997, 6,250 oxygen-tolerance tests were performed at the Naval Special Warfare Center and Naval Special Warfare Group One. Our review of these data found only six episodes of O2 toxicity for an incidence of 0.096%, an incidence considerably lower than the rate of 1.9% reported in an earlier review using data from the Naval Safety Center. Additionally, we reviewed data from the Naval Safety Center from 1986 to 1997 and found only one episode of O2 toxicity among 157,930 LAR V dives. Many factors other than individual sensitivity to HBO2 may contribute to the occurrence of O2 toxicity episodes during combat swimmer operations. The authors conclude that O2 tolerance testing of U. S. Navy SEAL candidates is not a useful screening test and recommend discontinuation of this test.

Divers may be exposed to intense noise underwater. Two cases of neurologic disturbances during experimental exposures to 15 min of continuous underwater sound are described. Sound exposure in the first case consisted of a warble tone with center frequency of 240 Hz and a sound pressure level of 160 dB re 1 microPa. Symptoms during exposure consisted of somnolence, lightheadedness, and an inability to concentrate. No apparent effect on hearing was noted. In the second case, a center frequency of 1,000 Hz at 181 dB was used. Lightheadedness, inability to concentrate, agitation, and head vibrations were noted during the exposure. The diver also exhibited a temporary auditory threshold shift of 19.2 dB. In both cases, overt symptoms resolved within 30 min after exposure, but both divers reported recurrent symptoms days to weeks after the exposures. Medical histories and examinations, assessment of dive profiles, and breathing gas analysis failed to support a source other than the sound exposures to account for the symptoms observed. Potential mechanisms for the described symptoms are discussed.

Diving is a high-risk sport. There are approximately between 1 to 3 million recreational scuba divers in the USA (with over a quarter-million learning scuba annually); there are about 1 million in Europe and over 50,000 in the United Kingdom. In this population 3-9 deaths/100,000 occur annually in the US alone, and those surviving diving injuries far exceeds this. Diving morbidity can be from near-drowning, from gas bubbles, from barotrauma or from environmental hazards. In reality, the most common cause of death in divers is drowning (60%), followed by pulmonary-related illnesses. The mean number of annual diving fatalities in the USA from 1970 to 1993 was 103.5 (sd 24.0) and the median was 106. This article will focus primarily upon pressure effects on the health of a diver. There are two principle ways pressure can affect us: by direct mechanical effects and by changing the partial pressures of inspired gases. Dysbarism is a general term used to describe pathology from altered environmental pressure, and has two main forms: barotrauma from the uncontrolled expansion of gas within gas-filled body compartments and decompression sickness from too rapid a return to atmospheric pressure after breathing air under increased pressures. Greater than 90% of the human body is either water or bone, which is incompressible; the areas directly affected by pressure changes thus are those that are filled with air or gas. These sites include the middle ear, the eustachian tube, the sinuses, the thorax, and the gastrointestinal tract. Air in these cavities is compressed when the ambient pressure rises because the pressure of inhaled air must equilibrate with the ambient pressure.

HPNS (high pressure neurological syndrome) is considered to be reversible condition of the nervous system caused by elevated (atmospheric) pressure. Clinical observations and experimental findings gave rise to the belief that this syndrome at least partly functions as a model of a dopamin dependent psychosis. Morphological alterations during or after HPNS in man and animals have not been reported so far. We treated rats for three hours with an increasing pressure of helium-oxygen mixture up to 61 ATA in a pressure chamber. This pressure was subsequently maintained for one hour and then released to zero within twenty seconds. The rats died within the first three seconds of pressure release due to complete deoxygenation. Brains were immediately removed and either cooled in liquid nitrogen or fixed in formalin. In both instances the central nervous tissue was excellently preserved. In paraffin embedded formalin fixed specimens, dark neurons in different brain regions were found, especially within parts of the dentate gyrus, the CA 4 subfield of the ammons horn, in dopaminergic brainstem nuclei and in some cortical pyramidal cells. In dopaminergic cells, tyrosine hydroxylase was found to be absent in cells transformed into dark neurons. These dark neurons which have long been recognized in neuropathology, probably represent reversibly damaged neurons transformed into the dark configuration by aldehyde fixation. They may correspond to early apoptosis or they may be the consequence of cytoskeletal disruption.

In the experiments conducted on mice which prior to compression in a heliox environment have been injected the blockers of various types of calcium channels (flunarezine, verapramil and nifedipine) as well as bemethyl (actoprotector) and oxymethacye (antioxidant) there escaped detection of noticeable effect of these drugs on developing the high pressure nervous syndrome (HPNS). On exposure to the hyperbaric nitrogen-oxygen environment verapromil (phenylalkulamine blocker of L-type calcium channels) had a protection effect with respect to a convulsive component of the nitrogen narcosis.

The mechanism by which 12 atm abs of a helium-oxygen gas mixture (heliox) antagonizes behavioral effects of ethanol is unknown. Although the threshold for pressure-reversal of general anesthesia and expression of the high pressure neurologic syndrome (HPNS) is well above 12 atm abs in mice, the ethanol antagonism by 12 atm abs heliox could result from similar underlying excitatory effects. To investigate this possibility, the behavior of water-injected control mice and the latency to convulsions in drug-injected mice were determined in 1 atm abs air and 12 atm abs heliox. Four convulsant drugs were tested: picrotoxin (2 mg/kg), dl-allylglycine (300 mg/kg), isoniazid (300 mg/kg), and l-methionine-dl-sulfoximine (170 mg/kg). Responses were videotaped to observe behavior and to measure latency to the onset of myoclonus and clonus. Results indicated no observable excitatory effects of 12 atm abs in control mice. The latency to myoclonus was significantly reduced by pressure in allylglycine-treated mice but not in mice treated with the other convulsants. Latency to clonus was not significantly altered by pressure, relative to latency at 1 atm abs heliox, for any drug tested. In conclusion, the present findings indicate that exposure to 12 atm abs heliox is not proconvulsant and, thus, the findings do not support the hypothesis that 12 atm abs heliox antagonizes ethanol indirectly via an increase in central nervous system excitability.

An established swine model of neurologic decompression illness (DCI) was adapted to investigate the influence of no-stop ascent profile shape on DCI risk after deep air and heliox dives. Pigs underwent a simulated air dive in a dry chamber to 200 fsw (613 kPa) for 24 min bottom time. They were then decompressed at either a linear rate of 20 fsw/min (61 kPa/min) or on a non-linear, fast-deep/slow-shallow profile. Both decompressions lasted 10 min. In the linear group, there were 11/20 cases of neurologic DCI, including 1 death and 8 severe cases, compared to 5/20 cases (1 severe) in the fast/slow group. Thirteen out of 20 from the linear group, vs. 6/20 of the non-linear group, had moderate or severe skin DCI affecting > 20% skin surface area. A similar study, but of paired, randomized, investigator-blind, and sequential design was performed with pigs breathing 80/20% heliox: Pigs were compressed to 250 fsw (766 kPa) for 8 min 50 s, then decompressed at either a linear 30 fsw/min (92 kPa/min), or on a fast/slow profile. Neurologic DCI occurred more frequently (P = 0.024) in the linear group (16/20; 1 death and 11 severe) than in the fast/slow group (8/20; 3 severe). Moderate or severe skin DCI affected 16/20 of the linear group compared to 3/20 of the fast/slow group (P = 0.0002). The study findings suggest that substantial reductions in DCI risk may be obtainable by manipulating the ascent profile after deep no-stop diving. This finding has potential application in both military and civil diving operations.

Involvement of the adrenergic mediator system in central mechanisms of hyperbaric nitrogen narcosis or the high pressure nervous syndrome (NSHP) produced by nitrogen or heliox gas mixtures under increased pressure was studied in mice and rabbit experiments with the use of pharmacological substances-analyzers. Accumulated data are indicative of lack of a significant role of the adrenergic system in the NSHP genesis and a protective effect of activation of the central but not peripheric adrenergic mediation in development of the behavioural and electrophysiological symptomatics of nitrogen narcosis. Mechanisms of NSHP and nitrogen narcosis and possible principles of pharmacological correction are under discussion.

Psychotic-like episodes in divers exposed to high pressure have been attributed to either the high-pressure neurological syndrome, confinement in pressure chamber, the subject's personality, or the addition of nitrogen or hydrogen to the basic helium-oxygen breathing mixture used for deep diving. Alternatively, it is suggested that these disorders are in fact paroxysmal narcotic symptoms that result from the sum of the individual narcotic potencies of each inert gas in the breathing mixture. This hypothesis is tested against a variety of lipid solubility theories of narcosis. The results clearly support the hypothesis and provide new information about the cellular interactions between inert gases at raised pressure and pressure itself.

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.

Suspended cells of the human neuroblastoma line SK-N-SH were exposed to elevated pressures of non-narcotic helium (He) and the narcotic gases nitrogen (N2), and argon (Ar) and stimulated with carbachol. He, 18 and 36 atmospheres absolute (ATA), equivalent to 544 and 1120 feet of seawater, potentiated the increase in [Ca2+]i induced by carbachol, as measured by Fura-2. Carbachol-stimulated increases in [Ca2+]i were not significantly altered from values in 1 ATA air by either N2 or Ar at the same pressures. The response to carbachol of cells exposed to 36 ATA of He and slowly decompressed to 1 ATA was indistinguishable from that of cells never exposed to pressure. Thus this pressure-potentiated increase in [Ca2+]i is compatible with excitation, is reversible and is not elicited by narcotic gases. It was observed, moreover, at pressures encountered by commercial deep-sea divers. The High Pressure Neurological Syndrome (HPNS) encountered by divers breathing He/O2 mixtures at high pressures, and its known antagonism by N2, may be due in part to effects on neuronal [Ca2+]i levels since an increase in these would most likely result in an excitatory response.

Diving deeper than 180 metres of seawater (msw) will impose neurological symptoms in most divers. Atactic signs and abnormal EEGs were found in five of 18 divers immediately after deep diving. Neuropsychological testing before and after deep diving in 64 divers revealed a reduction in autonomic reactivity (48%), increased hand tremor (27%) and impairment of spatial memory and reduced finger coordination (8%) after the dives. These results had not improved one year later. A follow-up study of 40 divers one to seven years after their last deep dive revealed that the divers experienced more problems of concentration and paresthesia in feet and hands than the controls. Two had had seizures, one had suffered episodes of transitory cerebral ischemia and one had experienced transitory global amnesia after the deep dives. In the future, oil installations at depths below 180 msw should be installed and maintained with remote control and robot technology.

Under continuous compression with normoxic helium-oxygen mixture up to 100 Ata with the velocity 1 Ata/min, guinea pigs developed successively tremor, myoclonias, seizures of clonic and tonic types. Blood supply of cerebral structures (cortex, black substance, caudate nucleus) during motor disorders increased depending on the stage of development of the high pressure neural syndrome. The role of cerebral circulation in the latter's pathogenesis is discussed.

In immersions over 20 ata, symptoms occur known as the high pressure neural syndrome (HPNS). Regular changes of the infraslow electrical activity were revealed in development of the HPNS: the waves of the 20-sec period start developing, the average oscillation amplitudes becoming considerably higher. The inter-lead correlation becomes more obvious.

We examined the effect of high pressure (10.1 MPa) on the sensitivity of the respiratory center to alterations in pH (range 5.8-7.6) which were obtained by varying either PCO2 or [HCO3-] in superfused Krebs solution. Isolated rat brainstem-spinal cord preparations were placed in a pressure chamber and respiratory-related motor neuron activity was recorded from severed ventral roots C1 and C5. At atmospheric pressure, respiratory burst frequency in both C1 and C5 varied inversely with pH. Only the time integral of a single C5 response was sensitive to acidification. High helium pressure reduced by 60% the sensitivity of the respiratory frequency to alteration in pH, while the time integral of both C1 and C5 responses became independent of PCO2, causing the relative respiratory drive between the two roots to change. These modifications in the chemoresponse of the respiratory center may contribute to the respiratory difficulties encountered under high pressure conditions.

When human divers or experimental animals are exposed to high pressure, they develop the High Pressure Neurological Syndrome (HPNS). Male Sprague-Dawley rats were exposed to high pressure in a conventional helium-oxygen breathing mixture to 80 bars. Pressure-induced behavioral motor disturbances including hyperlocomotor activity (HLA), tremor and myoclonia were monitored with a noninvasive piezoelectrical sensor device enabling a without discontinuity long-term analysis. New data were obtained on the development of the HPNS behavioral motor disturbances. Indeed, the present results suggest myoclonia would be more sensitive to constant high pressure exposure, while HLA and tremor would be more sensitive to increasing pressure. Moreover, myoclonia were found to occur significantly later in rats which developed epileptic seizures than in other. The present results constitute the quantitative basis of HPNS motor disturbances for future pharmacological pressure experiments.

Forty commercial saturation divers, mean age 34.9 (range 24-49) years, were examined one to seven years after their last deep dive (190-500 metres of seawater). Four had by then lost their divers' licence because of neurological problems. Twenty seven (68%) had been selected by neurological examination and electroencephalography before the deep dives. The control group consisted of 100 men, mean age 34.0 (range 22-48) years. The divers reported significantly more symptoms from the nervous system. Concentration difficulties and paraesthesia in feet and hands were common. They had more abnormal neurological findings by neurological examination compatible with dysfunction in the lumbar spinal cord or roots. They also had a larger proportion of abnormal electroencephalograms than the controls. The neurological symptoms and findings were highly significantly correlated with exposure to deep diving (depth included), but even more significantly correlated to air and saturation diving and prevalence of decompression sickness. Visual evoked potentials, brainstem auditory evoked potentials, and magnetic resonance imaging of the brain did not show more abnormal findings in the divers. Four (10%) divers had had episodes of cerebral dysfunction during or after the dives; two had had seizures, one had had transitory cerebral ischaemia and one had had transitory global amnesia. It is concluded that deep diving may have a long term effect on the nervous system of the divers.

Hyperbaric pressure induces hyperexcitability, tremor, and convulsions in intact animals by mechanisms that are not understood. High pressure induces spontaneous electrical discharges in the spinal ventral roots which we call "tremor-associated activity" (TAA). This study examined the nature of TAA, its likely origins, and its possible contribution in the cervical roots to respiratory difficulties. Activity was recorded extracellularly from the cut cervical ventral roots C1 and C5 in an in vitro brainstem-spinal cord preparation from newborn rats. Under hyperbaric conditions spontaneous TAA was observed either between the typical respiratory bursts in C1 and C5 or immediately after the burst itself. Stimulating the trigeminal nerve at 1 Hz induced a direct excitatory medullospinal reflex which, at high pressure, was followed by a conspicuous TAA. The TAA evoked by the dorsoventral root reflex in isolated spinal cord under hyperbaric conditions was similar to that evoked by the medullospinal reflex. These findings suggest that basic TAA originates at the level of the spinal cord and may be triggered by various synaptic inputs. They further suggest that pressure-induced abnormal activity of the motoneuron pool innervating various respiratory muscles may contribute to respiratory problems encountered under hyperbaric conditions.

In addition to the motor events associated with high pressure neurologic syndrome (HPNS), we have observed behavioral changes that resemble the 5-hydroxytryptamine (5-HT) syndrome in free-moving rats exposed to pressures up to 70 ATA. These include a flat body posture, head weaving, reciprocal forepaw treading, and hyperlocomotion. Such changes occur when brain 5-HT levels are raised or when 5-HT receptors are activated. We have therefore studied the behavior of rats at pressure treated either with saline or with one of the following drugs: p-chlorophenylalanine (pCPA) which depletes brain 5-HT by 85-90%, Wy 27587 which inhibits 5-HT reuptake, 5-hydroxytryptophan (5-HTP) and carbidopa which increase brain 5-HT synthesis, and quipazine which is a 5-HT receptor-agonist. After treatment, rats were individually exposed to pressure, and behavioral scores were made for 5 min every 10 ATA up to 70 ATA by an unbiased observer who was not aware of the treatment given. Analysis of all control rats indicated that only a flat body posture, forepaw treading, and hyperlocomotion were positively correlated with pressure, and these events were used in all subsequent analysis. Rats treated with pCPA with whole brain 5-HT levels reduced by 90% had scores significantly less than controls. Rats treated with Wy 27587 showed significantly increased scores. Rats treated with 5-HTP and quipazine failed to show a significant increase in scores. These results suggest that a modified form of the 5-HT syndrome occurs when rats are exposed to increased pressure, and the behavioral events seen are consistent with some activation of the 5-HT1A receptor subtype.

Inert gas narcotics increase intrinsic pressure tolerance (1,000Pc) in CD-1 mice but interfere with development of the protective responses raising seizure thresholds during slower compression (e.g., 60Pc). This secondary narcotic effect can block up to 40% of the total attainable increase in Pc. The narcosis susceptible moiety of this compression rate effect develops early, whereas a narcosis resistant remnant accounts for increase in Pc occurring after 90 min of compression or pressure exposure. Pressure conditioning by multiday pressure exposure entails increases in both 60Pc and 1,000Pc and in virtual annullment of the compression rate effect. The effect can be completely blocked by narcotic gases in the conditioning atmosphere. In addition to blocking part of the compression rate effect the presence of narcotic gases under these conditions can reverse the effects of previously established pressure conditioning. 60Pc regresses much more slowly under these conditions than 1,000Pc. Either reversal rate is much more rapid in air at 1 ATA than at 80 ATA under 0.9 atm N2O. The implications of these data are discussed with regard to evaluation of the hypothesis of antagonism between inert gas narcotics and high pressures and to elaboration of the monoamine hypothesis to account for the modification of the compression rate effect by narcotic gases.

Regional amino acid concentrations were measured in rat brain fixed by microwave irradiation at three levels of elevated atmospheric pressure corresponding to different phases of the high-pressure neurological syndrome [20 atmospheres absolute (ATA), no clinical signs; 60 ATA, tremor; 85 ATA, severe tremor and myoclonic jerks]. No changes in amino acid content occurred at 20 or 60 ATA. At 85 ATA glutamine content increased in hippocampus, striatum, cerebellum, and substantia nigra, and gamma-aminobutyric acid content increased in hippocampus. It is suggested that enhanced glutamate release in various subcortical structures contributes to the myoclonic activity observed at 85 ATA.

Neuropsychologic status of saturation divers was assessed before and after 300-500 msw dives (deep saturation diving--DSD group) and before and after 3.5 yr of ordinary saturation diving (saturation diving--SD group). Average baseline results showed the divers to be slightly superior to nondiving controls. Mild-to-moderate neuropsychologic changes (greater than 10% impairment) were found in measures of tremor, spatial memory, vigilance, and automatic reactivity in 20% of the divers after deep dives (DSD group). One year postdive no recovery was observed except for a vigilance test. In the SD group, 20% of the divers showed greater than 10% impairment after 3.5 yr of ordinary saturation diving. Significant reduction in autonomic reactivity was also found and there was a relationship between low autonomic reactivity before saturation diving and number of greater than 10% impairments. For the whole group (DSD + SD divers), negative correlations were found between saturation experience and results on memory and complex visuomotor tests. Years of diving from first to last examination was positively correlated with number of greater than 10% impairments and with reduction in autonomic reactivity. No similar correlations were found to dive variables after about 3 yr of air diving. The mild-to-moderate changes seen in some divers, therefore, seem to be the effects of saturation diving. Since one deep dive may cause an effect similar to the effect of 3.5 yr of ordinary saturation diving, there is reason to believe that repeated deep diving may lead to more pronounced neuropsychologic impairment.

Bennett (1975) reported that signs and symptoms of the High Pressure Nervous Syndrome (HPNS) appeared including nausea, dizziness, tremors of the hands and arms, increased slow wave activity in electroencephalogram, especially in the theta band (4-7 Hz) with depression of alpha (8-13 Hz) and beta (20 Hz and higher) on compression with oxygen-helium to depths greater than 500 ft (16 ATA). Earlier studies have indicated that the HPNS may be controlled by use of an increased nitrogen partial pressure, slowing compression rate or excluding subject who has higher susceptibility to HPNS. For determining the effect of slowing compression rate, it was changed to new compression profile of linear compression to 31 ATA with intermediate stops in SEADRAGON-VI carried out at JAMSTEC in 1983. All divers to compressed to 31 ATA using the new rate complained few and slight signs and symptoms involved HPNS than ever experienced.