The cost of decompression illness: the case of lobster and sea cucumber fishery in Yucatan, Mexico.

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.

Observed decompression sickness and venous bubbles following 18-msw dive profiles using RN Table 11.

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.

Evaluating the risk of decompression sickness for a yo-yo dive using a rat model.

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.

Detection of venous gas emboli after repetitive breath-hold dives: case report.

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.

MRI of the central nervous system in rats following heliox saturation decompression.

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.

Neurological complications of underwater diving.

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.

Decompression illness in goats following simulated submarine escape: 1993-2006.

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.

Submarine 'safe to escape' studies in man.

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.

A retrospective cohort study of lidocaine in divers with neurological decompression illness.

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.

Recreational technical diving part 2: decompression from deep technical dives.

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.

Is glucose-6-phosphate dehydrogenase deficiency a risk factor for hyperbaric oxygen exposure?

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.

Hyperbaric pressure effects on voltage-dependent Ca+2 channels: relevance to HPNS.

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.

Estimates of N2 narcosis and O2 toxicity during submarine escapes from 600 to 1,000 fsw.

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.

Síndrome neurológico de alta presiónimag / High pressure neurological syndrome

La presión, como la temperatura, es una variable termodinámica que afecta los estados de la materia.La alta presión es una característica medioambiental de las profundidades del mar, donde las presiones aumentan a razón de 0,1 MPa (1 atm) cada 10 m. Humanos expuestos a alta presión, generalmente buzos profesionales, sufren trastornos neurológicos proporcionales a esa exposición. Desarrollo. El sistema nervioso es uno de los tejidos más sensibles a los efectosde la presión. Su alteración, conocida como el síndrome neurológico de alta presión (SNAP), comienza a mostrar signos a unos 1,3 MPa (120 m) y se acentúa a profundidades mayores. El SNAP se manifiesta con temblores en las extremidades distales,náuseas y/o moderados trastornos psicomotores. Consecuencias más graves son temblores proximales, vómitos, hiperreflexia,somnolencia y compromiso cognitivo. Estadios graves del SNAP presentan fasciculaciones, mioclonos y, en casos extremos, psicosis, crisis convulsivas focalizadas o generalizadas. El SNAP muestra un electroencefalograma caracterizado por disminución de ondas de alta frecuencia (alfa y beta) e incremento de ondas lentas, modificaciones en potenciales evocadosauditivos, visuales y somatosensoriales, disminución de conducción nerviosa y cambios en latencia de reflejos. Estudios en animales de experimentación demostraron que estos signos son progresivos y directamente dependientes de la presión. A nivelneuronal y de redes, el SNAP muestra depresión de transmisión sináptica y, paradójicamente, hiperexcitabilidad. Conclusión.El SNAP se asocia con exposición a alta presión y su medioambiente tecnológico. Estudios experimentales sugieren hipótesis etiológicas y perspectivas terapéuticas y de prevención

Pressure is a thermodynamic variable that, like temperature, affects the states of matter. High pressureis 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 totheir exposure. Development. 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 severeconsequences 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 frequencyactivity (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 haveshown 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. Conclusion. HPNS is associatedwith exposure to high pressure and its related technological means. Experimental findings suggest etiological hypotheses, prevention and therapeutic approaches for this syndrome

Postural control in a simulated saturation dive to 240 msw.

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.

High pressure modulation of NMDA receptor dependent excitability.

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.

Recent neurochemical basis of inert gas narcosis and pressure effects.

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.

Nitric oxide amplifies the excitatory to inhibitory neurotransmitter imbalance accelerating oxygen seizures.

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.

CNS manifestations of HPNS: revisited.

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.