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.

Viewpoint: the type A- and the type B-variants of Decompression Sickness.

BACKGROUND: Symptoms of neurological decompression incidents (DCS/AGE) can be severe or mild. It is unknown if these differences of symptom presentation represent different clinical entities or if they represent just the spectrum of DCS/AGE. METHODS: 267 cases with DCS/AGE were compared retrospectively and classified into two subgroups, the Type A-DCS/AGE for cases with a severe and often stroke-like symptomatology and the Type B-DCS/AGE for those with milder and sometimes even doubtful neurological symptoms. The main outcome measures were the number of hyperbaric treatments (HTs) needed and the clinical outcome. RESULTS: 42 patients with DCS/AGE were classified as Type A- and 225 patients met the criteria for a Type B-DCS/AGE. Patients with Type A-lesions were more severely affected, needed more hyperbaric treatments and had a less favorable outcome than patients with the Type B-variant. CONCLUSIONS: The Type A- and the Type B-DCS/AGE are likely to be different entities with better clinical outcome in the Type B-variant and possibly significant differences in the underlying pathophysiologies of both variants. Future studies with a particular focus on the up to now inadequately investigated Type B-DCS/AGE are necessary to elucidate such differences in the pathophysiology.

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

Diving and marine medicine review part II: diving diseases.

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.

Changes in sleep patterns during He-O2 saturation dives.

During simulated hyperbaric saturation diving experiments of He-O2 mixture at the depths of 150, 180 and 230 m the standard polysomnography of four divers, as well as their subjective feelings of fatigue, were recorded for 268 nights. In all three diving conditions, during the bottom period and the decompression period, wakes after sleep onset and Stage 1 sleep increased while Stage 4 sleep decreased. In deeper diving conditions stage 4 sleep tended to decrease and subjective feelings of fatigue increased. When the results are considered it can be assumed that the deeper the diving depths, the increased sleep disturbances and fatigue. However, it is believed that a fundamental sleep pattern will be maintained.

High-pressure neurological syndrome (HPNS).

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.

Development of anxiety symptoms during a deep diving experiment.

Six commercial divers were investigated for anxiety responses during a 29-day, open-sea world record dive at 500 meters of depth. Three of six (50%) divers developed anxiety. The authors emphasize the importance of research on personality traits as possible predictors for the development of anxiety during deep dives of exceptional depth and duration of confinement.

[Acute and chronic effects of deep diving on the nervous system]. / Akutte og kroniske effekter på nervesystemet ved dypdykking.

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.

Topographic electroencephalographic studies in a hyperbaric environment--specific reference to high pressure nervous syndrome.

Hyperbaric chamber dives at various equivalent depths below sea level, i.e. 7, 14, 19 and 31 atmosphere absolute (ATA) with helium-oxygen or helium-nitrogen-oxygen have been performed at the Japan Marine Science and Technology Center. A two-dimensional (topographic) display of the scalp EEG was used during simulated underwater experiments to determine; 1) Whether there are any characteristic EEG patterns in high pressure nervous syndrome (HPNS), 2) the relationship between the EEG changes and the compression rate, and 3) the relationship between the EEG changes and the characteristic signs and symptoms of HPNS. A two-way analysis of variance and a distribution analysis technique revealed that the topographic brain patterns depended on the diving depth and indicated the most affected brain areas during compression and decompression. Significant correlations between the diving depth and the EEG potentials were observed at different brain locations. Alpha waves showed a diffuse cortical distribution. Theta wave activity was more localized in the frontal midline region. These waves developed paroxysmally in relatively brief bursts supplanting or intermixing with normal background EEG rhythms. In our subjects, frontal midline theta activity was associated mostly with some of the characteristic features of HPNS, such as a transient episode of laughter or euphoria at depths greater than 21 ATA. An intimate correlation between frontal midline theta wave and laughter was observed. Frontal midline theta waves may be related to emotional activities induced by helium under high pressure. There were significant individual variations in susceptibility and subjective signs and symptoms. The EEG is of great value in studying man's physiological reactions in an undersea environment and also very important in selecting divers who are relatively more tolerant of a severe hyperbaric environment.