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Decompression illness (DCI) is well known in compressed-air diving but has been considered anecdotal in breath-hold divers. Nonetheless, reported cases and field studies of the Japanese Ama, commercial or professional breath-hold divers, support DCI as a clinical entity. Clinical characteristics of DCI in Ama divers mainly suggest neurological involvement, especially stroke-like cerebral events with sparing of the spinal cord. Female Ama divers achieving deep depths have rarely experienced a panic-like neurosis from anxiety disorders. Neuroradiological studies of Ama divers have shown symptomatic and/or asymptomatic ischaemic lesions situated in the basal ganglia, brainstem, and deep and superficial cerebral white matter, suggesting arterial insufficiency. The underlying mechanism(s) of brain damage in breath-hold diving remain to be elucidated; one of the plausible mechanisms is arterialization of venous nitrogen bubbles passing through right to left shunts in the heart or lungs. Although the treatment for DCI in Ama divers has not been specifically established, oxygen breathing should be given as soon as possible for injured divers. The strategy for prevention of diving-related disorders includes reducing extreme diving schedules, prolonging surface intervals and avoiding long periods of repetitive diving. This review discusses the clinical manifestations of diving-related disorders in Ama divers and the controversial mechanisms.

Introduction: The aims of this study were to investigate the potential impact of age, sex and body mass index (BMI) upon the incidence of arrhythmias pre- and post- diving, and to identify the prevalence of left ventricular hypertrophy (LVH) in older recreational divers. Methods: Divers aged ≥ 40 years participating in group dive trips had ECG rhythm and echocardiograph recordings before and after diving. Arrhythmias were confirmed by an experienced human reader. LVH was identified by two-dimensional echocardiography. Weighted (0.5 fractional) values were used to account for participation by seven divers in 14 trips. Results: Seventy-seven divers undertook 84 dive trips and recorded 677 dives. Among divers with no pre-trip arrhythmias (n = 55), we observed that 6.5 (12%) recorded post-trip arrhythmias and the median increase was 1.0 arrhythmia. In divers with pre-trip arrhythmias, 14.5 had a median of 1.0 fewer post-trip arrhythmias, 2.0 had no change and 5.5 had a median of 16.0 greater. Age, but neither sex nor BMI, was associated with change in the number of arrhythmias before and after dive trips (P = 0.02). The relative risk for experiencing a change in the frequency of arrhythmias after a diver trip, was 2.1 for each additional 10 years of age (95% CI 1.1, 4.0). Of the 60 divers with imaging of their heart, five had left ventricular hypertrophy. Conclusions: We observed a higher than expected prevalence of arrhythmias. Divers with pre-trip arrhythmias tended to be older than divers without pre-trip arrhythmias (P = 0.02). The prevalence of LVH in our cohort was one quarter of that found post-mortem in scuba fatalities.

It is widely accepted that bubbles are a necessary but insufficient condition for the development of decompression sickness. However, open questions remain regarding the precise formation and behavior of these bubbles after an ambient pressure reduction (decompression), primarily due to the inherent difficulty of directly observing this phenomenon in vivo. In decompression research, information about these bubbles after a decompression is gathered via means of ultrasound acquisitions. The ability to draw conclusions regarding decompression research using ultrasound is highly influenced by the variability of the methodologies and equipment utilized by different research groups. These differences play a significant role in the quality of the data and thus the interpretation of the results. The purpose of this review is to provide a technical overview of the use of ultrasound in decompression research, particularly Doppler and brightness (B)-mode ultrasound. Further, we will discuss the strengths and limitations of these technologies and how new advancements are improving our ability to understand bubble behavior post-decompression

Decompression illness in breath‐hold diving is a rare dysbaric disease mainly characterized by stroke‐like neurological disorders. The early use of DWI‐MRI combined with ADC map in suspected cases can help in the early diagnosis and treatment.

Nitrogen (N2) accumulation in the blood and tissues can occur due to breath-hold (BH) diving. Post-dive venous gas emboli have been documented in commercial BH divers (Ama) after repetitive dives with short surface intervals. Hence, BH diving can theoretically cause decompression illness (DCI). “Taravana,” the diving syndrome described in Polynesian pearl divers by Cross in the 1960s, is likely DCI. It manifests mainly with cerebral involvements, especially stroke-like brain attacks with the spinal cord spared. Neuroradiological studies on Ama divers showed symptomatic and asymptomatic ischemic lesions in the cerebral cortex, subcortex, basal ganglia, brainstem, and cerebellum. These lesions localized in the external watershed areas and deep perforating arteries are compatible with cerebral arterial gas embolism. The underlying mechanisms remain to be elucidated. We consider that the most plausible mechanisms are arterialized venous gas bubbles passing through the lungs, bubbles mixed with thrombi occlude cerebral arteries and then expand from N2 influx from the occluded arteries and the brain. The first aid normobaric oxygen appears beneficial. DCI prevention strategy includes avoiding long-lasting repetitive dives for more than several hours, prolonging the surface intervals. This article provides an overview of clinical manifestations of DCI following repetitive BH dives and discusses possible mechanisms based on clinical and neuroimaging studies.

Background This study aimed to characterize the physiological demands of working dives on volunteer divers at a public aquarium in the USA. Aims To estimate the workloads associated with volunteer dives in a US aquarium. Methods Participants completed a medical and diving history questionnaire. Measurements included blood pressure before and after diving and continuous ECG (Holter) monitoring during diving. Dive profiles were recorded using loggers. Mean workload was estimated from total air consumption. Results Twenty-seven divers recorded 49 air dives over 5 days. Two-thirds were male and ages ranged from 40 to 78 years. Typically, each diver made two dives with a 30-60 min surface interval. Mean heart rate while diving was 100 beats per minute (bpm). Mean estimated workload during the dives recorded during this study was 5.8 metabolic equivalents (METS), with a range from 4.1 to 10.5. The highest mean recorded heart rate was 120 bpm over 40 min, vacuuming the floor in the shark exhibit. Conclusions Given the mean age of this sample and the prevalence of cardiovascular risk factors (body mass index, high cholesterol and hypertension), it may be prudent for aquariums to regularly monitor SAC/kg and heart rate in volunteer divers, to identify which tasks require the highest workload intensity. Divers with existing cardiovascular risk factors might then be employed in dives with lighter workloads. In conclusion, volunteer dives at this aquarium required a mean workload intensity that was described by recreational divers as moderate. The highest workload, at 10 METS for 23 min, would be considered by many recreational divers as exhausting.

Objectives This study investigates morbidity and mortality suffered by divers in the USA and Canada. Study design Prospectively recruited probability-weighted sample for estimating the national burden of injury and a weighted retrospective survey for estimating exposure. Methods The National Electronic Surveillance System and Canadian Hospitals Injury Reporting and Prevention Program (CHIRPP) were searched for scuba diving injuries. The Divers Alert Network diving fatality database was searched for deaths, and Sports and Fitness Industry Association estimates for diving were obtained from annual surveys. Results In the USA, there were an estimated 1394 emergency department (ED) presentations annually for scuba-related injuries. The majority (80%) were treated and/or released. There were an estimated 306 million dives made by the US residents 2006–2015 and concurrently 563 recreational diving deaths, a fatality rate of 0.18 per 105 dives and 1.8 per 105 diver-years. There were 658 diving deaths in the US 2006–2015 and 13,943 ED presentations for scuba injuries, giving a ratio of 47 diving deaths in the USA for every 1000 ED presentations. There were 98 cases of scuba-related injuries identified in the CHIRPP data. The prevalence of scuba-related injuries for patients aged 3–17 years was 1.5 per 105 cases, and the prevalence of scuba-related injuries to patients 18–62 years was 16.5 per 105 cases. Discussion In Canada and the USA, only one out of every 10,000 ED presentations is due to a scuba-related injury. That there are 47 deaths for every 1000 ED presentations for scuba injuries speaks to the relatively unforgiving environment in which scuba diving takes place. For 1.8 deaths per million recreational dives, mortality in scuba diving is nonetheless relatively low.

The diagnosis of decompression illness (DCI), which is based on a history of decompression and clinical findings, can sometimes be confounded with other vascular events of the central nervous system. The authors report three cases of divers who were urgently transported to a hyperbaric facility for hyperbaric oxygen treatment of DCI which at admission turned out to be something else. The first case, a 45-year-old experienced diver with unconsciousness, was clinically diagnosed as having experienced subarachnoid hemorrhage, which was confirmed by CT scan. The second case, a 49-year-old fisherman with a hemiparesis which occurred during diving, was diagnosed as cerebral stroke, resulting in putaminal hemorrhage. The third case, a 54-year-old fisherman with sensory numbness, ataxic gait and urinary retention following sudden post-dive onset of upper back pain, was diagnosed as spinal epidural hematoma; he also showed blood collection in the spinal canal. Neurological insults following scuba diving can present clinically with confusing features of cerebral and/or spinal DCI. We emphasize the importance of considering cerebral and/or spinal vascular diseases as unusual causes of neurological deficits after or during diving.

The first diver certification programme for recreational 'enriched air nitrox' (EAN) diving was released in 1985. Concerns were expressed that many EAN divers might suffer central nervous system (CNS) oxygen toxicity seizures and drown.US fatalities on open-circuit scuba occurring between 2004-2013, where the breathing gas was either air or EAN, were identified. Causes of death and preceding circumstances were examined by a medical examiner experienced in diving autopsies. Case notes were searched for witnessed seizures at elevated partial pressures of oxygen.The dataset comprised 344 air divers (86%) and 55 divers breathing EAN (14%). EAN divers' fatal dives were deeper than air divers' (28 msw vs 18 msw, p0.0001). Despite this, of the 249 cases where a cause of death was established, only three EAN divers were considered to have possibly died following CNS oxygen toxicity seizures at depth (ppO2 132, 142 and 193 kPa).The analysis of recreational diving fatalities in the US over 10 years found just one death likely from CNS oxygen toxicity among EAN divers. A further two possible, although unlikely, cases were also found. Fears of commonplace CNS oxygen toxicity seizures while EAN diving have not apparently been realized.

Cardiovascular factors among uninjured active adult recreational scuba divers in the USA are described. Scuba diving as an activity was included in 2011, 2013, and 2015 Behavioral Risk Factor Surveillance System data. One-third of active US scuba divers were aged ≥50 years and/or reported prior high cholesterol, around half were overweight, more than half reported having smoked cigarettes, and 32% reported hypertension or borderline hypertension. High cholesterol, hypertension, high body mass index, and smoking status should all be addressed during routine diving fitness physician assessments, to reduce the risk of mortality while diving.

Introduction Persistent (patent) foramen ovale (PFO) is a recognized risk for decompression sickness (DCS) in divers, which may be mitigated by conservative diving or by PFO closure. Our study aimed to compare the effectiveness of these two risk mitigation interventions. Methods This was a prospective study on divers who tested positive for PFO or an atrial septal defect (ASD) and either decided to continue diving without closure ('conservative group'), or to close their PFO/ASD and continue diving ('closure group'). Divers' characteristics, medical history, history of diving and history of DCS were reported at enrollment and annually after that. The outcome measures were the incidence rate of DCS, frequency and intensity of diving activities, and adverse events of closure. Results Divers in both groups dived less and had a lower incidence rate of confirmed DCS than before the intervention. In the closure group (n = 42) the incidence rate of confirmed DCS decreased significantly. Divers with a large PFO experienced the greatest reduction in total DCS. In the conservative group (n = 23), the post-intervention decrease in confirmed DCS incidence rate was not significant. Of note, not all divers returned to diving after closure. Seven subjects reported mild adverse events associated with closure; one subject reported a serious adverse event. Conclusions PFO closure should be considered on an individual basis. In particular, individuals who are healthy, have a significant DCS burden, a large PFO or seek to pursue advanced diving may benefit from closure.

BACKGROUND: Scuba diving mishaps, caused by equipment problems or human errors, increase the occurrence of injuries and fatalities while diving. Pre-dive checklists may mitigate mishaps. This study evaluated the effect of using a pre-dive checklist on the incidence of diving mishaps in recreational divers. METHODS: A multi-location cluster-randomized trial with parallel groups and allocation concealment was conducted between 1 June and 17 August 2012. The participants had to be at least 18 years of age, permitted to dive by the dive operator and planning to dive on the day of participation. They were recruited at the pier and dive boats at four locations. The intervention group received a pre-dive checklist and post-dive log. The control group received a post-dive log only. The outcomes, self-reported major and minor mishaps, were prompted by a post-dive questionnaire. Mishap rates per 100 dives were compared using Poisson regression with generalized estimating equations. Intent-to-treat, per-protocol and marginal structural model analyses were conducted. RESULTS: A total of 1043 divers (intervention = 617; control = 426) made 2041 dives, on 70 location-days (intervention = 40; control = 30) at four locations. Compared with the control group, the incidence of major mishaps decreased in the intervention group by 36%, minor mishaps by 26% and all mishaps by 32%. On average, there was one fewer mishap in every 25 intervention dives. CONCLUSIONS: In this trial, pre-dive checklist use prevented mishaps which could lead to injuries and fatalities. Pre-dive checklists can increase diving safety and their use should be promoted. TRIAL REGISTRATION: ClinicalTrials.gov ID NCT01960738. Language: en

Background Experience with commercial heliox diving at high altitude is limited. The purpose of this study was to evaluate the effects of acute high-altitude exposure on fitness to dive and the safety of decompression after heliox diving while using U.S. Navy heliox decompression tables with Cross correction. Method Four professional male divers were consecutively decompressed in a hypo- and hyperbaric chamber to altitudes of 3000 m (9842.5 ft), 4000 m (13,123.4 ft), and 5200 m (17,060.4 ft) during the 8-d study. The dive profiles tested were to 30 m (98.4 ft) for 60 min at all three altitudes and, in addition, a dive to 50 m (164 ft) for 60 min at 5200 m altitude. The decompression followed the U.S. Navy heliox decompression table. The safety of decompression was evaluated by precordial Doppler venous gas emboli (VGE) monitoring during the decompression stages and postdive monitoring of the divers for symptoms of decompression sickness (DCS). Effects of altitude exposure were measured as subjective rating and EEG signs of sleepiness and fatigue, clinical symptoms of high altitude disease, and fitness to dive. Results A total of 24 person-dives were conducted. There were no VGE detected during the decompression and no postdive symptoms of decompression illness. Both the EEG findings and subjective evaluation indicated increased sleepiness and fatigue at 3000 m, 4000 m, and 5200 m, all compared with the sea level baseline. During the diving phase, both the EEG findings and subjective evaluation scores returned to the baseline and the divers successfully completed diving. Discussion Diving at high altitude with a short acclimatization period appears safe despite divers exhibiting clinical symptoms and EEG signs of impairment by hypoxia at high altitude. Despite a small number of dives, the results of this study indicate that our application of U.S. Navy standard heliox decompression tables with Cross correction is effective and could be used for underwater constructions up to 5200 m altitude, with due caution.Shi L, Zhang Y, Tetsuo K, Shi Z, Fang Y, Denoble PJ, Li Y. Simulated high altitude helium-oxygen diving. Aerosp Med Hum Perform. 2017; 88(12):1088-1093.

BACKGROUND Scuba diver fitness is paramount to confront environmental stressors of diving. However, the diving population is aging and the increasing prevalence of diseases may be a concern for diver fitness. PURPOSE The purpose of this study is to assess the demographics, lifestyle factors, disease prevalence, and healthcare access and utilization of Divers Alert Network (DAN) members and compare them with those from the general population. METHODS DAN membership health survey (DMHS) was administered online in 2011 to DAN members in the United States (US). Health status of DMHS respondents was compared with the general US population data from the Center for Disease Control and Prevention's Behavioral Risk Factor Surveillance System using two-sided student's t-tests and Mantel-Haenszel chi-square tests. Univariate and multivariate logistic regression analyses were conducted to identify factors associated with healthcare utilization among the DMHS participants. RESULTS Compared to the general US population, the DMHS population had lower prevalence of asthma, heart attack, angina, stroke, diabetes, hypertension, hypercholesterolemia, and disabilities (p

Background Recreational scuba diving involves the use of complex instruments and specialized skills in an unforgiving environment. Errors in dive preparation in such an environment may lead to unsafe conditions, mishaps, injuries and fatalities. Diving mishaps can be major and minor based on their potential to cause injury and the severity of the resulting injury. The objective of this study is to assess the incidence of diving mishaps and unsafe conditions, and their associations with the participants’ routine use of their own checklists. Methods Between June and August 2012, 426 divers participated in the control group of a randomized trial to evaluate the effectiveness of an intervention pre-dive checklist. The current nested analysis prospectively follows the control participants, who did not receive the intervention checklist. Poisson regression models with generalized estimating equations were used to estimate rate ratios comparing written checklist use with memorized and no checklist use. Results The overall incidence of major mishaps and minor mishaps was 11.2 and 18.2 per 100 dives, respectively. Only 8% participants reported written checklist use, 71% reported using memorized checklists, and 21% did not use any checklist. The rate ratio for written checklist use as compared to using a memorized or no checklist was 0.47 (95%CI: 0.27, 0.83) for all mishaps (major and minor combined), and 0.31 (95% CI: 0.10, 0.93) for major mishaps. The rate of mishaps among memorized checklist users was similar to no checklist users. Conclusion This study reinforces the utility of written checklists to prevent mishaps and, potentially, injuries and fatalities.

Acclimatization (an adaptive change in response to repeated environmental exposure) to diving could reduce decompression stress. A decrease in post-dive circulating venous gas emboli (VGE or bubbles) would represent positive acclimatization. The purpose of this study was to determine whether four days of daily diving alter post-dive bubble grades. 16 male divers performed identical no-decompression air dives on 4 consecutive days to 18 meters of sea water for 47 min bottom times. VGE monitoring was performed with transthoracic echocardiography every 20 min for 120 min post-dive. Completion of identical daily dives resulted in progressively decreasing odds (or logit risk) of having relatively higher grade bubbles on consecutive days. The odds on Day 4 were half that of Day 1 (OR 0.50, 95% CI: 0.34, 0.73). The odds ratio for a >III bubble grade on Day 4 was 0.37 (95% CI: 0.20, 0.70) when compared to Day 1. The current study indicates that repetitive daily diving may reduce bubble formation, representing a positive (protective) acclimatization to diving. Further work is required to evaluate the impact of additional days of diving and multiple dive days and to determine if the effect is sufficient to alter the absolute risk of decompression sickness.

During SCUBA diving decompression, there is a significant gas bubble production in systemic veins, with rather frequent bubble crossover to arterial side even in asymptomatic divers. The aim of the current study was to investigate potential changes in humoral markers of endothelial and brain damage (endothelin-1, neuron-specific enolase and S-100β) after repetitive SCUBA diving with concomitant assessment of venous gas bubble production and subsequent arterialization. Sixteen male divers performed four open-water no-decompression dives to 18 msw (meters of sea water) lasting 49 min in consecutive days during which they performed moderate-level exercise. Before and after dives 1 and 4 blood was drawn, and bubble production and potential arterialization were echocardiographically evaluated. In addition, a control dive to 5 msw was performed with same duration, water temperature and exercise load. SCUBA diving to 18 msw caused significant bubble production with arterializations in six divers after dive 1 and in four divers after dive 4. Blood levels of endothelin-1 and neuron-specific enolase did not change after diving, but levels of S-100β were significantly elevated after both dives to 18 msw and a control dive. Creatine kinase activity following a control dive was also significantly increased. Although serum S-100β levels were increased after diving, concomitant increase of creatine kinase during control, almost bubble- free, dive suggests the extracranial release of S-100β, most likely from skeletal muscles. Therefore, despite the significant bubble production and sporadic arterialization after open-water dives to 18 msw, the current study found no signs of damage to neurons or the blood-brain barrier.

Adult male recreational diver fatalities ( n = 698) in North America from 2004 to 2013 were examined. Compared with non-harvesters, boat (86 vs 59%), solo (26 vs 13%) and night diving (10 vs 3%) were more common among harvesters. Of the divers who were low-on or out-of air, 20% were harvesters and 11% non-harvesters (OR = 2.0, P = 0.03).

The goal of this study was to evaluate annexin V-positive microparticles (MPs) and neutrophil activation in humans following decompression from open-water SCUBA diving with the hypothesis that changes are related to intravascular bubble formation. Sixteen male volunteer divers followed a uniform profile of four daily SCUBA dives to 18 m of sea water for 47 min. Blood was obtained prior to and at 80 min following the first and fourth dives to evaluate the impact of repetitive diving, and intravascular bubbles were quantified by trans-thoracic echocardiography carried out at 20-min intervals for 2 h after each dive. MPs increased by 3.4-fold after each dive, neutrophil activation occurred as assessed by surface expression of myeloperoxidase and the CD18 component of β2-integrins, and there was an increased presence of the platelet-derived CD41 protein on the neutrophil surface indicating interactions with platelet membranes. Intravascular bubbles were detected in all divers. Surprisingly, significant inverse correlations were found among postdiving bubble scores and MPs, most consistently at 80 min or more after the dive on the fourth day. There were significant positive correlations between MPs and platelet-neutrophil interactions after the first dive and between platelet-neutrophil interactions and neutrophil activation documented as an elevation in β2-integrin expression after the fourth dive. We conclude that MPs- and neutrophil-related events in humans are consistent with findings in an animal decompression model. Whether there are causal relationships among bubbles, MPs, platelet-neutrophil interactions, and neutrophil activation remains obscure and requires additional study.

An increasing number of recreational self- contained underwater breathing apparatus (SCUBA) divers use trimix of oxygen, helium, and nitrogen for dives deeper than 60 m of sea water. Although it was seldom linked to the development of pulmonary edema, whether SCUBA diving affects the extravascular lung water (EVLW) accumulation is largely unexplored. Methods: Seven divers performed six dives on consecutive days using compressed gas mixture of oxygen, helium, and nitrogen (trimix), with diving depths ranging from 55 to 80 m. The echocardiographic parameters (bubble grade, lung comets, mean pulmonary arterial pressure (PAP), and left ventricular function) and the blood levels of the N-terminal part of pro- brain natriuretic peptide (NT-proBNP) were assessed before and after each dive. Results: Venous gas bubbling was detected after each dive with mean probability of decompression sickness ranging from 1.77% to 3.12%. After each dive, several ultrasonographically detected lung comets rose significantly, which was paralleled by increased pulmonary artery pressure (PAP) and decreased left ventricular contractility (reduced ejection fraction at higher end-systolic and enddiastolic volumes) as well as the elevated NT-proBNP. The number of ultrasound lung comets and mean PAP did not return to baseline values after each dive. Conclusions: This is the first report that asymptomatic SCUBA dives are associated with accumulation of EVLW with concomitant increase in PAP, diminished left ventricular contractility, and increased release of NT- proBNP, suggesting a significant cardiopulmonary strain. EVLW and PAP did not return to baseline during repetitive dives, indicating possible cumulative effect with increasing the risk for pulmonary edema.

Protective effect of hydrogen (H2) gas on cardiac ischemia-reperfusion (I/R) injury has been demonstrated previously. This study was designed to test the hypothesis that hydrogen-rich saline (saline saturated with molecular hydrogen), which is easy to use, induces cardioprotection against ischemia (30 min) and reperfusion (24 h) injury in rats. Adult male Sprague-Dawley rats underwent 30-min occlusion of the left anterior descending (LAD) coronary artery and 24-h reperfusion. Intraperitoneal injection of hydrogen-rich saline before reperfusion significantly decreased plasma and myocardium malondialdehyde (MDA) concentration, decreased cardiac cell apoptosis, and myocardial 8-hydroxydeoxyguanosine (8-OHdG) in area at risk zones (AAR), suppressed the activity of caspase-3, and reduced infarct size. The heart function parameters including left ventricular systolic pressure (LVSP), left ventricular diastolic pressure (LVDP), +(dP/dt)max and −(dP/dt)max were also significantly improved 24 h after reperfusion. It is concluded that hydrogen-rich saline is a novel, simple, safe, and effective method to attenuate myocardial I/R injury.

The rate and pattern of lever pressing were studied in 18 rats during 24-h sessions in which responding resulted in intravenous infusions of nicotine. There were four indications of the positive reinforcing effect of nicotine: (1) a greater number of lever presses when nicotine was response-contingent compared to when saline was available; (2) a greater number of responses on the lever resulting in an infusion of nicotine than on the control lever; (3) systematic decreases in the number of contingent nicotine infusions when nicotine was delivered noncontingently; and (4) systematic changes in the frequency of lever pressing as a function of dose. Under a fixed ratio 1 (FR 1) schedule, the number of infusions first increased and then decreased as the dose of nicotine was decreased (64, 32, 16, and 8 microg/kg infusion) and nicotine intake (mg/kg every 24 h) was directly related to the infusion dose. As the FR size was increased from 1 to 6, the number of lever presses increased and the number of infusions (32 microg/kg) remained stable. At FR values greater than 6, both the number of lever presses and infusions decreased. Presession injections of mecamylamine (0.75, 1.5, and 3.0 mg/kg, s.c.) decreased the number of infusions in a dose-related manner. Presession injections of hexamethonium (1.5 and 3.0 mg/kg, s.c.) or naloxone (0.75, 1.5, and 3.0 mg/kg, s.c.) did not alter the within- or between-session patterns of nicotine self-administration. Under the conditions of the present experiment, nicotine served as an effective reinforcer and the behavior was shown to be sensitive to both FR size and infusion dose. In addition, the results suggest that nicotine self-administration involves central nicotinic receptors and that opioid receptor antagonism has no effect on nicotine's reinforcing effects in rats.

Decompression sickness (DCS), which is caused by inert gas bubbles in tissues, is an injury of concern for scuba divers, compressed air workers, astronauts, and aviators. Case reports for 3322 air and N2-O2 dives, resulting in 190 DCS events, were retrospectively analyzed and the outcomes were scored as (1) serious neurological, (2) cardiopulmonary, (3) mild neurological, (4) pain, (5) lymphatic or skin, and (6) constitutional or nonspecific manifestations. Following standard U.S. Navy medical definitions, the data were grouped into mild-Type I (manifestations 4-6)-and serious-Type II (manifestations 1-3). Additionally, we considered an alternative grouping of mild-Type A (manifestations 3-6)-and serious-Type B (manifestations 1 and 2). The current U.S. Navy guidance allows for a 2% probability of mild DCS and a 0.1% probability of serious DCS. We developed a hierarchical trinomial (3-state) probabilistic DCS model that simultaneously predicts the probability of mild and serious DCS given a dive exposure. Both the Type I/II and Type A/B discriminations of mild and serious DCS resulted in a highly significant (p << 0.01) improvement in trinomial model fit over the binomial (2-state) model. With the Type I/II definition, we found that the predicted probability of 'mild' DCS resulted in a longer allowable bottom time for the same 2% limit. However, for the 0.1% serious DCS limit, we found a vastly decreased allowable bottom dive time for all dive depths. If the Type A/B scoring was assigned to outcome severity, the no decompression limits (NDL) for air dives were still controlled by the acceptable serious DCS risk limit rather than the acceptable mild DCS risk limit. However, in this case, longer NDL limits were allowed than with the Type I/II scoring. The trinomial model mild and serious probabilities agree reasonably well with the current air NDL only with the Type A/B scoring and when 0.2% risk of serious DCS is allowed.

BACKGROUND: Acute decompression illness (DCI) involving the brain (Cerebral DCI) is one of the most serious forms of diving-related injuries which may leave residual brain damage. Cerebral DCI occurs in compressed air and in breath-hold divers, likewise. We conducted this study to investigate whether long-term breath-hold divers who may be exposed to repeated symptomatic and asymptomatic brain injuries, show brain damage on magnetic resonance imaging (MRI). SUBJECTS AND METHODS: Our study subjects were 12 commercial breath-hold divers (Ama) with long histories of diving work in a district of Japan. We obtained information on their diving practices and the presence or absence of medical problems, especially DCI events. All participants were examined with MRI to determine the prevalence of brain lesions. RESULTS: Out of 12 Ama divers (mean age: 54.9±5.1 years), four had histories of cerebral DCI events, and 11 divers demonstrated ischemic lesions of the brain on MRI studies. The lesions were situated in the cortical and/or subcortical area (9 cases), white matters (4 cases), the basal ganglia (4 cases), and the thalamus (1 case). Subdural fluid collections were seen in 2 cases. CONCLUSION: These results suggest that commercial breath-hold divers are at a risk of clinical or subclinical brain injury which may affect the long-term neuropsychological health of divers. Language: en

Introduction The term decompression illness (DCI) describes maladies resulting from inadequate decompression, but there is little consensus concerning clinically useful DCI subclasses. Our aim was to explore an objective DCI classification using multivariate statistics to assess naturally associated clusters of DCI manifestations. We also evaluated their mapping onto other DCI classifications and investigated the association with therapeutic outcome. Methods We defined the optimal number of clusters using "two-step" cluster analysis and Bayesian information criterion with confirmation by hierarchical clustering with squared Euclidian distances and Ward's method. The data were 1929 DCI cases reported by hyperbaric chambers to the Divers Alert Network (DAN America) from 1999-2003. Results Four robust and highly significant clusters of DCI manifestations were demonstrated containing 300, 741, 333, and 555 patients. Each cluster had characteristic manifestations. Cluster 1 was effectively pain only. For Cluster 2, characteristic manifestations included numbness, paresthesia, and decreased skin sensitivity; for Cluster 3, malaise, paralysis, muscular weakness, and bladder-bowel dysfunction; and for Cluster 4, hearing loss, localized skin swelling, tinnitus, skin rash and mottling, confusion, dyspnea/chokes, muscular problems, vision problems, altered consciousness, headache, vertigo, nausea, fatigue, dizziness, and abnormal sensations. Discussion Internal reliability was confirmed by arbitrarily dividing the dataset into two parts and repeating the analysis. The clusters mapped poorly onto traditional DCI categories (AGE, Type I DCS, Type II DCS), but more specifically onto the Perceived Severity Index (PSI). All three classification methods (DCI, Cluster, PSI) predicted complete relief of manifestations equally well. We conclude that cluster analysis is an objective method for classifying DCI manifestations independent of clinical judgment.

omegaWe review the terminology of decompression illness (DCI), investigations of residual symptoms of decompression sickness (DCS), and application of survival analysis for investigating DCI severity and resolution. The Type 1 and Type 2 DCS classifications were introduced in 1960 for compressed air workers and adapted for diving and altitude exposure with modifications based on clinical judgment concerning severity and therapy. In practice, these proved ambiguous, leading to recommendations that manifestations, not cases, be classified. A subsequent approach assigned individual scores to manifestations and correlated total case scores with the presence of residual symptoms after therapy. The next step used logistic regression to find the statistical association of manifestations to residual symptoms at a single point in time. Survival analysis, a common statistical method in clinical trials and longitudinal epidemiological studies, is a logical extension of logistic regression. The method applies to a continuum of resolution times, allows for time varying information, can manage cases lost to follow-up (censored), and has potential for investigating questions such as optimal therapy and DCI severity. There are operational implications as well. Appropriate definitions of mild and serious manifestations are essential for computing probabilistic decompression procedures where severity determines the DCS probability that is acceptable. Application of survival analysis to DCI data would require more specific case information than is commonly recorded.

Fatality records for American cave-diving fatalities (n = 368) occurring between 1969 and 2007 were examined and circumstances preceding each death categorized. Safety rules breached were noted in each case. The number of deaths per year peaked in the mid-1970s and has diminished since. Drowning was the most frequent cause of death, most often after running out of gas, which usually followed getting lost or starting the dive with insufficient gas. Compared with untrained divers, trained divers tended to be older, died at deeper depths and further inside caves, carried more cylinders of gas and more often died alone. Untrained divers were more likely to have dived without a guideline, without appropriate number of lights, and/or without adequate gas for the planned dive. Since running out of gas was associated with the greatest number of fatalities for trained divers, we recommend that gas management rules should receive the greatest emphasis in cave diving courses. Cave divers visit environments with inherent hazards that include flowing water, low or no visibility, a confusing number of possible exits, restrictions

Prospective study.To evaluate the formation of venous gas bubbles following open-sea scuba dives in persons with chronic spinal cord injury (SCI) and in able-bodied diving instructors (C) and to assess the risk for decompression sickness (DCS).Field study at the Island of Krk, Croatia.Gas bubbles were monitored with an ultrasound scanner 40 min after surfacing. The probability of DCS (P((DCS))) was estimated from the recorded depth-time profile using a decompression model.Divers completed six dives in 3 days using a modified Bühlmann decompression model, and none developed signs of DCS. Mean P((DCS)) was similar in both groups, SCI (0.51+/-0.2%) and C (0.64+/-0.27%), and was seen to increase with subsequent dives. Number of bubbles (bubbles per cm(2)) was low in both groups on all 3 days of diving.We have used the P((DCS)) as a severity index of diving exposure. Overall, the severity of exposure in SCI subjects was consistent with the range of typical recreational dives, suggesting that the diving profile used is very safe.

DuP 996, 3,3,-Bis(4-pyridinylmethyl)-1-phenylindolin-2-one, a potent in vitro and in vivo releaser of acetylcholine (ACh), dopamine (DA), and serotonin (5HT) in rat brain, significantly enhanced the performance of rats and mice in several behavioral test procedures. At doses of 0.01–0.1 mg/kg s.c. DuP 996 protected against a hypoxia-induced passive avoidance deficit in rats. In active avoidance procedures, DuP 996 enhanced acquisition of responses: in rats, at doses between 0.085 and 0.85 mg/kg s.c. and 0.25 and 0.85 mg/kg p.o.; in mice, at doses between 0.85 and 2.5 mg/kg s.c. These effects occurred without any alteration of sensitivity to foot-shock. In addition, Dup 996 prevented a CO2-induced retention deficit of a passive avoidance response when administered prior to acquisition testing. In a test for acquisition of lever pressing for food in the rat, DuP 996 increased the proportion of animals acquiring this response. Thus, DuP 996 was active in both the shock- and appetitive-motivated procedures and was shown to enhance performance levels when administered post-training as well as before training trials. These results suggest that DuP 996 may be useful in the treatment of cognition dysfunction.

The aim of this study was to determine whether venous gas embolism after a single air dive, evaluated using precordial Doppler monitoring, was associated with alterations in spirometry, lung volumes, arterial blood gases, or pulmonary diffusing capacity for carbon monoxide (DLCO). Postdive time course monitoring of pulmonary function was undertaken in 10 professional divers exposed to absolute air pressure of 5.5 bar for 25 min in a dry walk-in chamber. The US Navy decompression table was followed. Venous bubbles were detected by precordial Doppler monitoring. Two types of decompression were used: air and 100% O2 applied for 21 min during decompression stops. Spirometry, flow-volume, and body plethysmography parameters were unchanged after the dive with air decompression (AD) as well as with O2 decompression (OD). A significant reduction in arterial PO2, on average 20 Torr, was found after the dive with AD. DLCO was decreased in all divers 20, 40, 60, and 80 min after diving with AD (P < 0.001), whereas it was not significantly decreased after diving with OD. Maximal DLCO decrease of approximately 15% occurred 20 min postdive. In AD diving, maximum bubble grade for each individual vs. maximum DLCO reduction correlated significantly (r = 0.85, P = 0.002), as well as DLCO vs. arterial PO2 (r = 0.64, P = 0.017). In conclusion, a reduction in pulmonary diffusing capacity is observed in parallel with the appearance of venous bubbles detected by precordial Doppler. We suggest that bubbles cause pulmonary microembolization, triggering a complex sequence of events that remains to be resolved. Measuring DLCO complements Doppler bubble detection in postdiving assessment of pulmonary function.

The behavioral effects of intraventricularly (IVT) administered (-)-nicotine on food-maintained behavior were studied. Rats responded by pressing a lever under various fixed ratio (FR) schedules. Infusion of 5 microgram of (-)-nicotine suppressed responding under an FR 16 schedule for 11-13 min. The effect was inversely related to the ratio size (16, 32, 64 responses per food delivery), but it was directly related to the infused (-)-nicotine dose (0.312, 0.624, 1.25, 2.5, 5.0, 10.0 microgram) when ratio size was held constant. Responses rates following the (-)-nicotine-induced suppression were similar to those obtained prior to infusion. The behavioral effects of (-)-nicotine were blocked, in a dose-related manner, by the centrally acting nicotinic-cholinergic antagonist, mecamylamine (0.05-3.0 mg/kg) but not by ther peripherally acting antagonist, hexamethonium (0.5-3.0 mg/kg), suggesting that the behavioral effects of IVT infusions of (-)-nicotine are mediated by central nicotine-cholinergic receptors.

The number of liquid deliveries and pattern of concurrent pentobarbital and water drinking were studied in three food deprived rhesus monkeys during daily 3-hr sessions. During the daily sessions, deliveries of approximately 0.6 ml of each liquid occured under fixed-ratio (FR) schedules of lip contact responses. Between sessions water was freely available. Session drinking was studied as a function of pentobarbital concentration (1.0, 1.41, 2.0, and 4.0 mg/ml) and FR size (4, 8, 16 and 32 lip contacts per delivery). The number of drug deliveries decreased with increases in drug concentration. Drug intake ranged from 21 to 52 mg/kg of body wt./3-hr session. At all concentrations and FR values tested, the number of pentobarbital deliveries substantially exceeded the number of water deliveries. The positive reinforcing effect of the pentobarbital was indicated by a consistent choice of drug over water irrespective of the side position of pentobarbital and by higher rates of drug responding. Pentobarbital drinking occured in a negatively accelerated pattern whereas water drinking did not have any consistent pattern. Marked intoxication followed bouts of drug drinking.

The effect of several doses of systemically administered N-methyl-D-aspartate (NMDA) was studied on step-through passive avoidance (PA) retention in rats. Retention of single trial PA was significantly reduced by preacquisition (30 minutes) doses of NMDA (3, 10, 30, and 50 mg/kg SC). Preacquisition amnesia was found when NMDA (30 mg/kg SC) was administered between two and 60 minutes. At shorter and longer pretreatment times (0.5 and 180 minutes) NMDA (30 mg/kg SC) did not disrupt retention testing. Across the same dose range and pretreatment times, NMDA failed to interfere with PA retention when given after acquisition or before retention testing. The results suggest that systemic NMDA administration can interfere with the acquisition of PA response but does not alter consolidation of information or retrieval.

The alcohol withdrawal syndrome includes a broad spectrinn of severity. The milder stages of the syndrome include such symptoms as slight tremor, malaise and general irritability, and the more severe stages of the syndome are characterized by delirium tremors. While the nature of the underlying mechanisms is not established, the evidence presently available suggests that there may well be different mechanisms for different manifestations associated with withdrawal.

Responding by 4 monkeys was maintained under a fixed ratio 10 (FR 10) schedule for either food, intravenous sucrose or alcohol. The 20 hr sessions were divided so that food was available during hours 1, 6, 11, 16 and alcohol or sucrose during hours 2–5, 7–10, 12–15, and 17–20. All animals failed to maintain responding for isocaloric sucrose but continued to respond for food during those sessions. Responding under alcohol conditions was positively accelerated in 2 animals that were not previously exposed to alcohol, whereas prior exposure to alcohol produced maximal response rates during the first alcohol test session. The effects of alcohol in all monkeys were to suppress responding maintained by food and this suppression could not be produced with programmed infusions of isocaloric sucrose.

Rats provided with unlimited access to intravenous doses of ethanol (30, 60, 90, 180, and 360 mg/kg/infusion) failed to initiate and maintain lever pressing that resulted in ethanol delivery. When pentobarbital (0.5 mg/kg/infusion) was substituted for ethanol, lever pressing increased. There were three indications of the positive reinforcing effects of pentobarbital: (1) a greater number of lever presses occurred when pentobarbital was response-contingent than when saline was available (2) a greater number of responses were made on the pentobarbital lever than on a control “activity” lever; and (3) systematic changes in lever pressing were a function of pentobarbital dose (0.125, 0.25, 0.5, 1.0, and 2.0 mg/kg/infusion). Sequential substitution of ethanol (30, 90, 360 mg/kg/infusion) for pentobarbital failed to maintain lever pressing. However, access to combinations of ethanol (1, 3, 10, 30, 60 mg/kg/infusion) and a nonreinforcing dose of pentobarbital (0.125 or 0.25 mg/kg/infusion) did maintain lever pressing. As the dose of ethanol increased, the daily number of infusion first increased then decreased. Following a history of self-administration of ethanol-pentobarbital combinations, a retest of ethanol alone (10 or 30 mg/kg/infusions) followed by pentobarbital alone (0.125 or 0.25 mg/kg/infusion) failed to maintain lever pressing.

Two groups of male hooded rats (N=9) were given either ethanol or sucrose solutions as their only source of fluid for six months. Thirty days after the ethanol treatment, the rats were reduced to 85% of their free-feeding weights and allowed to obtain 45 mg food pellets on an FR 1 schedule for five consecutive days. Subsequently, the rats were tested on four DRL schedules (6, 12, 18, 24 sec). There was no difference between the two groups on FR 1 or DRL 6 sec schedules; however, when the DRL interval was lengthened to 12, 18, and 24 sec, the ethanol group required more sessions than the sucrose group to reach criterion performance. After increases in the DRL interval, the modal interresponse time of the ethanol group shifted more slowly than that of the sucrose group.