Narcosis is potentially one of the most dangerous conditions to affect the scuba diver below about . Except for occasional amnesia of events at depth, the effects of narcosis are entirely removed on ascent and therefore pose no problem in themselves, even for repeated, chronic or acute exposure. Nevertheless, the severity of narcosis is unpredictable and it can be fatal while diving, as the result of illogical behavior in a dangerous environment.

Tests have shown that all divers are affected by nitrogen narcosis, though some experience lesser effects than others. Even though it is possible that some divers can manage better than others because of learning to cope with the subjective impairment, the underlying behavioral effects remain. These effects are particularly dangerous because a diver may feel they are not experiencing narcosis, yet still be affected by it.

Hydrogen narcosis (also known as the hydrogen effect) is the psychotropic state induced by breathing hydrogen at high pressures. Hydrogen narcosis produces symptoms such as hallucinations, disorientation, and confusion, which are similar to hallucinogenic drugs. It can be experienced by deep-sea divers who dive to below sea level breathing hydrogen mixtures. However, hydrogen has far less narcotic effect than nitrogen (which causes the better known nitrogen narcosis) and is very rarely used in diving. In tests of the effect of hydrogen narcosis, where divers dived to with a hydrogen–helium–oxygen (Hydreliox) mixture containing 49% hydrogen, it was found that while the narcotic effect of hydrogen was detectable, the neurological symptoms of high-pressure nervous syndrome were only moderate.

The cause of narcosis is related to the increased solubility of gases in body tissues, as a result of the elevated pressures at depth (Henry's law). Modern theories have suggested that inert gases dissolving in the lipid bilayer of cell membranes cause narcosis. More recently, researchers have been looking at neurotransmitter receptor protein mechanisms as a possible cause of narcosis. The breathing gas mix entering the diver's lungs will have the same pressure as the surrounding water, known as the ambient pressure. After any change of depth, the pressure of gases in the blood passing through the brain catches up with ambient pressure within a minute or two, which results in a delayed narcotic effect after descending to a new depth. Rapid compression potentiates narcosis owing to carbon dioxide retention.

A divers' cognition may be affected on dives as shallow as , but the changes are not usually noticeable. There is no reliable method to predict the depth at which narcosis becomes noticeable, or the severity of the effect on an individual diver, as it may vary from dive to dive even on the same day.

Significant impairment due to narcosis is an increasing risk below depths of about , corresponding to an ambient pressure of about . Most sport scuba training organizations recommend depths of no more than because of the risk of narcosis. When breathing air at depths of – an ambient pressure of about – narcosis in most divers leads to hallucinations, loss of memory, and unconsciousness. A number of divers have died in attempts to set air depth records below . Because of these incidents, "Guinness World Records" no longer reports on this figure.

Narcosis has been compared with altitude sickness regarding its variability of onset (though not its symptoms); its effects depend on many factors, with variations between individuals. Thermal cold, stress, heavy work, fatigue, and carbon dioxide retention all increase the risk and severity of narcosis. Carbon dioxide has a high narcotic potential and also causes increased blood flow to the brain, increasing the effects of other gases. Increased risk of narcosis results from increasing the amount of carbon dioxide retained through heavy exercise, shallow or skip breathing, or because of poor gas exchange in the lungs.

Narcosis is known to be additive to even minimal alcohol intoxication, and also to the effects of other drugs such as cannabis (which is more likely than alcohol to have effects that last into a day of abstinence from use). Other sedative and analgesic drugs, such as opiate narcotics and benzodiazepines, add to narcosis.

The following environmental factors have been shown to increase the risk of DCS:

- the magnitude of the pressure reduction ratio – a large pressure reduction ratio is more likely to cause DCS than a small one.

- repetitive exposures – repetitive dives within a short period of time (a few hours) increase the risk of developing DCS. Repetitive ascents to altitudes above within similar short periods increase the risk of developing altitude DCS.

- the rate of ascent – the faster the ascent the greater the risk of developing DCS. The US Navy Dive Manual indicates that ascent rates greater than about when diving increase the chance of DCS, while recreational dive tables such as the Bühlmann tables require an ascent rate of with the last taking at least one minute. An individual exposed to a rapid decompression (high rate of ascent) above has a greater risk of altitude DCS than being exposed to the same altitude but at a lower rate of ascent.

- the duration of exposure – the longer the duration of the dive, the greater is the risk of DCS. Longer flights, especially to altitudes of and above, carry a greater risk of altitude DCS.

- underwater diving before flying – divers who ascend to altitude soon after a dive increase their risk of developing DCS even if the dive itself was within the dive table safe limits. Dive tables make provisions for post-dive time at surface level before flying to allow any residual excess nitrogen to outgas. However, the pressure maintained inside even a pressurized aircraft may be as low as the pressure equivalent to an altitude of above sea level. Therefore, the assumption that the dive table surface interval occurs at normal atmospheric pressure is invalidated by flying during that surface interval, and an otherwise-safe dive may then exceed the dive table limits.

- diving before travelling to altitude – DCS can occur without flying if the person moves to a high-altitude location on land immediately after diving, for example, scuba divers in Eritrea who drive from the coast to the Asmara plateau at increase their risk of DCS.

- diving at altitude – diving in water whose surface altitude is above — for example, Lake Titicaca is at — without using versions of decompression tables or dive computers that are modified for high-altitude.

Although the occurrence of DCS is not easily predictable, many predisposing factors are known. They may be considered as either environmental or individual.

Decompression sickness and arterial gas embolism in recreational diving are associated with certain demographic, environmental, and dive style factors. A statistical study published in 2005 tested potential risk factors: age, gender, body mass index, smoking, asthma, diabetes, cardiovascular disease, previous decompression illness, years since certification, dives in the last year, number of diving days, number of dives in a repetitive series, last dive depth, nitrox use, and drysuit use. No significant associations with risk of decompression sickness or arterial gas embolism were found for asthma, diabetes, cardiovascular disease, smoking, or body mass index. Increased depth, previous DCI, larger number of consecutive days diving, and being male were associated with higher risk for decompression sickness and arterial gas embolism. Nitrox and drysuit use, greater frequency of diving in the past year, increasing age, and years since certification were associated with lower risk, possibly as indicators of more extensive training and experience.

Obesity hypoventilation syndrome is associated with a reduced quality of life, and people with the condition incur increased healthcare costs, largely due to hospital admissions including observation and treatment on intensive care units. OHS often occurs together with several other disabling medical conditions, such as asthma (in 18–24%) and type 2 diabetes (in 30–32%). Its main complication of heart failure affects 21–32% of patients.

Those with abnormalities severe enough to warrant treatment have an increased risk of death reported to be 23% over 18 months and 46% over 50 months. This risk is reduced to less than 10% in those receiving treatment with PAP. Treatment also reduces the need for hospital admissions and reduces healthcare costs.

The exact prevalence of obesity hypoventilation syndrome is unknown, and it is thought that many people with symptoms of OHS have not been diagnosed. About a third of all people with morbid obesity (a body mass index exceeding 40 kg/m) have elevated carbon dioxide levels in the blood.

When examining groups of people with obstructive sleep apnea, researchers have found that 10–20% of them meet the criteria for OHS as well. The risk of OHS is much higher in those with more severe obesity, i.e. a body mass index (BMI) of 40 kg/m or higher. It is twice as common in men compared to women. The average age at diagnosis is 52. American Black people are more likely to be obese than American whites, and are therefore more likely to develop OHS, but obese Asians are more likely than people of other ethnicities to have OHS at a lower BMI as a result of physical characteristics.

It is anticipated that rates of OHS will rise as the prevalence of obesity rises. This may also explain why OHS is more commonly reported in the United States, where obesity is more common than in other countries.

High pressure nervous syndrome is rarely of importance to recreational divers. Breathing any gas at great depths (hundreds of feet) can cause seizures. Interestingly it was discovered because divers were using gas mixtures without nitrogen to be able to go to great depths without experiencing nitrogen narcosis. It turns out that nitrogen prevents HPNS. The answer? Add very small amounts of nitrogen to gas mixes when diving at great depth, small enough to avoid nitrogen narcosis, but sufficient to prevent HPNS.

Barotrauma is injury caused by pressure effects on gas spaces. This may occur during ascent or descent. The ears are the most commonly affected body part. The most serious injury is lung barotrauma, which can result in pneumothorax, pneumomediastinum, pneumopericardium, subcutaneous emphysema, and arterial gas embolism. All divers, commercial air travelers, people traveling overland between different altitudes, and people who work in pressurized environments have had to deal with some degree of barotrauma effect upon their ears, sinuses, and other air spaces. At the most extreme, barotrauma can cause ruptured eardrums, bleeding sinuses, exploding tooth cavities, and the lung injuries described above. This is the reason why divers follow a procedure of not holding their breath during ascent. By breathing continuously, they keep the airways open and avoid pressure differences between their lungs and ambient pressure.

The clinical course of BVVL can vary from one patient to another. There have been cases with progressive deterioration, deterioration followed by periods of stabilization, and deterioration with abrupt periods of increasing severity.

The syndrome has previously been considered to have a high mortality rate but the initial response of most patients to the Riboflavin protocol are very encouraging and seem to indicate a significantly improved life expectancy could be achievable. There are three documented cases of BVVL where the patient died within the first five years of the disease. On the contrary, most patients have survived more than 10 years after the onset of their first symptom, and several cases have survived 20–30 years after the onset of their first symptom.

Families with multiple cases of BVVL and, more generally, multiple cases of infantile progressive bulbar palsy can show variability in age of disease onset and survival. Dipti and Childs described such a situation in which a family had five children that had Infantile PBP. In this family, three siblings showed sensorineural deafness and other symptoms of BVVL at an older age. The other two siblings showed symptoms of Fazio-Londe disease and died before the age of two.

As of 2015, there are approximately 70 known cases of Brown-Vialetto-Van-Laere syndrome worldwide. BVVL was first described in a Portuguese family, and has since been described in a number of ethnic groups. Reports have shown that BVVL infects females more than males at a rate of 5:1 respectively. However, males usually exhibit more severe symptoms, an earlier onset of deafness and a tendency to die earlier in life.