The most straightforward way to avoid nitrogen narcosis is for a diver to limit the depth of dives. Since narcosis becomes more severe as depth increases, a diver keeping to shallower depths can avoid serious narcosis. Most recreational dive schools will only certify basic divers to depths of , and at these depths narcosis does not present a significant risk. Further training is normally required for certification up to on air, and this training should include a discussion of narcosis, its effects, and cure. Some diver training agencies offer specialized training to prepare recreational divers to go to depths of , often consisting of further theory and some practice in deep dives under close supervision. Scuba organizations that train for diving beyond recreational depths, may forbid diving with gases that cause too much narcosis at depth in the average diver, and strongly encourage the use of other breathing gas mixes containing helium in place of some or all of the nitrogen in air – such as trimix and heliox – because helium has no narcotic effect. The use of these gases forms part of technical diving and requires further training and certification.

While the individual diver cannot predict exactly at what depth the onset of narcosis will occur on a given day, the first symptoms of narcosis for any given diver are often more predictable and personal. For example, one diver may have trouble with eye focus (close accommodation for middle-aged divers), another may experience feelings of euphoria, and another feelings of claustrophobia. Some divers report that they have hearing changes, and that the sound their exhaled bubbles make becomes different. Specialist training may help divers to identify these personal onset signs, which may then be used as a signal to ascend to avoid the narcosis, although severe narcosis may interfere with the judgement necessary to take preventive action.

Deep dives should be made only after a gradual training to test the individual diver's sensitivity to increasing depths, with careful supervision and logging of reactions. Diving organizations such as Global Underwater Explorers (GUE) emphasize that such sessions are for the purpose of gaining experience in recognizing the onset symptoms of narcosis for an individual , which are somewhat more repeatable than for the average group of divers. Scientific evidence does not show that a diver can train to overcome any measure of narcosis at a given depth or become tolerant of it.

Equivalent narcotic depth (END) is a commonly used way of expressing the narcotic effect of different breathing gases. The National Oceanic and Atmospheric Administration (NOAA) Diving Manual now states that oxygen and nitrogen should be considered equally narcotic. Standard tables, based on relative lipid solubilities, list conversion factors for narcotic effect of other gases. For example, hydrogen at a given pressure has a narcotic effect equivalent to nitrogen at 0.55 times that pressure, so in principle it should be usable at more than twice the depth. Argon, however, has 2.33 times the narcotic effect of nitrogen, and is a poor choice as a breathing gas for diving (it is used as a drysuit inflation gas, owing to its low thermal conductivity). Some gases have other dangerous effects when breathed at pressure; for example, high-pressure oxygen can lead to oxygen toxicity. Although helium is the least intoxicating of the breathing gases, at greater depths it can cause high pressure nervous syndrome, a still mysterious but apparently unrelated phenomenon. Inert gas narcosis is only one factor influencing the choice of gas mixture; the risks of decompression sickness and oxygen toxicity, cost, and other factors are also important.

Because of similar and additive effects, divers should avoid sedating medications and drugs, such as marijuana and alcohol before any dive. A hangover, combined with the reduced physical capacity that goes with it, makes nitrogen narcosis more likely. Experts recommend total abstinence from alcohol for at least 12 hours before diving, and longer for other drugs. Abstinence time needed for marijuana is unknown, but owing to the much longer half-life of the active agent of this drug in the body, it is likely to be longer than for alcohol.

The management of narcosis is simply to ascend to shallower depths; the effects then disappear within minutes. In the event of complications or other conditions being present, ascending is always the correct initial response. Should problems remain, then it is necessary to abort the dive. The decompression schedule can still be followed unless other conditions require emergency assistance.

The symptoms of narcosis may be caused by other factors during a dive: ear problems causing disorientation or nausea; early signs of oxygen toxicity causing visual disturbances; or hypothermia causing rapid breathing and shivering. Nevertheless, the presence of any of these symptoms should imply narcosis. Alleviation of the effects upon ascending to a shallower depth will confirm the diagnosis. Given the setting, other likely conditions do not produce reversible effects. In the rare event of misdiagnosis when another condition is causing the symptoms, the initial management – ascending closer to the surface – is still essential.

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.

Formal criteria for diagnosis of OHS are:

- Body mass index over 30 kg/m (a measure of obesity, obtained by taking one's weight in kilograms and dividing it by one's height in meters squared)

- Arterial carbon dioxide level over 45 mmHg or 6.0 kPa as determined by arterial blood gas measurement

- No alternative explanation for hypoventilation, such as use of narcotics, severe obstructive or interstitial lung disease, severe chest wall disorders such as kyphoscoliosis, severe hypothyroidism (underactive thyroid), neuromuscular disease or congenital central hypoventilation syndrome

If OHS is suspected, various tests are required for its confirmation. The most important initial test is the demonstration of elevated carbon dioxide in the blood. This requires an arterial blood gas determination, which involves taking a blood sample from an artery, usually the radial artery. Given that it would be complicated to perform this test on every patient with sleep-related breathing problems, some suggest that measuring bicarbonate levels in normal (venous) blood would be a reasonable screening test. If this is elevated (27 mmol/l or higher), blood gasses should be measured.

To distinguish various subtypes, polysomnography is required. This usually requires brief admission to a hospital with a specialized sleep medicine department where a number of different measurements are conducted while the subject is asleep; this includes electroencephalography (electronic registration of electrical activity in the brain), electrocardiography (same for electrical activity in the heart), pulse oximetry (measurement of oxygen levels) and often other modalities. Blood tests are also recommended for the identification of hypothyroidism and polycythemia.

To distinguish between OHS and various other lung diseases that can cause similar symptoms, medical imaging of the lungs (such as a chest X-ray or CT/CAT scan), spirometry, electrocardiography and echocardiography may be performed. Echo- and electrocardiography may also show strain on the right side of the heart caused by OHS, and spirometry may show a restrictive pattern related to obesity.

Decompression sickness should be suspected if any of the symptoms associated with the condition occurs following a drop in pressure, in particular, within 24 hours of diving. In 1995, 95% of all cases reported to Divers Alert Network had shown symptoms within 24 hours. An alternative diagnosis should be suspected if severe symptoms begin more than six hours following decompression without an altitude exposure or if any symptom occurs more than 24 hours after surfacing. The diagnosis is confirmed if the symptoms are relieved by recompression. Although MRI or CT can frequently identify bubbles in DCS, they are not as good at determining the diagnosis as a proper history of the event and description of the symptoms.

Immediate treatment with 100% oxygen, followed by recompression in a hyperbaric chamber, will in most cases result in no long-term effects. However, permanent long-term injury from DCS is possible. Three-month follow-ups on diving accidents reported to DAN in 1987 showed 14.3% of the 268 divers surveyed had ongoing symptoms of Type II DCS, and 7% from Type I DCS. Long-term follow-ups showed similar results, with 16% having permanent neurological sequelae.

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.

Dysbarism refers to medical conditions resulting from changes in ambient pressure. Various activities are associated with pressure changes. underwater diving is the most frequently cited example, but pressure changes also affect people who work in other pressurized environments (for example, caisson workers), and people who move between different altitudes.

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.

Diagnosis requires a neurological examination and neuroimaging can be helpful.

BVVL can be differentially diagnosed from similar conditions like Fazio-Londe syndrome and amyotrophic lateral sclerosis, in that those two conditions don't involve sensorineural hearing loss, while BVVL, Madras motor neuron disease, Nathalie syndrome, and Boltshauser syndrome do. Nathalie syndrome does not involve lower cranial nerve symptoms, so it can be excluded if those are present. If there is evidence of lower motor neuron involvement, Boltshauser syndrome can be excluded. Finally, if there is a family history of the condition, then BVVL is more likely than MMND, as MMND tends to be sporadic.

Genetic testing is able to identify genetic mutations underying BVVL.

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.