<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Decompression sickness and explain in detail? [/INST] Decompression sickness (abbreviated DCS; also called divers disease, the bends, aerobullosis, and caisson disease) is a medical condition caused by dissolved gases emerging from solution as bubbles inside the body tissues during decompression. DCS most commonly occurs during or soon after a decompression ascent from underwater diving, but can also result from other causes of depressurisation, such as emerging from a caisson, decompression from saturation, flying in an unpressurised aircraft at high altitude, and extravehicular activity from spacecraft. DCS and arterial gas embolism are collectively referred to as decompression illness.
Since bubbles can form in or migrate to any part of the body, DCS can produce many symptoms, and its effects may vary from joint pain and rashes to paralysis and death. DCS often causes air bubbles to settle in major joints like knees or elbows, causing individuals to bend over in excruciating pain, hence its common name, the bends. Individual susceptibility can vary from day to day, and different individuals under the same conditions may be affected differently or not at all. The classification of types of DCS according to symptoms has evolved since its original description in the 19th century. The severity of symptoms varies from barely noticeable to rapidly fatal.
The risk of DCS caused by diving can be managed through proper decompression procedures, and contracting the condition has become uncommon. Its potential severity has driven much research to prevent it, and divers almost universally use dive tables or dive computers to limit their exposure and to monitor their ascent speed. If DCS is suspected, it is treated by hyperbaric oxygen therapy in a recompression chamber. Where a chamber is not accessible within a reasonable time frame, in-water recompression may be indicated for a narrow range of presentations, if there are suitably skilled personnel and appropriate equipment available on site. Diagnosis is confirmed by a positive response to the treatment. Early treatment results in a significantly higher chance of successful recovery.

Classification
DCS is classified by symptoms. The earliest descriptions of DCS used the terms: "bends" for joint or skeletal pain; "chokes" for breathing problems; and "staggers" for neurological problems. In 1960, Golding et al. introduced a simpler classification using the term "Type I (simple)" for symptoms involving only the skin, musculoskeletal system, or lymphatic system, and "Type II (serious)" for symptoms where other organs (such as the central nervous system) are involved. Type II DCS is considered more serious and usually has worse outcomes. This system, with minor modifications, may still be used today. Following changes to treatment methods, this classification is now much less useful in diagnosis, since neurological symptoms may develop after the initial presentation, and both Type I and Type II DCS have the same initial management.

Decompression illness and dysbarism
The term dysbarism encompasses decompression sickness, arterial gas embolism, and barotrauma, whereas decompression sickness and arterial gas embolism are commonly classified together as decompression illness when a precise diagnosis cannot be made. DCS and arterial gas embolism are treated very similarly because they are both the result of gas bubbles in the body. The U.S. Navy prescribes identical treatment for Type II DCS and arterial gas embolism. Their spectra of symptoms also overlap, although the symptoms from arterial gas embolism are generally more severe because they often arise from an infarction (blockage of blood supply and tissue death).

Signs and symptoms
While bubbles can form anywhere in the body, DCS is most frequently observed in the shoulders, elbows, knees, and ankles. Joint pain ("the bends") accounts for about 60% to 70% of all altitude DCS cases, with the shoulder being the most common site for altitude and bounce diving, and the knees and hip joints for saturation and compressed air work. Neurological symptoms are present in 10% to 15% of DCS cases with headache and visual disturbances being the most common symptom. Skin manifestations are present in about 10% to 15% of cases. Pulmonary DCS ("the chokes") is very rare in divers and has been observed much less frequently in aviators since the introduction of oxygen pre-breathing protocols. The table below shows symptoms for different DCS types.

Frequency
The relative frequencies of different symptoms of DCS observed by the U.S. Navy are as follows:

Onset
Although onset of DCS can occur rapidly after a dive, in more than half of all cases symptoms do not begin to appear for at least an hour. In extreme cases, symptoms may occur before the dive has been completed. The U.S. Navy and Technical Diving International, a leading technical diver training organization, have published a table that documents time to onset of first symptoms. The table does not differentiate between types of DCS, or types of symptom.

Causes
DCS is caused by a reduction in ambient pressure that results in the formation of bubbles of inert gases within tissues of the body. It may happen when leaving a high-pressure environment, ascending from depth, or ascending to altitude. A closely related condition of bubble formation in body tissues due to isobaric counterdiffusion can occur with no change of pressure.

Ascent from depth
DCS is best known as a diving disorder that affects divers having breathed gas that is at a higher pressure than the surface pressure, owing to the pressure of the surrounding water. The risk of DCS increases when diving for extended periods or at greater depth, without ascending gradually and making the decompression stops needed to slowly reduce the excess pressure of inert gases dissolved in the body. The specific risk factors are not well understood and some divers may be more susceptible than others under identical conditions. DCS has been confirmed in rare cases of breath-holding divers who have made a sequence of many deep dives with short surface intervals, and may be the cause of the disease called taravana by South Pacific island natives who for centuries have dived by breath-holding for food and pearls.Two principal factors control the risk of a diver developing DCS:

the rate and duration of gas absorption under pressure – the deeper or longer the dive the more gas is absorbed into body tissue in higher concentrations than normal (Henrys Law);
the rate and duration of outgassing on depressurization – the faster the ascent and the shorter the interval between dives the less time there is for absorbed gas to be offloaded safely through the lungs, causing these gases to come out of solution and form "micro bubbles" in the blood.Even when the change in pressure causes no immediate symptoms, rapid pressure change can cause permanent bone injury called dysbaric osteonecrosis (DON). DON can develop from a single exposure to rapid decompression.

Leaving a high-pressure environment
When workers leave a pressurized caisson or a mine that has been pressurized to keep water out, they will experience a significant reduction in ambient pressure. A similar pressure reduction occurs when astronauts exit a space vehicle to perform a space-walk or extra-vehicular activity, where the pressure in their spacesuit is lower than the pressure in the vehicle.The original name for DCS was "caisson disease". This term was introduced in the 19th century, when caissons under pressure were used to keep water from flooding large engineering excavations below the water table, such as bridge supports and tunnels. Workers spending time in high ambient pressure conditions are at risk when they return to the lower pressure outside the caisson if the pressure is not reduced slowly. DCS was a major factor during construction of Eads Bridge, when 15 workers died from what was then a mysterious illness, and later during construction of the Brooklyn Bridge, where it incapacitated the project leader Washington Roebling. On the other side of the Manhattan island during construction of the Hudson River Tunnel contractors agent Ernest William Moir noted in 1889 that workers were dying due to decompression sickness and pioneered the use of an airlock chamber for treatment.

Ascent to altitude
The most common health risk on ascent to altitude is not decompression sickness but altitude sickness, or acute mountain sickness (AMS), which has an entirely different and unrelated set of causes and symptoms. AMS results not from the formation of bubbles from dissolved gasses in the body but from exposure to a low partial pressure of oxygen and alkalosis. However, passengers in unpressurized aircraft at high altitude may also be at some risk of DCS.Altitude DCS became a problem in the 1930s with the development of high-altitude balloon and aircraft flights but not as great a problem as AMS, which drove the development of pressurized cabins, which coincidentally controlled DCS. Commercial aircraft are now required to maintain the cabin at or below a pressure altitude of 2,400 m (7,900 ft) even when flying above 12,000 m (39,000 ft). Symptoms of DCS in healthy individuals are subsequently very rare unless there is a loss of pressurization or the individual has been diving recently. Divers who drive up a mountain or fly shortly after diving are at particular risk even in a pressurized aircraft because the regulatory cabin altitude of 2,400 m (7,900 ft) represents only 73% of sea level pressure.Generally, the higher the altitude the greater the risk of altitude DCS but there is no specific, maximum, safe altitude below which it never occurs. There are very few symptoms at or below 5,500 m (18,000 ft) unless patients had predisposing medical conditions or had dived recently. There is a correlation between increased altitudes above 5,500 m (18,000 ft) and the frequency of altitude DCS but there is no direct relationship with the severity of the various types of DCS. A US Air Force study reports that there are few occurrences between 5,500 m (18,000 ft) and 7,500 m (24,600 ft) and 87% of incidents occurred at or above 7,500 m (24,600 ft).  High-altitude parachutists may reduce the risk of altitude DCS if they flush nitrogen from the body by pre-breathing pure oxygen.

Predisposing factors
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.

Environmental
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 5,500 metres (18,000 ft) 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 U.S. Navy Diving Manual indicates that ascent rates greater than about 20 m/min (66 ft/min) when diving increase the chance of DCS, while recreational dive tables such as the Bühlmann tables require an ascent rate of 10 m/min (33 ft/min) with the last 6 m (20 ft) taking at least one minute.  An individual exposed to a rapid decompression (high rate of ascent) above 5,500 metres (18,000 ft) 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 5,500 m (18,000 ft) 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 2,400 m (7,900 ft) 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 2,400 m (7,900 ft) increase their risk of DCS.
diving at altitude – diving in water whose surface pressure is significantly below sea level pressure — for example, Lake Titicaca is at 3,800 m (12,500 ft). Versions of decompression tables for altitudes exceeding 300 m (980 ft), or dive computers with high-altitude settings or surface pressure sensors may be used to reduce this risk.

Individual
The following individual factors have been identified as possibly contributing to increased risk of DCS:

dehydration – Studies by Walder concluded that decompression sickness could be reduced in aviators when the serum surface tension was raised by drinking isotonic saline, and the high surface tension of water is generally regarded as helpful in controlling bubble size. Maintaining proper hydration is recommended. There is no convincing evidence that overhydration has any benefits, and it is implicated in immersion pulmonary oedema.
patent foramen ovale – a hole between the atrial chambers of the heart in the fetus is normally closed by a flap with the first breaths at birth. In about 20% of adults the flap does not completely seal, however, allowing blood through the hole when coughing or during activities that raise chest pressure. In diving, this can allow venous blood with microbubbles of inert gas to bypass the lungs, where the bubbles would otherwise be filtered out by the lung capillary system, and return directly to the arterial system (including arteries to the brain, spinal cord and heart). In the arterial system, bubbles (arterial gas embolism) are far more dangerous because they block circulation and cause infarction (tissue death, due to local loss of blood flow). In the brain, infarction results in stroke, and in the spinal cord it may result in paralysis.
a persons age – there are some reports indicating a higher risk of altitude DCS with increasing age.
previous injury – there is some indication that recent joint or limb injuries may predispose individuals to developing decompression-related bubbles.
ambient temperature – there is some evidence suggesting that individual exposure to very cold ambient temperatures may increase the risk of altitude DCS. Decompression sickness risk can be reduced by increased ambient temperature during decompression following dives in cold water.
body type – typically, a person who has a high body fat content is at greater risk of DCS. This is due to nitrogens five times greater solubility in fat than in water, leading to greater amounts of total body dissolved nitrogen during time at pressure. Fat represents about 15–25 percent of a healthy adults body, but stores about half of the total amount of nitrogen (about 1 litre) at normal pressures.
alcohol consumption – although alcohol consumption increases dehydration and therefore may increase susceptibility to DCS, a 2005 study found no evidence that alcohol consumption increases the incidence of DCS.

Mechanism
Depressurisation causes inert gases, which were dissolved under higher pressure, to come out of physical solution and form gas bubbles within the body. These bubbles produce the symptoms of decompression sickness. Bubbles may form whenever the body experiences a reduction in pressure, but not all bubbles result in DCS. The amount of gas dissolved in a liquid is described by Henrys Law, which indicates that when the pressure of a gas in contact with a liquid is decreased, the amount of that gas dissolved in the liquid will also decrease proportionately.
On ascent from a dive, inert gas comes out of solution in a process called "outgassing" or "offgassing". Under normal conditions, most offgassing occurs by gas exchange in the lungs. If inert gas comes out of solution too quickly to allow outgassing in the lungs then bubbles may form in the blood or within the solid tissues of the body. The formation of bubbles in the skin or joints results in milder symptoms, while large numbers of bubbles in the venous blood can cause lung damage. The most severe types of DCS interrupt — and ultimately damage — spinal cord function, leading to paralysis, sensory dysfunction, or death. In the presence of a right-to-left shunt of the heart, such as a patent foramen ovale, venous bubbles may enter the arterial system, resulting in an arterial gas embolism. A similar effect, known as ebullism, may occur during explosive decompression, when water vapour forms bubbles in body fluids due to a dramatic reduction in environmental pressure.

Inert gases
The main inert gas in air is nitrogen, but nitrogen is not the only gas that can cause DCS. Breathing gas mixtures such as trimix and heliox include helium, which can also cause decompression sickness. Helium both enters and leaves the body faster than nitrogen, so different decompression schedules are required, but, since helium does not cause narcosis, it is preferred over nitrogen in gas mixtures for deep diving.
There is some debate as to the decompression requirements for helium during short-duration dives. Most divers do longer decompressions; however, some groups like the WKPP have been experimenting with the use of shorter decompression times by including deep stops. The balance of evidence as of 2020 does not indicate that deep stops increase decompression efficiency.
Any inert gas that is breathed under pressure can form bubbles when the ambient pressure decreases. Very deep dives have been made using hydrogen-oxygen mixtures (hydrox), but controlled decompression is still required to avoid DCS.

Isobaric counterdiffusion
DCS can also be caused at a constant ambient pressure when switching between gas mixtures containing different proportions of inert gas. This is known as isobaric counterdiffusion, and presents a problem for very deep dives. For example, after using a very helium-rich trimix at the deepest part of the dive, a diver will switch to mixtures containing progressively less helium and more oxygen and nitrogen during the ascent. Nitrogen diffuses into tissues 2.65 times slower than helium but is about 4.5 times more soluble. Switching between gas mixtures that have very different fractions of nitrogen and helium can result in "fast" tissues (those tissues that have a good blood supply) actually increasing their total inert gas loading. This is often found to provoke inner ear decompression sickness, as the ear seems particularly sensitive to this effect.

Bubble formation
The location of micronuclei or where bubbles initially form is not known. The most likely mechanisms for bubble formation are tribonucleation, when two surfaces make and break contact (such as in joints), and heterogeneous nucleation, where bubbles are created at a site based on a surface in contact with the liquid. Homogeneous nucleation, where bubbles form within the liquid itself is less likely because it requires much greater pressure differences than experienced in decompression. The spontaneous formation of nanobubbles on hydrophobic surfaces is a possible source of micronuclei, but it is not yet clear if these can grow large enough to cause symptoms as they are very stable.Once microbubbles have formed, they can grow by either a reduction in pressure or by diffusion of gas into the gas from its surroundings. In the body, bubbles may be located within tissues or carried along with the bloodstream. The speed of blood flow within a blood vessel and the rate of delivery of blood to capillaries (perfusion) are the main factors that determine whether dissolved gas is taken up by tissue bubbles or circulation bubbles for bubble growth.

Pathophysiology
The primary provoking agent in decompression sickness is bubble formation from excess dissolved gases. Various hypotheses have been put forward for the nucleation and growth of bubbles in tissues, and for the level of supersaturation which will support bubble growth. The earliest bubble formation detected is subclinical intravascular bubbles detectable by doppler ultrasound in the venous systemic circulation. The presence of these "silent" bubbles is no guarantee that they will persist and grow to be symptomatic.Vascular bubbles formed in the systemic capillaries may be trapped in the lung capillaries, temporarily blocking them. If this is severe, the symptom called "chokes" may occur. If the diver has a patent foramen ovale (or a shunt in the pulmonary circulation), bubbles may pass through it and bypass the pulmonary circulation to enter the arterial blood. If these bubbles are not absorbed in the arterial plasma and lodge in systemic capillaries they will block the flow of oxygenated blood to the tissues supplied by those capillaries, and those tissues will be starved of oxygen. Moon and Kisslo (1988) concluded that "the evidence suggests that the risk of serious neurological DCI or early onset DCI is increased in divers with a resting right-to-left shunt through a PFO. There is, at present, no evidence that PFO is related to mild or late onset bends. Bubbles form within other tissues as well as the blood vessels. Inert gas can diffuse into bubble nuclei between tissues. In this case, the bubbles can distort and permanently damage the tissue. As they grow, the bubbles may also compress nerves, causing pain. Extravascular or autochthonous bubbles usually form in slow tissues such as joints, tendons and muscle sheaths. Direct expansion causes tissue damage, with the release of histamines and their associated affects. Biochemical damage may be as important as, or more important than mechanical effects.Bubble size and growth may be affected by several factors - gas exchange with adjacent tissues, the presence of surfactants, coalescence and disintegration by collision. Vascular bubbles may cause direct blockage, aggregate platelets and red blood cells, and trigger the coagulation process, causing local and downstream clotting.Arteries may be blocked by intravascular fat aggregation. Platelets accumulate in the vicinity of bubbles. Endothelial damage may be a mechanical effect of bubble pressure on the vessel walls, a toxic effect of stabilised platelet aggregates and possibly toxic effects due to the association of lipids with the air bubbles. Protein molecules may be denatured by reorientation of the secondary and tertiary structure when non-polar groups protrude into the bubble gas and hydrophilic groups remain in the surrounding blood, which may generate a cascade of pathophysiological events with consequent production of clinical signs of decompression sickness.The physiological effects of a reduction in environmental pressure depend on the rate of bubble growth, the site, and surface activity. A sudden release of sufficient pressure in saturated tissue results in a complete disruption of cellular organelles, while a more gradual reduction in pressure may allow accumulation of a smaller number of larger bubbles, some of which may not produce clinical signs, but still cause physiological effects typical of a blood/gas interface and mechanical effects. Gas is dissolved in all tissues, but decompression sickness is only clinically recognised in the central nervous system, bone, ears, teeth, skin and lungs.Necrosis has frequently been reported in the lower cervical, thoracic, and upper lumbar regions of the spinal cord. A catastrophic pressure reduction from saturation produces explosive mechanical disruption of cells by local effervescence, while a more gradual pressure loss tends to produce discrete bubbles accumulated in the white matter, surrounded by a protein layer. Typical acute spinal decompression injury occurs in the columns of white matter. Infarcts are characterised by a region of oedema, haemorrhage and early myelin degeneration, and are typically centred on small blood vessels. The lesions are generally discrete. Oedema usually extends to the adjacent grey matter. Microthrombi are found in the blood vessels associated with the infarcts.Following the acute changes there is an invasion of lipid phagocytes and degeneration of adjacent neural fibres with vascular hyperplasia at the edges of the infarcts. The lipid phagocytes are later replaced by a cellular reaction of astrocytes. Vessels in surrounding areas remain patent but are collagenised. Distribution of spinal cord lesions may be related to vascular supply. There is still uncertainty regarding the aetiology of decompression sickness damage to the spinal cord.Dysbaric osteonecrosis lesions are typically bilateral and usually occur at both ends of the femur and at the proximal end of the humerus Symptoms are usually only present when a joint surface is involved, which typically does not occur until a long time after the causative exposure to a hyperbaric environment. The initial damage is attributed to the formation of bubbles, and one episode can be sufficient, however incidence is sporadic and generally associated with relatively long periods of hyperbaric exposure and aetiology is uncertain. Early identification of lesions by radiography is not possible, but over time areas of radiographic opacity develop in association with the damaged bone.

Diagnosis
Diagnosis of decompression sickness relies almost entirely on clinical presentation, as there are no laboratory tests that can incontrovertibly confirm or reject the diagnosis. Various blood tests have been proposed, but they are not specific for decompression sickness, they are of uncertain utility and are not in general use.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. This window can be extended to 36 hours for ascent to altitude and 48 hours for prolonged exposure to altitude following diving. 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.

Test of pressure
There is no gold standard for diagnosis, and DCI experts are rare. Most of the chambers open to treatment of recreational divers and reporting to Divers Alert Network see fewer than 10 cases per year, making it difficult for the attending doctors to develop experience in diagnosis. A method used by commercial diving supervisors when considering whether to recompress as first aid when they have a chamber on site, is known as the test of pressure. The diver is checked for contraindications to recompression, and if none are present, recompressed. If the symptoms resolve or reduce during recompression, it is considered likely that a treatment schedule will be effective. The test is not entirely reliable, and both false positives and false negatives are possible, however in the commercial diving environment it is often considered worth treating when there is doubt, and very early recompression has a history of very high success rates and reduced number of treatments needed for complete resolution and minimal sequelae.

Differential diagnosis
Symptoms of DCS and arterial gas embolism can be virtually indistinguishable. The most reliable way to tell the difference is based on the dive profile followed, as the probability of DCS depends on duration of exposure and magnitude of pressure, whereas AGE depends entirely on the performance of the ascent. In many cases it is not possible to distinguish between the two, but as the treatment is the same in such cases it does not usually matter.Other conditions which may be confused with DCS include skin symptoms cutis marmorata due to DCS and skin barotrauma due to dry suit squeeze, for which no treatment is necessary. Dry suit squeeze produces lines of redness with possible bruising where the skin was pinched between folds of the suit, while the mottled effect of cutis marmorata is usually on skin where there is subcutaneous fat, and has no linear pattern.Transient episodes of severe neurological incapacitation with rapid spontaneous recovery shortly after a dive may be attributed to hypothermia, but may be symptomatic of short term CNS involvement, which may have residual problems or relapses. These cases are thought to be under-diagnosed.Inner ear decompression sickness (IEDCS) can be confused with inner ear barotrauma (IEBt), alternobaric vertigo, caloric vertigo and reverse squeeze. A history of difficulty in equalising the ears during the dive makes ear barotrauma more likely, but does not always eliminate the possibility of inner ear DCS, which is usually associated with deep, mixed gas dives with decompression stops. Both conditions may exist concurrently, and it can be difficult to distinguish whether a person has IEDCS, IEBt, or both.
Numbness and tingling are associated with spinal DCS, but can also be caused by pressure on nerves (compression neurapraxia). In DCS the numbness or tingling is generally confined to one or a series of dermatomes, while pressure on a nerve tends to produce characteristic areas of numbness associated with the specific nerve on only one side of the body distal to the pressure point. A loss of strength or function is likely to be a medical emergency. A loss of feeling that lasts more than a minute or two indicates a need for immediate medical attention. It is only partial sensory changes, or paraesthesias, where this distinction between trivial and more serious injuries applies.Large areas of numbness with associated weakness or paralysis, especially if a whole limb is affected, are indicative of probable brain involvement and require urgent medical attention. Paraesthesias or weakness involving a dermatome indicate probable spinal cord or spinal nerve root involvement. Although it is possible that this may have other causes, such as an injured intervertebral disk, these symptoms indicate an urgent need for medical assessment. In combination with weakness, paralysis or loss of bowel or bladder control, they indicate a medical emergency.

Prevention
Underwater diving
To prevent the excess formation of bubbles that can lead to decompression sickness, divers limit their ascent rate—the recommended ascent rate used by popular decompression models is about 10 metres (33 ft) per minute—and follow a decompression schedule as necessary. This schedule may require the diver to ascend to a particular depth, and remain at that depth until sufficient inert gas has been eliminated from the body to allow further ascent. Each of these is termed a "decompression stop", and a schedule for a given bottom time and depth may contain one or more stops, or none at all. Dives that contain no decompression stops are called "no-stop dives", but divers usually schedule a short "safety stop" at 3 to 6 m (10 to 20 ft),  depending on the training agency or dive computer.The decompression schedule may be derived from decompression tables, decompression software, or from dive computers, and these are generally based upon a mathematical model of the bodys uptake and release of inert gas as pressure changes. These models, such as the Bühlmann decompression algorithm, are modified to fit empirical data and provide a decompression schedule for a given depth and dive duration using a specified breathing gas mixture.Since divers on the surface after a dive may still have excess inert gas in their bodies, decompression from any subsequent dive before this excess is eliminated needs to modify the schedule to take account of the residual gas load from the previous dive. This will result in a shorter allowable time under water without obligatory decompression stops, or an increased decompression time during the subsequent dive. The total elimination of excess gas may take many hours, and tables will indicate the time at normal pressures that is required, which may be up to 18 hours.Decompression time can be significantly shortened by breathing mixtures containing much less inert gas during the decompression phase of the dive (or pure oxygen at stops in 6 metres (20 ft) of water or less). The reason is that the inert gas outgases at a rate proportional to the difference between the partial pressure of inert gas in the divers body and its partial pressure in the breathing gas; whereas the likelihood of bubble formation depends on the difference between the inert gas partial pressure in the divers body and the ambient pressure. Reduction in decompression requirements can also be gained by breathing a nitrox mix during the dive, since less nitrogen will be taken into the body than during the same dive done on air.Following a decompression schedule does not completely protect against DCS. The algorithms used are designed to reduce the probability of DCS to a very low level, but do not reduce it to zero. The mathematical implications of all current decompression models are that provided that no tissue is ingassing, longer decompression stops will decrease decompression risk, or at worst not increase it. Efficient decompression requires the diver to ascend fast enough to establish as high a decompression gradient, in as many tissues, as safely possible, without provoking the development of symptomatic bubbles. This is facilitated by the highest acceptably safe oxygen partial pressure in the breathing gas, and avoiding gas changes that could cause counterdiffusion bubble formation or growth. The development of schedules that are both safe and efficient has been complicated by the large number of variables and uncertainties, including personal variation in response under varying environmental conditions and workload, attributed to variations of body type, fitness and other risk factors.

Exposure to altitude
One of the most significant breakthroughs in the prevention of altitude DCS is oxygen pre-breathing. Breathing pure oxygen significantly reduces the nitrogen loads in body tissues by reducing the partial pressure of nitrogen in the lungs, which induces diffusion of nitrogen from the blood into the breathing gas, and this effect eventually lowers the concentration of nitrogen in the other tissues of the body. If continued for long enough, and without interruption, this provides effective protection upon exposure to low-barometric pressure environments. However, breathing pure oxygen during flight alone (ascent, en route, descent) does not decrease the risk of altitude DCS as the time required for ascent is generally not sufficient to significantly desaturate the slower tissues.Pure aviator oxygen which has moisture removed to prevent freezing of valves at altitude is readily available and routinely used in general aviation mountain flying and at high altitudes. Most small general aviation aircraft are not pressurized, therefore oxygen use is an FAA requirement at higher altitudes.
Although pure oxygen pre-breathing is an effective method to protect against altitude DCS, it is logistically complicated and expensive for the protection of civil aviation flyers, either commercial or private. Therefore, it is currently used only by military flight crews and astronauts for protection during high-altitude and space operations. It is also used by flight test crews involved with certifying aircraft, and may also be used for high-altitude parachute jumps.
Astronauts aboard the International Space Station preparing for extra-vehicular activity (EVA) "camp out" at low atmospheric pressure, 10.2 psi (0.70 bar), spending eight sleeping hours in the Quest airlock chamber before their spacewalk. During the EVA they breathe 100% oxygen in their spacesuits, which operate at 4.3 psi (0.30 bar), although research has examined the possibility of using 100% O2 at 9.5 psi (0.66 bar) in the suits to lessen the pressure reduction, and hence the risk of DCS.

Treatment
Recompression on air was shown to be an effective treatment for minor DCS symptoms by Keays in 1909. Evidence of the effectiveness of recompression therapy utilizing oxygen was first shown by Yarbrough and Behnke, and has since become the standard of care for treatment of DCS. Recompression is normally carried out in a recompression chamber. At a dive site, a riskier alternative is in-water recompression.Oxygen first aid has been used as an emergency treatment for diving injuries for years. Particularly if given within the first four hours of surfacing, it increases the success of recompression therapy as well as decreasing the number of recompression treatments required. Most fully closed-circuit diving rebreathers can deliver sustained high concentrations of oxygen-rich breathing gas and could be used as a means of supplying oxygen if dedicated equipment is not available.It is beneficial to give fluids, as this helps reduce dehydration. It is no longer recommended to administer aspirin, unless advised to do so by medical personnel, as analgesics may mask symptoms. People should be made comfortable and placed in the supine position (horizontal), or the recovery position if vomiting occurs. In the past, both the Trendelenburg position and the left lateral decubitus position (Durants maneuver) have been suggested as beneficial where air emboli are suspected, but are no longer recommended for extended periods, owing to concerns regarding cerebral edema.

First aid
All cases of decompression sickness should be treated initially with the highest available concentration of oxygen until hyperbaric oxygen therapy (100% oxygen delivered in a hyperbaric chamber) can be provided. Mild cases of the "bends" and some skin symptoms may disappear during descent from high altitude; however, it is recommended that these cases still be evaluated. Neurological symptoms, pulmonary symptoms, and mottled or marbled skin lesions should be treated with hyperbaric oxygen therapy if seen within 10 to 14 days of development. Early recompression has a history of better outcomes and less treatment being needed.Normobaric oxygen administered at as close to 100% as practicable is known to be beneficial based on observed bubble reduction and symptom resolution. For this reason diver training in oxygen administration, and a system for administering a high percentage of inspired oxygen at quantities sufficient for plausible evacuation scenarios is desirable. Where oxygenation may be compromised the administration rate should be adjusted to ensure that the best practicable supplementation is maintained until supplies can be replenished.A horizontal position is preferable during evacuation if possible, with the recovery position recommended for unconscious divers, as there is evidence that inert gas washout is improved in horizontal subjects, and that large arterial bubbles tend to distribute towards the head in upright positions. A head down position is thought to be harmful in DCS.Oral hydration is recommended in fully conscious persons, and fluids should ideally be isotonic, without alcohol, carbonation or caffeine, as diving is known to cause dehydration, and rehydration is known to reduce post-dive venous gas emboli.Intravascular rehydration is recommended if suitably competent responders are present. Glucose free isotonic crystalloid solutions are preferred. Case evidence shows that aggressive rehydration can be life-saving in severe cases.If there are no contraindications, a non-steroidal anti-inflammatory drug along with hyperbatic oxygen is likely to improve rate of recovery. Corticosteroids, pentoxyphylline, aspirin, lidocaine and nicergoline have been used in early management of DCS, but there is insufficient evidence on their effectiveness.Divers should be kept comfortably warm, but not overheated, as warm subjects are known to eliminate gas more quickly, but overheating aggravates neurological injury.

Delay of recompression
Observational evidence shows that outcomes after recompression are likely to be better after immediate recompression, which is only possible when on-site recompression is possible, although the 2004 workshop on decompression came to the conclusion that for cases with mild symptoms, a delay before recompression is unlikely to cause any worsening of long-term outcomes.In more serious cases recompression should be done as soon as safely possible. There is some evidence that delays longer than six hours result in slower or less complete recovery, and the number of treatments required may be increased.

Transport of a symptomatic diver
Exposing a case of decompression sickness to reduced ambient pressure will cause the bubbles to expand if not constrained by a rigid local tissue environment. This can aggravate the symptoms, and should be avoided if reasonably practicable. If a diver with DCS is transported by air, cabin pressure should be kept as close to sea level atmospheric pressure as possible, preferably not more than 150 m, either by cabin pressurisation or by remaining at low altitude throughout the flight. The risk of deterioration at higher altitudes must be considered against the risk of deterioration if not transported. Some divers with symptoms or signs of mild decompression sickness may be evacuated by pressurised commercial airliner for further treatment after a surface interval of at least 24 hours. The 2004 workshop considered it unlikely for this to cause a worse outcome. Most experience has been for short flights of less than two hours. There is little known about the effects of longer flights. Where possible, pre-flight and in-flight oxygen breathing at the highest available percentage is considered best practice. Similar precautions apply to surface transport through higher altitudes.

In-water recompression
Recompression and hyperbaric oxygen administered in a recompression chamber is recognised as the definitive treatment for DCI, but when there is no readily available access to a suitable hyperbaric chamber, and if symptoms are significant or progressing, in-water recompression (IWR) with oxygen is a medically recognised option where a group of divers including the symptomatic diver already have relevant training and equipment that provides a sufficient understanding of the associated risks and allows the involved parties to collectively accept responsibility for a decision to proceed with IWR.In-water recompression (IWR) or underwater oxygen treatment is the emergency treatment of decompression sickness by returning the diver underwater to help the gas bubbles in the tissues, which are causing the symptoms, to resolve. It is a procedure that exposes the diver to significant risk which should be compared with the risk associated with the other available options. Some authorities recommend that it is only to be used when the time to travel to the nearest recompression chamber is too long to save the victims life, others take a more pragmatic approach, and accept that in some circumstances IWR is the best available option. The risks may not be justified for case of mild symptoms likely to resolve spontaneously, or for cases where the diver is likely to be unsafe in the water, but in-water recompression may be justified in cases where severe outcomes are likely, if conducted by a competent and suitably equipped team.Carrying out in-water recompression when there is a nearby recompression chamber or without suitable equipment and training is never a desirable option. The risk of the procedure is due to the diver suffering from DCS being seriously ill and may become paralysed, unconscious or stop breathing while under water. Any one of these events is likely to result in the diver drowning or asphyxiating or suffering further injury during a subsequent rescue to the surface. This risk can be reduced by improving airway security by using surface supplied gas and a helmet or full-face mask.Several schedules have been published for in-water recompression treatment, but little data on their efficacy is available.The decision of whether or not to attempt IWR is dependent on identifying the diver whose condition is serious enough to justify the risk, but whose clinical condition does not indicate that the risk is unacceptable. The risk may not be justified for mild DCI, if spontaneous recovery is probable whether the diver is recompressed or not, and surface oxygen is indicated for these cases. However, in these cases the risk of the recompression is also low, and early abandonment is also unlikely to cause further harm.

Contraindications
Some signs of decompression illness which suggest a risk of permanent injury are nevertheless considered contraindications for IWR.  Hearing loss and vertigo displayed in isolation with no other symptoms of DCI can have been caused by inner ear barotrauma rather than DCI, and inner ear barotrauma is generally considered a contraindication for recompression. Even when caused by DCI, vertigo can make in-water treatment hazardous if accompanied by nausea and vomiting. A diver with a deteriorating level of consciousness or with a persisting reduced level of consciousness should also not be recompressed in-water nor should a diver who does not want to go back down, or with a  history of oxygen toxicity in the preceding dives, or any physical injury or incapacitation which may make the procedure unsafe.

Definitive treatment
The duration of recompression treatment depends on the severity of symptoms, the dive history, the type of recompression therapy used and the patients response to the treatment. One of the more frequently used treatment schedules is the US Navy Table 6, which provides hyperbaric oxygen therapy with a maximum pressure equivalent to 60 feet (18 m) of seawater (2.8 bar PO2) for a total time under pressure of 288 minutes, of which 240 minutes are on oxygen and the balance are air breaks to minimise the possibility of oxygen toxicity.A multiplace chamber is the preferred facility for treatment of decompression sickness as it allows direct physical access to the patient by medical personnel, but monoplace chambers are more widely available and should be used for treatment if a multiplace chamber is not available or transportation would cause significant delay in treatment, as the interval between onset of symptoms and recompression is important to the quality of recovery. It may be necessary to modify the optimum treatment schedule to allow use of a monoplace chamber, but this is usually better than delaying treatment. A US Navy treatment table 5 can be safely performed without air breaks if a built-in breathing system is not available. In most cases the patient can be adequately treated in a monoplace chamber at the receiving hospital.

Altitude decompression sickness
Treatment and management may vary depending on the grade or form of decompression sickness and the treating facility or organization. First aid at altitude is oxygen at the highest practicable concentration and earliest and largest practicable reduction in cabin altitude.
Ground-level 100% oxygen therapy is suggested for 2 hours following type-1 decompression sickness that occurs at altitude, if it resolves upon descent. In more severe cases, hyperbaric oxygen therapy following standard recompression protocols is indicated. Decompression sickness in aviation most commonly follows flights in non-pressurized aircraft, flights with cabin pressure fluctuations, or in individuals who fly after diving. Cases have also been reported after the use of altitude chambers. These are relatively rare clinical events.

Prognosis
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.Long term effects are dependent on both initial injury, and treatment. While almost all cases will resolve more quickly with treatment, milder cases may resolve adequately over time without recompression, where the damage is minor and the damage is not significantly aggravated by lack of treatment. In some cases the cost, inconvenience, and risk to the patient may make it appropriate not to evacuate to a hyperbaric treatment facility. These cases should be assessed by a specialist in diving medicine, which can generally be done remotely by telephone or internet.For joint pain, the likely tissues affected depend on the symptoms, and the urgency of hyperbaric treatment will depend largely on the tissues involved.
Sharp, localised pain that is affected by movement suggests tendon or muscle injury, both of which will usually fully resolve with oxygen and anti-inflammatory medication.
Sharp, localised pain that is not affected by movement suggests local inflammation, which will also usually fully resolve with oxygen and anti-inflammatory medication.
Deep, non-localised pain affected by movement suggests joint capsule tension, which is likely to fully resolve with oxygen and anti-inflammatory medication, though recompression will help it to resolve faster.
Deep, non-localised pain not affected by movement suggests bone medulla involvement, with ischaemia due to blood vessel blockage and swelling inside the bone, which is mechanistically associated with osteonecrosis, and therefore it has been strongly recommended that these symptoms are treated with hyperbaric oxygen.

Epidemiology
The incidence of decompression sickness is rare, estimated at 2.8 to 4 cases per 10,000 dives, with the risk 2.6 times greater for males than females. DCS affects approximately 1,000 U.S. scuba divers per year. In 1999, the Divers Alert Network (DAN) created "Project Dive Exploration" to collect data on dive profiles and incidents. From 1998 to 2002, they recorded 50,150 dives, from which 28 recompressions were required — although these will almost certainly contain incidents of arterial gas embolism (AGE) — a rate of about 0.05%.Around 2013, Honduras had the highest number of decompression-related deaths and disabilities in the world, caused by unsafe practices in lobster diving among the indigenous Miskito people, who face great economic pressures. At that time it was estimated that in the country over 2000 divers had been injured and 300 others had died since the 1970s.

Timeline
1670: Robert Boyle demonstrated that a reduction in ambient pressure could lead to bubble formation in living tissue. This description of a bubble forming in the eye of a viper subjected to a near vacuum was the first recorded description of decompression sickness.
1769: Giovanni Morgagni described the post mortem findings of air in cerebral circulation and surmised that this was the cause of death.
1840: Charles Pasley, who was involved in the recovery of the sunken warship HMS Royal George, commented that, of those having made frequent dives, "not a man escaped the repeated attacks of rheumatism and cold".
1841: First documented case of decompression sickness, reported by a mining engineer who observed pain and muscle cramps among coal miners working in mine shafts air-pressurized to keep water out.
1854: Decompression sickness reported and one resulting death of caisson workers on the Royal Albert Bridge.
1867: Panamanian pearl divers using the revolutionary Sub Marine Explorer submersible repeatedly experienced "fever" due to rapid ascents. Continued sickness led to the vessels abandonment in 1869.
1870: Bauer published outcomes of 25 paralyzed caisson workers.
From 1870 to 1910, all prominent features were established. Explanations at the time included: cold or exhaustion causing reflex spinal cord damage; electricity cause by friction on compression; or organ congestion; and vascular stasis caused by decompression.
1871: The Eads Bridge in St Louis employed 352 compressed air workers including Alphonse Jaminet as the physician in charge. There were 30 seriously injured and 12 fatalities. Jaminet himself developed decompression sickness and his personal description was the first such recorded. According to Divers Alert Network, in its Inert Gas Exchange, Bubbles and Decompression Theory course, this is where "bends" was first used to refer to DCS.
1872: The similarity between decompression sickness and iatrogenic air embolism as well as the relationship between inadequate decompression and decompression sickness was noted by Friedburg. He suggested that intravascular gas was released by rapid decompression and recommended: slow compression and decompression; four-hour working shifts; limit to maximum pressure of 44.1 psig (4 atm); using only healthy workers; and recompression treatment for severe cases.
1873: Andrew Smith first used the term "caisson disease" describing 110 cases of decompression sickness as the physician in charge during construction of the Brooklyn Bridge. The project employed 600 compressed air workers. Recompression treatment was not used. The project chief engineer Washington Roebling had caisson disease, and endured the after-effects of the disease for the rest of his life. During this project, decompression sickness became known as "The Grecian Bends" or simply "the bends" because affected individuals characteristically bent forward at the hips: this is possibly reminiscent of a then popular womens fashion and dance maneuver known as the Grecian Bend.
1890 During construction of the Hudson River Tunnel contractors agent Ernest William Moir pioneered the use of an airlock chamber for treatment.
1900: Leonard Hill used a frog model to prove that decompression causes bubbles and that recompression resolves them. Hill advocated linear or uniform decompression profiles. This type of decompression is used today by saturation divers. His work was financed by Augustus Siebe and the Siebe Gorman Company.
1904: Tunnel building to and from Manhattan Island caused over 3,000 injuries and over 30 deaths which led to laws requiring PSI limits and decompression rules for "sandhogs" in the United States.
1904: Siebe and Gorman in conjunction with Leonard Hill developed and produced a closed bell in which a diver can be decompressed at the surface.
1908: "The Prevention of Compressed Air Illness" was published by JS Haldane, Boycott and Damant recommending staged decompression. These tables were accepted for use by the Royal Navy.
1914–16: Experimental decompression chambers were in use on land and aboard ship.
1924: The US Navy published the first standardized recompression procedure.
1930s: Albert R Behnke separated the symptoms of Arterial Gas Embolism (AGE) from those of DCS.
1935: Behnke et al. experimented with oxygen for recompression therapy.
1937: Behnke introduced the "no-stop" decompression tables.
1941: Altitude DCS is treated with hyperbaric oxygen for the first time.
1944: US Navy published hyperbaric treatment tables "Long Air Recompression Table with Oxygen" and "Short Oxygen Recompression Table", both using 100% oxygen below 60 fsw (18 msw)
1945: Field results showed that the 1944 oxygen treatment table was not yet satisfactory, so a series of tests were conducted by staff from the Navy Medical Research Institute and the Navy Experimental Diving Unit using human subjects to verify and modify the treatment tables. Tests were conducted using the 100-foot air-oxygen treatment table and the 100-foot air treatment table, which were found to be satisfactory. Other tables were extended until they produced satisfactory results. The resulting tables were used as the standard treatment for the next 20 years, and these tables and slight modifications were adopted by other navies and industry. Over time, evidence accumulated that the success of these table for severe decompression sickness was not very good.
1957: Robert Workman established a new method for calculation of decompression requirements (M-values).
1959: The "SOS Decompression Meter", a submersible mechanical device that simulated nitrogen uptake and release, was introduced.
1960: FC Golding et al. split the classification of DCS into Type 1 and 2.
1965: Low success rates of the existing US Navy treatment tables led to the development of the oxygen treatment table by Goodman and Workman in 1965, variations of which are still in general use as the definitive treatment for most cases of decompression sickness.
1965: LeMessurier and Hills published a paper on A thermodynamic approach arising from a study on Torres Strait diving techniques which suggests that decompression by conventional models results in bubble formation which is then eliminated by re-dissolving at the decompression stops.
1976 – M.P </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Auditory hallucination and explain in detail? [/INST] An auditory hallucination, or paracusia, is a form of hallucination that involves perceiving sounds without auditory stimulus. While experiencing an auditory hallucination, the affected person would hear a sound or sounds which did not come from the natural environment.
A common form of auditory hallucination involves hearing one or more voices without a speaker present, known as an auditory verbal hallucination. This may be associated with psychotic disorders, most notably schizophrenia, and this phenomenon is often used to diagnose these conditions.  However, individuals without any psychiatric disease whatsoever may hear voices, including those under the influence of mind-altering substances, such as cannabis, cocaine, amphetamines, and PCP.
There are three main categories into which the hearing of talking voices often fall: a person hearing a voice speak ones thoughts, a person hearing one or more voices arguing, or a person hearing a voice narrating their own actions. These three categories do not account for all types of auditory hallucinations.
Hallucinations of music also occur. In these, people more often hear snippets of songs that they know, or the music they hear may be original. They may occur in mentally sound people and with no known cause. Other types of auditory hallucinations include exploding head syndrome and musical ear syndrome.  In the latter, people will hear music playing in their mind, usually songs they are familiar with. These hallucinations can be caused by: lesions on the brain stem (often resulting from a stroke), sleep disorders such as narcolepsy, tumors, encephalitis, or abscesses. This should be distinguished from the commonly experienced phenomenon of getting a song stuck in ones head. Reports have also mentioned that it is also possible to get musical hallucinations from listening to music for long periods of time. Other causes include hearing loss and epileptic activity.In the past, the cause of auditory hallucinations was attributed to cognitive suppression by way of executive function failure of the frontoparietal sulcus. Newer research has found that they coincide with the left superior temporal gyrus, suggesting that they are better attributed to speech misrepresentations. It is assumed through research that the neural pathways involved in normal speech perception and production, which are lateralized to the left temporal lobe, also underlie auditory hallucinations. Auditory hallucinations correspond with spontaneous neural activity of the left temporal lobe, and the subsequent primary auditory cortex. The perception of auditory hallucinations corresponds to the experience of actual external hearing, despite the absence of any sound itself.

Causes
In 2015 a small survey reported voice hearing in persons with a wide variety of DSM-5 diagnoses, including:

Bipolar disorder
Borderline personality disorder
Depression (mixed)
Dissociative identity disorder
Generalized anxiety disorder
Major depression
Obsessive compulsive disorder
Post-traumatic stress disorder
Psychosis (NOS)
Schizoaffective disorder
Schizophrenia
Substance-induced psychosisHowever, numerous persons surveyed reported no diagnosis. In his popular 2012 book Hallucinations, neurologist Oliver Sacks describes voice hearing in patients with a wide variety of medical conditions, as well as his own personal experience of hearing voices. Genetic correlations have been identified with auditory hallucinations, but most work with non-psychotic causes of auditory hallucinations is still ongoing.

Schizophrenia
In people with psychosis, the premier cause of auditory hallucinations is schizophrenia, and these are known as auditory verbal hallucinations (AVHs). In schizophrenia, people show a consistent increase in activity of the thalamic and striatal subcortical nuclei, hypothalamus, and paralimbic regions; confirmed by PET and fMRI scans.  Other research shows an enlargement of temporal white matter, frontal gray matter, and temporal gray matter volumes (those areas crucial to both inner and outer speech) when compared to control groups.  This implies that functional and structural abnormalities in the brain, both of which may have a genetic component, can induce auditory hallucinations.Auditory verbal hallucinations attributed to an external source, rather than internal, are considered the defining factor for the diagnosis of schizophrenia. The voices heard are generally destructive and emotive, adding to the state of artificial reality and disorientation seen in psychotic patients. The causal basis of hallucinations has been explored on the cellular receptor level. The glutamate hypothesis, proposed as a possible cause for schizophrenia, may also have implications in auditory hallucinations, which are suspected to be triggered by altered glutamatergic transmission.Studies using dichotic listening methods suggest that people with schizophrenia have major deficits in the functioning of the left temporal lobe by showing that patients do not generally exhibit what is a functionally normal right ear advantage. Inhibitory control of hallucinations in patients has been shown to involve failure of top-down regulation of resting-state networks and up-regulation of effort networks, further impeding normal cognitive functioning.Not all who experience hallucinations find them to be distressing. The relationship between an individual and their hallucinations is personal, and everyone interacts with their troubles in different ways. There are those who hear solely malevolent voices, solely benevolent voices, those that hear a mix of the two, and those that see them as either malevolent or benevolent and not believing the voice.

Mood disorders and dementias
Mood disorders such as bipolar disorder and major depression have also been known to correlate with auditory hallucinations, but tend to be milder than their psychosis-induced counterpart. Auditory hallucinations are a relatively common sequelae of major neurocognitive disorders (formerly dementia) such as Alzheimers disease.

Transient causes
Auditory hallucinations have been known to manifest as a result of intense stress, sleep deprivation, and drug use. Auditory hallucinations can also occur in mentally healthy individuals during the altered state of consciousness while falling asleep (hypnagogic hallucinations) and waking up (hypnopompic hallucinations).High caffeine consumption has been linked to an increase in the likelihood of experiencing auditory hallucinations. A study conducted by the La Trobe University School of Psychological Sciences revealed that as few as five cups of coffee a day could trigger the phenomenon. Intoxication of psychoactive drugs such as PCP, amphetamines, cocaine, marijuana and other substances can produce hallucinations in general, especially in high doses. Withdrawal from certain drugs such as alcohol, sedatives, hypnotics, anxiolytics, and opioids can also produce hallucinations, including auditory.

Pathophysiology
The following areas of the brain have been found to be active during auditory hallucinations, through the use of fMRIs.

Transverse temporal gyri (Heschls gyri): found within the primary auditory cortex.
Left temporal lobe: processes semantics in speech and vision, including primary auditory cortex.
Brocas area: speech and language comprehension.
Superior temporal gyrus: contains primary auditory cortex.
Primary auditory cortex: processes hearing and speech perception.
Globus pallidus: Regulation of voluntary movement.

Treatments
Medication
The primary means of treating auditory hallucinations is antipsychotic medications which affect dopamine metabolism. If the primary diagnosis is a mood disorder (with psychotic features), adjunctive medications are often used (e.g., antidepressants or mood stabilizers). These medical approaches may allow the person to function normally but are not a cure as they do not eradicate the underlying thought disorder.

Therapy
Cognitive behavioral therapy has been shown to help decrease the frequency and distressfulness of auditory hallucinations, particularly when other psychotic symptoms were presenting.  Enhanced supportive therapy has been shown to reduce the frequency of auditory hallucinations, the violent resistance the patient displayed towards said hallucinations, and an overall decrease in the perceived malignancy of the hallucinations.  Other cognitive and behavioural therapies have been used with mixed success.Another key to therapy is to help patients see that they do not need to obey the voices that they are hearing. It has been seen in patients with schizophrenia and auditory hallucinations that therapy might help confer insight into recognising and choosing to not obey the voices that they hear.

Others
Between 25% and 30% of schizophrenia patients do not respond to antipsychotic medication which has led researchers to look for alternate sources to help them. Two common methods to help are electroconvulsive therapy and repetitive transcranial magnetic stimulation (rTMS).  Electroconvulsive therapy or ECT has been shown to reduce psychotic symptoms associated with schizophrenia, mania, and depression, and is often used in psychiatric hospitals.
Transcranial magnetic stimulation when used to treat auditory hallucinations in patients with schizophrenia is done at a low frequency of 1 Hertz to the left temporoparietal cortex.

History
Ancient history
Presentation
In the ancient world, auditory hallucinations were often viewed as either a gift or curse by God or the gods (depending on the specific culture). According to the Greek historian Plutarch, during the reign of Tiberius (A.D. 14–37), a sailor named Thamus heard a voice cry out to him from across the water, "Thamus, are you there? When you reach Palodes, take care to proclaim that the great god Pan is dead."The oracles of ancient Greece were known to experience auditory hallucinations while breathing in certain neurologically active vapors (such as the smoke from bay leaves), while the more pervasive delusions and symptomatology were often viewed as possession by demonic forces as punishment for misdeeds.

Treatments
Treatment in the ancient world is ill-documented, but there are some cases of therapeutics being used to attempt treatment, while the common treatment was sacrifice and prayer in an attempt to placate the gods. During the Middle Ages, those with auditory hallucinations were sometimes subjected to trepanning or trial as a witch. In other cases of extreme symptomatology, individuals were seen as being reduced to animals by a curse; these individuals were either left on the streets or imprisoned in insane asylums. It was the latter response that eventually led to modern psychiatric hospitals.

Pre-modern
Presentation
Auditory hallucinations were rethought during the enlightenment.  As a result, the predominant theory in the western world beginning in the late 18th century was that auditory hallucinations were the result of a disease in the brain (e.g., mania), and treated as such.

Treatments
There were no effective treatments for hallucinations at this time. Conventional thought was that clean food, water, and air would allow the body to heal itself (sanatorium). Beginning in the 16th century insane asylums were first introduced in order to remove "the mad dogs" from the streets. These asylums acted as prisons until the late 18th century. This is when doctors began the attempt to treat patients. Often attending doctors would douse patients in cold water, starve them, or spin patients on a wheel. Soon, this gave way to brain-specific treatments with the most famous examples including lobotomy, shock therapy, and branding the skull with a hot iron.

Society and culture
Notable cases
Robert Schumann, a famous music composer, spent the end of his life experiencing auditory hallucinations. Schumanns diaries state that he suffered perpetually from imagining that he had the note A5 sounding in his ears. The musical hallucinations became increasingly complex. One night he claimed to have been visited by the ghost of Schubert and wrote down the music that he was hearing. Thereafter, he began making claims that he could hear an angelic choir singing to him. As his condition worsened, the angelic voices developed into demonic ones.Brian Wilson, songwriter and co-founder of the Beach Boys, has schizoaffective disorder that presents itself in the form of disembodied voices. They formed a major component of Bill Pohlads Love & Mercy (2014), a biographical film which depicts Wilsons hallucinations as a source of musical inspiration, constructing songs that were partly designed to converse with them. Wilson has said of the voices: "Mostly [theyre] derogatory. Some of its cheerful. Most of it isnt." To combat them, his psychiatrist advised that he "talk humorously to them", which he says has helped "a little bit".The onset of delusional thinking is most often described as being gradual and insidious. Patients have described an interest in psychic phenomena progressing to increasingly unusual preoccupations and then to bizarre beliefs "in which I believed wholeheartedly". One author wrote of their hallucinations: "they deceive, derange and force me into a world of crippling paranoia". In many cases, the delusional beliefs could be seen as fairly rational explanations for abnormal experiences: "I increasingly heard voices (which Id always call loud thoughts)... I concluded that other people were putting these loud thoughts into my head". Some cases have been described as an "auditory ransom note".

Cultural effects
According to research on hallucinations, both with participants from the general population and people diagnosed with schizophrenia, psychosis and related mental illnesses, there is a relationship between culture and hallucinations. In relation to hallucinations, the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) states that "transient hallucinatory experiences may occur without a mental disorder"; put differently, short or temporary hallucinations are not exclusive to being diagnosed with a mental disorder.In a study of 1,080 people with a schizophrenia diagnosis from seven countries of origin: Austria, Poland, Lithuania, Georgia, Pakistan, Nigeria and Ghana, researchers found that 74.8% of the total participants (n = 1,080) disclosed having experienced more auditory hallucinations in the last year than any other hallucinations from the date of the interview. Further, the study found the highest rates of both auditory hallucinations and visual hallucinations in both of the West African countries, Ghana and Nigeria. In the Ghana sample, n = 76, auditory hallucinations were reported by 90.8% and visual hallucinations were reported by 53.9% of participants. In the Nigeria sample, n = 324, auditory hallucinations were reported by 85.4%, and visual hallucinations were reported by 50.8% of participants. These findings are in line with other studies that have found that visual hallucinations were reported more in traditional cultures.
A 2015 published study, "Hearing Voices in Different Cultures: A Social Kindling Hypothesis" compared the experiences of three groups of 20 participants who met the criteria for schizophrenia (n = 60) from three places, including San Mateo, California (USA), Accra, Ghana (Africa), and Chennai, India (South Asia). In this study, researchers found distinct differences among the participants experience with voices. In the San Mateo, CA sample all but three of the participants referred to their experience of hearing voices with "diagnostic labels, and even [used] diagnostic criteria readily", they also connected "hearing voices" with being "crazy". For the Accra, Ghana sample, almost no participants referenced a diagnosis and instead they spoke about voices as having "a spiritual meaning and as well as a psychiatric one". In the Chennai, India sample, similarly to the Ghana interviewees, most of the participants did not reference a diagnosis and for many of these participants, the voices they heard were of people they knew and people they were related to, "voices of kin". Another key finding that was identified in this research study is that "voice-hearing experience outside the West may be less harsh". Finally, researchers found that "different cultural expectations about the mind, or about the way people expect thoughts and feelings to be private or accessible to spirits or persons" could be attributed to the differences they found across the participants.

In a qualitative study of 57 self-identified Māori participants subcategorized within one or more of the following groups including: "tangata Māori (people seeking wellness/service users), Kaumatua/Kuia (elders), Kai mahi (cultural support workers), Managers of mental health services, clinicians (psychiatrists, nurses, and psychologists) and students (undergraduate and postgraduate psychology students)", researchers interviewed participants and asked them about "[1] their understanding of experiences that could be considered to be psychotic or labelled schizophrenic, [2] what questions they would ask someone who came seeking help and [3] they we asked about their understanding of the terms schizophrenia and psychosis". The participants were also people who either had worked with psychosis or schizophrenia or had experienced psychosis or schizophrenia. In this study, researchers found that the participants understood these experiences labelled "psychotic" or "schizophrenic" through multiple models. Taken directly from the article, the researchers wrote that there is "no one Māori way of understanding psychotic experiences". Instead, as part of understanding these experiences, the participants combined both "biological explanations and Māori spiritual beliefs", with a preference for cultural and psychosocial explanations. For example, 19 participants spoke about psychotic experiences as sometimes being a sign of matakite (giftedness). One of the Kaumatua/Kuia (elders) was quoted as saying:"I never wanted to accept it, I said no it isnt, it isnt [matakite] but it wouldnt stop and in truth I knew what I had to do, help my people, I didnt want the responsibility but here I am. They helped me understand it and told me what to do with it."An important finding highlighted in this study is that studies done by the World Health Organization (WHO) have found that "developing countries (non-Western) experience far higher rates of recovery from schizophrenia than Western countries". The researchers further articulate that these findings may be due to culturally specific meaning created about the experience of schizophrenia, psychosis, and hearing voices as well as "positive expectations around recovery".
Research has found that auditory hallucinations and hallucinations more broadly are not necessarily a symptom of "severe mental health" and instead might be more commonplace than assumed and also experienced by people in the general population. According to a literature review, "The prevalence of voice-hearers in the general population: A literature review", which compared 17 studies on auditory hallucinations in participants from nine countries, found that "differences in the prevalence of [voice-hearing in the adult general population] can be attributed to true variations based on gender, ethnicity and environmental context". The studies took place from 1894 to 2007 and the nine countries in which the studies took place were the United Kingdom, Philippines, United States, Sweden, France, Germany, Italy, Netherlands, and New Zealand. The same literature review highlighted that "studies that [analyzed] their data by gender report[ed] a higher frequency of women reporting hallucinatory experiences of some kind". Although generally speaking hallucinations (including auditory) are strongly related to psychotic diagnoses and schizophrenia, the presence of hallucinations does not exclusively mean that someone has a psychotic or schizophrenic episode or diagnosis.

Audible thoughts
General information
Audible thoughts, also called thought sonorisation, is a kind of auditory verbal hallucination. People with this hallucination constantly hear a voice narrating ones own thoughts out loud. This idea was first defined by Kurt Schneider, who included this symptom as one of the "first-rank symptoms" in diagnosing schizophrenia. Although the diagnostic reliability of "first-rank symptoms" has long been questioned, this idea remains important for its historical and descriptive value in psychiatry. Audible thoughts is a positive symptom of schizophrenia according to DSM-5, however, this hallucination is not exclusively found among people with schizophrenia, but also among patients of bipolar disorder in their manic phase.

Types
Patients who experience audible thoughts will hear the voice repeating their own thoughts either as or after the thought comes into their minds. The first kind of audible thought, the voice and the thought appear simultaneously, was named by German psychiatry August Cramer as Gedankenlautwerden, a German word stands for "thoughts become aloud".Example of Gedankenlautwerden:
A 35-year-old painter heard a quiet voice with an Oxford accent. The volume was slightly lower than that of normal conversation and could be heard equally well with either ear. The voice would say, I cant stand that man, the way he holds his brush he looks like a poof. He immediately experienced whatever the voice was saying as his own thoughts, to the exclusion of all other thoughts.And the second kind in which the voice comes after the thought appears is called echo de la pensée in French, namely thought echo.Example of thought echo:
A 32-year-old housewife complained of a mans voice. The voice would repeat almost all the patients goal-directed thinking, even banalest thoughts. The patient would think I must put the kettle on, and after a pause of not more than one second the voice would say I must put the kettle on.If categorized by patients subjective feelings about where the voices come from, audible thoughts can be either external or internal. Patients reporting an internal origin of the hallucination claim that the voices are coming from somewhere inside their body, mainly in their own heads, while those reporting an external origin feel the voice as coming from the environment. The external origins vary in the patients description:  some hear the voice in front of their ears, some attribute the ambient surrounding noise, like running water or wind, as the source. This sometimes influences patients behaviours as they believe people around them can also hear these audible thoughts, therefore they may avoid social events and public places to prevent others from hearing their thoughts. Besides, study suggests that the locus of the voice may change as the patients hallucinations develop. Theres a trend of internalization of external perceptions, which means patients will locate the source of their hallucination from external objects to internal subjectivity over time.

Phenomenological study
According to the study conducted by Tony Nayani and Anthony David in 1996, about half of the patients(46%) with audible thoughts claimed that the hallucination has somehow taken the place of their conscience in making decisions and judgement. They tend to follow the voices instructions when confronting dilemmas in their daily lives. The study also suggests that a majority of the patients, both male and female, labeled the sounds they heard as male voices. However, younger patients tend to hear younger voices, which suggests that the voices in the hallucination may share age with the patients but not gender. Whats more, voices in the hallucination usually differ from the patients own voices in accents. They reported the voices they heard as coming from different regions or social classes with them.Some patients may develop skills to control their hallucinations to a certain extent through some kind of cognitive focusing. They cant eliminate the voices, but through cognitive focusing or suggestive behaviours (e.g. swallowing), they can control the onset and offset of their hallucination.

Pathophysiology
Studies have suggested that damage to specific brain areas may relate to the formation of audible thought. Patients who attribute the hallucination to an external locus are more likely to report the voice coming from the right. This unilateral characteristic can be explained by either contralateral temporal lobe disease or ipsilateral ear disease. Researchers also came up with hypotheses that audible thought may result from damage in the right hemisphere, which causes the malfunction of prosodic construction. If this happens, the left hemisphere may misinterpret the patients own thoughts as alien, leading the patients to misconceive their thoughts as coming from another voice.

Research
A good amount of the research done has focused primarily on patients with schizophrenia, and beyond that drug-resistant auditory hallucinations.

Auditory verbal hallucinations as symptoms of disordered speech
There is now substantial evidence that auditory verbal hallucinations (AVHs) in psychotic patients are manifestations of disorganized speech capacity at least as much as, and even more than, being genuinely auditory phenomena. Such evidence comes mainly from research carried out on the neuroimaging of AVHs, on the so-called "inner" and "subvocal" speech, on "voices" experienced by deaf patients, and on the phenomenology of AVHs. Interestingly, this evidence is in line with clinical insights of the classical psychiatric school (de Clérambault) as well as of (Lacanian) psychoanalysis. According to the latter, the experience of the voice is linked more to speech as a chain of articulated signifying elements than to sensorium itself.

Non-psychotic symptomatology
There is on-going research that supports the prevalence of auditory hallucinations, with a lack of other conventional psychotic symptoms (such as delusions, or paranoia), particularly in pre-pubertal children.  These studies indicate a remarkably high percentage of children (up to 14% of the population sampled) experienced sounds or voices without any external cause, although "sounds" are not considered by psychiatrists to be examples of auditory hallucinations. Differentiating actual auditory hallucinations from "sounds" or a normal internal dialogue is important since the latter phenomena are not indicative of mental illness.

Methods
To explore the auditory hallucinations in schizophrenia, experimental neurocognitive use approaches such as dichotic listening, structural fMRI, and functional fMRI. Together, they allow insight into how the brain reacts to auditory stimuli, be they external or internal. Such methods allowed researchers to find a correlation between a decreased gray matter of the left temporal lobe and difficulties in processing external sound stimuli in hallucinating patients.Functional neuroimaging has shown increased blood and oxygen flow to speech-related areas of the left temporal lobe, including Brocas area and the thalamus.

Causes
The causes of auditory hallucinations are unclear.
It is suspected that deficits in the left temporal lobe attribute that lead to spontaneous neural activity cause speech misrepresentations that account for auditory hallucinations.Charles Fernyhough, of the University of Durham, poses one theory among many but stands as a reasonable example of the literature.  Given standing evidence towards the involvement of the inner voice in auditory hallucinations, he proposes two alternative hypotheses on the origins of auditory hallucinations in the non-psychotic.  They both rely on an understanding of the internalization process of the inner voice.

Internalization of the inner voice
The internalization process of the inner voice is the process of creating an inner voice during early childhood and can be separated into four distinct levels.Level one (external dialogue) involves the capacity to maintain an external dialogue with another person, i.e. a toddler talking with their parent(s).
Level two (private speech) involves the capacity to maintain a private external dialogue, as seen in children voicing the actions of play using dolls or other toys, or someone talking to themselves while repeating something they had written down.
Level three (expanded inner speech) is the first internal level in speech.  This involves the capacity to carry out internal monologues, as seen in reading to oneself or going over a list silently.
Level four (condensed inner speech) is the final level in the internalization process.  It involves the capacity to think in terms of pure meaning without the need to put thoughts into words in order to grasp the meaning of the thought.

Disruption to internalization
A disruption could occur during the normal process of internalizing ones inner voice, where the individual would not interpret their own voice as belonging to them; a problem that would be interpreted as a level one to level four error.

Re-expansion
Alternatively, the disruption could occur during the process of re-externalizing ones inner voice, resulting in an apparent second voice that seems alien to the individual; a problem that would be interpreted as a level four to level one error.

Treatments
Psychopharmacological treatments include antipsychotic medications. Meta-analyses show that cognitive behavioral therapy and metacognitive training also reduce the severity of hallucinations. Psychology research shows that the first step in treatment is for the patient to realize that the voices they hear are a creation of their own mind. This realization allows patients to reclaim a measure of control over their lives.

See also
Auditory imagery
Earworm
Hearing Voices Network
Hypnagogic hallucinations
Intrusive thought
Microwave auditory effect
Speech synthesis
Tinnitus

References
Further reading
Johnson FH (1978). The anatomy of hallucinations. Chicago: Nelson-Hall Co </s>