The subject of mouthpiece pressure is closely related to the issue of embouchure collapse/embouchure overuse.

It has long been argued that excessive mouthpiece pressure is a cause of embouchure problems and can be a factor in causing embouchure collapse. However, the pressure of the mouthpiece is not static during playing: it increases the higher in the register a player plays and the louder volume level. Also, a little mouthpiece pressure is essential to provide a seal between the player's embouchure and the instrument; without this, all the air would escape before entering the instrument and no sound would be emitted (brass instruments are dependent on an airflow to produce sound).

Embouchure collapse is far more common among trumpet and horn players. Both of these instruments have mouthpieces with a small circumference, and therefore the pressure is presumably greater, as the force of the mouthpiece on the face is more concentrated. This is in accordance with the principle of physics that pressure is the amount of force divided by the area on which the force is exerted.

As a result of a lack of scientific evidence (no scientific study into mouthpiece pressure as a cause of embouchure collapse has ever been done), the equally valid argument that all brass players can suffer embouchure collapse, and the subjective (not static) nature of mouthpiece pressure, knowledge of mouthpiece pressure as a cause of embouchure collapse is limited.

Embouchure collapse caused by focal dystonia can be diagnosed medically; embouchure collapse caused by embouchure overuse, however, is generally speaking not considered to be a specifically medical issue. A difficulty in diagnosis is that when a brass player describes the symptoms to a doctor or dentist (as is often the case), the medical practitioner does not fully understand what the patient means. This is because brass players learn their embouchure by "feel," and therefore words have a limited ability to describe embouchure problems, especially if the person listening to the description is not a brass player and has a limited knowledge of the embouchure.

Also, in less severe cases, the player may only be able to feel what is wrong while playing. Many players with an embouchure problem will, once they have realized that it is more than a simple case of tired lips, wish to refrain from playing. The fact that around 24 muscles are employed in forming a brass embouchure, and that each will change slightly as a player struggles to play when experiencing embouchure problems, mean that what players describe as being wrong will have not only worsened their condition when they play, but will be different each time they do so.

In the severest cases, the pain caused by embouchure overuse can be felt even when not playing; in some cases, other symptoms will manifest, such as loss of tissue and damaged nerves. This, however, occurs only in the rarest and most extreme circumstances and usually signals the end of the player's career.

The exact cause of Kienböck's is not known, though there are thought to be a number of factors predisposing a person to Kienböck's.

Recent studies have made a correlation between Kienböck's sufferers and Western European ancestry, but no definitive link can be positively confirmed.

The necrosis of the lunate bone can frequently be traced to a trauma to the wrist, like a compound fracture, which could cause the lunate's blood supply to be interrupted. Blood flows to the lunate through several arteries, each supplying a percentage. When one of these pathways is severed, the likelihood the patient will develop necrosis increases.

Despite a preponderance of evidence, no particular cause has been conclusively verified.

Data exists on the internet that most people suffering from Kienböck's are affected in their dominant hand, though about one-third of sufferers report the condition in their non-dominant hand. In very few cases have there been people that have acquired it in both wrists.

Kienböck's disease is classified as a "rare disorder," meaning that it affects fewer than 200,000 people in the U.S. population.

Many Kienböck's patients are frustrated by the lack of consensus among hand surgeons about optimal treatments for Kienböck's. No matter what the disease's stage of progression, there is no one best treatment, and the decision is often based partially, or even mostly, on incidental factors such as the patient's pain tolerance, the patient's desire to return to active use of the hand (such as in manual occupations), and the surgeon's level of expertise with different treatments.

Though, since each case of Kienböck's is different, the makeup of the wrist and arm bones are important factors which are individualized to each patient. Therefore, one surgery will never be able to solve all the problems associated with the disease. Thus, no consensus can be reached among surgeons.

Kienböck's disease is a disorder of the wrist. It is named for Dr. Robert Kienböck, a radiologist in Vienna, Austria who described osteomalacia of the lunate in 1910.

It is breakdown of the lunate bone, a carpal bone in the wrist that articulates with the radius in the forearm. Specifically, Kienböck's disease is another name for avascular necrosis (death and fracture of bone tissue due to interruption of blood supply) with fragmentation and collapse of the lunate. This has classically been attributed to arterial disruption, but may also occur after events that produce venous congestion with elevated interosseous pressure.

Dysbaric osteonecrosis is a significant occupational hazard, occurring in 50% of commercial Japanese divers, 65% of Hawaiian fishermen and 16% of commercial and caisson divers in the UK.

Its relationship to compressed air is strong in that it may follow a single exposure to compressed air, may occur with no history of DCS but is usually associated with significant compressed air exposure. The distribution of lesions differs with the type of exposure - the juxta-articular lesions being more common in caisson workers than in divers.

There is a definite relationship between length of time exposed to extreme depths and the percentage of divers with bone lesions. Evidence does not suggest that dysbaric osteonecrosis is a significant risk in recreational scuba diving.

Crucial in the decision to breed would be the primary cause of FCKS in the litter, which may or may not be genetic. Some recovered FCKS adults have produced FCKS offspring in their turn (or lines that consistently produce flat kittens), and breeding from them is therefore inadvisable. However, repeat matings in which FCKS has appeared does not always result in further FCKS kittens. Queens and studs who consistently throw complete litters of kittens with the condition are generally neutered since a genetically linked cause for the condition can be introduced into lines that do not produce it by breeding with lines in which it is common. Isolated instances of single flat kittens in an otherwise healthy litter are unlikely to have a genetic component in the condition, and neutering of parents of such kittens is not usually necessary in pedigree breeding, especially since this may have detrimental effects on the gene pool.

If the cause of flattening is colic related to over-production of milk then this would not be cause for neutering. The only way to determine if the cause is digestive would be if the condition was alleviated in all cases by pinching the phrenic nerve and/or use of liquid paraffin to relieve colic resulting in improvement in the condition.

Line-breeding or inbreeding is highly inadvisable in lines where FCKS has appeared, and the practice may cause the condition to appear in lines where it has not previously been recorded.

Children younger than 6 have the best prognosis, since they have time for the dead bone to revascularize and remodel, with a good chance that the femoral head will recover and remain spherical after resolution of the disease. Children who have been diagnosed with Perthes' disease after the age of 10 are at a very high risk of developing osteoarthritis and coxa magna. When an LCP disease diagnosis occurs after age 8, a better outcome results with surgery rather than nonoperative treatments. Shape of femoral head at the time when Legg-Calve Perthes disease heals is the most important determinant of risk for degenerative arthritis; hence, the shape of femoral head and congruence of hip are most useful outcome measures.

It is currently not known what causes the disease, but it is believed to be connected to infestations of the parasitic worm "Onchocerca volvulus", which is prevalent in all outbreak areas, and a possible explanation involves the formation of antibodies against parasite antigen that are cross-reactive to leiomodin-1 in the hippocampus. "O. volvulus", a nematode, is carried by the black fly and causes river blindness. In 2004, most children suffering from nodding disease lived close to the Yei River, a hotbed for river blindness, and 93.7% of nodding disease sufferers were found to harbour the parasite — a far higher percentage than in children without the disease. A link between river blindness and normal cases of epilepsy, as well as retarded growth, had been proposed previously, although the evidence for this link is inconclusive. Of the connection between the worm and the disease, Scott Dowell, the lead investigator into the syndrome for the US Centers for Disease Control and Prevention (CDC), stated: "We know that ["Onchocerca volvulus"] is involved in some way, but it is a little puzzling because [the worm] is fairly common in areas that do not have nodding disease". Andrea Winkler, the first author of a 2008 Tanzanian study, has said of the connection: "We could not establish any hint that "Onchocerca volvulus" is actually going into the brain, but what we cannot exclude is that there is an autoimmune mechanism going on." In the most severely affected region of Uganda, infection with microfilariae in epileptic or nodding children ranged from 70% to 100%.

The CDC is investigating a possible connection with wartime chemical exposure. The team is also investigating whether a deficiency in vitamin B (pyridoxine) could be a cause, noting the seizures of pyridoxine-dependent epilepsy and this common deficiency in disease sufferers. Older theories include a 2002 toxicology report that postulated a connection with tainted monkey meat, as well as the eating of agricultural seeds provided by relief agencies that were covered in toxic chemicals.

First described by Preiser in 1910 in 5 patients, all with previous history of wrist trauma, and scaphoid fractures in 3 of them.

In some cases (particularly where whole litters are affected) FCKS can be due to genetic factors: certain bloodlines are known to produce a preponderance of kittens with the condition, and close matings very commonly produce it in the offspring. Isolated cases are more likely due to environmental factors or slight prematurity of the kittens concerned, and even complete litters suffering from FCKS may have no genetic component—repeat matings that have produced flat kittens in one instance have often not produced it again, and recovered FCKS that have been bred from have likewise not necessarily produced offspring that suffered from the condition.

Spinal shock was first defined by Whytt in 1750 as a loss of accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury (SCI) – most often a complete transection. Reflexes in the spinal cord below the level of injury are depressed (hyporeflexia) or absent (areflexia), while those above the level of the injury remain unaffected. The 'shock' in spinal shock does not refer to circulatory collapse, and should not be confused with neurogenic shock, which is life-threatening

Perthes' disease is one of the most common hip disorders in young children, occurring in roughly 5.5 of 100,000 children per year. The lifetime risk of a child developing the disease is about one per 1,200 individuals. Boys are affected about three to five times more often than girls. New cases of Perthes' disease rarely occur after age 14 years (if diagnosed after 14 years of age, then it is usually old disease from early in childhood or avascular necrosis from an alternative cause).

White northern Europeans appear to be affected more frequently than other races, though a paucity of reliable epidemiology exists in the Southern Hemisphere. Children of sufferers of the disease themselves may have a very slightly increased risk, though it is unclear if this is because of a genetic predisposition, or a shared environmental factor. It is most commonly seen in persons aged three to 12 years, with a median of six years of age. The UK incidence rates show an intriguing pattern with low incidence rates in London, and a progressive increase in disease in more northerly areas (maximal in Scotland). Some evidence suggests, at least in developed countries, more socioeconomically deprived communities have a greater risk of disease (a similar trend to diseases such as adult heart disease), though the reason for this remains unknown. One possible explanation that has been considered is tobacco smoke exposure, though this is significantly confounded by the strong socioeconomic gradient common to both smoking and Perthes' disease. Dietary factors of the child, and of the mother during pregnancy, are of interest to the research groups.

If the diver has not been exposed to excessive depth and decompression and presents as DON, there may be a predisposition for the condition. Diving should be restricted to shallow depths. Divers who have suffered from DON are at increased risk of future fracture of a juxta-articular lesion during a dive, and may face complications with future joint replacements. Because of the young age of the population normally affected, little data is available regarding joint replacement complications.

There is the potential for worsening of DON for any diving where there might be a need for decompression, experimental or helium diving. Physically stressful diving should probably be restricted, both in sport diving and work diving due to the possibility of unnecessary stress to the joint. Any diving should be less than 40 feet/12 meters. These risks are affected by the degree of disability and by the type of lesion (juxta-articular or shaft).

Preiser disease, or (idiopathic) avascular necrosis of the scaphoid, is a rare condition where ischemia and necrosis of the scaphoid bone occurs without previous fracture. It is thought to be caused by repetitive microtrauma or side effects of drugs (e.g., steroids or chemotherapy) in conjunction with existing defective vascular supply to the proximal pole of the scaphoid. MRI coupled with CT and X-ray are the methods of choice for diagnosis.

Preiser's disease is initially treated by immobilising the wrist with a cast. However, in most cases the avascular scaphoid will start to collapse leading to degeneration within the wrist joints. This often requires surgical intervention to prevent the progression of arthris. Two commonly performed procedures are:

1. Proximal row carpectomy (PRC), which involves removing the first row of the carpal bones, i.e. the scaphoid, lunate and triquetrum. The wrist is immobilised in a cast for six weeks after the surgery and then physiotherapy is started.

2. Scaphoid excision and 4-corner fusion, which is a procedure consisting of the removal of the scaphoid and fixation of the remaining wrist bones with a plate (called a "spider plate") or wires in order to provide stability. The plate usually is left inside the patient's wrist, while the wires (usually K-wires) have to be removed in a second surgery. This procedure of partial wrist fusion allows for limited wrist movement, whereas total wrist fusion immobilizes the wrist permanently. Following surgery it can take several months for affected patients to regain strength.

Unfortunately both of these operations are salvage procedures and movements in the wrist will be significantly reduced.

Nodding syndrome is debilitating both physically and mentally. In 2004, Peter Spencer stated: "It is, by all reports, a progressive disorder and a fatal disorder, perhaps with a duration of about three years or more." While a few children are said to have recovered from it, many have died from the illness. Seizures can also cause children to collapse, potentially causing injury or death.

Collapse is a sudden and often unannounced loss of postural tone (going weak), often but not necessarily accompanied by loss of consciousness.

If the episode was accompanied by a loss of consciousness, the term syncope is used. The main causes are cardiac (e.g. due to irregular heart beat, low blood pressure), seizures or a psychological cause. The main tool in distinguishing the causes is careful history on the events before, during and after the collapse, from the patient as well as from any possible witnesses. Other investigations may be performed to further strengthen the diagnosis, but many of these have a low yield.

Individuals suffering from Diogenes syndrome generally display signs of collectionism, hoarding, or compulsive disorder. Individuals who have suffered damage to the brain, particularly the frontal lobe, may be at more risk to developing the syndrome. The frontal lobes are of particular interest, because they are known to be involved in higher order cognitive processes, such as reasoning, decision-making and conflict monitoring.

Diogenes Syndrome tends to occur among the elderly. The behavioural patterns that is usually reflected by those living with this disorder are suffering from significant functional problem that is correlated with morbidity and mortality.

Although this is a congenital lesion, airway sounds typically begin at age 4–6 weeks. Until that age, inspiratory flow rates may not be high enough to generate the sounds. Symptoms typically peak at age 6–8 months and remit by age 2 years.

Late-onset laryngomalacia may be a distinct entity, which can present after age of 2 years

Diogenes syndrome is a disorder that involves hoarding of rubbish and severe self-neglect. In addition, the syndrome is characterized by domestic squalor, syllogomania, social alienation, and refusal of help. It has been shown that the syndrome is caused as a reaction to stress that was experienced by the patient. The time span in which the syndrome develops is undefined, though it is most accurately distinguished as a reaction to stress that occurs late in life.

In most instances, patients were observed to have an abnormal possessiveness and patterns of compilation in a disordered manner. These symptoms suggest damages on the prefrontal areas of the brain, due to its relation to decision making. Although in contrast, there have been some cases where the hoarded objects were arranged in a methodical manner, which may suggest a cause other than brain damage.

Although most patients have been observed to come from homes with poor conditions, and many had been faced with poverty for a long period of time, these similarities are not considered as a definite cause to the syndrome. Research showed that some of the participants with the condition had solid family backgrounds as well successful professional lives. Half of the patients were of higher intelligence level. This indicates the "Diogenes syndrome" does not exclusively affect those experiencing poverty or those who had traumatic childhood experiences.

The severe neglect that they bring on themselves usually results in physical collapse or mental breakdown. Most individuals who suffer from the syndrome do not get identified until they face this stage of collapse, due to their predilection to refuse help from others.

The patients are generally highly intelligent, and the personality traits that can be seen frequently in patients diagnosed with Diogenes syndrome are aggressiveness, stubbornness, suspicion of others, unpredictable mood swings, emotional instability and deformed perception of reality. Secondary DS is related to mental disorders. The direct relation of the patients' personalities to the syndrome is unclear, though the similarities in character suggest potential avenues for investigation.

Although laryngomalacia is not associated with a specific gene, there is evidence that some cases may be inherited. Relaxation or a lack of muscle tone in the upper airway may be a factor. It is often worse when the infant is on his or her back, because the floppy tissues can fall over the airway opening more easily in this position.

Sack–Barabas syndrome is rare and has an estimated prevalence of 1 in 100,000 to 200,000.

The initial clinical manifestation of vascular problems in patients with SBS is early, about 25% have their first symptoms at age 20 and more than 80% of patients have had at least one complication by the age of 40.

The median survival for one study of SBS patients was only 48 years.

Some horse organizations have instituted rules to attempt to eliminate this widespread disease. The American Quarter Horse Association (AQHA) mandates testing for foals descended from Impressive if both of the foal's parents were not homozygous negative (N/N) for the gene, and, since 2007, has not registered foals homozygous (H/H) for the gene. Since 2007, the Appaloosa Horse Club (ApHC) has required foals descended from Impressive to be tested, so that the results may be recorded on its certificate. The American Paint Horse Association (APHA) mandated that, after 2017, stallions must be tested for HYPP so that mare owners may make an informed decision before choosing a stallion for breeding to their mare.

Hyperkalemic periodic paralysis (HYPP, HyperKPP) is a genetic disorder. It occurs in humans, horses (where it is also known as Impressive syndrome, after an index case in a horse named Impressive, or possibly one of his ancestors), and perhaps other animals. It is an inherited autosomal dominant disorder that affects sodium channels in muscle cells and the ability to regulate potassium levels in the blood. It is most commonly associated with horses, but occurs in humans, where it may be called Gamstorp episodic adynamy. It is characterized by muscle hyperexcitability or weakness which, exacerbated by potassium, heat or cold, can lead to uncontrolled shaking followed by paralysis. Onset in humans usually occurs in early childhood, but still occurs with adults.

The mutation which causes this disorder is dominant on SCN4A with linkage to the sodium channel expressed in muscle. The mutation causes single amino acid changes in parts of the channel which are important for inactivation. In the presence of high potassium levels, including those induced by diet, sodium channels fail to inactivate properly.

Equine hyperkalemic periodic paralysis occurs in 1 in 50 Quarter Horses and can be traced to a single ancestor, a stallion named Impressive.

Collapsed veins are a common result of chronic use of intravenous injections. They are particularly common where injecting conditions are less than ideal, such as in the context of drug abuse.

Veins may become temporarily blocked if the internal lining of the vein swells in response to repeated injury or irritation. This may be caused by the needle, the substance injected, or donating plasma. Once the swelling subsides, the circulation will often become re-established.

Permanent vein collapse occurs as a consequence of:

- Long-term injecting

- Repeated injections, especially with blunt needles

- Poor technique

- Injection of substances which irritate the veins; in particular, injection of liquid methadone intended for oral use.

Smaller veins may collapse as a consequence of too much suction being used when pulling back against the plunger of the syringe to check that the needle is in the vein. This will pull the sides of the vein together and, especially if they are inflamed, they may stick together causing the vein to block. Removing the needle too quickly after injecting can have a similar effect.

Collapsed veins may never recover. Many smaller veins are created by the body to circulate the blood, but they are not adequate for injections or IVs.

Tracheobronchomalacia or TBM is a condition characterized by flaccidity of the tracheal support cartilage which leads to tracheal collapse. This condition can also affect the bronchi. There are two forms of this rare condition: primary TB and secondary TB. Primary TB is congenital and starts as early as two years old. It is mainly linked to genetic causes. Secondary TB is acquired and starts in adulthood. It is mainly developed after an accident or chronic inflammation.

On 28 May 2013, it was reported that a cure had been developed via a 3D printed windpipe. This cure has currently saved the lives of at least 3 infants.