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 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.

Operations that attempt to restore a blood supply to the lunate may be performed.

Depending on the stage the disease is in when it is discovered, varying treatments are applied.

If X-rays show a mostly intact lunate (not having lost a great deal of size, and not having been compressed into a triangular shape), but an MRI shows a lack of blood flow to the bone, then revascularization is normally attempted. Revascularization techniques, usually involving a bone graft taken elsewhere from the body — often held in place by an external fixator for a period of weeks or months — have been successful at stages as late as 3B, although their use at later stages (like most treatments for Kienböck's) is controversial.

One conservative treatment option would be using an Ultrasound Bone Stimulator, which uses low-intensity pulsed ultrasound to increase vascular endothelial growth factor (VEG-F) and increase blood flow to the bone.

Some Kienböck's patients present with an abnormally large difference in length between the radius and the ulna, termed "ulnar variance", which is hypothesized to cause undue pressure on the lunate, contributing to its avascularity. In cases with such a difference, "radial shortening" is commonly performed. In this procedure, the radius (the lateral long bone) is shortened by a given length, usually between 2 and 5 mm, to relieve the pressure on the dying lunate. A titanium plate is inserted to hold the newly shortened bone together.

During Stage 3, the lunate has begun to break apart due to the pressure of the surrounding bones. This causes sharp fragments of bone to float between the joints, causing excruciating pain. At this point, the lunate is ready for removal. The most frequently performed surgery is the "Proximal Row Carpectomy", where the lunate, scaphoid and triquetrum are extracted. This greatly limits the range of motion of the wrist, but pain relief can be achieved for longer than after the other surgeries.

Another surgical option for this stage is a titanium, silicon or pyrocarbon implant that takes place of the lunate, though doctors shy from this due to a tendency of the implant to smooth the edges of the surrounding bones, thus causing painful pinched nerves when the bones slip out of place.

After the lunate is removed, another procedure, "ulnar shortening" can be performed. This relieves pressure on the newly formed wrist joint of the pisiform, hamate and capitate. Depending on the surgeon, the procedure may be performed the same way as the "radial shortening" where a small section is removed, or the entire top of the ulna may be excised.

At Stage 4, the lunate has completely disintegrated and the other bones in the wrist have radiated downward to fill in the void. The hand now has a deformed, crippled appearance. The only procedure that can be done is the "total wrist fusion", where a plate is inserted on the top of the wrist from the radius to the carpals, effectively freezing all flexion and movement in the wrist. Rotation is still possible as it is controlled by the radius and ulna.

This is currently the last and most complete surgical option for Kienböck's sufferers.

Most of the treatments described here are not mutually exclusive — meaning that a single patient may receive many of them in his quest to relieve pain. For instance, some patients have had casting, bone graft, radial shortening, proximal row carpectomy, and wrist fusion, all on the same hand.

First described by David Lichtman et al. in 1977.

The purpose of this classification system is to guide treatment and to enable comparison of clinical outcomes.

1. Stage I Normal radiograph (possible lunate fracture).

2. Stage II Sclerosis of the lunate without collapse. (Portions of the lunate begin to deteriorate. This shows as a white blemish on x-rays.)

3. Stage IIIA Lunate collapse and fragmentation, in addition to proximal migration of the capitate.

4. Stage IIIB Lunate collapse and fragmentation, in addition to proximal migration of the capitate. In addition there is fixed flexion deformity of the scaphoid.

5. Stage IV Changes up to and including fragmentation, with radiocarpal and midcarpal arthritic changes.

Diagnosis is not very advanced and is based on the telltale nodding seizures of the victims. When stunted growth and mental disability are also present, probability of nodding syndrome is high. In the future, neurological scans may also be used in diagnosis. As there is no known cure for the disease, treatment has been directed at symptoms, and has included the use of anticonvulsants such as sodium valproate and phenobarbitol. Anti-malaria drugs have also been administered, to unknown effect.

X-rays of the hip may suggest and/or verify the diagnosis. X-rays usually demonstrate a flattened, and later fragmented, femoral head. A bone scan or MRI may be useful in making the diagnosis in those cases where X-rays are inconclusive. Usually, plain radiographic changes are delayed 6 weeks or more from clinical onset, so bone scintigraphy and MRI are done for early diagnosis. MRI results are more accurate, i.e. 97 to 99% against 88 to 93% in plain radiography. If MRI or bone scans are necessary, a positive diagnosis relies upon patchy areas of vascularity to the capital femoral epiphysis (the developing femoral head).

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.

It is difficult to determine whether a kitten that goes flat will survive or not. A good indicator is the weight of the kitten: those that continue to gain weight generally have a better chance of survival. Supplement feeding is therefore recommended in all cases, together with vitamin supplements, although many of these kittens will not accept hand feeding. Liquid Paraffin to alleviate colic seems to be significant in assisting normal feeding and weight-gain.

Another indicator to the severity of the case is the use of the stomach when breathing: normal kittens use only the ribcage, a flat-chested kitten may manage to breathe only using the ribcage, or may suck the gut upwards with every breath – if the latter is the case then the likelihood of survival seems to be lower, though still not sufficient to warrant immediate euthanasia. If the condition is stable (i.e. the flatness does not increase over time) or improving, the kitten is more likely to survive. If the condition worsens over several days, survival is less likely.

Kittens with FCKS may die (or have to be euthanased) very soon after onset. There are two points at which breeders report kittens that were otherwise doing well deteriorating and dying: at 10 days of age and at 3 weeks. Generally if the kitten is still flat, but survives the 3-week developmental stage, its prognosis is good. Many will have returned to a normal shape by this time. Those retaining some degree of flatness often grow out of the condition at any point in the ensuing 6 months, and the vast majority of survivors appear to lead normal lives with no side-effects, either physical or immunological.

FCKS kittens that survive but who have not been given any drug treatment or support other than supplementary feeding, generally recover over a period of 4–10 weeks, and are usually normal by 12 weeks of age, though some take as long as 6 months to normalise. In the very small number of kittens reported so far treated with steroids, antibiotics and liquid paraffin (to address colic) recovery is usually seen within a matter of days. Given the number of different types of FCKS these kittens (all with the minor form of the condition) may not be representative of all cases. More data is required for statistical analysis.

A small proportion of severe FCKS kittens are left with long-term respiratory problems, kyphosis, and in some cases cardiac issues caused by the compression of the thorax during the early developmental stages (particularly where the condition has been coupled with Pectus Excavatum). Cardiac issues are generally audible on physical examination; further indications include the kitten becoming breathless after play, less active than siblings, and failure to grow and develop normally.

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.

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).

The physician will ask some questions about the baby’s health problems and may recommend a flexible laryngoscopy to further evaluate the infant's condition.

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

Prevention is a more successful strategy than treatment. By using the most conservative decompression schedule reasonably practicable, and by minimizing the number of major decompression exposures, the risk of DON may be reduced. Prompt treatment of any symptoms of decompression sickness (DCS) with recompression and hyperbaric oxygen also reduce the risk of subsequent DON.

The use of steroids (Dexamethasone) coupled with an antibiotic (Amoxicillin) will support the kitten in a number of ways, the steroid enhancing maturation and the antibiotic addressing the possibility of underlying infection and compensating for the immuno-depressant properties of the steroid. The steroid will also encourage the kitten to feed more energetically, keeping its weight up. Several breeders believe that Taurine plays a part in the condition, and it may be that some cases are Taurine-related. These breeders give the queen large doses of Taurine (1000 mg) daily until the kittens recover – apparently within a few days. Given that most FCKS cases take weeks rather than days to recover, this supplement may be relevant.

Diagnosis is conducted according to the severity of the symptoms. Initially pulmonary function tests are administered. These tests include the lungs' capability of air intake and outtake, and gas flow of oxygen and carbon dioxide between the body and environment. Following these function tests a CT scan or bronchoscopy will be ordered. The results to the scan and bronchoscopy will display the status of the rare condition. A mild case of tracheobronchomalacia would be if the patient's trachea condenses 50% of its normal space when exhaling. Moderate tracheobronchomalacia would be 25% of the normal trachea space constricting and a severe case would be if the walls touch each other.

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

Laryngomalacia becomes symptomatic after the first few months of life (2–3 months), and the stridor may get louder over the first year, as the child moves air more vigorously. Most of the cases resolve spontaneously and less than 15% of the cases will need surgical intervention. Parents need to be supported and educated about the condition.

It is ethically difficult when it comes to dealing with diagnosed patients, for many of them deny their poor conditions and refuse to accept treatment. The main objectives of the doctors are to help improve the patient’s lifestyle and wellbeing, so health care professionals must decide whether or not to force treatment onto their patient.

In some cases, especially those including the inability to move, patients have to consent to help, since they cannot manage to look after themselves. Hospitals or nursing homes are often considered the best treatment under those conditions.

When under care, patients must be treated in a way in which they can learn to trust the health care professionals. In order to do this, the patients should be restricted in the number of visitors they are allowed, and be limited to 1 nurse or social worker. Some patients respond better to psychotherapy, while others to behavioral treatment or terminal care.

Results after hospitalization tend to be poor. Research on the mortality rate during hospitalization has shown that approximately half the patients die while in the hospital. A quarter of the patients are sent back home, while the other quarter are placed in long time care. Patients under care in hospitals and nursing homes often slide back into relapse or face death.

There are other approaches to improve the patient’s condition. Day care facilities have often been successful with maturing the patient’s physical and emotional state, as well as helping them with socialization. Other methods include services inside the patient’s home, such as the delivery of food.

To properly treat a patient with tracheobronchomalacia, the subtype must be determined (primary or secondary). After the type is named, the cause must be identified, whether it is from genetics, a trauma accident, or chronic tracheal illness. If a trauma case or chronic tracheal illnesses were the cause, the first steps of treatment would be to fix or help these underlying issues. If the cause is genetic or the previous underlying issues could not be fixed, other treatments would be assessed. More severe treatments include silicone stenting to prevent tracheal constriction, surgery to strengthen or attempt to rebuild the walls, continuous positive airway pressure that has a machine blow small amounts of air into the trachea to keep it open (mainly at night), or a tracheostomy, which is surgically put into your neck that leads to your trachea to help with breathing. People with tracheobronchomalacia who do not experience symptoms do not need treatment and are often undiagnosed.

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.

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.

The tests to verify Sack–Barabas syndrome are biochemical samples such as collagen typing (performed on a skin biopsy sample) or collagen gene mutation testing. There is no cure for Ehlers-Danlos syndrome, so individual problems and symptoms must be evaluated and cared for accordingly.

The key for managing Sack–Barabas syndrome is for the patient to be aware of their disease. Close follow up and planning of interventions can significantly prolong and maintain the quality of life of a patient with this disease.

Pregnant affected women must take special care due to the increased risk of premature death due to rupture of arteries, bowel or uterine rupture with a reported mortality rate of 50%.

Genetic counselling is recommended for prospective parents with a family history of Ehlers–Danlos syndrome. Affected parents should be aware of the type of Ehlers-Danlos syndrome they have and its mode of inheritance.

Diagnosis of degenerative disc disease will usually consist of an analysis of a patient's individual medical history, a physical exam designed to reveal muscle weakness, tenderness or poor range of motion, and an MRI scan to confirm the diagnosis and rule out other causes.

A study of aortic cross-clamping, a common procedure in cardiac surgery, demonstrated a strong potential benefit with further research ongoing.