The first case of eosinophilia–myalgia syndrome was reported to the Centers for Disease Control and Prevention (CDC) in November 1989, although some cases had occurred as early as 2–3 years before this. In total, more than 1,500 cases of EMS were reported to the CDC, as well as at least 37 EMS-associated deaths. After preliminary investigation revealed that the outbreak was linked to intake of tryptophan, the U.S. Food and Drug Administration (FDA) recalled tryptophan supplements in 1989 and banned most public sales in 1990, with other countries following suit.

Eosinophilia–myalgia syndrome (EMS) is an incurable and sometimes fatal flu-like neurological condition linked to the ingestion of the dietary supplement L-tryptophan. The risk of developing EMS increases with larger doses of tryptophan and increasing age. Some research suggests that certain genetic polymorphisms may be related to the development of EMS. The presence of eosinophilia is a core feature of EMS, along with unusually severe myalgia (muscle pain).

PPID shares similarities to Equine Metabolic Syndrome, which also causes regional adiposity, laminitis, and insulin resistance. Treatment and management may differ between the two endocrinopathies, making differentiation important. However, it is important to keep in mind that horses with EMS may develop PPID, therefore both diseases may occur simultaneously.

This test may also be referred to as a ‘’resting ACTH’’, ’’endogenous ACTH’’, or ‘’basal ACTH’’. The majority of ACTH produced in normal horses comes from corticotrope cells in the pars distalis, with only 2% thought to come from melanotropes in the pars intermedia. In horses with PPID, melanotropes produce abnormally high levels of ACTH. Basal plasma ACTH concentrations, which measure the blood levels of circulating ACTH, can therefore be useful in diagnosing the disease.

ACTH levels naturally fluctuate in healthy horses, with a significant rise occurring the in autumn (August through October) in North American horses. Horses with PPID have a similar, but much more significant, rise in the autumn. Therefore, a seasonally adjusted reference range must be used that correlates with the time of year the sample is taken. Failure to use a seasonally adjusted reference range may lead to false-positive results in normal horses if they are sampled in the fall. Autumnal testing is thought to be more sensitive and specific than testing at other times of the year, so is preferred. Basal plasma ACTH levels may increase if the horse is severely ill or under great stress or pain, such as if it has laminitis. However, such events must be fairly significant to confound the results. Additionally, ACTH levels may not be significantly increased early on in the disease, leading to false negatives.

Whilst diet has long been known to be linked to laminitis, there is emerging evidence that breed and body condition also play a role. Levels of hormones, particularly adiponectin, and serum insulin are also implicated, opening up new possibilities for developing early prognostic tests and risk assessments.

The mechanism remains unclear and is the subject of much research. Three conditions are thought to cause secondary laminitis:

- Sepsis/endotoxemia or generalized inflammation

- Endocrinopathy

- Trauma: concussion or excessive weight-bearing

- Inflammation

Inflammatory events that are associated with laminitis include sepsis, endotoxemia, retained placenta, carbohydrate overload (excessive grain or pasture), enterocolitis, pleuropneumonia, and contact with black walnut shavings. In these cases, there is an increase in blood flow to the hoof, bringing in damaging substances and inflammatory cells into the hoof.

- Endocrinopathy

Endocrinopathy is usually the result of improper insulin regulation, and is most commonly seen with pituitary pars intermedia dysfunction (also called equine Cushing's syndrome) and equine metabolic syndrome (EMS), as well as obesity and glucocorticoid administration. In cases of EMS, most episodes occur in the spring when the grass is lush.

- Trauma

Mechanical laminitis starts when the hoof wall is pulled away from the bone or lost, as a result of external influences. Mechanical laminitis can occur when a horse habitually paws, is ridden or driven on hard surfaces ("road founder"), or in cases of excessive weight-bearing due to compensation for the opposing limb, a process called "support limb laminitis". Support limb laminitis is most common in horses suffering from severe injury to one limb, such as fracture, resulting in a non-weight bearing state that forces them to take excessive load on the opposing limb. This causes decreased blood flow to the cells, decreasing oxygen and nutrient delivery, and thus altering their metabolism which results in laminitis.

Chlorine is a relatively common gas in industry with a variety of uses. It is used to disinfect water as well as being a part of the sanitation process for sewage and industrial waste. Chlorine is also used as a bleaching agent during the production of paper and cloth. Many household cleaning products, including bleach, contain chlorine. Given the volume and ease of chlorine for industrial and commercial use, exposure could occur from an accidental spill or a deliberate attack. The National Institute for Occupational Safety and Health recommends that a person wear splash proof goggles, a face shield and a respirator mask when working in the vicinity of chlorine gas. Because chlorine is a gas at room temperature, most exposure occurs via inhalation. Exposure may also occur through skin or eye contact or by ingesting chlorine-contaminated food or water. Chlorine is a strong oxidizing element causing the hydrogen to split from water in moist tissue, resulting in nascent oxygen and hydrogen chloride that cause corrosive tissue damage. Additionally oxidation of chlorine may form hypochlorous acid, which can penetrate cells and react with cytoplasmic proteins destroying cell structure. Chlorine’s odor provides early warning signs of exposure but causes olfactory fatigue or adaptations, reducing awareness of exposure at low concentrations. With increased exposure, symptoms may progress to labored respirations, severe coughing, chest tightness, wheezing, dyspnea, and broncospasm associated with a decrease in oxygen saturation level. . Severe exposure may result in changes in upper and lower airways resulting in an acute lung injury, which may not be present until several hours after exposure. A recent chlorine gas leak in Pune, India, landed 20 individuals in the hospital. Though that was an accidental exposure, chlorine gas has been used as a weapon of warfare since World War I, most recently in 2007 in Iraq.

Smoke inhalation injury, either by itself but more so in the presence of body surface burn, can result in severe lung-induced morbidity and mortality. The most common cause of death in burn centers is now respiratory failure. The September 11 attacks in 2001 and forest fires in U.S. states such as California and Nevada are examples of incidents that have caused smoke inhalation injury. Injury to the lungs and airways is not only due to deposition of fine particulate soot but also due to the gaseous components of smoke, which include phosgene, carbon monoxide, and sulfur dioxide.

A recent study by Salcido et al. (2010) ascertained rearrest in all initial and rearrest rhythms treated by any level of Emergency Medical Service (EMS), finding a rearrest rate of 36% and a lower but not significantly different rate of survival to hospital discharge in cases with rearrest compared to those without rearrest.

Rearrest may reduce the likelihood of survival when compared to patients who have had just one episode of cardiac arrest. Overall resuscitation rates have been estimated to be about 34%, however survival to hospital discharge rates are as low as 7%. This phenomenon may be contributed to rearrest.

About 10% of cases of moyamoya disease are familial, and some cases result from specific genetic mutations. Susceptibility to moyamoya disease-2 (MYMY2; 607151) is caused by variation in the RNF213 gene (613768) on chromosome 17q25. Moyamoya disease-5 (MYMY5; 614042) is caused by mutation in the ACTA2 gene (102620) on chromosome 10q23.3; and moyamoya disease-6 with achalasia (MYMY6; 615750) is caused by mutation in the GUCY1A3 gene (139396) on chromosome 4q32. Loci for the disorder have been mapped to chromosome 3p (MYMY1) and chromosome 8q23 (MYMY3; 608796). See also MYMY4 (300845), an X-linked recessive syndromic disorder characterized by moyamoya disease, short stature, hypergonadotropic hypogonadism, and facial dysmorphism. and linked to q25.3, on chromosome 17". (Online Mendelian Inheritance in Man, omim.org/entry/252350).

In Japan the overall incidence is higher (0.35 per 100,000). In North America, women in the third or fourth decade of life are most often affected, but the condition may also occur during infancy or childhood. These women frequently experience transient ischaemic attacks (TIA), cerebral hemorrhage, or may not experience any symptoms at all. They have a higher risk of recurrent stroke and may be experiencing a distinct underlying pathophysiology compared to patients from Japan.

Moyamoya disease can be either congenital or acquired. Patients with Down syndrome, sickle cell anemia, neurofibromatosis type 1, congenital heart disease, fibromuscular dysplasia, activated protein C resistance, or head trauma can develop moyamoya malformations. It is more common in women than in men, although about a third of those affected are male.

Moyamoya disease is a disease in which certain arteries in the brain are constricted. Blood flow is blocked by the constriction, and also by blood clots (thrombosis).

A collateral circulation develops around the blocked vessels to compensate for the blockage, but the collateral vessels are small, weak, and prone to bleeding, aneurysm and thrombosis. On conventional X-ray angiography, these collateral vessels have the appearance of a "puff of smoke" (described as "もやもや (moyamoya)" in Japanese).

When Moyamoya is diagnosed by itself, with no underlying correlational conditions, it is diagnosed as Moyamoya disease. This is also the case when the arterial constriction and collateral circulation are bilateral. Moyamoya syndrome is unilateral arterial constriction, or occurs when one of the several specified conditions is also present. This may also be considered as Moyamoya being secondary to the primary condition.

Mainly, occlusion of the distal internal carotid artery occurs. On angiography, a "puff of smoke" appearance is seen, and the treatment of choice is surgical bypass.

The risk factors for SCD are similar to those of coronary artery disease and include age, cigarette smoking, high blood pressure, high cholesterol, lack of physical exercise, obesity, diabetes, and family history. A prior episode of sudden cardiac arrest also increases the risk of future episodes.

Current cigarette smokers with coronary artery disease were found to have a two to threefold increase in the risk of sudden death between ages 30 and 59. Furthermore, it was found that former smokers risk was closer to that of those who had never smoked.

Comas can last from several days to several weeks. In more severe cases a coma may last for over five weeks, while some have lasted as long as several years. After this time, some patients gradually come out of the coma, some progress to a vegetative state, and others die. Some patients who have entered a vegetative state go on to regain a degree of awareness. Others remain in a vegetative state for years or even decades (the longest recorded period being 42 years).

The outcome for coma and vegetative state depends on the cause, location, severity and extent of neurological damage. A deeper coma alone does not necessarily mean a slimmer chance of recovery, because some people in deep coma recover well while others in a so-called milder coma sometimes fail to improve.

People may emerge from a coma with a combination of physical, intellectual, and psychological difficulties that need special attention. Recovery usually occurs gradually—patients acquire more and more ability to respond. Some patients never progress beyond very basic responses, but many recover full awareness. Regaining consciousness is not instant: in the first days, patients are only awake for a few minutes, and duration of time awake gradually increases. This is unlike the situation in many movies where people who awake from comas are instantly able to continue their normal lives. In reality, the coma patient awakes sometimes in a profound state of confusion, not knowing how they got there and sometimes suffering from dysarthria, the inability to articulate any speech, and with many other disabilities.

Predicted chances of recovery are variable owing to different techniques used to measure the extent of neurological damage. All the predictions are based on statistical rates with some level of chance for recovery present: a person with a low chance of recovery may still awaken. Time is the best general predictor of a chance of recovery: after four months of coma caused by brain damage, the chance of partial recovery is less than 15%, and the chance of full recovery is very low.

The most common cause of death for a person in a vegetative state is secondary infection such as pneumonia, which can occur in patients who lie still for extended periods.

There are reports of patients coming out of coma after long periods of time. After 19 years in a minimally conscious state, Terry Wallis spontaneously began speaking and regained awareness of his surroundings.

A brain-damaged man, trapped in a coma-like state for six years, was brought back to consciousness in 2003 by doctors who planted electrodes deep inside his brain. The method, called deep brain stimulation (DBS) successfully roused communication, complex movement and eating ability in the 38-year-old American man who suffered a traumatic brain injury. His injuries left him in a minimally conscious state (MCS), a condition akin to a coma but characterized by occasional, but brief, evidence of environmental and self-awareness that coma patients lack.

Comas lasting seconds to minutes result in post-traumatic amnesia (PTA) that lasts hours to days; recovery plateau occurs over days to weeks.

Comas that last hours to days result in PTA lasting days to weeks; recovery plateau occurs over months.

Comas lasting weeks result in PTA that lasts months; recovery plateau occurs over months to years.

Structural heart disease not related to CAD (i.e. hypertrophic cardiomyopathy, congenital coronary artery anomalies, myocarditis) account for 10% of all SCDs. Examples of these include: cardiomyopathy, cardiac rhythm disturbances, myocarditis, hypertensive heart disease, and congestive heart failure.

Left ventricular hypertrophy is thought to be a leading cause of SCD in the adult population. This is most commonly the result of longstanding high blood pressure which has caused secondary damage to the wall of the main pumping chamber of the heart, the left ventricle.

A 1999 review of SCDs in the United States found that this accounted for over 30% of SCDs for those under 30 years. A study of military recruits age 18-35 found that this accounted for over 40% of SCDs.

Congestive heart failure increases the risk of SCD fivefold.

Coma is a state of unconsciousness in which a person cannot be awakened; fails to respond normally to painful stimuli, light, or sound; lacks a normal wake-sleep cycle; and does not initiate voluntary actions. A person in a state of coma is described as being "comatose". A distinction is made in the medical community between a real coma and a medically induced coma, the former is a result of circumstances beyond the control of the medical community, while the latter is a means by which medical professionals may allow a patient's injuries to heal in a controlled environment.

A comatose person exhibits a complete absence of wakefulness and is unable to consciously feel, speak, hear, or move. For a patient to maintain consciousness, two important neurological components must function. The first is the cerebral cortex—the gray matter that forms the outer layer of the brain. The other is a structure located in the brainstem, called reticular activating system (RAS).

Injury to either or both of these components is sufficient to cause a patient to experience a coma. The cerebral cortex is a group of tight, dense, "gray matter" composed of the nuclei of the neurons whose axons then form the "white matter," and is responsible for perception, relay of the sensory input via the thalamic pathway, and many other neurological functions, including complex thinking.

RAS, on the other hand, is a more primitive structure in the brainstem which includes the reticular formation (RF). The RAS area of the brain has two tracts, the ascending and descending tract. Made up of a system of acetylcholine-producing neurons, the ascending track, or ascending reticular activating system (ARAS), works to arouse and wake up the brain, from the RF, through the thalamus, and then finally to the cerebral cortex. A failure in ARAS functioning may then lead to a coma. The word is from the Greek "koma", meaning "deep sleep."