Coma may result from a variety of conditions, including intoxication (such as drug abuse, overdose or misuse of over the counter medications, prescribed medication, or controlled substances), metabolic abnormalities, central nervous system diseases, acute neurologic injuries such as strokes or herniations, hypoxia, hypothermia, hypoglycemia, eclampsia or traumatic injuries such as head trauma caused by falls, drowning accidents, or vehicle collisions. It may also be deliberately induced by pharmaceutical agents during major neurosurgery, to preserve higher brain functions following brain trauma, or to save the patient from extreme pain during healing of injuries or diseases.

Forty percent of comatose states result from drug poisoning. Drugs damage or weaken the synaptic functioning in the ARAS and keep the system from properly functioning to arouse the brain. Secondary effects of drugs, which include abnormal heart rate and blood pressure, as well as abnormal breathing and sweating, may also indirectly harm the functioning of the ARAS and lead to a coma. Seizures and hallucinations have shown to also play a major role in ARAS malfunction. Given that drug poisoning is the cause for a large portion of patients in a coma, hospitals first test all comatose patients by observing pupil size and eye movement, through the vestibular-ocular reflex.

The second most common cause of coma, which makes up about 25% of comatose patients, occurs from lack of oxygen, generally resulting from cardiac arrest. The Central Nervous System (CNS) requires a great deal of oxygen for its neurons. Oxygen deprivation in the brain, also known as hypoxia, causes neuronal extracellular sodium and calcium to decrease and intracellular calcium to increase, which harms neuron communication. Lack of oxygen in the brain also causes ATP exhaustion and cellular breakdown from cytoskeleton damage and nitric oxide production.

Twenty percent of comatose states result from the side effects of a stroke. During a stroke, blood flow to part of the brain is restricted or blocked. An ischemic stroke, brain hemorrhage, or tumor may cause such cessation of blood flow. Lack of blood to cells in the brain prevents oxygen from getting to the neurons, and consequently causes cells to become disrupted and eventually die. As brain cells die, brain tissue continues to deteriorate, which may affect functioning of the ARAS.

The remaining 15% of comatose cases result from trauma, excessive blood loss, malnutrition, hypothermia, hyperthermia, abnormal glucose levels, and many other biological disorders.

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.

When the soporous condition is stipulated by the cerebral circulation or a concussion and other neurological diseases, the patient should be put to bed. Administer a dehydrating agent (20 ml 40% glucose solution intravenously, 10 ml of 2.4% aminophylline solution with 10 ml 40% glucose solution by slow intravenous injection or 1-2ml 12% solution of aminophylline intramuscularly, 10 ml of 25% solution of magnesium sulfate intramuscularly, 50 mg hypothiazide inside) and vasodilators (1-2 ml of 2% papaverine solution subcutaneously, 1 ml of 1% solution of nicotinic acid intravenously).

Lesions of the ascending reticular activation system on height of the pons and metencephalon have been shown to cause stupor. The incidence is higher after left-sided lesions.

If not stimulated externally, a patient with stupor will be in a sleepy state most of the time. In some extreme cases of severe depressive disorders the patient can become motionless, lose their appetite and become mute. Short periods of restricted responsivity can be achieved by intense stimulation (e.g. pain, bright light, loud noise, shock).

Soporous states can be observed in the presence of traumatic, vascular, inflammatory, neoplastic, and toxic lesions of the brain.

Initial treatment is aimed at providing symptomatic relief. Benzodiazepines are the first line of treatment, and high doses are often required. A test dose of intramuscular lorazepam will often result in marked improvement within half an hour. In France, zolpidem has also been used in diagnosis, and response may occur within the same time period. Ultimately the underlying cause needs to be treated.

Electroconvulsive therapy (ECT) is an effective treatment for catatonia. Antipsychotics should be used with care as they can worsen catatonia and are the cause of neuroleptic malignant syndrome, a dangerous condition that can mimic catatonia and requires immediate discontinuation of the antipsychotic.

Excessive glutamate activity is believed to be involved in catatonia; when first-line treatment options fail, NMDA antagonists such as amantadine or memantine are used. Amantadine may have an increased incidence of tolerance with prolonged use and can cause psychosis, due to its additional effects on the dopamine system. Memantine has a more targeted pharmacological profile for the glutamate system, reduced incidence of psychosis and may therefore be preferred for individuals who cannot tolerate amantadine. Topiramate is another treatment option for resistant catatonia; it produces its therapeutic effects by producing glutamate antagonism via modulation of AMPA receptors.

Only 25% of people who experience seizures or status epilepticus have epilepsy. The following is a list of possible causes:

- Stroke

- Hemorrhage

- Intoxicants or adverse reactions to drugs

- Insufficient dosage or sudden withdrawal of a medication (especially anticonvulsants)

- Consumption of alcoholic beverages while on an anticonvulsant, or alcohol withdrawal

- Dieting or fasting while on an anticonvulsant

- Starting on a new medication that reduces the effectiveness of the anticonvulsant or changes drug metabolism, decreasing its half-life, leading to decreased blood concentrations

- Developing a resistance to an anticonvulsant already being used

- Gastroenteritis while on an anticonvulsant, where lower levels of anticonvulsant may exist in the bloodstream due to vomiting of gastric contents or reduced absorption due to mucosal edema

- Developing a new, unrelated condition in which seizures are coincidentally also a symptom, but are not controlled by an anticonvulsant already used

- Metabolic disturbances—such as affected kidney and liver

- Sleep deprivation of more than a short duration is often the cause of a (usually, but not always, temporary) loss of seizure control.

Between 10 and 30% of people who have status epilepticus die within 30 days. The great majority of these people have an underlying brain condition causing their status seizure such as brain tumor, brain infection, brain trauma, or stroke. However, people with diagnosed epilepsy who have a status seizure also have an increased risk of death if their condition is not stabilized quickly, their medication and sleep regimen adapted and adhered to, and stress and other stimulant (seizure trigger) levels controlled.

However, with optimal neurological care, adherence to the medication regimen, and a good prognosis (no other underlying uncontrolled brain or other organic disease), the person—even people who have been diagnosed with epilepsy—in otherwise good health can survive with minimal or no brain damage, and can decrease risk of death and even avoid future seizures.

Alcohol consumption increases the risk of hypothermia by its action as a vasodilator. It increases blood flow to the skin and extremities, making a person "feel" warm, while increasing heat loss. Between 33% and 73% of hypothermia cases are complicated by alcohol.

In the UK, 28,354 cases of hypothermia were treated in 2012-13 – an increase of 25% from the previous year. Some cases of hypothermia death, as well as other preventable deaths, happen because poor people cannot easily afford to keep warm. Rising fuel bills have increased the numbers who have difficulty paying for adequate heating in the UK. Some pensioners and disabled people are at risk because they do not work and cannot easily get out of their homes. Better heat insulation can help.

Catatonia is a state of psycho-motor immobility and behavioral abnormality manifested by stupor. It was first described in 1874 by Karl Ludwig Kahlbaum, in ("Catatonia or Tension Insanity").

Though catatonia has historically been related to schizophrenia (catatonic schizophrenia), it is now known that catatonic symptoms are nonspecific and may be observed in other mental disorders and neurological conditions. In the fifth edition of the "Diagnostic and Statistical Manual of Mental Disorders" (DSM), catatonia is not recognized as a separate disorder, but is associated with psychiatric conditions such as schizophrenia (catatonic type), bipolar disorder, post-traumatic stress disorder, depression and other mental disorders, narcolepsy, as well as drug abuse or overdose (or both). It may also be seen in many medical disorders including infections (such as encephalitis), autoimmune disorders, focal neurologic lesions (including strokes), metabolic disturbances, alcohol withdrawal and abrupt or overly rapid benzodiazepine withdrawal. In the fifth edition of the DSM, it is written that a variety of medical conditions may cause catatonia, especially neurological conditions: encephalitis, cerebrovascular disease, neoplasms, head injury. Moreover, metabolic conditions: homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, hypercalcaemia.

It can be an adverse reaction to prescribed medication. It bears similarity to conditions such as encephalitis lethargica and neuroleptic malignant syndrome. There are a variety of treatments available; benzodiazepines are a first-line treatment strategy. Electroconvulsive therapy is also sometimes used. There is growing evidence for the effectiveness of NMDA receptor antagonists for benzodiazepine-resistant catatonia. Antipsychotics are sometimes employed but require caution as they can worsen symptoms and have serious adverse effects.

Waxy flexibility is a psychomotor symptom of catatonia as associated with schizophrenia, bipolar disorder, or other mental disorders which leads to a decreased response to stimuli and a tendency to remain in an immobile posture. Attempts to reposition the patient are met by "slight, even resistance", and after being repositioned the patient will typically remain in the new position. Waxy flexibility rarely occurs in cases of delirium. The presence of waxy flexibility along with at least two other catatonic symptoms such as stupor or negativism are enough to warrant a diagnosis of catatonia.

For instance, if one were to move the arm of someone with waxy flexibility, they would keep their arm where one moved it until it was moved again, as if it were made from wax. Further alteration of an individual's posture is similar to bending a candle. Although waxy flexibility has historically been linked to schizophrenia, there are also other disorders which it may be associated with, for example, mood disorder with catatonic behaviour.

Electroconvulsive therapy is often used as a treatment for catatonia. A study has found that catatonic patients suffering from waxy flexibility responded faster to electroconvulsive therapy, compared to patients with different catatonic symptoms.

Complex partial status epilepticus (CPSE) is one of the non-convulsive forms of status epilepticus, a rare form of epilepsy defined by its recurrent nature. CPSE is characterized by seizures involving long-lasting stupor, staring and unresponsiveness. Sometimes this is accompanied by motor automatisms, such as eye twitching.

The symptoms of sedative/hypnotic toxidrome include ataxia, blurred vision, coma, confusion, delirium, deterioration of central nervous system functions, diplopia, dysesthesias, hallucinations, nystagmus, paresthesias, sedation, slurred speech, and stupor. Apnea is a potential complication. Substances that may cause this toxidrome include anticonvulsants, barbiturates, benzodiazepines, gamma-Hydroxybutyric acid, Methaqualone, and ethanol. While most sedative-hypnotics are anticonvulsant, some such as GHB and methaqualone instead lower the seizure threshold, and so can cause paradoxical seizures in overdose.

As is the case with other non-convulsive status epilepticus forms, CPSE is dangerously underdiagnosed. This is due to the potentially fatal yet veiled nature of the symptoms. Usually, an electroencephalogram, or EEG, is needed to confirm a neurologist's suspicions. The EEG is also needed to differentiate between absence status epilepticus (which affects the entire brain), and CPSE, which only affects one region.

The symptoms of an opiate toxidrome include the classic triad of coma, pinpoint pupils, and respiratory depression as well as altered mental states, shock, pulmonary edema and unresponsiveness. Complications include bradycardia, hypotension, and hypothermia. Substances that may cause this toxidrome are opioids.

Treatment consists of high-dose lorazepam or in some cases ECT. The response to the treatment is usually good, especially if detected early

Autistic catatonia is a rare type of disorder that affects roughly 10 percent of all adults with autism spectrum disorder. Most of them are not severely affected but a few exhibit stupor and severe excitement, which is the most extreme form of the disorder. Full expression of excitement could be a sign of comorbid Bipolar disorder but more research is needed.

More than 40 symptoms has been identified to be a result of the disorder, but some of the symptoms overlap with those of autism spectrum disorder, making diagnosing difficult even for a seasoned professional. In a few cases stupor and hyperactivity can continue for weeks or even months.

During the excitement phase individuals show combativeness and can have delusions and hallucinations and can also pose a danger to themselves or others and can make marked destruction of property..In the later stages of medium and even more in the severe and if left untreatead lethal state they will also experience autonomic instability! (Behav Sci (Basel). 2015 Dec; 5(4): 576–588.

Published online 2015 Dec 9. doi: 10.3390/bs5040576

Childhood schizophrenia increases the risk for autistic catatonia later in life dramatically. There seems to be a common font of brain pathology for psychosis, catatonia and autism.

Obstructive sleep apnea (OSA) affects around 4% of men and 2% of women in the United States. In general, this disorder is more prevalent among men. However, this difference tends to diminish with age. Women experience the highest risk for OSA during pregnancy. Also, they tend to report experiencing depression and insomnia in conjunction with obstructive sleep apnea. In a meta-analysis of the various Asian countries, India and China present the highest prevalence of the disorder. Specifically, about 13.7% of the Indian population and 7% of Hong-Kong's population is estimated to have OSA. The two groups experience daytime OSA symptoms such as difficulties concentrating, mood swings, or high blood pressure, at similar rates (prevalence of 3.5% and 3.57%, respectively).

The condition is rare, with only 80 established cases reported in medical literature and incomplete evidence of a further 200.

According to one meta-analysis, the two most prevalent sleep disorders among children are confusional arousals and sleep walking. An estimated 17.3% of kids between 3 and 13 years old experience confusional arousals. About 17% of children sleep walk, with the disorder being more common among boys than girls. The peak ages of sleep walking are from 8 to 12 years old. A different systematic review offers a high range of prevalence rates of sleep bruxism for children. Between 15.29 and 38.6% of preschoolers grind their teeth at least one night a week. All but one of the included studies reports decreasing bruxist prevalence as age increased as well as a higher prevalence among boys than girls.

Another systematic review noted 7-16% of young adults suffer from delayed sleep phase disorder. This disorder reaches peak prevalence when people are in their 20's. Between 20 and 26% of adolescents report a sleep onset latency of >30 minutes. Also, 7-36% have difficulty initiating sleep. Asian teens tend to have a higher prevalence of all of these adverse sleep outcomes than their North American and European counterparts.

Patients with hypertensive encephalopathy who are promptly treated usually recover without deficit. However, if treatment is not administered, the condition can lead to death.

There is no known single cause or causes of schizophrenia, however, it is a heritable disorder.

Several environmental factors, including perinatal complications and prenatal maternal infections could cause schizophrenia. These factors in a greater severity or frequency could result in an earlier onset of schizophrenia. Maybe a genetic predisposition is a important factor too, familial illness reported for childhood-onset schizophrenic patients.

Environmental factors associated with the development of schizophrenia include the living environment, drug use, and prenatal stressors.

Maternal stress has been associated with an increased risk of schizophrenia, possibly in association with reelin. Maternal Stress has been observed to lead to hypermethylation and therefore under-expression of reelin, which in animal models leads to reduction in GABAergic neurons, a common finding in schizophrenia. Maternal nutritional deficiencies, such as those observed during a famine, as well as maternal obesity have also been identified as possible risk factors for schizophrenia. Both maternal stress and infection have been demonstrated to alter fetal neurodevelopment through pro-inflammatory proteins such as IL-8 and TNF.

Parenting style seems to have no major effect, although people with supportive parents do better than those with critical or hostile parents. Childhood trauma, death of a parent, and being bullied or abused increase the risk of psychosis. Living in an urban environment during childhood or as an adult has consistently been found to increase the risk of schizophrenia by a factor of two, even after taking into account drug use, ethnic group, and size of social group. Other factors that play an important role include social isolation and immigration related to social adversity, racial discrimination, family dysfunction, unemployment, and poor housing conditions.

It has been hypothesized that in some people, development of schizophrenia is related to intestinal tract dysfunction such as seen with non-celiac gluten sensitivity or abnormalities in the intestinal flora. A subgroup of persons with schizophrenia present an immune response to gluten different from that found in people with celiac, with elevated levels of certain serum biomarkers of gluten sensitivity such as anti-gliadin IgG or anti-gliadin IgA antibodies.