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.

In those with cirrhosis, the risk of developing hepatic encephalopathy is 20% per year, and at any time about 30–45% of people with cirrhosis exhibit evidence of overt encephalopathy. The prevalence of minimal hepatic encephalopathy detectable on formal neuropsychological testing is 60–80%; this increases the likelihood of developing overt encephalopathy in the future. Once hepatic encephalopathy has developed, the prognosis is determined largely by other markers of liver failure, such as the levels of albumin (a protein produced by the liver), the prothrombin time (a test of coagulation, which relies on proteins produced in the liver), the presence of ascites and the level of bilirubin (a breakdown product of hemoglobin which is conjugated and excreted by the liver). Together with the severity of encephalopathy, these markers have been incorporated into the Child-Pugh score; this score determines the one- and two-year survival and may assist in a decision to offer liver transplantation.

In acute liver failure, the development of severe encephalopathy strongly predicts short-term mortality, and is almost as important as the nature of the underlying cause of the liver failure in determining the prognosis. Historically, widely used criteria for offering liver transplantation, such as King's College Criteria, are of limited use and recent guidelines discourage excessive reliance on these criteria. The occurrence of hepatic encephalopathy in people with Wilson's disease (hereditary copper accumulation) and mushroom poisoning indicates an urgent need for a liver transplant.

A number of measures have been attempted to prevent seizures in those at risk. Following traumatic brain injury anticonvulsants decrease the risk of early seizures but not late seizures.

In those with a history of febrile seizures, medications (both antipyretics and anticonvulsants) have not been found effective for prevention. Some, in fact, may cause harm.

There is no clear evidence that antiepileptic drugs are effective or not effective at preventing seizures following a craniotomy, following subdural hematoma, after a stroke, or after subarachnoid haemorrhage, for both people who have had a previous seizure, and those who have not.

Following a first seizure, the risk of more seizures in the next two years is 40%–50%. The greatest predictors of more seizures are problems either on the electroencephalogram or on imaging of the brain. In adults, after 6 months of being seizure-free after a first seizure, the risk of a subsequent seizure in the next year is less than 20% regardless of treatment. Up to 7% of seizures that present to the emergency department (ER) are in status epilepticus. In those with a status epilepticus, mortality is between 10% and 40%. Those who have a seizure that is provoked (occurring close in time to an acute brain event or toxic exposure) have a low risk of re-occurrence, but have a higher risk of death compared to those with epilepsy.

Panayiotopoulos syndrome is remarkably benign in terms of its evolution. The risk of developing epilepsy in adult life is probably no more than of the general population. Most patients have one or 2-5 seizures. Only a third of patients may have more than 5 seizures, and these may be frequent, but outcome is again favorable. However, one fifth of patients may develop other types of infrequent, usually rolandic seizures during childhood and early teens. These are also age-related and remit before the age of 16 years. Atypical evolutions with absences and drop attacks are exceptional. Children with pre-existing neurobehavioral disorders tend to be pharmacoresistant and have frequent seizures though these also remit with age.

Formal neuropsychological assessment of children with Panayiotopoulos syndrome showed that these children have normal IQ and they are not on any significant risk of developing cognitive and behavioural aberrations, which when they occur they are usually mild and reversible. Prognosis of cognitive function is good even for patients with atypical evolutions.

However, though Panayiotopoulos syndrome is benign in terms of its evolution, autonomic seizures are potentially life-threatening in the rare context of cardiorespiratory arrest.

Panayiotopoulos syndrome probably affects 13% of children aged 3 to 6 years who have had 1 or more afebrile seizures and 6% of such children in the 1- to 15-year age group. All races and both sexes are affected.

Treatment is in the form of anti-epileptic drugs, such as barbiturates, benzodiazepines and topiramate.

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.

In a small proportion of cases, the encephalopathy is caused directly by liver failure; this is more likely in acute liver failure. More commonly, especially in chronic liver disease, hepatic encephalopathy is triggered by an additional cause, and identifying these triggers can be important to treat the episode effectively.

Hepatic encephalopathy may also occur after the creation of a transjugular intrahepatic portosystemic shunt (TIPS). This is used in the treatment of refractory ascites, bleeding from oesophageal varices and hepatorenal syndrome. TIPS-related encephalopathy occurs in about 30% of cases, with the risk being higher in those with previous episodes of encephalopathy, higher age, female sex and liver disease due to causes other than alcohol.

The mortality rate ranges from 3–7% in a mean follow up period of 8.5 to 9.7 years. Death is often related to accidents.

Jeavons syndrome is a lifelong disorder, even if seizures are well controlled with antiepileptic drugs. Men have a better prognosis than women. There is a tendency for photosensitivity to disappear in middle age, but eyelid myoclonia persists. It is highly resistant to treatment and occurs many times a day, often without apparent absences and even without demonstrable photosensitivity.

The prognosis for Rolandic seizures is invariably excellent, with probably less than 2% risk of developing absence seizures and less often GTCS in adult life.

Remission usually occurs within 2–4 years from onset and before the age of 16 years. The total number of seizures is low, the majority of patients having fewer than 10 seizures; 10–20% have just a single seizure. About 10–20% may have frequent seizures, but these also remit with age.

Children with Rolandic seizures may develop usually mild and reversible linguistic, cognitive and behavioural abnormalities during the active phase of the disease. These may be worse in children with onset of seizures before 8 years of age, high rate of occurrence and multifocal EEG spikes.

The development, social adaptation and occupations of adults with a previous history of Rolandic seizures were found normal.

Toxic encephalopathy is often irreversible. If the source of the problem is treated by removing the toxic chemical from the system, further damage can be prevented, but prolonged exposure to toxic chemicals can quickly destroy the brain. Long term studies have demonstrated residual cognitive impairment (primarily attention and information-processing impairment resulting in dysfunction in working memory) up to 10 years following cessation of exposure. Severe cases of toxic encephalopathy can be life-threatening.

The cause of FIRES is not known. It does not happen twice in the same family, but the medical community does not know if it is genetic. It happens in boys more than girls. After the initial status, life expectancy is not affected directly. Issues such as overdose of medications or infections at a food tube site are examples of things that would be secondary to the status.

LGS is seen in approximately 4% of children with epilepsy, and is more common in males than in females. Usual onset is between the ages of three and five. Children can have no neurological problems prior diagnosis, or have other forms of epilepsy. West syndrome is diagnosed in 20% of patients before it evolves into LGS at about 2 years old.

Mild and moderate cerebral hypoxia generally has no impact beyond the episode of hypoxia; on the other hand, the outcome of severe cerebral hypoxia will depend on the success of damage control, amount of brain tissue deprived of oxygen, and the speed with which oxygen was restored.

If cerebral hypoxia was localized to a specific part of the brain, brain damage will be localized to that region. A general consequence may be epilepsy. The long-term effects will depend on the purpose of that portion of the brain. Damage to the Broca's area and the Wernicke's area of the brain (left side) typically causes problems with speech and language. Damage to the right side of the brain may interfere with the ability to express emotions or interpret what one sees. Damage on either side can cause paralysis of the opposite side of the body.

The effects of certain kinds of severe generalized hypoxias may take time to develop. For example, the long-term effects of serious carbon monoxide poisoning usually may take several weeks to appear. Recent research suggests this may be due to an autoimmune response caused by carbon monoxide-induced changes in the myelin sheath surrounding neurons.

If hypoxia results in coma, the length of unconsciousness is often indicative of long-term damage. In some cases coma can give the brain an opportunity to heal and regenerate, but, in general, the longer a coma, the greater the likelihood that the person will remain in a vegetative state until death. Even if the patient wakes up, brain damage is likely to be significant enough to prevent a return to normal functioning.

Long-term comas can have a significant impact on a patient's families. Families of coma victims often have idealized images of the outcome based on Hollywood movie depictions of coma. Adjusting to the realities of ventilators, feeding tubes, bedsores, and muscle wasting may be difficult. Treatment decision often involve complex ethical choices and can strain family dynamics.

The age of onset ranges from 1 to 14 years with 75% starting between 7–10 years. There is a 1.5 male predominance, prevalence is around 15% in children aged 1–15 years with non-febrile seizures and incidence is 10–20/100,000 of children aged 0–15 years

The most potent precipitating factor is eye closure, whether voluntary, involuntary or reflex. Most and, in some patients, all of the seizures are induced immediately after closure of the eyes in the presence of uninterrupted (non-flickering) light. Eye closure in total darkness is ineffective.

Contrary to other forms of photosensitive epilepsies that are sensitive only to flickering lights, patients with Jeavons syndrome are also sensitive to bright, non-flickering lights. This is probably due to the enhancing effect of bright light on the sensitivity of eye closure.

In addition, chemicals, such as lead, that could instigate toxic encephalopathy are sometimes found in everyday products such as cleaning products, building materials, pesticides, air fresheners, and even perfumes. These harmful chemicals can be inhaled (in the case of air fresheners) or applied (in the case of perfumes). The substances diffuse into the brain rapidly, as they are lipophilic and readily transported across the blood–brain barrier. This is a result of increased membrane solubility and local blood flow, with central nervous system (CNS) solvent uptake being further increased with high levels of physical activity. When they are not detoxified immediately, the symptoms of toxic encephalopathy begin to emerge. However, in chronic situations, these effects may not become severe enough to be noticed until much later. Increased exposure time and increased concentration of the chemicals will worsen the effects of toxic encephalopathy, due to the associated structural CNS damage and direct functional impairment consequences.

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

An occurrence of Todd's paralysis indicates that a seizure has occurred. The prognosis for the patient depends upon the effects of the seizure, not the occurrence of the paralysis.

Hypertensive encephalopathy (HE) is general brain dysfunction due to significantly high blood pressure. Symptoms may include headache, vomiting, trouble with balance, and confusion. Onset is generally sudden. Complications can include seizures, posterior reversible encephalopathy syndrome, and bleeding in the back of the eye.

In hypertensive encephalopathy, generally the blood pressure is greater than 200/130 mmHg. Occasionally it can occur at a BP as low as 160/100 mmHg. This can occur in kidney failure, those who rapidly stop blood pressure medication, pheochromocytoma, and people on a monoamine oxidase inhibitor (MAOI) who eats foods with tyramine. When it occurs in pregnancy it is known as eclampsia. The diagnosis requires ruling out other possible causes.

The condition is generally treated with medications to relatively rapidly lower the blood pressure. This may be done with labetalol or sodium nitroprusside given by injection into a vein. In those who are pregnant, magnesium sulfate may be used. Other treatments may include anti seizure medications.

Hypertensive encephalopathy is uncommon. It is believed to occur more often in those without easy access to health care. The term was first used by Oppenheimer and Fishberg in 1928. It is classified as a type of hypertensive emergency.

The most common cause of is overly rapid correction of low blood sodium levels (hyponatremia). Apart from rapid correction of hyponatraemia, there are case reports of central pontine myelinolysis in association with hypokalaemia, anorexia nervosa when feeding is started, patients undergoing dialysis and burns victims. There is a case report of central pontine myelinolysis occurring in the context of re-feeding syndrome, in the absence of hyponatremia.

It has also been known to occur in patients suffering withdrawal symptoms of chronic alcoholism. In these instances, occurrence may be entirely unrelated to hyponatremia or rapid correction of hyponatremia. It could affect patients who take some prescription medicines that are able to cross the blood-brain barrier and cause abnormal thirst reception - in this scenario the CPM is caused by polydipsia leading to low blood sodium levels (hyponatremia).

In schizophrenic patients with psychogenic polydipsia, inadequate thirst reception leads to excessive water intake, severely diluting serum sodium. With this excessive thirst combined with psychotic symptoms, brain damage such as CPM may result from hyperosmolarity caused by excess intake of fluids, (primary polydipsia) although this is difficult to determine because such patients are often institutionalised and have a long history of mental health conditions.

It has been observed following hematopoietic stem cell transplantation.

CPM may also occur in patients prone to hyponatraemia affected by

- severe liver disease

- liver transplant

- alcoholism

- severe burns

- malnutrition

- anorexia

- severe electrolyte disorders

- AIDS

- hyperemesis gravidarum

- hyponatremia due to Peritoneal Dialysis

- Wernicke encephalopathy

The number cases of PRES that occur each year is not known. It may be somewhat more common in females.