Seizures in cats are caused by various onsets. Cats can have reactive, primary (idiopathic) or secondary seizures. Idiopathic seizures are not as common in cats as in dogs however a recent study conducted showed that of 91 feline seizures, 25% were suspected to have idiopathic epilepsy. In the same group of 91 cats, 50% were secondary seizures and 20% reactive.

Idiopathic epilepsy does not have a classification due to the fact there are no known causes of these seizures, however both reactive and symptomatic secondary epilepsy can be placed into classifications.

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.

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.

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.

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.

Genetics may play a role in the risk that a person will develop PTE; people with the ApoE-ε4 allele may be at higher risk for PTE. The haptoglobin Hp2-2 allele may be another genetic risk factor, possibly because it binds hemoglobin poorly and thus allows more iron to escape and damage tissues. However, most studies have found that having family members with epilepsy does not significantly increase the risk of PTS, suggesting that genetics are not a strong risk factor.

Studies have found that the incidence of PTE ranges between 1.9 and more than 30% of TBI sufferers, varying by severity of injury and by the amount of time after TBI for which the studies followed subjects.

Brain trauma is one of the strongest predisposing factors for epilepsy development, and is an especially important factor in young adults. Young adults, who are at the highest risk for head injury, also have the highest rate of PTE, which is the largest cause of new-onset epilepsy cases in young people. Children have a lower risk for developing epilepsy; 10% of children with severe TBI and 16–20% of similarly injured adults develop PTE. Being older than 65 is also a predictive factor in the development of epilepsy after brain trauma. One study found PTE to be more common in male TBI survivors than in females.

Consistent risk factors include:

- Severity of seizures, increased refractoriness of epilepsy and presence of generalized tonic-clonic seizures: the most consistent risk factor is an increased frequency of tonic–clonic seizures.

- Poor compliance. Lack of therapeutic levels of anti-epileptic drugs, non-adherence to treatment regimens, and frequent changes in regimens are risk factors for sudden death.

- Young age, and early age of seizures onset.

- Male gender

- Poly-therapy of epilepsy. It remains unclear whether this is an independent risk factor or a surrogate marker for severity of epilepsy.

- Being asleep during a seizure is likely to favour SUDEP occurrence.

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.

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.

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

Both medication and drug overdoses can result in seizures, as may certain medication and drug withdrawal. Common drugs involved include: antidepressants, antipsychotics, cocaine, insulin, and the local anaesthetic lidocaine. Difficulties with withdrawal seizures commonly occurs after prolonged alcohol or sedative use, a condition known as delirium tremens.

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.

West syndrome is a triad of developmental delay, seizures termed infantile spasms, and EEG demonstrating a pattern termed hypsarrhythmia. Onset occurs between three months and two years, with peak onset between eight and 9 months. West syndrome may arise from idiopathic, symptomatic, or cryptogenic causes. The most common cause is tuberous sclerosis. The prognosis varies with the underlying cause. In general, most surviving patients remain with significant cognitive impairment and continuing seizures and may evolve to another eponymic syndrome, Lennox-Gastaut syndrome. It can be classified as idiopathic, syndromic, or cryptogenic depending on cause and can arise from both focal or generalized epileptic lesions.

It is not possible to make a generalised prognosis for development due to the variability of causes, as mentioned above, the differing types of symptoms and cause. Each case must be considered individually.

The prognosis for children with idiopathic West syndrome are mostly more positive than for those with the cryptogenic or symptomatic forms. Idiopathic cases are less likely to show signs of developmental problems before the attacks begin, the attacks can often be treated more easily and effectively and there is a lower relapse rate. Children with this form of the syndrome are less likely to go on to develop other forms of epilepsy; around two in every five children develop at the same rate as healthy children.

In other cases, however, treatment of West syndrome is relatively difficult and the results of therapy often dissatisfying; for children with symptomatic and cryptogenic West syndrome, the prognosis is generally not positive, especially when they prove resistant to therapy.

Statistically, 5 out of every 100 children with West syndrome do not survive beyond five years of age, in some cases due to the cause of the syndrome, in others for reasons related to their medication. Only less than half of all children can become entirely free from attacks with the help of medication. Statistics show that treatment produces a satisfactory result in around three out of ten cases, with only one in every 25 children's cognitive and motoric development developing more or less normally.

A large proportion (up to 90%) of children suffer severe physical and cognitive impairments, even when treatment for the attacks is successful. This is not usually because of the epileptic fits, but rather because of the causes behind them (cerebral anomalies or their location or degree of severity). Severe, frequent attacks can (further) damage the brain.

Permanent damage often associated with West syndrome in the literature include cognitive disabilities, learning difficulties and behavioural problems, cerebral palsy (up to 5 out of 10 children), psychological disorders and often autism (in around 3 out of 10 children). Once more, the cause of each individual case of West syndrome must be considered when debating cause and effect.

As many as 6 out of 10 children with West syndrome suffer from epilepsy later in life. Sometimes West syndrome turns into a focal or other generalised epilepsy. Around half of all children develop Lennox-Gastaut syndrome.

The lack of generally recognized clinical recommendations available are a reflection of the dearth of data on the effectiveness of any particular clinical strategy, but on the basis of present evidence, the following may be relevant:

- Epileptic seizure control with the appropriate use of medication and lifestyle counseling is the focus of prevention.

- Reduction of stress, participation in physical exercises, and night supervision might minimize the risk of SUDEP.

- Knowledge of how to perform the appropriate first-aid responses to seizure by persons who live with epileptic people may prevent death.

- People associated with arrhythmias during seizures should be submitted to extensive cardiac investigation with a view to determining the indication for on-demand cardiac pacing.

- Successful epilepsy surgery may reduce the risk of SUDEP, but this depends on the outcome in terms of seizure control.

- The use of anti suffocation pillows have been advocated by some practitioners to improve respiration while sleeping, but their effectiveness remain unproven because experimental studies are lacking.

- Providing information to individuals and relatives about SUDEP is beneficial.

Temporal lobe epilepsy (TLE) is not a classic syndrome but mentioned here because it is the most common epilepsy of adults. It is a symptomatic localization-related epilepsy and in most cases the epileptogenic region is found in the midline (mesial) temporal structures (e.g., the hippocampus, amygdala, and parahippocampal gyrus). Seizures begin in late childhood and adolescence. Most of these patients have focal seizures sometimes preceded by an aura, and some TLE patients also have secondary generalized tonic-clonic seizures. Often seizures do not sufficiently respond to medical treatment with anticonvulsants and epilepsy surgery may be considered.

Generalized epilepsy, also known as primary generalized epilepsy or idiopathic epilepsy, is a form of epilepsy characterised by generalised seizures with no apparent cause. Generalized seizures, as opposed to focal seizures, are a type of seizure that impairs consciousness and distorts the electrical activity of the whole or a larger portion of the brain (which can be seen, for example, on electroencephalography, EEG).

Generalized epilepsy is "primary" because the epilepsy is the originally diagnosed condition itself, as opposed to "secondary" epilepsy, which occurs as a symptom of a diagnosed condition.

Most people with PNES (75%) are women, with onset in the late teens to early twenties being typical.

Some studies have reported an elevated frequency of childhood abuse in people with PNES. However, others that have controlled for other demographic factors have failed to find a higher rate of reported childhood abuse than in a comparable groups with organic disease (usually epilepsy).

A number of studies have also reported a high incidence of abnormal personality traits or personality disorders in people with PNES such as borderline personality. However, again, when an appropriate control group is used, the incidence of such characteristics it not always higher in PNES than in similar illnesses arising due to organic disease (e.g., epilepsy).

Other risk factors for PNES include having a diagnosis of epilepsy, having recently had a head injury or recently undergone neurosurgery.

It is still unknown which bio-chemical mechanisms lead to the occurrence of West syndrome. It is conjectured that it is a malfunction of neurotransmitter function, or more precisely, a malfunction in the regulation of the GABA transmission process. Another possibility being researched is a hyper-production of the Corticotropin-releasing hormone (CRH). It is possible that more than one factor is involved. Both hypotheses are supported by the effect of certain medications used to treat West syndrome.

Cases of epilepsy have been historically divided into three different groups: symptomatic, cryptogenic, and unknown. The International League Against Epilepsy (ILAE) recommended in 2011 to abandon these terms for reasons of clarity and instead try to place individual cases into one of the following 3 groups: genetic, structural/metabolic, and unknown. The new terms are more immediately clear in their meaning, except that the structural and metabolic group includes cases that have a genetic component that does not always directly lead to the condition. Only the genetic grouping has a known direct genetic cause. "Unknown" cases may be of "unknown" genetic, structural, metabolic, or other unknown cause.

The old terminology was defined by the ILAE as follows:

- symptomatic: the epilepsy is the consequence of a known or suspected disorder of the central nervous system.

- cryptogenic: this refers to a disorder whose cause is hidden or occult. Cryptogenic epilepsies are presumed to be symptomatic.

- idiopathic: there is no underlying cause other than a possible hereditary predisposition.

The remainder of this section will refer to the older terminology.

Most generalized epilepsy starts during childhood. While some patients outgrow their epilepsy during adolescence and no longer need medication, in others, the condition remains for life, thereby requiring lifelong medication and monitoring.

Though there is limited evidence, outcomes appear to be relatively poor with a review of outcome studies finding that two thirds of PNES patients continue to experience episodes and more than half are dependent on social security at three-year followup. This outcome data was obtained in a referral-based academic epilepsy center and loss to follow-up was considerable; the authors point out ways in which this may have biased their outcome data. Outcome was shown to be better in patients with higher IQ, social status, greater educational attainments, younger age of onset and diagnosis, attacks with less dramatic features, and fewer additional somatoform complaints.

No single cause of OS has been identified. In most cases, there is severe atrophy of both hemispheres of the brain. Less often, the root of the disorder is an underlying metabolic syndrome. Although it was initially published that no genetic connection had been established, several genes have since associated with Ohtahara syndrome. It can be associated with mutations in "ARX", "CDKL5", "SLC25A22", "STXBP1", "SPTAN1", "KCNQ2", "ARHGEF9", "PCDH19", "PNKP", "SCN2A", "PLCB1", "SCN8A", and likely others.

Treatment outlook is poor. Anticonvulsant drugs and glucocorticoid steroids may be used to try to control the seizures, but their effectiveness is limited. Most therapies are related to symptoms and day-to-day living.

The National Institute of Health Office and Rare Disease Research characterizes PCDH19 gene-related epilepsy as a rare disorder. Rare diseases, by definition, are diseases that affect fewer than 200,000 people in the United States. Since the mutation associated with PCDH19 gene-related epilepsy was only recently identified in 2008, the true incidence of the disease is generally unknown.

Although formal epidemiologic data is not available, results from diagnostic screening indicates that approximately 1 out of 10 girls who have seizure onset before five years of age may have PCDH19 gene mutations. Additionally, PCDH19 screening of several large cohorts of females with early onset febrile-related epilepsy has resulted in a rate of approximately 10% of mutation-positive individuals.