Seven anti-epileptic drugs are approved for use in cases of suspected primary generalized epilepsy:

- Felbamate

- Levetiracetam

- Zonisamide

- Topiramate

- Valproate

- Lamotrigine

- Perampanel

Valproate, a relatively old drug, is often considered the first-line treatment. It is highly effective, but its association with fetal malformations when taken in pregnancy limits its use in young women.

All anti-epileptic drugs (including the above) can be used in cases of partial seizures.

No high quality evidence has shown any drug very useful as of 2013. Rufinamide, lamotrigine, topiramate and felbamate may be useful.

LGS seizures are often treatment resistant, but this does not mean that treatment is futile. Options include anticonvulsants, anesthetics, steroids such as prednisone, immunoglobulins, and various other pharmacological agents that have been reported to work in individual patients.

Many antiepileptic drugs are used for the management of canine epilepsy. Oral phenobarbital, in particular, and imepitoin are considered to be the most effective antiepileptic drugs and usually used as ‘first line’ treatment. Other anti-epileptics such as zonisamide, primidone, gabapentin, pregabalin, sodium valproate, felbamate and topiramate may also be effective and used in various combinations. A crucial part of the treatment of pets with epilepsy is owner education to ensure compliance and successful management.

The first line treatment of choice for someone who is actively seizing is a benzodiazepine, most guidelines recommend lorazepam. This may be repeated if there is no effect after 10 minutes. If there is no effect after two doses, barbiturates or propofol may be used. Benzodiazepines given by a non-intravenous route appear to be better than those given by intravenous as the intravenous takes time to start.

Ongoing anti-epileptic medications are not typically recommended after a first seizure except in those with structural lesions in the brain. They are generally recommended after a second one has occurred. Approximately 70% of people can obtain full control with continuous use of medication. Typically one type of anticonvulsant is preferred. Following a first seizure, while immediate treatment with an anti-seizure drug lowers the probability of seizure recurrence up to five years it does not change the risk of death and there are potential side effects.

In seizures related to toxins, up to two doses of benzodiazepines should be used. If this is not effective pyridoxine is recommended. Phenytoin should generally not be used.

There is a lack of evidence for preventative anti-epileptic medications in the management of seizures related to intracranial venous thrombosis.

Anticonvulsants are the most successful medication in reducing and preventing seizures from reoccurring. The goal of these medications in being able to reduce the reoccurrence of seizures is to be able to limit the amount of rapid and extensive firing of neurons so that a focal region of neurons cannot become over-activated thereby initiating a seizure. Although anticonvulsants are able to reduce the amount of seizures that occur in the brain, no medication has been discovered to date that is able to prevent the development of epilepsy following a head injury. There are a wide range of anticonvulsants that have both different modes of action and different abilities in preventing certain types of seizures. Some of the anticonvulsants that are prescribed to patients today include: Carbamazepine (Tegretol), Phenytoin (Dilantin Kapseals), Gabapentin (Neurontin), Levetiracetam (Keppra), Lamotrigine (Lamictal), Topiramate (Topamax), Tiagabine (Gabitril), Zonisamide (Zonegran) and Pregabalin (Lyrica).

Lorazepam and clonazepam are front line treatment for severe convulsions, belonging to the benzodiazepine class of medications.

As of 2017, data on optimal treatment was limited. Therapies with hormones is the standard of care, namely adrenocorticotrophic hormone (ACTH), or oral

corticosteroids such as prednisone. Vigabatrin is also a common consideration, though there is a risk of visual field loss with long term use. The high cost of ACTH leads doctors to avoid it in the US; higher dose prednisone appears to generate equivalent outcomes.

As of 2017 data from clinical trials of the ketogenic diet for treating infantile spams was inconsistent; most trials were as a second-line therapy after failure of drug treatment, and as of 2017 it had not been explored as a first line treatment in an adequately designed clinical trial.

Helmets may be used to provide protection to the head during a seizure. Some claim that seizure response dogs, a form of service dog, can predict seizures. Evidence for this, however, is poor. At present there is not enough evidence to support the use of cannabis for the management of seizures, although this is an ongoing area of research. There is tentative evidence that a ketogenic diet may help in those who have epilepsy and is reasonable in those who do not improve following typical treatments.

Continuous prophylactic antiepileptic drug (AED) treatment may not be needed particularly for children with only 1-2 or brief seizures. This is probably best reserved for children whose seizures are unusually frequent, prolonged, distressing, or otherwise significantly interfering with the child’s life. There is no evidence of superiority of monotherapy with any particular common AED.

Autonomic status epilepticus in the acute stage needs thorough evaluation for proper diagnosis and assessment of the neurologic/autonomic state of the child. "Rescue" benzodiazepines are commonly used to terminate it. Aggressive treatment should be avoided because of the risk of iatrogenic complications, including cardiovascular arrest. There is some concern that intravenous lorazepam and/or diazepam may precipitate cardiovascular arrest. Early parental treatment is more effective than late emergency treatment. Buccal midazolam is probably the first choice medication for out of hospital termination of autonomic status epilepticus which should be administered as soon as the child shows evidence of onset of its habitual autonomic seizures.

Parental education about Panayiotopoulos syndrome is the cornerstone of correct management. The traumatizing, sometimes long-lasting effect on parents is significant particularly because autonomic seizures may last for many hours compounded by physicians’ uncertainty regarding diagnosis, management, and prognosis.

A modified Atkins diet describes the long term practice of the first phase of the popular Atkins diet the so-called induction phase to reduce seizures through ketosis. In this diet the fat content of the nutrition is slightly lower than in the ketogenic diet at around 60%, the protein content is around 30% and the carbohydrate content is around 10% rendering the diet less restrictive and more compatible with the daily life compared to the ketogenic diet. Several studies show that the modified Atkins diet produces a similar or slightly lower seizure reduction to the ketogenic diet. Some physicians, especially in the USA, recommend the modified Atkins diet because they assume that patients will adhere to it on the long-term because it is more compatible with daily life and the meals are more enjoyable. It has also been concluded in another study that the diet is well tolerated and effective in hard to treat childhood epilepsy.

At the hospital, physicians follow standard protocol for managing seizures. Cluster seizures are generally controlled by benzodiazepines such as diazepam, midazolam, lorazepam or clonazepam. The use of oxygen is recommended in the United States, but in Europe it is only recommended in cases of prolonged epileptic status.

In the 1960s it was discovered that when medium-chain triglycerides (MCT) fats are metabolized in the body more ketone bodies are produced then from metabolizing any other fat. Based on this mechanism the MCT ketogenic diet a modification of the ketogenic diet was developed and it has nearly replaced the classic ketogenic diet in the USA. In the MCT ketogenic diet MCT oil is added to ketogenic meals, which allows the carbohydrate content to be increased to around 15 to 20%. This way some patients find the meals more enjoyable. The success rate of the MCT ketogenic diet does not differ from the classic ketogenic diet however not all children can tolerate the necessary large amounts of MCT oil which is also very expensive.

Treatment varies according to the type and severity of the encephalopathy. Anticonvulsants may be prescribed to reduce or halt any seizures. Changes to diet and nutritional supplements may help some patients. In severe cases, dialysis or organ replacement surgery may be needed.

Sympathomimetic drugs can increase motivation, cognition, motor performance and alertness in patients with encephalopathy caused by brain injury, chronic infections, strokes, brain tumors.

Antiepileptic drugs (AEDs) are used in most cases to control seizures, however, PCDH19 gene-related epilepsy is generally associated with early-onset development of drug resistant seizures. Existing data supports the use of “rational polypharmacy,” which consists of a step-wise addition of AEDs until a patient responds favorably or experiences intolerable adverse events. In general, as in other types of uncontrolled epilepsy, the use of drugs with different mechanisms of action appears to be more effective than combining drugs with similar mechanisms of action.

No currently marketed AEDs have been extensively studied in PCDH19 gene-related epilepsy and there is no established treatment strategy for girls diagnosed with PCDH19 gene-related epilepsy. Patients may respond well to treatment with levetiracetam and in cases of drug resistance, stiripentol, which is not approved in the U.S. but is available through the FDA Expanded Access IND process.

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.

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.

Treatment for LKS usually consists of medications, such as anticonvulsants and corticosteroids (such as prednisone), and speech therapy, which should be started early. Some patients improve with the use of corticosteroids or adrenocorticotropin hormone (ACTH) which lead researches to believe that inflammation and vasospasm may play a role in some cases of acquired epileptic aphasia.

A controversial treatment option involves a surgical technique called multiple subpial transection in which multiple incisions are made through the cortex of the affected part of the brain beneath the pia mater, severing the axonal tracts in the subjacent white matter. The cortex is sliced in parallel lines to the midtemporal gyrus and perisylvian area to attenuate the spread of the epileptiform activity without causing cortical dysfunction. There is a study by Morrell "et al." in which results were reported for 14 patients with acquired epileptic aphasia who underwent multiple subpial transections. Seven of the fourteen patients recovered age-appropriate speech and no longer required speech therapy. Another 4 of the 14 displayed improvement of speech and understanding instructions given verbally, but they still required speech therapy. Eleven patients had language dysfunction for two or more years. Another study by Sawhney "et al." reported improvement in all three of their patients with acquired epileptic aphasia who underwent the same procedure.

Various hospitals contain programs designed to treat conditions such as LKS like the Children's Hospital Boston and its Augmentative Communication Program. It is known internationally for its work with children or adults who are non-speaking or severely impaired. Typically, a care team for children with LKS consists of a neurologist, a neuropsychologist, and a speech pathologist or audiologist. Some children with behavioral problems may also need to see a child psychologist and a psychopharmacologist. Speech therapy begins immediately at the time of diagnosis along with medical treatment that may include steroids and anti-epileptic or anti-convulsant medications.

Patient education has also proved to be helpful in treating LKS. Teaching them sign language is a helpful means of communication and if the child was able to read and write before the onset of LKS, that is extremely helpful too.

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.

Treating the underlying cause of the disorder may improve or reverse symptoms. However, in some cases, the encephalopathy may cause permanent structural changes and irreversible damage to the brain. These permanent deficits can be considered a form of stable dementia. Some encephalopathies can be fatal.

The treatment of PRES dependent on its cause. Anti-epileptic medication may also be appropriate.

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.

Currently, there is no cure for porencephaly because of the limited resources and knowledge about the neurological disorder. However, several treatment options are available. Treatment may include physical therapy, rehabilitation, medication for seizures or epilepsy, shunt (medical), or neurosurgery (removal of the cyst). According to the location, extent of the lesion, size of cavities, and severity of the disorder, combinations of treatment methods are imposed. In porencephaly patients, patients achieved good seizure control with appropriate drug therapy including valproate, carbamazepine, and clobazam. Also, anti-epileptic drugs served as another positive method of treatment.

In the past, treatment options were limited to supportive medical therapy. Nowadays neonatal encephalopathy is treated using hypothermia therapy.

The onset of Wernicke's encephalopathy is considered a medical emergency, and thus thiamine administration should be initiated immediately when the disease is suspected. Prompt administration of thiamine to patients with Wernicke's encephalopathy can prevent the disorder from developing into Wernicke–Korsakoff syndrome, or reduce its severity. Treatment can also reduce the progression of the deficits caused by WKS, but will not completely reverse existing deficits. WKS will continue to be present, at least partially, in 80% of patients. Patients suffering from WE should be given a minimum dose of 500 mg of thiamine hydrochloride, delivered by infusion over a 30-minute period for two to three days. If no response is seen then treatment should be discontinued but for those patients that do respond, treatment should be continued with a 250 mg dose delivered intravenously or intramuscularly for three to five days unless the patient stops improving. Such prompt administration of thiamine may be a life-saving measure. Banana bags, a bag of intravenous fluids containing vitamins and minerals, is one means of treatment.