Like many other types of seizures, gelastic seizures are hard to control for an extended period of time. The best outlook is for children suffering the seizures due to a benign tumor in their hypothalamus. The removal of these tumors can be effective not only for the frequency of the seizures, but also the behavioral and cognitive symptoms that come along with the syndrome. Cases have also been described where that antiepileptic drugs have stopped seizures fully.

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 the United States, about 40 cases of SE occur annually per 100,000 people. This includes about 10–20% of all first seizures.

Dravet syndrome is a severe form of epilepsy. It is a rare genetic disorder that affects an estimated 1 in every 20,000–40,000 births.

Epilepsy is a relatively common disorder, affecting between 0.5-1% of the population, and frontal lobe epilepsy accounts for about 1-2% of all epilepsies. The most common subdivision of epilepsy is symptomatic partial epilepsy, which causes simple partial seizures, and can be further divided into temporal and frontal lobe epilepsy. Although the exact number of cases of frontal lobe epilepsy is not currently known, it is known that FLE is the less common type of partial epilepsy, accounting for 20-30% of operative procedures involving intractable epilepsy. The disorder also has no gender or age bias, affecting males and females of all ages. In a recent study, the mean subject age with frontal lobe epilepsy was 28.5 years old, and the average age of epilepsy onset for left frontal epilepsy was 9.3 years old whereas for right frontal epilepsy it was 11.1 years old.

These syndromes are childhood absence epilepsy, epilepsy with myoclonic absences, juvenile absence epilepsy and juvenile myoclonic epilepsy. Other proposed syndromes are Jeavons syndrome (eyelid myoclonia with absences), and genetic generalised epilepsy with phantom absences.

These types of seizures are also known to occur to patients suffering with porphyria and can be triggered by stress or other porphyrin-inducing factors.

Treatment of patients with absence seizures only is mainly with valproic acid or ethosuximide, which are of equal efficacy controlling absences in around 75% of patients. Lamotrigine monotherapy is less effective, with nearly half of the patients becoming seizure free. This view has been recently confirmed by Glauser et al. (2010), who studied the effects of ethosuximide, valproic acid, and lamotrigine in children with newly diagnosed childhood absence epilepsy. Drug dosages were incrementally increased until the child was free of seizures, the maximal allowable dose was reached, or a criterion indicating treatment failure was met. The primary outcome was freedom from treatment failure after 16 weeks of therapy; the secondary outcome was attentional dysfunction. After 16 weeks of therapy, the freedom-from-failure rates for ethosuximide and valproic acid were similar and were higher than the rate for lamotrigine. There were no significant differences between the three drugs with regard to discontinuation because of adverse events. Attentional dysfunction was more common with valproic acid than with ethosuximide.

If monotherapy fails or unacceptable adverse reactions appear, replacement of one by another of the three antiepileptic drugs is the alternative. Adding small doses of lamotrigine to sodium valproate may be the best combination in resistant cases.

While ethosuximide is effective in treating only absence seizures, valproic acid is effective in treating multiple seizure types including tonic-clonic seizure and partial seizure, as such it may be a better choice if a patient is exhibiting multiple types of seizures.

Similarly, lamotrigine treats multiple seizure types including partial seizures and generalized seizures, therefore it is also an option for patients with multiple seizure types. Clonazepam (Klonopin, Rivotril) is effective in the short term but is not generally recommended for treatment of absence seizure because of the rapid development of tolerance and high frequency of side effects.

Deep brain stimulation of the anterior nuclei of the thalamus is approved for DRE in some countries in Europe, but has been and continues to only be used in a very few patients. After 5 years of DBS a seizure reduction of 69% and a 50%-responder rate of 68% was reported in a randomized-double blinded trial. The rate of serious device related events was 34% in this study.

Responsive neurostimulation (RNS) is approved for DRE in the USA and involves stimulation directly to 1 or 2 seizure foci when abnormal electrocorticographic activity is detected by the devices software. After 2 years of RNS a seizure reduction of 53% was reported in a randomized-double blinded trial as well as a rate of serious device related events of 2.5%.

Transcutaneous vagus nerve stimulation (tVNS) is approved for DRE in some European countries and involves externally stimulating the auricular branch of the vagus nerve in the ear. tVNS failed to demonstrate efficacy in a first randomized-double blinded trial: responder rates did not differ between active and control groups potentially indicating a placebo effect behind the 34% seizure reduction seen in the patients who completed the full follow-up period.

In Europe the ketogenic diet is the diet that is most commonly recommended by doctors for patients with epilepsy. In this diet the ratio of fat to carbohydrates and proteins is 4:1. That means that the fat content of the consumed food must be around 80%, the protein content must be around 15%, and the carbohydrate content must be around 5%. For comparison the average western diet consists of a carbohydrate content of over 50%. After one year on the ketogenic diet the success rate (seizure reduction over 50%) is between 30 and 50% and the dropout rate is around 45%. Although the ketogenic diet can be very effective some families report that it's not compatible with daily life on the long run because it's too restrictive as bread pasta and sweets are forbidden in the ketogenic diet. In puberty with increasing autonomy it can be difficult for adolescents to follow the diet strictly. For this reason a fat ratio of 3: 1 instead of 4: 1 can be recommended to make meals more palatable. Side effects of the ketogenic diet can be constipation, tiredness and after a long term diet, in one out of 20 patients, kidney stones.

Gelastic seizures are usually not responsive to pharmacotherapy. They can produce secondary seizure characteristics which may respond to medications or surgery. These options are not a guaranteed cure, and depend primarily on the individual patient’s pathology.

The treatment depends on the cause of the seizures. If the seizures are caused by a tumor, surgical removal can be attempted. However, surgical removal is not always an immediate cure, and there can be complications. Complications can include cerebral infarcts, and cognitive deterioration. Hormonal treatment can be attempted to help individuals with precocious puberty. Anti-epileptic drugs could be an option as well depending on the patient’s criteria. These drugs could include carbamazepine, clobazam, lamotrigine, levetiracetam, oxcarbazepine and topiramate. However, usually none of these medications are capable of stopping the seizures from occurring, and like any medication, there may be undesirable side effects. There is also a specialized form of radiotherapy that may be an option depending on the tumor type and location. Once again, there are very few areas in the world that offer this treatment. Gamma knife radiosurgery can be the treatment of choice when it comes to hypothalamic hamartomas. It is a low risk option due to its lower frequency of neurological deficits. It is recommended for patients with tumors that don’t come into contact with the optic chiasm.

Although the theory is controversial, there is a link between febrile seizures (seizures coinciding with episodes of fever in young children) and subsequent temporal lobe epilepsy, at least epidemiologically.

The causes of TLE include mesial temporal sclerosis, traumatic brain injury, brain infections, such as encephalitis and meningitis, hypoxic brain injury, stroke, cerebral tumours, and genetic syndromes. Temporal lobe epilepsy is not the result of psychiatric illness or fragility of the personality.

Over the past decade or so, researchers have been attempting to discover less invasive, safer and more efficient technologies that enable surgeons to remove epileptogenic focal zones without causing any damage to neighboring cortical areas. One such technology that has emerged and has great promise, is the use of gamma knife radiosurgery to either excise a brain tumor or repair a vascular malformation.

In Gamma Knife radiosurgery, intersecting gamma radiation beams are applied directly to the tumor site or vascular malformation site that had been established using neuroimaging. Although each beam itself is not strong enough to damage brain tissue, when the beams interesect they are strong enough to destroy the specific brain tissue that is to be excised. This process is extremely efficient and entirely non-invasive and is therefore much safer than actual neurosurgery itself.

Recently researchers and surgeons alike have begun to use Gamma Knife radiosurgery to treat cases of epilepsy by removing tumors responsible for causing the seizures. The early success rates in being able to alleviate seizures seem to be similar to those of temporal resective surgery however Gamma Knife radiosurgery has less associated risk factors. Current research on this topic is aimed at improving the technique in order to increase success rates as well as developing non-invasive forms of physiologic monitoring in order to determine the epileptogenic focus conclusively.

ADNFLE is a partial epilepsy disorder characterized by brief violent seizures during sleep. Seizures are complex, consisting of arm and leg movements, fist clenching, and vocalizations such as yelling and moaning. These seizures often occur in clusters and can first manifest in childhood. Diagnosis is often initially incorrectly made as nightmares, night terrors, parasomnias and various psychiatric disorders.

Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is an epileptic disorder that causes frequent violent seizures during sleep. These seizures often involve complex motor movements, such as hand clenching, arm raising/lowering, and knee bending. Vocalizations such as shouting, moaning, or crying are also common. ADNFLE is often misdiagnosed as nightmares. Attacks often occur in clusters and typically first manifest in childhood. There are four known loci for ADNFLE, three with known causative genes. These genes, "CHRNA4", "CHRNB2", and "CHRNA2", encode various nicotinic acetylcholine receptor α and β subunits.

PME accounts for less than 1% of epilepsy cases at specialist centres. The incidence and prevalence of PME is unknown, but there are considerable geography and ethnic variations amongst the specific genetic disorders. One cause, Unverricht Lundborg Disease, has an incidence of at least 1:20,000 in Finland.

Seizures in Dravet syndrome can be difficult to manage but may be reduced by anticonvulsant medications such as clobazam, stiripentol, topiramate and valproate. Because the course of the disorder varies from individual to individual, treatment protocols may vary. A diet high in fats and low in carbohydrates may also be beneficial, known as a ketogenic diet. Although diet adjustment can help, it does not eliminate the symptoms. Until a better form of treatment or cure is discovered, those with this disease will have myoclonic epilepsy for the rest of their lives.

Certain anticonvulsant drugs that are classed as Sodium Channel Blockers are now known to make seizures worse in most Dravet patients. These drugs include carbamazepine, gabapentin, lamotrigine, and phenytoin.

Treatments include cognitive rehabilitation through psychomotor and speech therapy. In addition, valproate is often administered to prevent recurrence of febrile seizures and benzodiazapine is used for long lasting seizures, but these treatments are usually insufficient.

Stiripentol was the only drug for which a double-blind placebo trial was performed and this drug showed efficacy in trials. It acts as a GABAergic agent and as a positive allosteric modulator of GABA receptor. Stiripentol, can improve focal refractory epilepsy, as well as Dravet's syndrome, supplemented with clobazam and valproate was approved in Europe in 2007 as a therapy for Dravet syndrome and has been found to reduce overall seizure rate by 70%. In cases with more drug resistant seizures, topiramate and the ketogenic diet are used as alternative treatments.

Cannabidiol (CBD) has received orphan drug status in the United States, for treatment of Dravet syndrome which will allow it to be studied.

Seizure frequency is reduced to four to six seizures per year. By this time, they are mentally and physically incapable to live without assistance due to the total mental degradation. Life expectancy is at least 50 years of age, which is shorter than the average worldwide age of 70.

Myoclonic seizures involve brief involuntary muscle twitching, and may become frequent enough to be disabling. Tonic-clonic seizures have two phases: the tonic phase may last a few seconds and involves the muscles tensing, and may lead to the person falling down; the clonic phase involves a convulsion of rapidly alternating muscle tensing and relaxing. Neurological dysfunction includes difficulty coordinating muscle movements (ataxia) and a decline in cognitive ability (dementia).

Life expectancy is only moderately affected by NE because the rate of disease progression is slow. Patients usually survive past 40-50 years of age.

Episodic ataxia (EA) is an autosomal dominant disorder characterized by sporadic bouts of ataxia (severe discoordination) with or without myokymia (continuous muscle movement). There are seven types recognised but the majority are due to two recognized entities. Ataxia can be provoked by stress, startle, or heavy exertion such as exercise. Symptoms can first appear in infancy. There are at least 6 loci for EA, of which 4 are known genes. Some patients with EA also have migraine or progressive cerebellar degenerative disorders, symptomatic of either familial hemiplegic migraine or spinocerebellar ataxia. Some patients respond to acetazolamide though others do not.

Also known as periodic vestibulocerebellar ataxia, type-4 episodic ataxia (EA4) is an extremely rare form of episodic ataxia differentiated from other forms by onset in the third to sixth generation of life, defective smooth pursuit and gaze-evoked nystagmus. Patients also present with vertigo and ataxia. There are only two known families with EA4, both located in North Carolina. The locus for EA4 is unknown.

Two international research studies are currently underway. The International Genetic Study done with the Spinner Laboratory at The Children's Hospital of Philadelphia studies the ring 20 chromosome at the molecular level. The Clinical Research Study collects clinical information from parents to create a database of about the full spectrum of patients with ring chromosome 20 syndrome.

PDE is inherited in an autosomal recessive manner and is estimated to affect around 1 in 400,000 to 700,000 births, though one study conducted in Germany estimated a prevalence of 1 in 20,000 births. The ALDH7A1 gene encodes for the enzyme antiquitin or α -aminoadipic semialdehyde dehydrogenase, which is involved with the catabolism of lysine.

Limited data is available for the long-term prognosis of ring chromosome 20 syndrome since only over 60 patients with this syndrome have been reported in published literature. Optimal control of seizures appears to be the determining factor, but early diagnosis and a comprehensive management plan with multidisciplinary support is also thought be to be important.