Depending on subtype, many patients find that acetazolamide therapy is useful in preventing attacks. In some cases, persistent attacks result in tendon shortening, for which surgery is required.

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.

Current available treatment is limited to treating the symptoms, not the cause. Seizure frequency can be regulated by the use of drugs such as Clonazepam (or other benzodiazepines) and Sodium Valproate. Clonazepam functions by increasing GABA activity at the GABA receptor. GABA is an inhibitory neurotransmitter and therefore, its increased activity hyperpolarizes cells. Clonazepam has been effective in minimising seizure activity, especially during puberty. Sodium valproate prevents the depolarization of the cell by blocking sodium ion channels and inhibitory GABA enzymes. Both of these anticonvulsants lead to depression of the central nervous system.

The most common drug used to treat AHC is flunarizine. Flunarizine functions by acting as a calcium channel blocker. Other drugs, in order of frequency of use are benzodiazepines, carbamazapine, barbiturates, and valproic acid. Flunarizine is prescribed for the purpose of reducing the severity of AHC attacks and the number of episodes, though it rarely stops attacks altogether. Minimizing the attacks may help reduce damage to the body from hemiplegic attacks and improve long-term outcomes as far as mental and physical disabilities are concerned.

Experts differ in their confidence in flunarizine's effectiveness. Some studies have found it to be very effective in reducing the duration, severity, and frequency of hemiplegic attacks. It is generally considered the best treatment available, but this drug is thought by some to be of little benefit to AHC patients. Many patients suffer adverse effects without seeing any improvement. Flunarizine also causes problems because it is difficult for patients to obtain, as it is not readily available in the United States.

Neonatal seizures are often controlled with phenobarbital administration. Recurrent seizures later in life are treated in the standard ways (covered in the main epilepsy article). Depending on the severity, some infants are sent home with heart and oxygen monitors that are hooked to the child with stick on electrodes to signal any seizure activity. Once a month the monitor readings are downloaded into a central location for the doctor to be able to read at a future date. This monitor is only kept as a safeguard as usually the medication wards off any seizures. Once the child is weaned off the phenobarbital, the monitor is no longer necessary.

Non-selective beta-blockers are the most effective in reducing the frequency and severity of PSH episodes. They help decrease the effect of circulating catecholamines and lower metabolic rates, which are high in patients during PSH episodes. Beta-blockers also help in reducing fever, diaphoresis, and in some cases dystonia. Propanolol is a common beta-blocker administered due to the fact that it penetrates the blood-brain barrier relatively well. Typically it is administered in doses of twenty milligrams to sixty milligrams every four to six hours in the treatment of PSH.

The two most common medications used in the treatment of paroxysmal sympathetic hyperactivity are morphine sulfate and beta-blockers. Morphine is useful in helping halt episodes that have started to occur. Beta-blockers are helpful in preventing the occurrence of 'sympathetic storms'. Other drugs that have been used and have in some cases been helpful are dopamine agonists, other various opiates, benzodiazepines, clonidine, and baclofen. Chlorpromazine and haloperidol, both dopamine antagonists, in some cases have worsened PSH symptoms. These drugs are in use currently for treatment; exact pathways are not known and wide-range helpfulness is speculative.

Currently, no treatment slows the neurodegeneration in any of the neuroacanthocytosis disorders. Medication may be administered to decrease the involuntary movements produced by these syndromes. Antipsychotics are used to block dopamine, anticonvulsants treat seizures and botulinum toxin injections may control dystonia. Patients usually receive speech, occupational and physical therapies to help with the complications associated with movement. Sometimes, physicians will prescribe antidepressants for the psychological problems that accompany neuroacanthocytosis. Some success has been reported with Deep brain stimulation.

Mouthguards and other physical protective devices may be useful in preventing damage to the lips and tongue due to the orofacial chorea and dystonia typical of chorea acanthocytosis.

Current research at the University of Utah is investigating whether sodium oxybate, also known as Gamma-Hydroxybutyric acid is an effective treatment for AHC. Thus far, only a small number of patients have been sampled, and no conclusive results are yet available. While some success has been had thus far with the drug, AHC patients have been known to respond well initially to other drugs, but then the effectiveness will decline over time. Currently, sodium oxybate is used as a narcolepsy-cataplexy treatment, though in the past it has been used controversially in nutritional supplements. This drug was chosen to test because of a possible link between the causes of narcolepsy-cataplexy and AHC.

Almost all patients respond positively to antiepileptic (anticonvulsant) drugs. One of the drugs most often mentioned in the literature is carbamazepine, and is the most widely used drug for treating PKD. Other anticonvulsants like valproic acid, phenytoin and clonazepam are common alternatives. Other categories of drugs have also been used, such as dopamine affecting drugs like Levodopa or Tetrabenazine. Individuals with the disorder can also modify their behavior to lessen their attacks without the influence of drug therapy. For example, decreasing stress to avoid precipitants can help patients decrease the number of attacks. In addition, avoiding any sudden movements can also prevent an attack. In order to prevent an attack, some individuals use their auras as a warning, while others purposefully perform slow gestures or movements prior to a triggering movement. Many, if not most, individuals end up growing out of the attacks with age, even without medicinal therapy, but some patients will go back to having attacks after a period of remission. In regards to secondary PKD, treatment of the primary condition can lessen the PKD attacks in those individuals.

PKD patients usually show a good response to anticonvulsants. Most commonly used medications are sodium blockers, carbamazepine and phenytoin. During a drug-testing study, patients reported a decreasing response to the latter use of anticonvulsants and switched to carbamazepine or phenytoin. Refraining from established triggers such as sudden movement has been shown to lessen attacks occurrences. Avoidance of predisposing factors such as stress, excitement, and fatigue also help manage attacks.

Most pharmacological treatments work poorly, but the best treatment is a low dosage of clonazepam, a muscle relaxant. Patients may also benefit from other benzodiazepines, phenobarbital, and other anticonvulsants such as valproic acid. Affected individuals have reported garlic to be effective for softening the attacks, but no studies have been done on this.

Treatment for PKND is more difficult than other Paroxysmal Dyskinesias. The majority of patients experience some relief from low dosages of clonazepam, a muscle relaxant and anticonvulsant. Similar to PKD, avoidance of stress, excitement, and fatigue will lower the frequency of PNKD attacks. Many patients also avoid known methyglyoxal containing foods and beverages such as alcohol, coffee, tea, and chocolate.

As there appeared to be a connection with PED and mutated GLUT1 transporters a possible treatment was looking at changing patients diets. A common treatment for another disorder with a mutated GLUT1 transporter is the ketogenic diet. The diet is a strict 3:1 ratio of fat (3) to protein and carbohydrates (1). This diet is thought to help restore the unbalance created by the decreased amount of glucose in the brain caused by the faulty GLUT1 transporter. This diet was administered to three patients who had been screened and found to have mutation in their SLC2A genes coding for GLUT1 and were experiencing PED symptoms. All three showed benefit from this treatment and a reduction in their PED episodes. They were able to exercise and run long distances for the first time in their lives. No other studies have been performed using this diet as many patients feel the advantages of the diet do not outweigh its disadvantages.

As some cases have noted that patients were able to alleviate or lessen their PED attacks with a sugary snack, another diet that was tried on patients was one rich in carbohydrates with additional frequent carbohydrate-containing snacks. Four patients with reported PED symptoms were put on this diet but no observable improvements were noted and in fact one patient even complained of worsening symptoms.

Additionally it has been observed that levodopa may reduce some symptoms associated with PED. This may demonstrate that PED is a precursor to Parkinson's disease. Acetazolamide was beneficial to some patients, but also worsened symptoms in others. Additionally, a modified version of the Atkin's diet helped to regulate glucose levels in the CSF. Patients with PED associated with insulinomas appeared to have symptoms resolved after consuming sugary drinks. Currently, there are no drugs that are particularly useful in completely curing all symptoms.

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.

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.

Patients with ICOE-G need prophylactic treatment mainly with carbamazepine or other antiepileptic drugs licensed for focal seizures. A slow reduction in the dose of medication 2 or 3 years after the last visual or other minor or major seizure should be advised, but if visual seizures reappear, treatment should be restored.

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

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).

No known treatment for BPT currently exists. However, the condition it is self-limiting and resolves after about eighteen months.

There is currently no cure for Costeff syndrome. Treatment is supportive, and thus focuses on management of the symptoms. The resulting visual impairment, spasticity, and movement disorders are treated in the same way as similar cases occurring in the general population.

Carbamazepine is at least partly effective at reducing the number or severity of attacks in the majority of PEPD patients. High doses of this drug may be required, perhaps explaining the lack of effect in some individuals. While other anti-epileptic drugs, gabapentin and topiramate, have limited effect in some patients, they have not been shown to be generally effective. Opiate derived analgesics are also largely ineffective, with only sporadic cases of beneficial effect.

There are several different treatment approaches to dealing with athetosis. The most common methods are the use of drugs, surgical intervention, and retraining movements of the afflicted person. It is suggested that training a person to relearn movements can be helpful in select situations. Though, generally, this type of treatment will not work, in certain cases it can be found to be very helpful in treating the symptom of athetosis.

Drugs can also be used in the treatment of athetosis, however their collective effectiveness is not very convincing. There is not a single drug that is a standard among treatment. Many different medicines can be used, including:

- Artane

- Cogentin

- Curare, though not practical due to respiratory paralysis

- Tetrabenazine

- Haloperidol

- Thiopropazate

- Diazepam

Most instances of drug use where the symptoms seem to be lessened tend to be in more mild cases of athetosis.

Treatment by surgical intervention can obviously have the most immediate impact, again however, it is not a cure-all. In patients that have cerebral palsy as the cause of their athetosis, it has been demonstrated that a subthalamotomy tends to help relieve the extent of athetosis in approximately half of patients. Additionally, late 19th and early 20th century surgical accounts state that athetosis can be relieved by the removal of a part of the cerebral motor cortex or by cutting a part of the posterior spinal roots. Patients who undergo surgical treatment to relieve the athetosis often see significant improvement in the control of their limbs and digits. While surgery is often very beneficial in the short term and can produce near immediate results, in the long term it has been seen that its effects are not incredibly long lasting.

As athetosis is relatively difficult to treat, efforts are being made to help those with the condition live and perform tasks more effectively and more efficiently. One such example of work that has been recently undertaken is a project to help those affected with athetosis to use a computer with more ease. Software for the control of the computer uses joysticks that perform linear filtering to aid in control.

An additional possible treatment option for those afflicted with the symptom is neurostimulation. Studies have begun, and in cerebral palsy patients affected with dystonia-choreoathetosis, it has been demonstrated that neurostimulation has been an effective treatment in lessening symptoms in patients. There has not been a tremendous amount of experimentation, though, in this as a possible treatment option.

"See the equivalent section in the main migraine article."

People with FHM are encouraged to avoid activities that may trigger their attacks. Minor head trauma is a common attack precipitant, so FHM sufferers should avoid contact sports. Acetazolamide or standard drugs are often used to treat attacks, though those leading to vasoconstriction should be avoided due to the risk of stroke.