Treatment plans will vary depending on the severity of the condition and its evidences in each patient.

Areas that will probably need to be evaluated and assessed include speech, vision, hearing and EEG. Treatment measures may include physical therapy, occupational therapy, Speech therapy, anti-seizure drugs and orthotic devices. Surgery may be needed to assuage spastic motor problems. Various supportive measures such as joint contractures that could prevent complications.

Genetic counseling may also be recommended

Most patients suffering from KTS have epilepsy that is resistant to anti-epileptic agents. Some patients showed a partial response to treatment, but very few were able to stop their epilepsy through treatment. One case was responsive to treatment using Phenobartbital and vigabatrin which are both anti-epileptic agents. Spasticity can be treated with baclofen, but not all patients are responsive to the treatment.

Many children affected by alternating hemiplegia also suffer from epilepsy. Seizures may occur during an attack but more often occur between attacks. Anti-epilepsy drugs are given to prevent or lessen the seizures, but the drugs often don’t work and have severe side effects that require the patient to discontinue use. Flunarizine, which blocks calcium channels, is an antiepilepsy drugs used in 50% of patients, and has been shown to shorten the duration of attacks as well as reducing the severity of the attacks. While Flunarizine does not stop the attacks, it is most common drug prescribed to treat those suffering from alternating hemiplegia.

Dennie–Marfan syndrome is a syndrome in which there is association of spastic paraplegia of the lower limbs and mental retardation in children with congenital syphilis. Both sexes are affected, and the onset of the disease can be acute or insidious, with slow progression from weakness to quadriplegia. Epilepsy, cataract, and nystagmus may be also be found.

The syndrome was described by Charles Clayton Dennie in 1929, and Antoine Marfan in 1936.

Sleep is also used as a management technique. An early indication of an episode is tiredness so medication such as melatonin or Buccal midazolam can be administered to induce sleep and avoid the episode.

Those suffering from alternating hemiplegia are often underweight and with the help of dietitians, a meal plan should be developed for times of attack when consumption of food may be difficult.

The syndrome primarily affects young males. Preliminary studies suggest that prevalence may be 1.8 per 10,000 live male births. 50% of those affected do not live beyond 25 years of age, with deaths attributed to the impaired immune function.

No specific treatment is known that would prevent, slow, or reverse HSP. Available therapies mainly consist of symptomatic medical management and promoting physical and emotional well-being. Therapeutics offered to HSP patients include:

- Baclofen – a voluntary muscle relaxant to relax muscles and reduce tone. This can be administered orally or intrathecally. (Studies in HSP )

- Tizanidine – to treat nocturnal or intermittent spasms (studies available )

- Diazepam and clonazepam – to decrease intensity of spasms

- Oxybutynin chloride – an involuntary muscle relaxant and spasmolytic agent, used to reduce spasticity of the bladder in patients with bladder control problems

- Tolterodine tartate – an involuntary muscle relaxant and spasmolytic agent, used to reduce spasticity of the bladder in patients with bladder control problems

- Botulinum toxin – to reduce muscle overactivity (existing studies for HSP patients)

- Antidepressants (such as selective serotonin re-uptake inhibitors, tricyclic antidepressants and monoamine oxidase inhibitors) – for patients experiencing clinical depression

- Physical therapy – to restore and maintain the ability to move; to reduce muscle tone; to maintain or improve range of motion and mobility; to increase strength and coordination; to prevent complications, such as frozen joints, contractures, or bedsores.

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.

The ketogenic diet is a high fat, low carbohydrate diet reserved for intractable childhood epilepsies. There are no published reports on the use of the ketogenic diet in patients with ring chromosome 20 syndrome. However, its efficacy and safety are well established in other difficult to control epilepsy syndromes.

No treatment is available to cure or slow down the progression of aspartylglucosaminuria. Bone marrow transplants have been conducted in hope that the bone marrow will produce the missing enzyme. The results of the tests thus far have shown to be inconclusive.

There is no known prevention of spinocerebellar ataxia. Those who are believed to be at risk can have genetic sequencing of known SCA loci performed to confirm inheritance of the disorder.

In 1974, Dr. Tönz brought an infant suffering from a fatal brain disease to the attention of Alfried Kohlschütter. The infant's symptoms included loss of motor skills, mental disability, epilepsy, and missing enamel. The infant also showed signs of myelin breakdown and did not produce the same amount of sweat as a normal person which resulted in the development of the term amelo-cerebro-hypohydrotic syndrome. A connection between the neurological and enamel symptoms is unknown.

Since ear infections and respiratory infections are common for children diagnosed with aspartylglucosaminuria, it is best to have regular checkups for both the ears and the respiratory tract.

Extreme sensitivity to the sun’s rays may develop; the best way to protect an individual diagnosed with aspartylglucosaminuria is to have them wear sunglasses, hats or caps to protect their eyes.

Epilepsy and insomnia can both be treated with medication.

It will be beneficial to children who are diagnosed with AGU to receive an education from a school with special teaching.

Treatment of Ramsay Hunt Syndrome Type 1 is specific to individual symptoms. Myoclonus and seizures may be treated with drugs like valproate.

Some have described this condition as difficult to characterize.

Bilateral frontoparietal polymicrogyria (BFPP) is a genetic disorder with autosomal recessive inheritance that causes a cortical malformation. Our brain has folds in the cortex to increase surface area called gyri and patients with polymicrogyri have an increase number of folds and smaller folds than usual. Polymicrogyria is defined as a cerebral malformation of cortical development in which the normal gyral pattern of the surface of the brain is replaced by an excessive number of small, fused gyri separated by shallow sulci and abnormal cortical lamination. From ongoing research, mutation in GPR56, a member of the adhesion G protein-coupled receptor (GPCR) family, results in BFPP. These mutations are located in different regions of the protein without any evidence of a relationship between the position of the mutation and phenotypic severity. It is also found that GPR56 plays a role in cortical pattering.

The treatment of 2-Hydroxyglutaric aciduria is based on seizure control, the prognosis depends on how severe the condition is.

MECP2 Duplication Syndrome (M2DS) is a rare disease that is characterized by severe intellectual disability and impaired motor function. It is an X-linked genetic disorder caused by the overexpression of MeCP2 protein.

Although HSP is a progressive condition, the prognosis for individuals with HSP varies greatly. It primarily affects the legs although there can be some upperbody involvement in some individuals. Some cases are seriously disabling while others are less disabling and are compatible with a productive and full life. The majority of individuals with HSP have a normal life expectancy.

Because pachygyria is a structural defect no treatments are currently available other than symptomatic treatments, especially for associated seizures. Another common treatment is a gastrostomy (insertion of a feeding tube) to reduce possible poor nutrition and repeated aspiration pneumonia.

There is currently no specific treatment for megalencephaly, however periodic head measurements may be assessed to determine the rate of brain growth.

Those individuals who develop neurological disorders may be prescribed anti-epileptic drugs for seizures. Studies have shown that reducing epilepsy can increase cell apoptosis and reduce the proliferation of neurons that ultimately leads to brain overgrowth.

It is named for James Ramsay Hunt who first described a form of progressive cerebellar dyssynergia associated with myoclonic epilepsy in 1921.

Since there are very few treatment methods focused on managing megalencephaly, future research is targeted at inhibiting mutation of the pathway. However, this next step could be met with several complications as understanding the underlying mechanism of the mutation is a difficult task. The genetic coding that initiates a single mutation is sporadic and patterns are hard to detect in many cases.

Even thought very little research has been done to create inhibitors of the PI3K-AKT pathway, several pharmaceutical companies have begun to focus their interests in designing a prevention method for this purpose.

Long term management is by use of anticonvulsant medication, principally valproate, stiripentol, topiramate or clobazam. Ketogenic diet has also been found useful in certain cases

Management of breakthrough seizures is by benzodiazepine such as midazolam.

Treatment is surgical with attention to form and volume. Surgery usually takes place before the age of one since it has been reported that the intellectual outcome is better.

Only symptomatic treatment for the management of disturbances can be indicated for affected individuals. The genetic origin of this disease would indicate gene therapy holds the most promise for future development of a cure. But at this time no specific treatments for Flynn–Aird syndrome exist.