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.

Response to treatment is variable and the long-term and functional outcome is unknown. To provide a basis for improving the understanding of the epidemiology, genotype/phenotype correlation and outcome of these diseases their impact on the quality of life of patients, and for evaluating diagnostic and therapeutic strategies a patient registry was established by the noncommercial International Working Group on Neurotransmitter Related Disorders (iNTD).

Treatment is limited. Drugs can alleviate the symptoms, such as sleep difficulties and epilepsy. Physiotherapy helps affected children retain the ability to remain upright for as long as possible, and prevents some of the pain.

Recent attempts to treat INCL with cystagon have been unsuccessful.

In most cases, between the age of 2 and 4 oculomotor signals are present. Between the age of 2 and 8, telangiectasias appears. Usually by the age of 10 the child needs a wheel chair. Individuals with autosomal recessive cerebellum ataxia usually survive till their 20s; in some cases individuals have survived till their 40s or 50s.

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.

Kufor–Rakeb syndrome is an autosomal recessive disorder of juvenile onset also known as Parkinson disease-9 (PARK9).

Symptoms include supranuclear gaze palsy, spasticity, and dementia.

It can be associated with "ATP13A2". It is named after Kufr Rakeb in Irbid, Jordan.

The disease is named after Dr. Masaya Segawa, who provided an early clinical description.

There is currently no treatment or cure for CARASIL. Most frequently, a combination of supportive care and medications to prevent the occurrence of stroke are recommended.

Treatment of ALS2-related disorders includes physical therapy and occupational therapy to promote mobility and independence and use of computer technologies and devices to facilitate writing and voice communication.

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.

There is currently no cure or standard procedure for treatment. A bone marrow transplant has been attempted on a child, but it made no improvement. Hydrocephalus may be seen in younger patients and can be relieved with surgery or by implanting a shunt to relieve pressure.

Parkinson-plus syndromes are usually more rapidly progressive and less likely to respond to antiparkinsonian medication than PD. However, the additional features of the diseases may respond to medications not used in PD.

Current therapy for Parkinson-plus syndromes is centered around a multidisciplinary treatment of symptoms.

These disorders have been linked to pesticide exposure.

Research is underway worldwide to increase scientific understanding of these disorders as well to identify prevention and treatment methods. Known genetic mutations provide a basis for studying some of the conditions.

The recurrence of DOOR in siblings and the finding of DOOR syndrome in a few families with consanguinity suggest that the condition is an autosomal recessive genetic condition. Mutations in TBC1D24 have been identified in 9 families.

Infantile neuronal ceroid lipofuscinoses (INCL) or Santavuori disease or Hagberg-Santavuori disease or Santavuori-Haltia disease or Infantile Finnish type neuronal ceroid lipofuscinosis or Balkan disease is a form of NCL and inherited as a recessive autosomal genetic trait. The disorder is progressive, degenerative and fatal, extremely rare worldwide – with approximately 60 official cases reported by 1982, perhaps 100 sufferers in total today – but relatively common in Finland due to the local founder effect.

A painkiller available in several European countries, Flupirtine, has been suggested to possibly slow down the progress of NCL, particularly in the juvenile and late infantile forms. No trial has been officially supported in this venue, however. Currently the drug is available to NCL families either from Germany, Duke University Medical Center in Durham, North Carolina, and the Hospital for Sick Children in Toronto, Ontario.

There is currently no cure for the disease but treatments to help the symptoms are available.

For early Unverricht–Lundborg disease patients, the disease would begin to progress early and lack of effective treatment meant a quick progression. In many cases the patient would require a wheelchair for mobility, and would die at a young age.

However, increased knowledge about the disease and improved treatment and medication has led to a dramatic improvement in prognosis for individuals with ULD. Antiepileptic drugs reduce the occurrence of seizures and myoclonus, which leads to a decrease in the damage caused in the brain due to seizures and the body due to falls resulting from the seizures. As a result, individuals with Unverricht–Lundborg disease are now much less likely to end up in a wheelchair, which eliminates the chance of complications involved with being a wheelchair user. All these factors have increased the outlook for patients. Due to the progressive nature of the disease, depression is prevalent, but support of family and friends as well as proper treatment can help. While early patients with ULD had a life expectancy of around 24 years, there have recently been reported cases of individuals living to near-normal ages.

Prognosis strongly depends on which subtype of disease it is. Some are deadly in infancy but most are late onset and mostly manageable.

Because lack of sialic acid appears to be part of the pathology of IBM caused by GNE mutations, clinical trials with sialic acid supplements, and with a precursor of sialic acid, N-Acetylmannosamine, have been conducted, and as of 2016 further trials were planned.

Berger, in 1876, first reported a case of 12-year-old child with progressive bulbar paralysis

In late 2007, it was reported by Dr. David Pearce et al. that Cellcept, an immunosuppressant medication commonly used in bone marrow transplants, may be useful in slowing down the progress of Juvenile NCL. Fundraising is currently underway to gather the funds needed to start a clinical trial to test the safety and efficiency of CellCept for Juvenile NCL.

Its occurrence is very rare. The infantile form from birth to 2 years of age. The average duration of the infantile form of the illness is usually about 3 years. Onset of the juvenile form presents between two and twelve years of age. Duration of this form is in most cases about 6 years. The adult form from twelve years and older. In younger patients, seizures, megalencephaly, developmental delay, and spasticity are usually present. Neonatal onset is also reported. Onset in adults is least frequent. In older patients, bulbar or pseudobulbar symptoms and spasticity predominate. Symptoms of the adult form may also resemble multiple sclerosis.

There are no more than 500 reported cases.

The standard treatment is chenodeoxycholic acid (CDCA) replacement therapy. Serum cholesterol levels are also followed. If hypercholesterolemia is not controlled with CDCA, an HMG-CoA reductase inhibitor ("statins" such as simvastatin) can also be used.

Valproic acid is the first line drug choice for reducing generalised seizures and myoclonus. Levetiracetam is also effective for both generalised seizures and myoclonus. Clonazepam and high-dose piracetam can alleviate myoclonus. Phenytoin can worsen seizures and may speed up neurodegeneration; carbamazepine, oxcarbazepine, tiagabine, vigabatrin, gabapentin and pregabalin may worsen myoclonus and myoclonic seizures. Other common medications to treat ULD include topiramate and zonisamide. If an individual with Unverricht–Lundborg disease is particularly sensitive to a certain type of stimulus, it is also beneficial to reduce the patient's exposure to that stimulus in order to reduce the likelihood of seizures. Since ULD is progressive and may not get better over time, depression has been documented in many cases, so providing a strong support group of friends, family, and even other individuals with ULD is very beneficial.