The treatment of Tourette's focuses on identifying and helping the individual manage the most troubling or impairing symptoms. Most cases of Tourette's are mild, and do not require pharmacological treatment; instead, psychobehavioral therapy, education, and reassurance may be sufficient. Treatments, where warranted, can be divided into those that target tics and comorbid conditions, which, when present, are often a larger source of impairment than the tics themselves. Not all people with tics have comorbid conditions, but when those conditions are present, they often take treatment priority.

There is no cure for Tourette's and no medication that works universally for all individuals without significant adverse effects. Knowledge, education and understanding are uppermost in management plans for tic disorders. The management of the symptoms of Tourette's may include pharmacological, behavioral and psychological therapies. While pharmacological intervention is reserved for more severe symptoms, other treatments (such as supportive psychotherapy or cognitive behavioral therapy) may help to avoid or ameliorate depression and social isolation, and to improve family support. Educating a patient, family, and surrounding community (such as friends, school, and church) is a key treatment strategy, and may be all that is required in mild cases.

Medication is available to help when symptoms interfere with functioning. The classes of medication with the most proven efficacy in treating tics—typical and atypical neuroleptics including risperidone (trade name Risperdal), ziprasidone (Geodon), haloperidol (Haldol), pimozide (Orap) and fluphenazine (Prolixin)—can have long-term and short-term adverse effects. The antihypertensive agents clonidine (trade name Catapres) and guanfacine (Tenex) are also used to treat tics; studies show variable efficacy, but a lower side effect profile than the neuroleptics. Stimulants and other medications may be useful in treating ADHD when it co-occurs with tic disorders. Drugs from several other classes of medications can be used when stimulant trials fail, including guanfacine (trade name Tenex), atomoxetine (Strattera) and tricyclic antidepressants. Clomipramine (Anafranil), a tricyclic, and SSRIs—a class of antidepressants including fluoxetine (Prozac), sertraline (Zoloft), and fluvoxamine (Luvox)—may be prescribed when a Tourette's patient also has symptoms of obsessive–compulsive disorder. Several other medications have been tried, but evidence to support their use is unconvincing.

Because children with tics often present to physicians when their tics are most severe, and because of the waxing and waning nature of tics, it is recommended that medication not be started immediately or changed often. Frequently, the tics subside with explanation, reassurance, understanding of the condition and a supportive environment. When medication is used, the goal is not to eliminate symptoms: it should be used at the lowest possible dose that manages symptoms without adverse effects, given that these may be more disturbing than the symptoms for which they were prescribed.

Cognitive behavioral therapy (CBT) is a useful treatment when OCD is present, and there is increasing evidence supporting the use of habit reversal (HRT) in the treatment of tics. There is evidence that HRT reduces tic severity, but there are methodological limitations in the studies, and a need for more trained specialists and better large-scale studies.

Relaxation techniques, such as exercise, yoga or meditation, may be useful in relieving the stress that may aggravate tics, but the majority of behavioral interventions (such as relaxation training and biofeedback, with the exception of habit reversal) have not been systematically evaluated and are not empirically supported therapies for Tourette's. Deep brain stimulation has been used to treat adults with severe Tourette's that does not respond to conventional treatment, but it is regarded as an invasive, experimental procedure that is unlikely to become widespread.

, studies on the impact of dietary interventions on the symptoms of Tourette's are scarce and methodologically poor, and a single dietary pattern has not been established. Anecdotal reports suggest that certain dietary interventions may relieve symptoms, such as gluten-free and low-sugar diets.

Methylphenidate, commonly used to treat ADHD, has been used in conjunction with levodopa to treat hypokinesia in the short term. The two work together to increase dopamine levels in the striatum and prefrontal cortex. Methylphenidate mainly inhibits dopamine and noradrenaline reuptake by blocking presynaptic transporters, and levodopa increases the amount of dopamine, generally improving hypokinesic gait. Some patients, however, have adverse reactions of nausea and headache to the treatment and the long-term effects of the drug treatment still need to be assessed.

PED patients usually avoid prolonged, continuous exertion to prevent occurrence of attacks. Use of anticonvulsants such as benzodiazepines show little to no success in PED patients. A few cases have shown that patients were able to lessen their attacks with a high carbohydrate snack. A new approach to managing PED is the ketogenic diet, which alters the primary cerebral energy metabolism from glucose to ketone bodies. Reports have shown that the ketonic diet protects against seizures in epilepsy. In PED, it is probable that ketones will provide sufficient energy for the basal ganglia, which is normally deficient in patients with PED.

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.

There is no standard course of treatment for chorea. Treatment depends on the type of chorea and the associated disease. Although there are many drugs that can control it, no cure has yet been identified.

New treatments include increasing the number of dopamine cells by transplanting stem cells into the basal ganglia or stimulating endogenous stem cell production and movement to the basal ganglia. The successful integration of stem cells can relieve hypokinetic symptoms and decrease the necessary dose of dopaminergic drugs. However, a variety of complications, including possible tumor formation, inappropriate cell migration, rejection of cells by the immune system, and cerebral hemorrhage are possible, causing many physicians to believe the risks outweigh the possible benefits.

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.

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.

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.

Lesionsing is the intentional destruction of neuronal cells in a particular area used for therapeutic purposes. Though this seems dangerous, vast improvements have been achieved in patients with movement disorders. The exact process generally involves unilateral lesioning in the sensorimotor territory of the GPi. This process is called pallidotomy. It is believed that the success of pallidotomies in reducing the effects of movement disorders may result from the interruption of abnormal neuronal activity in the GPi. This ablation technique can be viewed as simply removing a faulty piece of a circuit. With the damaged piece of the circuit removed, the healthy area of the circuit can continue normal function.

There is no known cure for MSA and management is primarily supportive.

Ongoing care from a neurologist specializing in "movement disorders" is recommended as the complex symptoms of MSA are often not familiar to less-specialized health care professionals.

One particularly serious problem, the drop in blood pressure upon standing up (with risk of fainting and thus injury from falling) often responds to fludrocortisone, a synthetic mineralocorticoid. Another common drug treatment is midodrine (an alpha-agonist). Non-drug treatments include "head-up tilt" (elevating the head of the whole bed by about 10 degrees), salt tablets or increasing salt in the diet, generous intake of fluids, and pressure (elastic) stockings. Avoidance of triggers of low blood pressure (such as hot weather, alcohol, and dehydration) are crucial.

Hospice/homecare services can be very useful as disability progresses.

Levodopa (L-Dopa), a drug used in the treatment of Parkinson's disease, improves parkinsonian symptoms in a small percentage of MSA patients. A recent trial reported that only 1.5% of MSA patients experienced a less than 50% improvement when taking levodopa, and even this was a transient effect lasting less than one year. Poor response to L-Dopa has been suggested as a possible element in the differential diagnosis of MSA from Parkinson's disease.

A November, 2008 study conducted in Europe failed to find an effect for the drug riluzole in treating MSA or PSP.

Treatment depends upon the underlying disorder. Movement disorders have been known to be associated with a variety of autoimmune diseases.

Management by rehabilitation professionals (physiatrists, physiotherapists, occupational therapists, speech therapists, and others) for problems with walking/movement, daily tasks, and speech problems is essential.

Physiotherapy can help to maintain the patient’s mobility and will help to prevent contractures. Instructing patients in gait training will help to improve their mobility and decrease their risk of falls. A physiotherapist may also prescribe mobility aids such as a cane or a walker to increase the patient’s safety. Other ways a physiotherapist can help to improve the patient’s safety are to teach them to move and transfer from sitting to standing slowly to decrease risk of falls and limit the effect of postural hypotension. Instruction in ankle pumping helps to return blood in the legs to the systemic circulation. To further control the postural hypotension, raising the head of the bed by 8 in (20.3 cm) while sleeping may be indicated as well as the use of elastic compression garments.

Speech and language therapists may assist in assessing, treating and supporting speech (dysarthria) and swallowing difficulties (dysphagia). Early intervention of swallowing difficulties is particularly useful to allow for discussion around tube feeding further in the disease progression.{doubtful - citation needed} At some point in the progression of the disease, fluid and food modification may be suggested. Speech changes mean that alternative communication may be needed, for example communication aids or word charts.

Social workers and occupational therapists can also help with coping with disability through the provision of equipment and home adaptations, services for caregivers and access to healthcare services, both for the person with MSA as well as family caregivers.

There is no cure for XDP and medical treatment offers only temporary relief. Some authors have reported benzodiazepines and anticholinergic agents in the early stages of the disease. Botulinum toxin injections have been used to relieve focal dystonia. Deep brain stimulation has shown promise in the few cases treated surgically.

Many disorders of the basal ganglia are due to the dysfunction of a localized area. For this reason gene therapy seems viable for neurodegenerative disorders. Gene therapy is performed by replacing diseased phenotypes with new genetic material. This process is still in the early stages but early results are promising. An example of this therapy might involve implanting cells genetically modified to express tyrosine hydroxylase which, in the body, could be converted to dopamine. Increasing dopamine levels in the basal ganglia could possibly offset the effects of the Parkinson’s Disease.

Tetrabenazine was approved in 2008 for treatment of chorea in Huntington's disease in the US. Other drugs that help to reduce chorea include neuroleptics and benzodiazepines. Compounds such as amantadine or remacemide are still under investigation but have shown preliminary positive results. Hypokinesia and rigidity, especially in juvenile cases, can be treated with antiparkinsonian drugs, and myoclonic hyperkinesia can be treated with valproic acid.

Psychiatric symptoms can be treated with medications similar to those used in the general population. Selective serotonin reuptake inhibitors and mirtazapine have been recommended for depression, while atypical antipsychotic drugs are recommended for psychosis and behavioral problems. Specialist neuropsychiatric input is recommended as people may require long-term treatment with multiple medications in combination.

When treating hemiballismus, it is first important to treat whatever may be causing the manifestation of this disorder. This could be hyperglycemia, infections, or neoplastic lesions. Some patients may not even need treatment because the disorder is not severe and can be self – limited.

Dopamine Blockers

When pharmacological treatment is necessary, the most standard type of drug to use is an antidopaminergic drug. Blocking dopamine is effective in about ninety percent of patients. Perphenazine, pimozide, haloperidol, and chlorpromazine are standard choices for treatment. Scientists are still unsure as to why this form of treatment works, as dopamine has not been directly linked to hemiballismus.

Anticonvulsants

An anticonvulsant called topiramate has helped patients in three cases and may be a viable treatment for the future.

ITB Therapy

Intrathecal baclofen (ITB) therapy is used to treat a variety of movement disorders such as cerebral palsy and multiple sclerosis. It can also be a possibility to help treat hemiballismus. In one case, before ITB the patient had an average of 10-12 ballism episodes of the right lower limb per hour. During episodes, the right hip would flex up to about 90 degrees, with a fully extended knee. After an ITB pump was implanted and the correct dosage was found, the frequency of ballistic right leg movements decreased to about three per day, and the right hip flexed to only 30 degrees. The patient was also able to better isolate individual distal joint movements in the right lower limb. The patient currently receives 202.4 microg/day of ITB and continues to benefit almost 6 years after the ITB pump was implanted.

Botulinum Injections

New uses for botulinum toxin have included treatment of hemiballismus. However, this is still in the early stages of testing. This treatment deals with the muscular manifestations of hemiballismus as opposed to the neurological causes.

Tetrabenazine

Tetrabenazine has been used to treat other movement disorders, but is now being used to treat hemiballismus. Patients using this medication have had a dramatic response. However, lowering the dosage leads to a return of symptoms. This drug works by depleting dopamine.

Antipsychotics

In one case, a patient had not been responding to haloperidol, thus the physician tried olanzapine. The patient made a significant recovery. More research is being performed on the use of these types of drugs in treating hemiballismus.

Functional Neurosurgery

Surgery as a treatment should only be used on patients with severe hemiballismus that has not responded to treatment. Lesioning of the globus pallidus or deep brain stimulation of the globus pallidus are procedures that can be used on humans. Usually, lesioning is favored over deep brain stimulation because of the maintenance required to continue stimulating the brain correctly and effectively.

There is no cure for HD, but there are treatments available to reduce the severity of some of its symptoms. For many of these treatments, evidence to confirm their effectiveness in treating symptoms of HD specifically are incomplete. As the disease progresses the ability to care for oneself declines, and carefully managed multidisciplinary caregiving becomes increasingly necessary. Although there have been relatively few studies of exercises and therapies that help rehabilitate cognitive symptoms of HD, there is some evidence for the usefulness of physical therapy, occupational therapy, and speech therapy. An association between caffeine intake and earlier age of onset in Huntington's disease has been found but, since this finding was based on retrospective questionnaire data rather than a blinded, randomized trial or case-control study, this work is a poor basis for guiding lifestyle decisions.

There have been no major breakthroughs in the treatment of PKAN, with most pharmacologic treatments focusing on the easing or temporary relieving of PKAN’s symptoms. Iron chelating agents have been used somewhat successfully in retarding the disorder, but they have not been a significant success.

Current research focuses on the future use of high dose pantothenate, the PANK2 enzyme substrate, in possibly alleviating symptoms as well as the further development of iron chelating agents that may be better aimed at reaching the central nervous system and working to better remove excess iron from the individual’s system.

Complications may result from the medication used to treat symptoms. Immobility from the disease can also lead to skin breakdown, respiratory infections, and blood clots, among others.

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.

Due to neuroferritinopathy’s genetic etiology, the disorder is not currently curable. Furthermore, progression of the disorder is unable to be effectively halted. Therefore current treatment focuses on managing symptoms of the disorder.

No medication is available to treat all symptoms. Botox has been shown to help with focal dystonia. The dopamine depleter Tetrabenazine shown to help with involuntary movements. Symptoms affecting movement (dystonia) have also been treated with L-Dopa, orphenadrine, benzhexol, sulpiride, diazepam, clonazepam, and deanol. Parkinsonian symptoms were not decreased by L-Dopa. Iron supplements should be avoided.

The treatment to battle the disease chorea-acanthocytosis is completely symptomatic. For example, Botulinum toxin injections can help to control orolingual dystonia.

Deep Brain Stimulation is a treatment that has varied effects on the people suffering from the symptoms of this disease, for some it has helped in a large way and for other people it did not help whatsoever, it is more effective on specific symptoms of the disease. Patients with chorea-acanthocytosis should undergo a cardiac evaluation every 5 years to look for cardiomyopathy.

SR deficiency is currently being treated using a combination therapy of levodopa and carbidopa. These treatments are also used for individuals suffering from Parkinson's. The treatment is noninvasive and only requires the patient to take oral tablets 3 or 4 times a day, where the dosage of levodopa and carbidopa is determined by the severity of the symptoms. Levodopa is in a class of medications called central nervous system agents where its main function is to become dopamine in the brain. Carbidopa is in a class of medications called decarboxylase inhibitors and it works by preventing levodopa from being broken down before it reaches the brain. This treatment is effective in mitigating motor symptoms, but it does not totally eradicate them and it is not as effective on cognitive problems. Patients who have been diagnosed with SR deficiency and have undergone this treatment have shown improvements with most motor impairments including oculogyric crises, dystonia, balance, and coordination.

For those whose RLS disrupts or prevents sleep or regular daily activities, medication may be useful. Evidence supports the use of dopamine agonists including: pramipexole, ropinirole, rotigotine, and cabergoline. They reduce symptoms, improve sleep quality and quality of life. Levodopa is also effective. One review found pramipexole to be better than ropinirole.

There are, however, issues with the use of dopamine agonists including augmentation. This is a medical condition where the drug itself causes symptoms to increase in severity and/or occur earlier in the day. Dopamine agonists may also cause rebound when symptoms increase as the drug wears off. In many cases, the longer dopamine agonists have been used the higher the risk of augmentation and rebound as well as the severity of the symptoms. Also, a recent study indicated that dopamine agonists used in restless leg syndrome can lead to an increase in compulsive gambling.

- Gabapentin or pregabalin, a non-dopaminergic treatment for moderate to severe primary RLS

- Opioids are only indicated in severe cases that do not respond to other measures due to their high rate of side effects.

Benzodiazepines, such as diazepam or clonazepam, are not generally recommended, and their effectiveness is unknown. They however are sometimes still used as a second line, as add on agents. Quinine is not recommended due to its risk of serious side effects involving the blood.

There is no cure for PMD, nor is there a standard course of treatment. Treatment, which is symptomatic and supportive, may include medication for seizures and spasticity. Regular evaluations by physical medicine and rehabilitation, orthopedic, developmental and neurologic specialists should be made to ensure optimal therapy and educational resources. The prognosis for those with Pelizaeus–Merzbacher disease is highly variable, with children with the most severe form (so-called connatal) usually not surviving to adolescence, but survival into the sixth or even seventh decades is possible, especially with attentive care. Genetic counseling should be provided to the family of a child with PMD.

In December 2008, StemCells Inc., a biotech company in Palo Alto, received clearance from the U.S. Food and Drug Administration (FDA) to conduct Phase I clinical trials in PMD to assess the safety of transplanting human neural stem cells as a potential treatment for PMD. The trial was initiated in November 2009 at the University of California, San Francisco (UCSF) Children's Hospital.