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.

Before prescribing medication for these conditions which often resolve spontaneously, recommendations have pointed to improved skin hygiene, good hydration via fluids, good nutrition, and installation of padded bed rails with use of proper mattresses. Pharmacological treatments include the typical neuroleptic agents such as fluphenazine, pimozide, haloperidol and perphenazine which block dopamine receptors; these are the first line of treatment for hemiballismus. Quetiapine, sulpiride and olanzapine, the atypical neuroleptic agents, are less likely to yield drug-induced parkinsonism and tardive dyskinesia. Tetrabenazine works by depleting presynaptic dopamine and blocking postsynaptic dopamine receptors, while reserpine depletes the presynaptic catecholamine and serotonin stores; both of these drugs treat hemiballismus successfully but may cause depression, hypotension and parkinsonism. Sodium valproate and clonazepam have been successful in a limited number of cases. Stereotactic ventral intermediate thalamotomy and use of a thalamic stimulator have been shown to be effective in treating these conditions.

Treatment of primary dystonia is aimed at reducing symptoms such as involuntary movements, pain, contracture, embarrassment, and to restore normal posture and improve the patient’s function. This treatment is therefore not neuroprotective. According to the European Federation of Neurological Sciences and Movement Disorder Society, there is no evidence-based recommendation for treating primary dystonia with antidopaminergic or anticholinergic drugs although recommendations have been based on empirical evidence. Anticholinergic drugs prove to be most effective in treating generalized and segmental dystonia, especially if dose starts out low and increases gradually. Generalized dystonia has also been treated with such muscle relaxants as the benzodiazepines. Another muscle relaxant, baclofen, can help reduce spasticity seen in cerebral palsy such as dystonia in the leg and trunk. Treatment of secondary dystonia by administering levodopa in dopamine-responsive dystonia, copper chelation in Wilson’s disease, or stopping the administration of drugs that may induce dystonia have been proven effective in a small number of cases. Physical therapy has been used to improve posture and prevent contractures via braces and casting, although in some cases, immobilization of limbs can induce dystonia, which is by definition known as peripherally induced dystonia. There are not many clinical trials that show significant efficacy for particular drugs, so medical of dystonia must be planned on a case-by-case basis. Botulinum toxin B, or Myobloc, has been approved by the US Food and Drug Administration to treat cervical dystonia due to level A evidential support by the scientific community. Surgery known as GPi DBS (Globus Pallidus Pars Interna Deep Brain Stimulation) has come to be popular in treating phasic forms of dystonia, although cases involving posturing and tonic contractions have improved to a lesser extent with this surgery. A follow-up study has found that movement score improvements observed one year after the surgery was maintained after three years in 58% of the cases. It has also been proven effective in treating cervical and cranial-cervical dystonia.

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.

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.

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.

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

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.

The most common acquired causes of chorea are cerebrovascular disease and, in the developing world, HIV infection - usually through its association with cryptococcal disease.

Sydenham's chorea occurs as a complication of streptococcal infection. Twenty percent (20%) of children and adolescents with rheumatic fever develop Sydenham's chorea as a complication. It is increasingly rare, which may be partially due to penicillin, improved social conditions, and/or a natural reduction in the bacteria ( Streptococcus ) it has stemmed from. Psychological symptoms may precede or accompany this acquired chorea and may be relapsing and remitting. The broader spectrum of paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection can cause chorea and are collectively referred to as PANDAS.

Chorea gravidarum refers to choreic symptoms that occur during pregnancy. If left untreated, the disease resolves in 30% of patients before delivery but, in the other 70%, it persists. The symptoms then progressively disappear in the next few days following the delivery.

Chorea may also be caused by drugs (commonly levodopa, anti-convulsants and anti-psychotics).

Other acquired causes include systemic lupus erythematosus, antiphospholipid syndrome, thyrotoxicosis, polycythaemia rubra vera, transmissible spongiform encephalopathies and coeliac disease.

Movement disorders are clinical syndromes with either an excess of movement or a paucity of voluntary and involuntary movements, unrelated to weakness or spasticity. Movement disorders are synonymous with basal ganglia or extrapyramidal diseases. Movement disorders are conventionally divided into two major categories- "hyperkinetic" and "hypokinetic".

Hyperkinetic movement disorders refer to dyskinesia, or excessive, often repetitive, involuntary movements that intrude upon the normal flow of motor activity.

Hypokinetic movement disorders refer to akinesia (lack of movement), hypokinesia (reduced amplitude of movements), bradykinesia (slow movement) and rigidity. In primary movement disorders, the abnormal movement is the primary manifestation of the disorder. In secondary movement disorders, the abnormal movement is a manifestation of another systemic or neurological disorder.

There is no cure for the alien hand syndrome. However, the symptoms can be reduced and managed to some degree by keeping the alien hand occupied and involved in a task, for example by giving it an object to hold in its grasp. Specific learned tasks can restore voluntary control of the hand to a significant degree. One patient with the "frontal" form of alien hand who would reach out to grasp onto different objects (e.g., door handles) as he was walking was given a cane to hold in the alien hand while walking, even though he really did not need a cane for its usual purpose of assisting with balance and facilitating ambulation. With the cane firmly in the grasp of the alien hand, it would generally not release the grasp and drop the cane in order to reach out to grasp onto a different object. Other techniques proven to be effective includes; wedging the hand between the legs or slapping it; warm water application and visual or tactile contact. Additionally, Wu et al. found that an irritating alarm activated by biofeedback reduced the time the alien hand held an object.

In the presence of unilateral damage to a single cerebral hemisphere, there is generally a gradual reduction in the frequency of alien behaviors observed over time and a gradual restoration of voluntary control over the affected hand. Actually, when AHS originates from focal injury of acute onset, recovery usually occurs within a year. One theory is that neuroplasticity in the bihemispheric and subcortical brain systems involved in voluntary movement production can serve to re-establish the connection between the executive production process and the internal self-generation and registration process. Exactly how this may occur is not well understood, but a process of gradual recovery from alien hand syndrome when the damage is confined to a single cerebral hemisphere has been reported. In some instances, patients may resort to constraining the wayward, undesirable and sometimes embarrassing actions of the impaired hand by voluntarily grasping onto the forearm of the impaired hand using the intact hand. This observed behavior has been termed "self-restriction" or "self-grasping".

In another approach, the patient is trained to perform a specific task, such as moving the alien hand to contact a specific object or a highly salient environmental target, which is a movement that the patient can learn to generate voluntarily through focused training in order to effectively override the alien behavior. It is possible that some of this training produces a re-organization of premotor systems within the damaged hemisphere, or, alternatively, that ipsilateral control of the limb from the intact hemisphere may be expanded.

Another method involves simultaneously "muffling" the action of the alien hand and limiting the sensory feedback coming back to the hand from environmental contact by placing it in a restrictive "cloak" such as a specialized soft foam hand orthosis or, alternatively, an everyday oven mitt. Other patients have reported using an orthotic device to restrict perseverative grasping or restraining the alien hand by securing it to the bed pole. Of course, this can limit the degree to which the hand can participate in addressing functional goals for the patient and may be considered to be an unjustifiable restraint.

Theoretically, this approach could slow down the process through which voluntary control of the hand is restored if the neuroplasticity that underlies recovery involves the recurrent exercise of voluntary will to control the actions of the hand in a functional context and the associated experiential reinforcement through successful willful suppression of the alien behavior.

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.

Over time, the approach to CP management has shifted away from narrow attempts to fix individual physical problems such as spasticity in a particular limb to making such treatments part of a larger goal of maximizing the person's independence and community engagement. Much of childhood therapy is aimed at improving gait and walking. Approximately 60% of people with CP are able to walk independently or with aids at adulthood. However, the evidence base for the effectiveness of intervention programs reflecting the philosophy of independence has not yet caught up: effective interventions for body structures and functions have a strong evidence base, but evidence is lacking for effective interventions targeted toward participation, environment, or personal factors. There is also no good evidence to show that an intervention that is effective at the body-specific level will result in an improvement at the activity level, or vice versa. Although such cross-over benefit might happen, not enough high-quality studies have been done to demonstrate it.

Because cerebral palsy has "varying severity and complexity" across the lifespan, it can be considered a collection of conditions for management purposes. A multidisciplinary approach for cerebral palsy management is recommended, focusing on "maximising individual function, choice and independence" in line with the International Classification of Functioning, Disability and Health's goals. The team may include a paediatrician, a health visitor, a social worker, a physiotherapist, an orthotist, a speech and language therapist, an occupational therapist, a teacher specialising in helping children with visual impairment, an educational psychologist, an orthopaedic surgeon, a neurologist and a neurosurgeon.

Various forms of therapy are available to people living with cerebral palsy as well as caregivers and parents. Treatment may include one or more of the following: physical therapy; occupational therapy; speech therapy; water therapy; drugs to control seizures, alleviate pain, or relax muscle spasms (e.g. benzodiazepines); surgery to correct anatomical abnormalities or release tight muscles; braces and other orthotic devices; rolling walkers; and communication aids such as computers with attached voice synthesisers. A Cochrane review published in 2004 found a trend toward benefit of speech and language therapy for children with cerebral palsy, but noted the need for high quality research. A 2013 systematic review found that many of the therapies used to treat CP have no good evidence base; the treatments with the best evidence are medications (anticonvulsants, botulinum toxin, bisphosphonates, diazepam), therapy (bimanual training, casting, constraint-induced movement therapy, context-focused therapy, fitness training, goal-directed training, hip surveillance, home programmes, occupational therapy after botulinum toxin, pressure care) and surgery (selective dorsal rhizotomy).

There is no treatment known to slow or stop the progression of the neurologic problems. Treatment of A-T is symptomatic and supportive. Physical, occupational and speech therapies and exercise may help maintain function but will not slow the course of neurodegeneration. Therapeutic exercises should not be used to the point of fatigue and should not interfere with activities of daily life. Certain anti-Parkinson and anti-epileptic drugs maybe useful in the management of symptoms, but should be prescribed in consultation with a neurologist.

Oral intake may be aided by teaching persons with A-T how to drink, chew and swallow more safely. The propriety of treatments for swallowing problems should be determined following evaluation by an expert in the field of speech-language pathology. Dieticians may help treat nutrition problems by recommending dietary modifications, including high calorie foods or food supplements.

A feeding (gastrostomy) tube is recommended when any of the following occur:

- A child cannot eat enough to grow or a person of any age cannot eat enough to maintain weight;

- Aspiration is problematic;

- Mealtimes are stressful or too long, interfering with other activities.

Feeding tubes can decrease the risk of aspiration by enabling persons to avoid liquids or foods that are difficult to swallow and provide adequate calories without the stress and time commitment of prolonged meals. Gastrostomy tubes do not prevent people from eating by mouth. Once a tube is in place, the general goal should be to maintain weight at the 10-25th percentile.

Nucleoside bypass therapy is an experimental treatment aimed to restore the normal levels of deoxyribonucleotides (dNTPs) in mitochondria.

Because the causes of CP are varied, a broad range of preventative interventions have been investigated.

Electronic fetal monitoring has not helped to prevent CP, and in 2014 the American College of Obstetricians and Gynecologists, the Royal Australian and New Zealand College of Obstetricians and Gynaecologists, and the Society of Obstetricians and Gynaecologists of Canada have acknowledged that there are no long-term benefits of electronic fetal monitoring. Prior to this, electronic fetal monitoring was widely used to prop up obstetric litigation.

In those at risk of an early delivery, magnesium sulphate appears to decrease the risk of cerebral palsy. It is unclear if it helps those who are born at term. In those at high risk of preterm labor a review found that moderate to severe CP was reduced by the administration of magnesium sulphate, and that adverse effects on the babies from the magnesium sulphate were not significant. Mothers who received magnesium sulphate could experience side effects such as respiratory depression and nausea. Caffeine is used to treat apnea of prematurity and reduces the risk of cerebral palsy in premature babies, but there are also concerns of long term negative effects. A moderate level of evidence has been shown for giving women antibiotics during preterm labour when their waters had not broken was associated with an increased risk of cerebral palsy in the child. Additionally, allowing a preterm birth to proceed rather than trying to delay the birth also had a moderate level of evidence for increased risk of cerebral palsy in the child.

Cooling high-risk full-term babies shortly after birth may reduce disability, but this may only be useful for some forms of the brain damage that causes CP.

Choreoathetosis is the occurrence of involuntary movements in a combination of chorea (irregular migrating contractions) and athetosis (twisting and writhing).

It is caused by many different diseases and agents. It is a symptom of several diseases, including Lesch-Nyhan Syndrome, phenylketonuria, and Huntington disease.

Choreoathetosis is also a common presentation of dyskinesia as a side effect of levodopa-carbidopa in the treatment of Parkinson disease.

The long-term prognosis of Costeff syndrome is unknown, though it appears to have no effect on life expectancy at least up to the fourth decade of life. However, as mentioned previously, movement problems can often be severe enough to confine individuals to a wheelchair at an early age, and both visual acuity and spasticity tend to worsen over time.

There are no treatments for MDDS, but some of the symptoms can be managed. For survivors living with MDDS, there are drugs to control epilepsy, and physical therapy can help with muscle control. Liver transplants may benefit people with liver involvement.

Paroxysmal Nonkinesigenic Dyskinesia (PNKD) is an episodic movement disorder first described by Mount and Reback in 1940 under the name "Familial paroxysmal choreoathetosis". It is a rare hereditary disease that affects various muscular and nervous systems in the body, passing to roughly fifty percent of the offspring.

Alien hand syndrome (AHS) is a condition in which a person experiences their limbs acting seemingly on their own, without control over the actions. The term is used for a variety of clinical conditions and most commonly affects the left hand. There are many similar names used to describe the various forms of the condition but they are often used inappropriately. The afflicted person may sometimes reach for objects and manipulate them without wanting to do so, even to the point of having to use the controllable hand to restrain the alien hand. While under normal circumstances, thought, as intent, and action can be assumed to be deeply mutually entangled, the occurrence of alien hand syndrome can be usefully conceptualized as a phenomenon reflecting a functional "disentanglement" between thought and action.

Alien hand syndrome is best documented in cases where a person has had the two hemispheres of their brain surgically separated, a procedure sometimes used to relieve the symptoms of extreme cases of epilepsy and epileptic psychosis, e.g., temporal lobe epilepsy. It also occurs in some cases after brain surgery, stroke, infection, tumor, aneurysm, migraine and specific degenerative brain conditions such as Alzheimer's disease and Creutzfeldt–Jakob disease. Other areas of the brain that are associated with alien hand syndrome are the frontal, occipital, and parietal lobes.

This disease has not been shown to be life-threatening or the cause of death in patients. However, treatment is necessary to maintain a healthy lifestyle.

Since this condition is generally agreed upon to be hereditary, nothing can be done to prevent HGF. However, in some cases where it can develop as a result of rare multi-system syndromes, such as: Zimmerman-Laband, Jones, Ramon Syndrome, Rutherford Syndrome, Juvenile Hyaline Fibromatosis, Systemic Infantile Hyalinosis, and Mannosidosis, it is best for one to simply monitors the possible progression for HGF with regular dental check-ups.

If the patient's disease is treated by means of surgery, it is recommended that the patient undergoes post-surgical therapies for maintenance and periodic monitoring of gums for the sake of the possibility of re-occurrence of HGF.