Ataxia usually goes away without any treatment. In cases where an underlying cause is identified, your doctor will treat the underlying cause. In extremely rare cases, you may have continuing and disabling symptoms. Treatment includes corticosteroids, Intravenous immunoglobulin, or plasma exchange therapy. Drug treatment to improve muscle coordination has a low success rate. However, the following drugs may be prescribed: clonazepam, amantadine, gabapentin, or buspirone. Occupational or physical therapy may also alleviate lack of coordination. Changes to diet and nutritional supplements may also help. Treatment will depend on the cause. If the acute cerebellar ataxia is due to bleeding, surgery may be needed. For a stroke, medication to thin the blood can be given. Infections may need to be treated with antibiotics. Steroids may be needed for swelling (inflammation) of the cerebellum (such as from multiple sclerosis). Cerebellar ataxia caused by a recent viral infection may not need treatment.

Supportive treatment is the only intervention for acute cerebellar ataxia of childhood. Symptoms may last as long as 2 or 3 months.

Although no specific treatment exists, the disease can be managed with anticonvulsants, physiotherapy, etc.

There is no known definitive cure for OMS. However, several drugs have proven to be effective in its treatment.

Some of medication used to treat the symptoms are:

- ACTH has shown improvements in symptoms but can result in an incomplete recovery with residual deficits.

- Corticosteroids (such as "prednisone" or "methylprednisolone") used at high dosages (500 mg - 2 g per day intravenously for a course of 3 to 5 days) can accelerate regression of symptoms. Subsequent very gradual tapering with pills generally follows. Most patients require high doses for months to years before tapering.

- Intravenous Immunoglobulins (IVIg) are often used with varying results.

- Several other immunosuppressive drugs, such as cyclophosphamide and azathioprine, may be helpful in some cases.

- Chemotherapy for neuroblastoma may be effective, although data is contradictory and unconvincing at this point in time.

- Rituximab has been used with encouraging results.

- Other medications are used to treat symptoms without influencing the nature of the disease (symptomatic treatment):

- Trazodone can be useful against irritability and sleep problems

- Additional treatment options include plasmapheresis for severe, steroid-unresponsive relapses.

The National Organization for Rare Disorders (NORD) recommends FLAIR therapy consisting of a three-agent protocol involving front-loaded high-dose ACTH, IVIg, and rituximab that was developed by the National Pediatric Myoclonus Center, and has the best-documented outcomes. Almost all patients (80-90%) show improvement with this treatment and the relapse rate appears to be about 20%.

A more detailed summary of current treatment options can be found at Treatment Options

The following medications should probably be avoided:

- Midazolam - Can cause irritability.

- Melatonin - Is known to stimulate the immune system.

- Also, see for more details

If people are found to have a tumor, the long-term prognosis is generally better and the chance of relapse is much lower. This is because the tumour can be removed surgically, thus eradicating the source of autoantibodies. In general, early diagnosis and aggressive treatment is believed to improve patient outcomes, but this remains impossible to know without data from randomized controlled trials. Given that the majority of patients are initially seen by psychiatrists, it is critical that all physicians (especially psychiatrists) consider anti-NMDA receptor encephalitis as a possible cause of acute psychosis in young patients with no past neuropsychiatric history.

- If a tumor is detected, its removal should occur in conjunction with first-line immunotherapy. This involves steroids to suppress the immune system, intravenous immunoglobulin, and plasmapheresis to physically remove autoantibodies. A study of 577 patients showed that over four weeks, about half the patients improved after receiving first-line immunotherapy.

- Second-line immunotherapy includes rituximab, a monoclonal antibody that targets the CD20 receptor on the surface of B cells, thus destroying the self-reactive B cells. Cyclophosphamide, an alkylating agent that cross-links DNA and is used to treat both cancer and autoimmune diseases, has sometimes proven useful when other therapies have failed.

- Other medications, such as alemtuzumab, remain experimental.

There is currently no cure for SCA 6; however, there are supportive treatments that may be useful in managing symptoms.

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.

People whose condition was caused by a recent viral infection should make a full recovery without treatment in a few months. Fine motor skills, such as handwriting, typically have to be practised in order to restore them to their former ability. In more serious cases, strokes, bleeding or infections may sometimes cause permanent symptoms.

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.

The recovery process from anti-NMDA encephalitis can take many months. The symptoms reappear in reverse order: The patient may begin to experience psychosis again, leading many people to falsely believe the patient is not recovering. As the recovery process continues on, the psychosis fades. Lastly, the person's social behavior and executive functions begin to improve.

Physiotherapy intervention aims to improve balance and gait of OPCA patients, by stimulating neuroplastic changes in the atrophied neural structure. A challenge-oriented treatment program has previously been shown to be beneficial for individuals with ataxia from OPCA. The treatment program was composed of repetitive training with task challenges (e.g. obstacle course) and/or novel motor skills acquisition over a 12-week period under the supervision of a physiotherapist. Task challenges were progressed only when the patient showed mastery of a task.

Overground harness systems may be used to allow OPCA patients to challenge their balance without chance of falling. Furthermore, home exercise programs and/or aquatic exercises are used to allow more repetitions to facilitate balance learning. Treatment programs should be frequently monitored and adjusted based on a patient's progress. Outcome measures such as the Berg Balance Scale, Dynamic Gait Index and activities-specific balance confidence scales are useful to assess patient’s progress over time.

In terms of a cure there is currently none available, however for the disease to manifest itself, it requires mutant gene expression. Manipulating the use of protein homoestasis regulators can be therapuetic agents, or a treatment to try and correct an altered function that makes up the pathology is one current idea put forth by Bushart, et al. There is some evidence that for SCA1 and two other polyQ disorders that the pathology can be reversed after the disease is underway. There is no effective treatments that could alter the progression of this disease, therefore care is given, like occupational and physical therapy for gait dysfunction and speech therapy.

Treatment for lateral medullary syndrome involves focusing on relief of symptoms and active rehabilitation to help patients return to their daily activities. Speech Therapy is a very common form of rehabilitation that many patients undergo. Depressed mood and withdrawal from society can be seen in patients following the initial onslaught of symptoms.

In more severe cases, a feeding tube may need to be inserted through the mouth or a gastrostomy may be necessary if swallowing is impaired. In some cases, medication may be used to reduce or eliminate residual pain. Some studies have reported success in mitigating the chronic neuropathic pain associated with the syndrome with anti-epileptics such as gabapentin. Long term treatment generally involves the use of antiplatelets like aspirin or clopidogrel and statin regimen for the rest of their lives in order to minimize the risk of another stroke. Warfarin is used if atrial fibrillation is present. Other medications may be necessary in order to suppress high blood pressure and risk factors associated with strokes. A blood thinner may be prescribed to a patient in order to break up the infarction and reestablish blood flow and to try to prevent future infarctions.

One of the most unusual and difficult to treat symptoms that occur due to Wallenberg syndrome are interminable, violent hiccups. The hiccups can be so severe that patients often struggle to eat, sleep and carry on conversations. Depending on the severity of the blockage caused by the stroke, the hiccups can last for weeks. Unfortunately there are very few successful medications available to mediate the inconvenience of constant hiccups.

For dysphagia symptoms, Repetitive transcranial magnetic stimulation has been shown to assist in rehabilitation. Overall, traditional stroke assessment and outcomes are used to treat patients, since lateral medullary syndrome is often a cause of a stroke in the lateral medulla.

Treatment for this disorder can be disconcerting because some individuals will always have residual symptoms due to the severity of the blockage as well as the location of the infarction. Two patients may present with the same initial symptoms right after the stroke has occurred, but after several months one patient may fully recover while the other is still severely handicapped. This variation in outcome may be due to but not limited to the size of the infarction, the location of the infarction, and how much damage resulted from it.

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.

There is no cure for GSS, nor is there any known treatment to slow the progression of the disease. However, therapies and medication are aimed at treating or slowing down the effects of the symptoms. Their goal is to try to improve the patient's quality of life as much as possible. Despite there being no cure for GSS, it is possible to undergo testing for the presence of the underlying genetic mutation. Testing for GSS involves a blood and DNA examination in order to attempt to detect the mutated gene at certain codons. If the genetic mutation is present, the patient will eventually be afflicted by GSS, and, due to the genetic nature of the disease, the offspring of the patient are predisposed to a higher risk of inheriting the mutation.

Like many mitochondrial diseases, there is no cure for MERRF, no matter the means for diagnosis of the disease. The treatment is primarily symptomatic. High doses of Coenzyme Q10, B complex vitamins and L-Carnitine are the drugs that patients are treated with in order to account for the altered metabolic processed resulting in the disease. There is very little success with these treatments as therapies in hopes of improving mitochondrial function. The treatment only alleviates symptoms and these do not prevent the disease from progressing. Patients with concomitant disease, such as diabetes, deafness or cardiac disease, are treated in combination to manage symptoms.

There is no cure for Machado-Joseph Disease. However, treatments are available for some symptoms. For example, spasticity can be reduced with antispasmodic drugs, such as baclofen. The Parkinsonian symptoms can be treated with levodopa therapy. Prism glasses can reduce diplopic symptoms. Physiotherapy/Physical Therapy and/or occupational therapy can help patients by prescribing mobility aids to increase the patients' independence, providing gait training, and prescribing exercises to maintain the mobility of various joints and general health to decrease the likelihood of falls or injuries as a result of falls. Walkers and wheelchairs can greatly help the patient with everyday tasks. Some patients will experience difficulties with speech and swallowing, therefore a Speech-Language Pathologist can assist the patients to improve their communicating abilities and their issues with swallowing.

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.

Idebenone, an antioxidant, was recently removed from the Canadian market in 2013 due to lack of effectiveness. A Cochrane review on antioxidants and other pharmacological treatment of patients with Friedreich ataxia concluded that there is limited but not persuasive evidence of efficacy.

Different medications are tried in an effort to find a combination that is effective for a specific person. Not all people will respond well to the same medications. Medications that have had positive results in some include: diphenhydramine, benzatropine and atropine. anti-Parkinsons agents (such as ropinirole and bromocriptine), and muscle relaxants (such as diazepam).

- Anticholinergics

Medications such as anticholinergics (benztropine), which act as inhibitors of the neurotransmitter acetylcholine, may provide some relief. In the case of an acute dystonic reaction, diphenhydramine is sometimes used (though this drug is well known as an antihistamine, in this context it is being used primarily for its anticholinergic role).. See also Procyclidine.

- Baclofen

A baclofen pump has been used to treat patients of all ages exhibiting muscle spasticity along with dystonia. The pump delivers baclofen via a catheter to the thecal space surrounding the spinal cord. The pump itself is placed in the abdomen. It can be refilled periodically by access through the skin. Baclofen can also be taken in tablet form

- Botulin toxin injection

Botulinum toxin injections into affected muscles have proved quite successful in providing some relief for around 3–6 months, depending on the kind of dystonia. Botox or Dysport injections have the advantage of ready availability (the same form is used for cosmetic surgery) and the effects are not permanent. There is a risk of temporary paralysis of the muscles being injected or the leaking of the toxin into adjacent muscle groups, causing weakness or paralysis in them. The injections have to be repeated, as the effects wear off and around 15% of recipients will develop immunity to the toxin. There is a Type A and a Type B toxin approved for treatment of dystonia; often, those that develop resistance to Type A may be able to use Type B.

- Muscle relaxants

Clonazepam, an anti-seizure medicine, is also sometimes prescribed. However, for most, their effects are limited and side-effects like mental confusion, sedation, mood swings, and short-term memory loss occur.

- Parkinsonian drugs

Dopamine agonists: One type of dystonia, dopamine-responsive dystonia, can be completely treated with regular doses of L-DOPA in a form such as Sinemet (carbidopa/levodopa). Although this does not remove the condition, it does alleviate the symptoms most of the time. (In contrast, dopamine antagonists can sometimes cause dystonia.)

Ketogenic Diet

A Ketogenic diet consisting of 70% fats (focusing on medium chain triglycerides and unsaturated fats), 20% protein and 10% carbohydrates (any sugar) has shown strong promise as a treatment for Dystonia.

"For many years, it was thought that postural and balance disorders in cerebellar ataxia were not treatable. However, the results of several recent studies suggest that rehabilitation can relieve postural disorders in patients with cerebellar ataxia...There is now moderate level evidence that rehabilitation is efficient to improve postural capacities of patients with cerebellar ataxia – particularly in patients with degenerative ataxia or multiple sclerosis. Intensive rehabilitation programs with balance and coordination exercises are necessary. Although techniques such as virtual reality, biofeedback, treadmill exercises with supported bodyweight and torso weighting appear to be of value, their specific efficacy has to be further investigated. Drugs have only been studied in degenerative ataxia, and the level of evidence is low."

One approach is that it can be ameliorated to varying degrees by means of Frenkel exercises.

One main objective of the treatment is to re-establish the physiological inhibition exerted by the cerebellar cortex over cerebellar nuclei. Research using Transcranial direct-current stimulation (TCDCS) and Transcranial magnetic stimulation (TMS) shows promising results.

Additionally, mild to moderate cerebellar ataxia may be treatable with buspirone.

It is thought that the buspirone increases the serotonin levels in the cerebellum and so decreases ataxia.

Nicotinamide administration on patients was associated with a sustained improvement in frataxin concentrations towards those seen in asymptomatic carriers during 8 weeks of daily dosing. The daily oral administration of 3.8 g nicotinamide resulted in a 1.5-times increase, whereas 7.5 g resulted in a doubling of frataxin protein concentration.

There is no cure for spinocerebellar ataxia, which is currently considered to be a progressive and irreversible disease, although not all types cause equally severe disability.

In general, treatments are directed towards alleviating symptoms, not the disease itself. Many patients with hereditary or idiopathic forms of ataxia have other symptoms in addition to ataxia. Medications or other therapies might be appropriate for some of these symptoms, which could include tremor, stiffness, depression, spasticity, and sleep disorders, among others. Both onset of initial symptoms and duration of disease are variable. If the disease is caused by a polyglutamine trinucleotide repeat CAG expansion, a longer expansion may lead to an earlier onset and a more radical progression of clinical symptoms. Typically, a person afflicted with this disease will eventually be unable to perform daily tasks (ADLs). However, rehabilitation therapists can help patients to maximize their ability of self-care and delay deterioration to certain extent. Researchers are exploring multiple avenues for a cure including RNAi and the use of Stem Cells and several other avenues.

On January 18, 2017 BioBlast Pharma announced completion of Phase 2a clinical trials of their medication, Trehalose, in the treatment of SCA3. BioBlast has received FDA Fast Track status and Orphan Drug status for their treatment. The information provided by BioBlast in their research indicates that they hope this treatment may prove efficacious in other SCA treatments that have similar pathology related to PolyA and PolyQ diseases.

In addition, Dr. Beverly Davidson has been working on a methodology using RNAi technology to find a potential cure for over 2 decades. Her research began in the mid-1990s and progressed to work with mouse models about a decade later and most recently has moved to a study with non-human primates. The results from her most recent research "are supportive of clinical application of this gene therapy". Dr. Davidson along with Dr. Pedro Gonzalez-Alegre are currently working to move this technique into a Phase 1 clinical trial.

Finally, another gene transfer technology discovered in 2011 has also been shown by Dr. Davidson to hold great promise and offers yet another avenue to a potential future cure.

Recurrent sinus and lung infections can lead to the development of chronic lung disease. Such infections should be treated with appropriate antibiotics to prevent and limit lung injury. Administration of antibiotics should be considered when children and adults have prolonged respiratory symptoms (greater than 7 days), even following what was presumed to have been a viral infection. To help prevent respiratory illnesses from common respiratory pathogens, annual influenza vaccinations should be given and pneumococcal vaccines should be administered when appropriate. Antibiotic treatment should also be considered in children with chronic coughs that are productive of mucous, those who do not respond to aggressive pulmonary clearance techniques and in children with muco-purulent secretions from the sinuses or chest. A wet cough can also be associated with chronic aspiration which should be ruled out through proper diagnostic studies, however aspiration and respiratory infections are not necessarily exclusive of each other. In children and adults with bronchiectasis, chronic antibiotic therapy should be considered to slow chronic lung disease progression.

Culturing of the sinuses may be needed to direct antibiotic therapy. This can be done by an Ear Nose and Throat (ENT) specialist. In addition, diagnostic bronchoscopy may be necessary in people who have recurrent pneumonias, especially those who do not respond or respond incompletely to a course of antibiotics.

Clearance of bronchial secretions is essential for good pulmonary health and can help limit injury from acute and chronic lung infections. Children and adults with increased bronchial secretions can benefit from routine chest therapy using the manual method, an a cappella device or a chest physiotherapy vest. Chest physiotherapy can help bring up mucous from the lower bronchial tree, however an adequate cough is needed to remove secretions. In people who have decreased lung reserve and a weak cough, use of an insufflator-exsufflator (cough-assist) device may be useful as a maintenance therapy or during acute respiratory illnesses to help remove bronchial secretions from the upper airways. Evaluation by a Pulmonology specialist however, should first be done to properly assess patient suitability.

Children and adults with chronic dry cough, increased work of breathing (fast respiratory rate, shortness of breath at rest or with activities) and absence of an infectious process to explain respiratory symptoms should be evaluated for interstitial lung disease or another intrapulmonary process. Evaluation by a Pulmonologist and a CT scan of the chest should be considered in individuals with symptoms of interstitial lung disease or to rule other non-infectious pulmonary processes. People diagnosed with interstitial lung disease may benefit from systemic steroids.

Physical therapists can assist patients in maintaining their level of independence through therapeutic exercise programmes. One recent research report demonstrated a gain of 2 SARA points (Scale for the Assessment and Rating of Ataxia) from physical therapy. In general, physical therapy emphasises postural balance and gait training for ataxia patients. General conditioning such as range-of-motion exercises and muscle strengthening would also be included in therapeutic exercise programmes. Research showed that spinocerebellar ataxia 2 (SCA2) patients with a mild stage of the disease gained significant improvement in static balance and neurological indices after six months of a physical therapy exercise training program. Occupational therapists may assist patients with incoordination or ataxia issues through the use of adaptive devices. Such devices may include a cane, crutches, walker, or wheelchair for those with impaired gait. Other devices are available to assist with writing, feeding, and self care if hand and arm coordination are impaired. A randomised clinical trial revealed that an intensive rehabilitation program with physical and occupational therapies for patients with degenerative cerebellar diseases can significantly improve functional gains in ataxia, gait, and activities of daily living. Some level of improvement was shown to be maintained 24 weeks post-treatment. Speech language pathologists may use both behavioral intervention strategies as well as augmentative and alternative communication devices to help patients with impaired speech.