Treatment consists of physical rehabilitation programs designed to improve overall function, increase strength and improve balance. The ultimate goal is to increase the patient's degree of independence, thus improving the patient's quality of life. Exercise typically begins with simple movements, gradually transitioning into more complex actions. Various aspects of treatment are assessed based on the individual patient's condition, utilizing many assessment tools:

- Functional Reach Test

- External Perturbation Test – Push, Release

- External Perturbation Test – Pull

- Clinical Sensory Integration Test

- Single Leg Stance Test

- Five Times Sit to Stand Test

Various scales are also utilized

- Brief Ataxia Rating Scale

- Friedreich's Ataxia Impact Scale

- Scale For Assessment and Rating of Ataxia

Currently there is no cure for dysmetria itself as it is actually a symptom of an underlying disorder. However, isoniazid and clonazepam have been used to treat dysmetria. Frenkel exercises treat dysmetria. There have also been numerous reported cases of chiropractic neurology as an effective holistic treatment for dysmetria. Cannabis has been used in trials in the U.K. and displayed some success, though it is not legal to use in some U.S. states.

Researchers now are testing different possibilities for treating dysmetria and ataxia. One opportunity for treatment is called rehearsal by eye movement. It is believed that visually guided movements require both lower- and higher-order visual functioning by first identifying a target location and then moving to acquire what is sought after. In one study, researchers used visually guided stepping which is parallel to visually guided arm movements to test this treatment. The patients suffered from saccadic dysmetria which in turn caused them to overshoot their movements 3. The patients first walked normally and were then told to twice review the area that was to be walked through 3. After rehearsal with eye movements, the patients improved their motor performance. Researchers believe that prior rehearsal with the eyes might be enough for a patient who suffers from motor dysmetria as a result of saccadic dysmetria to complete a motor task with enhanced spatial awareness.

Research has also been done for those patients who suffer from MS. Deep brain stimulation (DBS) remains a viable possibility for some MS patients though the long-term effects of this treatment are currently under review. The subjects who have undergone this treatment had no major relapse for six months and disabling motor function problems. Most subjects benefited from the implantation of the electrodes and some reported that their movement disorder was gone after surgery. However, these results are limiting at this time because of the small range of subjects who were used for the experiment and it is unknown whether this is a viable option for all MS patients who suffer from motor control problems.

Bruns apraxia, or frontal ataxia is a gait apraxia found in patients with bilateral frontal lobe disorders. It is characterised by an inability to initiate the process of walking, despite the power and coordination of the legs being normal when tested in the seated or lying position. The gait is broad-based with short steps with a tendency to fall backwards. It was originally described in patients with frontal lobe tumours, but is now more commonly seen in patients with cerebrovascular disease.

It is named after Ludwig Bruns.

"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.

Individuals with cerebellar ataxia have full cognitive awareness: it is usually only the physical deterioration that prohibits them from participating in activities of daily living and any other relevant or desired interests. One of the most significant barriers in the lives of these individuals is dysarthria. Due to their cognitive stability, it is important that people who spend time with individuals with this disease are able to communicate as fully as possible with them. This is necessary in order to improve their day-to-day interactions.

Behavioral intervention is successful when it involves engaging knowledge of the interests and general backgrounds of individuals with cerebellar ataxia. Communication maximizing strategies are also useful, such as exaggeration of articulatory gestures, giving full attention to their responses, repeating where necessary, and slowing down speaking rate. Another intervention technique for speech is to focus on optimizing respiratory and vocal resources as well as training compensatory strategies.

These listed intervention techniques can improve quality of life in individuals with this disease and can be helpful for professionals/clinicians in the field as well as loved ones of those affected.

Dysdiadochokinesia, dysdiadochokinesis, dysdiadokokinesia, dysdiadokokinesis (from Greek "δυς" "dys" "bad", "διάδοχος" "diadochos" "succeeding", "κίνησις" "kinesis" "movement"), often abbreviated as DDK, is the medical term for an impaired ability to perform rapid, alternating movements (i.e., diadochokinesia). Complete inability is called adiadochokinesia.

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.

Dysdiadochokinesia is a feature of cerebellar ataxia and may be the result of lesions to either the cerebellar hemispheres or the frontal lobe (of the cerebrum), it can also be a combination of both. It is thought to be caused by the inability to switch on and switch off antagonising muscle groups in a coordinated fashion due to hypotonia, secondary to the central lesion.

Dysdiadochokinesia is also seen in Friedreich's ataxia and multiple sclerosis, as a cerebellar symptom (including ataxia, intention tremor and dysarthria). It is also a feature of ataxic dysarthria. Dysdiadochokinesia often presents in motor speech disorders (dysarthria), therefore testing for dysdiadochokinesia can be used for a differential diagnosis.

Dysdiadochokinesia has been linked to a mutation in "SLC18A2", which encodes vesicular monoamine transporter 2 (VMAT2).

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.

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.

The National Institute of Neurological Disorders and Stroke (NINDS) conducts and supports research on various movement disorders, including opsoclonus myoclonus. These studies are focused on finding ways to prevent, treat, and cure these disorders, as well as increasing knowledge about them.

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.

Oculomotor apraxia (OMA), also known as Cogan ocular motor apraxia or saccadic initiation failure (SIF) is the absence or defect of controlled, voluntary, and purposeful eye movement. It was first described in 1952 by the American ophthalmologist David Glendenning Cogan. People with this condition have difficulty moving their eyes horizontally and moving them quickly. The main difficulty is in saccade initiation, but there is also impaired cancellation of the vestibulo-ocular reflex. Patients have to turn their head in order to compensate for the lack of eye movement initiation in order to follow an object or see objects in their peripheral vision, but they often exceed their target. There is controversy regarding whether OMA should be considered an apraxia, since apraxia is the inability to perform a learned or skilled motor action to command, and saccade initiation is neither a learned nor a skilled action.

Tandem gait is a gait (method of walking or running) where the toes of the back foot touch the heel of the front foot at each step. Neurologists sometimes ask patients to walk in a straight line using tandem gait as a test to help diagnose ataxia, especially truncal ataxia, because sufferers of these disorders will have an unsteady gait. However, the results are not definitive, because many disorders or problems can cause unsteady gait (such as vision difficulties and problems with the motor neurons or associative cortex). Therefore, inability to walk correctly in tandem gait does not prove the presence of ataxia.

Profoundly affected tandem gait with no other perceptible deficits is a defining feature of posterior vermal split syndrome.

Suspects may also be asked to perform a tandem gait walk during the "walk and turn" part of a field sobriety test.

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.

40 cases were diagnosed in northern Italy between 1940 and 1990. The gene frequency for this autosomal recessive condition was estimated at 1 in 218. In 1989, 16 cases on EOCA were diagnosed in children with a mean onset age of 7.1 In 1990, 20 patients affected by EOCA were studied. It was found that the ataxia of this study's participants affected the pyramidal tracts and peripheral nerves.

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

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.

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

Motor disorders are disorders of the nervous system that cause abnormal and involuntary movements. They can result from damage to the motor system.

Motor disorders are defined in the fifth edition of the "Diagnostic and Statistical Manual of Mental Disorders" (DSM-5) – published in 2013 to replace the fourth text revision (DSM-IV-TR) – as a new sub-category of neurodevelopmental disorders. The DSM-5 motor disorders include developmental coordination disorder, stereotypic movement disorder, and the tic disorders including Tourette syndrome.

Stomping gait (or sensory ataxia gait) is a form of gait abnormality.

Dystonia is a neurological motor disorder that affects muscles and causes involuntary muscle spasms, and it occurs when the part of the brain called the basal ganglia malfunctions. The basal ganglia is located in the cerebrum and is responsible for controlling the coordination, speed, and fluidity of movement as well as suppressing involuntary or unwanted movements. Dystonias can be classified by the affected part(s) of the body.

1. General Dystonia - affects most or all of the body.

2. Focal Dystonia - localized to a specific part of the body.

3. Multifocal Dystonia - localized to two or more unrelated parts of the body.

4. Segmental Dystonia - localized to two or more adjacent parts of the body.

5. Hemidystonia - Involves the arm and leg on the same side of the body.

Body parts usually affected by focal dystonias include the neck, lower face, eyelids, or hands.

Typical treatments for dystonia include medication, surgery, and botox injections. Botox can reduce involuntary movements by blocking signals between muscles and nerves. When all other treatments are unsuccessful, surgery is usually used as a last resort (“Movement Disorders”).

Harding ataxia, also known as Early onset cerebellar ataxia with retained reflexes (EOCARR), is an autosomal recessive cerebellar ataxia originally described by Harding in 1981. This form of cerebellar ataxia is similar to Friedreich ataxia including that it results in poor reflexes and balance, but differs in several ways, including the absence of diabetes mellitus, optic atrophy, cardiomyopathy, skeletal abnormalities, and the fact that tendon reflexes in the arms and knees remain intact. This form of ataxia is characterized by onset in the first 20 years, and is less severe than Friedreich ataxia. Additional cases were diagnosed in 1989, 1990, 1991, and 1998.

Episodic ataxia (EA) is an autosomal dominant disorder characterized by sporadic bouts of ataxia (severe discoordination) with or without myokymia (continuous muscle movement). There are seven types recognised but the majority are due to two recognized entities. Ataxia can be provoked by stress, startle, or heavy exertion such as exercise. Symptoms can first appear in infancy. There are at least 6 loci for EA, of which 4 are known genes. Some patients with EA also have migraine or progressive cerebellar degenerative disorders, symptomatic of either familial hemiplegic migraine or spinocerebellar ataxia. Some patients respond to acetazolamide though others do not.