Diagnosis of any cerebellar disorder or syndrome should be made by a qualified neurologist. Prior to referring a patient to a neurologist, a general practitioner or MS nurse will perform a finger-to-nose test. The clinician will raise a finger in front of the patient and ask him to touch it with his finger and then touch his nose with his forefinger several times. This shows a patient’s ability to judge the position of a target. Other tests that could be performed are similar in nature and include a heel to shin test in which proximal overshoot characterizes dysmetria and an inability to draw an imaginary circle with the arms or legs without any decomposition of movement. After a positive result in the finger-to-nose test, a neurologist will do a magnetic resonance image (MRI) to determine any damage to the cerebellum.

Cerebellar patients encounter difficulties to adapt to unexpected changes of the inertia of the limbs. This can be used to increase dysmetria and confirm a diagnosis of cerebellar dysfunction. Patients also show an abnormal response to changes in damping. These findings confirm a role of the cerebellum in predictions.

Diagnosis consists of a variety of tests, including but not limited to:

- Measurement of orthostatic blood pressure

- Coordination

- rapid, alternating movements

- stroking of heel from along the opposite shin from knee to ankle

- finger-to-nose testing.

- Primary sensory modalities are examined with the following methods, searching for focal sensory loss, graded distal sensory loss, or levels of decreased sensation, hyperesthesia or dysesthesia.

- light touch

- pin-prick

- temperature

- position

- vibration

- Focused gait examination, which examines stationary position and walking abnormalities. Walking generally exposes any faults within the complex neurological communication between systems as weight is shifted from one foot to the other.

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.

Abnormalities in diadochokinesia can be seen in the upper extremity, lower extremity and in speech. The deficits become visible in the rate of alternation, the completeness of the sequence, and in the variation in amplitude involving both motor coordination and sequencing. Average rate can be used as a measure of performance when testing for dysdiadochokinesia.

Dysdiadochokinesia is demonstrated clinically by asking the patient to tap the palm of one hand with the fingers of the other, then rapidly turn over the fingers and tap the palm with the back of them, repeatedly. This movement is known as a pronation/supination test of the upper extremity. A simpler method using this same concept is to ask the patient to demonstrate the movement of trying a doorknob or screwing in a light bulb. When testing for this condition in legs, ask the patient to tap your hand as quickly as possible with the ball of each foot in turn. Movements tend to be slow or awkward. The feet normally perform less well than the hands. When testing for dysdiadochokinesia with speech the patient is asked to repeat syllables such as /pə/, /tə/, and /kə/; variation, excess loudness, and irregular articular breakdown are signs of dysdiadochokinesia.

Clinical diagnosis is conducted on individuals with age onset between late teens and late forties who show the initial characteristics for the recessive autosomal cerebellar ataxia.

The following tests are performed:

- MRI brain screening for cerebellum atrophy.

- Molecular genetic testing for SYNE-1 sequence analysis.

- Electrophysiologic studies for polyneurotherapy

- Neurological examination

Prenatal diagnosis and preimplantation genetic diagnosis (PGD) can be performed to identify the mothers carrying the recessive genes for cerebellar ataxia.

Different types of ataxia:

- congenital ataxias (developmental disorders)

- ataxias with metabolic disorders

- ataxias with a DNA repair defect

- degenerative ataxias

- ataxia associated with other features.

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.

"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.

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).

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.

A diagnosis of Friedreich's ataxia requires a careful clinical examination, which includes a medical history and a thorough physical exam, in particular looking for balance difficulty, loss of proprioception, absence of reflexes, and signs of neurological problems. Genetic testing now provides a conclusive diagnosis. Other tests that may aid in the diagnosis or management of the disorder include:

- Electromyogram (EMG), which measures the electrical activity of muscle cells,

nerve conduction studies, which measure the speed with which nerves transmit impulses

- Electrocardiogram (ECG), which gives a graphic presentation of the electrical activity or beat pattern of the heart

- Echocardiogram, which records the position and motion of the heart muscle

- Blood tests to check for elevated glucose levels and vitamin E levels

- Magnetic resonance imaging (MRI) or computed tomography (CT) scans, tests which provide brain and spinal cord images that are useful for ruling out other neurological conditions

Because OMS is so rare and occurs at an average age of 19 months (6 to 36 months), a diagnosis can be slow. Some cases have been diagnosed as having been caused by a virus. After a diagnosis of OMS is made, an associated neuroblastoma is discovered in half of cases, with median delay of 3 months.

The interictal EEG pattern is usually normal.

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.

Type 1 (AOA1) usually has an onset of symptoms during childhood. It is an autosomal recessive cerebellar ataxia (ARCA) associated with hypoalbuminemia and hypercholesterolemia. Mutations in the gene APTX, which encodes for aprataxin, have been identified to be responsible for AOA1. Elevated creatine kinase is occasionally present, in addition to a sensorimotor axonal neuropathy, as shown by nerve conduction velocity studies. In addition, MRI studies have shown cerebellar atrophy, mild brainstem atrophy, and, in advanced cases, cortical atrophy

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.

Currently there are no clinically established laboratory investigations available to predict prognosis or therapeutic response.

Tumors in children who develop OMS tend to be more mature, showing favorable histology and absence of n-myc oncogene amplification than similar tumors in children without symptoms of OMS. Involvement of local lymph nodes is common, but these children rarely have distant metastases and their prognosis, in terms of direct morbidity and mortality effects from the tumor, is excellent. The three-year survival rate for children with non-metastatic neuroblastoma and OMS was 100% according to Children’s Cancer Group data (gathered from 675 patients diagnosed between 1980 and 1994); three-year survival in comparable patients with OMS was 77%. Although the symptoms of OMS are typically steroid-responsive and recovery from acute symptoms of OMS can be quite good, children often suffer lifelong neurologic sequelae that impair motor, cognitive, language, and behavioral development.

Most children will experience a relapsing form of OMS, though a minority will have a monophasic course and may be more likely to recover without residual deficits. Viral infection may play a role in the reactivation of disease in some patients who had previously experienced remission, possibly by expanding the memory B cell population. Studies have generally asserted that 70-80% of children with OMS will have long-term neurologic, cognitive, behavioral, developmental, and academic impairment. Since neurologic and developmental difficulties have not been reported as a consequence of neuroblastoma or its treatment, it is thought that these are exclusively due to the immune mechanism underlying OMS.

One study concludes that: ""Patients with OMA and neuroblastoma have excellent survival but a high risk of neurologic sequelae. Favourable disease stage correlates with a higher risk for development of neurologic sequelae. The role of anti-neuronal antibodies in late sequelae of OMA needs further clarification"."

Another study states that: ""Residual behavioral, language, and cognitive problems occurred in the majority"."

In diagnosing autosomal dominant cerebellar ataxia the individuals clinical history or their past health examinations, a current physical examination to check for any physical abnormalities, and a genetic screening of the patients genes and the genealogy of the family are done. The large category of cerebellar ataxia is caused by a deterioration of neurons in the cerebellum, therefore magnetic resonance imaging (MRI) is used to detect any structural abnormality such as lesions which are the primary cause of the ataxia. Computed tomography (CT) scans can also be used to view neuronal deterioration, but the MRI provides a more accurate and detailed picture.

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.

Ataxia with oculomotor apraxia type 2 (AOA2) has its onset during adolescence. It is characterized by cerebellar atrophy and peripheral neuropathy. Sufferers of Type 2 have high amounts of another protein called alpha-fetoprotein (AFP), and may also have high amounts of the protein creatine phosphokinase (CPK). Mutations in the SETX gene are the cause of the disease. AOA2 shows cerebellar atrophy, loss of Purkinje cells, and demyelination. In particular, there is a failure of the cerebrocerebellar circuit in AOA2 that has been shown to be responsible for the weaker coordination of complex cognitive functions such as working memory, executive functions, speech, and sequence learning. Although there is no sign of mental retardation or severe dementia, even after long disease duration, research on families with possible AOA2 have shown mild cognitive impairment as indexed by the Mini-Mental State Examination (MMSE) and the Mattis Dementia Rating Scale. These impairments appear to be mostly due to a deficit in initiation and concept subtests.

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.

For a prognosis, treatment, and any other information, please consult your doctor.

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.

Treatment for this rare genetic disorder can be physical therapy, there have been antibiotics found to be affective, and surgery has been found to be another solution.

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.