Unlike ataxias of cerebellar origin, Bruns apraxia exhibits many frontal lobe ataxia characteristics, with some or all present.

- Difficulty in initiating movement

- Poor truncal mobility

- Falls due to minor balance disturbances

- Greatly hindered postural responses

- Characteristic magnetic gait, the inability to raise one's foot off of the floor.

- Wide base, poor balance control when in stance

- Short stride

- En bloc turns

Often patients with frontal lobe ataxia may experience minute cognitive changes that accompany the gait disturbances, such as frontal dementia and presentation of frontal release signs (Plantar reflex). Urinary incontinence may also be present.

Bruns apraxia can be distinguished from Parkinsonian ataxia and cerebellar ataxia in a number of ways. Patients typically afflicted with Parkinsonian ataxia typically have irregular arm swing, a symptom not typically present in frontal ataxia. Walking stride in cerebellar ataxia varies dramatically, accompanied by erratic foot placement and sudden, uncontrolled lurching, not generally characteristic of Bruns apraxia.

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.

Dysmetria () refers to a lack of coordination of movement typified by the undershoot or overshoot of intended position with the hand, arm, leg, or eye. It is a type of ataxia. It is sometimes described as an inability to judge distance or scale.

Hypermetria and hypometria refer, respectively, to overshooting and undershooting the intended position.

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.

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).

The actual cause of dysmetria is thought to be caused by lesions in the cerebellum or by lesions in the proprioceptive nerves that lead to the cerebellum that coordinate visual, spatial and other sensory information with motor control. Damage to the proprioceptive nerves does not allow the cerebellum to accurately judge where the hand, arm, leg, or eye should move. These lesions are often caused by strokes, multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), or tumors.

According to the research article cited above, motor control is a learning process that utilizes APPGs. Disruption of APPGs is possibly the cause of ataxia and dysmetria and upon identification of the motor primitives, clinicians may be able to isolate the specific areas responsible for the cerebellar problems.

There are two types of cerebellar disorders that produce dysmetria, specifically midline cerebellar syndromes and hemispheric cerebellar syndromes. Midline cerebellar syndromes can cause ocular dysmetria, which is a condition in which the pupils of the eye overshoot. Ocular dysmetria makes it difficult to focus vision onto one object. Hemispheric cerebellar syndromes cause dysmetria in the typical motor sense that many think of when hearing the term dysmetria.

A common motor syndrome that causes dysmetria is cerebellar motor syndrome, which also marked by impairments in gait (also known as ataxia), disordered eye movements, tremor, difficulty swallowing and poor articulation. As stated above, cerebellar cognitive affective syndrome (CCAS) also causes dysmetria.

Cerebellar ataxia can occur as a result of many diseases and presents with symptoms of an inability to coordinate balance, gait, extremity and eye movements. Lesions to the cerebellum can cause dyssynergia, dysmetria, dysdiadochokinesia, dysarthria and ataxia of stance and gait. Deficits are observed with movements on the same side of the body as the lesion (ipsilateral). Clinicians often use visual observation of people performing motor tasks in order to look for signs of ataxia.

Damage to the cerebellum, particularly to the cerebrocerebellum area and the cerebellar vermis, is very often associated with clinical depression and often with alcoholism. Due to difficulties in mobility, self-care, everyday activities, and pain/discomfort, those with cerebellar ataxia are more likely to be diagnosed with anxiety and depression. Almost a third of patients with isolated, late onset cerebellar ataxia go on to develop multiple system atrophy.

In recent years the cerebellum's role has been observed as not purely motor. It is intimately combined with intellect, emotion and planning.

Tremor is the uncontrollable shaking of an arm or a leg. Twitches or jerks of body parts may occur due to a startling sound or unexpected, sudden pain. Spasms and contractions are temporary abnormal resting positions of hands or feet. Spasms are temporary while contractions could be permanent. Gait problems are problems with the way one walks or runs. This can mean an unsteady pace or dragging of the feet along with other possible irregularities (Stone).

Motor disorders are malfunctions of the nervous system that cause involuntary or uncontrollable movements or actions of the body (Stone). These disorders can cause lack of intended movement or an excess of involuntary movement (Mandal). Symptoms of motor disorders include tremors, jerks, twitches, spasms, contractions, or gait problems.

Typically, episodic ataxia presents as bouts of ataxia induced by startle, stress, or exertion. Some patients also have continuous tremors of various motor groups, known as myokymia. Other patients have nystagmus, vertigo, tinnitus, diplopia or seizures.

Episodic ataxia type-3 (EA3) is similar to EA1 but often also presents with tinnitus and vertigo. Patients typically present with bouts of ataxia lasting less than 30 minutes and occurring once or twice daily. During attacks, they also have vertigo, nausea, vomiting, tinnitus and diplopia. These attacks are sometimes accompanied by headaches and precipitated by stress, fatigue, movement and arousal after sleep. Attacks generally begin in early childhood and last throughout the patients' lifetime. Acetazolamide administration has proved successful in some patients. As EA3 is extremely rare, there is currently no known causative gene. The locus for this disorder has been mapped to the long arm of chromosome 1 (1q42).

Onset of symptoms usually occur in early adulthood and is characterized by intention tremor, progressive ataxia, convulsions, and myoclonic epileptic jerks.

Tremors usually affect one extremity, primarily the upper limb, and eventually involve the entire voluntary motor system. Overall, the lower extremity is usually disturbed less often than the upper extremity.

Additional features of the syndrome include: an unsteady gait, seizures, muscular hypotonia, reduced muscular coordination, asthenia, adiadochokinesia and errors with estimating range, direction, and force of voluntary movements. Mental deterioration can occur, however it is rare.

Even though OMA is not always associated with developmental issues, children with this condition often have hypotonia, decreased muscle tone, and show developmental delays. Some common delays are seen in speech, reading and motor development

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.

Telangiectasias are widened blood vessels that can develop anywhere on the skin, mucous membranes, whites of the eyes, and even in the brain. Telangiectasias are associated with multiple systemic signs, the most serious of which are unusual sensitivity to ionizing radiation, excessive chromosomal breakage, and a deficiency in the immune system. Ataxia telangiectasia results from defects in the ataxia telangiectasia mutated gene, which can cause abnormal cell death in various places of the body, including brain areas related to coordinated movement of the eyes. Patients with ataxia telangiectasia have prolonged vertical and horizontal saccade latencies and hypometric saccades, and, although not all, some patients show head thrusts.

Most cases of autosomal recessive cerebellar ataxia are early onset, usually around the age of 20. People with this type of ataxia share many characteristic symptoms including:

- frequent falls due to poor balance

- imprecise hand coordination

- postural or kinetic tremor of extremities or trunk

- dysarthria

- dysphasia

- vertigo

- diplopia

- lower extremity tendon reflexes

- dysmetria

- minor abnormalities in ocular saccades

- attention defects

- impaired verbal working memory and visuospatial skills

- Normal life expectancy

Autosomal recessive ataxias are generally associated with a loss of proprioception and vibration sense. Arreflexia is more common in autosomal recessive ataxia than autosomal dominant ataxias. Also, they tend to have more involvement outside of the nervous system. Mutations in subunit of the mitochondrial DNA polymerase (POLG) have been found to be a potential cause of autosomal recessive cerebellar ataxia.

OPCA is characterized by progressive cerebellar ataxia, leading to clumsiness in body movements, veering from midline when walking, wide-based stance, and falls without signs of paralysis or weakness. Clinical presentation can vary greatly between patients, but mostly affects speech, balance and walking. Other possible neurological problems include spasmodic dysphonia, hypertonia, hyperreflexia, rigidity, dysarthria, dysphagia and neck dystonic posture.

Deep brain stimulation may provide relief from some symptoms of Benedikt syndrome, particularly the tremors associated with the disorder.

Autosomal recessive cerebellar ataxia type 1 (ARCA1) is a condition characterized by progressive problems with movement. Signs and symptoms of the disorder first appear in early to mid-adulthood. People with this condition initially experience impaired speech (dysarthria), problems with coordination and balance (ataxia), or both. They may also have difficulty with movements that involve judging distance or scale (dysmetria). Other features of ARCA1 include abnormal eye movements (nystagmus) and problems following the movements of objects with their eyes. The movement problems are slowly progressive, often resulting in the need for a cane, walker, or wheelchair.

ARSACS is usually diagnosed in early childhood, approximately 12–24 months of age when a child begins to take their first steps. At this time it manifests as a lack of coordination and balance resulting in frequent falls. Some of the signs and symptoms include:

- Stiffness of the legs

- Appendicular and trunk ataxia

- Hollow foot and hand deformities

- Ataxic dysarthria

- Distal muscle wasting

- Horizontal gaze nystagmus

- Spasticity

It is characterized by the presence of an oculomotor nerve (CN III) palsy and cerebellar ataxia including tremor and involuntary choreoathetotic movements. Neuroanatomical structures affected include CNIII nucleus, Red nucleus, corticospinal tracts, brachium conjunctivum, and the superior cerebellar peduncle decussation. It has a very similar cause, morphology and signs and symptoms to Weber's syndrome; the main difference between the two being that Weber's is more associated with hemiplegia (i.e. paralysis), and Benedikt's with hemiataxia (i.e. disturbed coordination of movements). It is also similar to Claude's syndrome, but is distinguishable in that Benedikt's has more predominant tremor and choreoathetotic movements while Claude's is more marked by the ataxia.

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

Symptoms include:

- opsoclonus (rapid, involuntary, multivectorial (horizontal and vertical), unpredictable, conjugate fast eye movements without intersaccadic [quick rotation of the eyes] intervals)

- myoclonus (brief, involuntary twitching of a muscle or a group of muscles)

- cerebellar ataxia, both truncal and appendicular

- aphasia (a language disorder in which there is an impairment of speech and of comprehension of speech, caused by brain damage)

- mutism (a language disorder in which a person does not speak despite evidence of speech ability in the past, often part of a larger neurological or psychiatric disorder)

- lethargy

- irritability or malaise

- drooling

- strabismus (a condition in which the eyes are not properly aligned with each other)

- vomiting

- sleep disturbances

About half of all OMS cases occur in association with neuroblastoma (a cancer of the sympathetic nervous system usually occurring in infants and children).

In most cases OMS starts with an acute flare-up of physical symptoms within days or weeks, but some less obvious symptoms such as irritability and malaise may begin weeks or months earlier.