|Classification and external resources|
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.
There are many causes of cerebellar ataxia including direct injury, alcohol use, and genetic disease.
Misfunction of the sodium-potassium pump may be a factor in some cerebellar ataxias. The Na+
pump has been shown to control and set the intrinsic activity mode of cerebellar Purkinje neurons. This suggests that the pump might not simply be a homeostatic, "housekeeping" molecule for ionic gradients; but could be a computational element in the cerebellum and the brain. Indeed, an ouabain block of Na+
pumps in the cerebellum of a live mouse results in it displaying ataxia and dystonia. Ataxia is observed for lower ouabain concentrations, dystonia is observed at higher ouabain concentrations.
Considering nicotine's apparent protective effect on other parts of the brain, surprisingly nicotine is toxic to the cerebellum.
Damage to the cerebellum, particularly to the cerebrocerebellum area and the cerebellar vermis, is almost always 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. 
In recent years the cerebellum's role has been observed as not purely motor. It is intimately combined with intellect, emotion and planning.
It is widely thought that cerebellar ataxia is untreatable.
One approach is that it can be ameliorated to varying degrees by means of Frenkel exercises.
Additionally, mild to moderate cerebellar ataxia is treated by buspirone.
It is thought that the buspirone increases the serotonin levels in the cerebellum and so decreases ataxia.
Implications for Intervention
Individuals with cerebellar ataxia have full cognitive awareness: it's 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.
- Autosomal recessive cerebellar ataxia
- Sensory ataxia
- Spinocerebellar ataxia
- Vestibulocerebellar syndrome
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