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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 (unilaterally). 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. 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, incorrectly, that cerebellar ataxia is untreatable.
However, it can be ameliorated to varying degrees by means of Frenkel exercises.
- Autosomal recessive cerebellar ataxia
- Sensory ataxia
- Spinocerebellar ataxia
- Vestibulocerebellar syndrome
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