Cerebellar Lesions

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Cerebellar Lesions According to an article by Rhawn Joseph, Ph.D., each of the deep cerebellar nuclei maintains a semi-independent map of the human body (2000). The cerebellum is tonically active, and is presumed to exert a stabilizing influence on motor function; accordingly, it is functionally responsible for coordination and smooth fine tuning of movement, in addition to influencing timing. Not only is the cerebellum associated with motor functioning, but, importantly, also with classical conditioning: e.g., the learning of new motor programs (Joseph, 2000). It is associated with the acquisition if finely skilled movements, such as playing an instrument, playing a sport, and performance dance. Interestingly, as motor information is acquired, it takes time for the cerebellum to acquire control over the specific task. With the notion of “practice makes perfect,” task control shifts from conscious cortical control (active, practicing memory) to the subconscious realm and control of the cerebellum. Hence, the cerebellum plays an integrated and important part in complex learning and memory (Joseph, 2000.) During early learning stages, cerebellar climbing fibers are activated, and mossy fibers seem to modulate and to monitor ongoing and related activity in the learning context. Lesions occurring in the cerebellum have the unfortunate effect of abolishing conditioned response acquisition and retention. Such lesions and/or diseases cause motor incoordination called ataxia, with symptoms of tremors, instability and teetering, and an inability to maintain regular movement of tempo (nanonline.org). There are three known major cerebellar syndromes. The vestibulocerebellar cortex controls movement of the eyes and body relating to gravity and turning of the head in space; damage to this area results in ataxia gait and stance, as described above. The spinocerebellar system, which receives information via rapid spinocerebellar pathways during the duration of movement, modulates and smoothes that movement. Lesions occurring in the spinocerebellar system are a result of chronic alcoholism and thiamine deficiency (nanonline.org, Joseph, 2000), and results in difficulty producing rapid and smooth movements. There occurs a prominent shuffle, wide gait, and hesitating steps, with ataxia, tremor and difficulty in lower limb coordination. Lastly, lesions of the cerebrocerebellum (neocerebellum) have blatant effects on well- learned volitional movements, as it has direct pathways with cerebral cortex motor control regions. Several symptoms exist to suggest cerebellar lesions. Joseph (2000) reports a study by Gordon Holmes (1971, 1939) that investigated cerebellar disturbances following gunshot wounds. Deficits involved voluntary/skilled motor function, gait ataxia, dysarthria (loss of proprioceptive input), asynergia (loss of

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