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For paraneoplastic cerebellar degeneration, the average age of onset is 50 years, generally affecting a greater population of males than females. [2] Nutritional and alcoholic cerebellar degeneration, being more prevalent than paraneoplastic cerebellar degeneration, affects individuals with a thiamine deficiency and dipsomaniacs, respectively. [2]
Alcoholic polyneuropathy usually has a gradual onset over months or even years, although axonal degeneration often begins before an individual experiences any symptoms. [ 2 ] The disease typically involves sensory issues and motor loss, as well as painful physical perceptions, though all sensory modalities may be involved. [ 3 ]
Alcohol-related brain damage [1] [2] alters both the structure and function of the brain as a result of the direct neurotoxic effects of alcohol intoxication or acute alcohol withdrawal. Increased alcohol intake is associated with damage to brain regions including the frontal lobe , [ 3 ] limbic system , and cerebellum , [ 4 ] with widespread ...
Heavy alcohol consumption also damages the nerves in arms and legs, i.e. peripheral neuropathy, as well as the cerebellum that controls coordination thereby leading to the development of cerebellar ataxia. These patients frequently have problems with sensation in their extremities and may demonstrate unsteadiness on their feet. [3]
Cerebellar ataxia with neuropathy and vestibular areflexia syndrome (CANVAS) is an autosomal recessive late-onset heredodegenerative multisystem neurological disease. The symptoms include poor balance and difficulty walking. Chronic cough and difficulty swallowing may also be present.
The classic triad of symptoms found in Wernicke encephalopathy is: [11] ophthalmoplegia (later expanded to other eye movement disorders, most commonly affecting the lateral rectus muscle. [11] Lateral nystagmus is most commonly seen although lateral rectus palsy, usually bilateral, may be seen). ataxia (later expanded to imbalance or any ...