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Clinical abnormalities in multiple sclerosis (MS) have traditionally been attributed to inflammation, demyelination, or degeneration of axons within the brain and spinal cord. Among those symptoms, clinical deficits due to cerebellar dysfunction, including loss of coordination, ataxia, tremor, and dysarthria, can reduce function substantially, are less likely to remit, and are more likely to be associated with progressive MS in the future.1 Interestingly, cerebellar signs and symptoms are sometimes seen in patients in whom structural lesions or inflammation of the cerebellum cannot be detected. These symptoms can be paroxysmal, similar to trigeminal neuralgia in patients with MS, which preferentially responds to sodium channel blockers. What is the basis for these clinical deficits?
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- © 2016 American Academy of Neurology
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