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Symptoms and Signs – Differential Diagnosis of Spinocerebellar Ataxia
• Acquired vitamin E deficiency: differs from SCAs in that patients almost always have a clinically evident disorder of fat malabsorption.
• Creutzfeldt-Jakob disease: differs from the SCAs in that the ataxia progresses relatively rapidly and is accompanied by dementia and myoclonus.
• Mitochondrial encephalomyopathies
• Multiple sclerosis, other central nervous system inflammatory diseases: differ from SCAs in that ataxia, when present, usually presents acutely to subacutely.
• Multiple systems atrophy: differs from the SCAs in that age at onset n present.
• Paraneoplastic cerebellar degeneration: differs from SCAs in that the ataxia progresses relatively rapidly.
• Posterior fossa mass lesions
• Sensory ataxias: differ from the SCAs in that the primary defect is not one of cerebellar function but of sensory inputs into the cerebellum. They can be the result of peripheral neuropathies or spinal cord disease that involves the posterior columns.
• Superficial siderosis: differs from the SCAs in that it also often produces sensorineural hearing loss, anosmia, dementia, and bladder disturbance.
• Toxin exposure (alcohol, phenytoin, organic mercury)
• Wilson’s disease: differs from the SCAs in that there is often accompanying parkinsonism, psychiatric manifestations, and hepatic dysfunction.
is usually later and parkinsonism, long tract signs, and orthostatic hypotension are ofte• Friedreich’s ataxia: differs from the SCAs in that inheritance is autosomal recessive, it almost always begins in childhood or adolescence, and it is associated with early lower limb areflexia.
• Acquired vitamin E deficiency: differs from SCAs in that patients almost always have a clinically evident disorder of fat malabsorption.
• Creutzfeldt-Jakob disease: differs from the SCAs in that the ataxia progresses relatively rapidly and is accompanied by dementia and myoclonus.
• Mitochondrial encephalomyopathies
• Multiple sclerosis, other central nervous system inflammatory diseases: differ from SCAs in that ataxia, when present, usually presents acutely to subacutely.
• Multiple systems atrophy: differs from the SCAs in that age at onset n present.
• Paraneoplastic cerebellar degeneration: differs from SCAs in that the ataxia progresses relatively rapidly.
• Posterior fossa mass lesions
• Sensory ataxias: differ from the SCAs in that the primary defect is not one of cerebellar function but of sensory inputs into the cerebellum. They can be the result of peripheral neuropathies or spinal cord disease that involves the posterior columns.
• Superficial siderosis: differs from the SCAs in that it also often produces sensorineural hearing loss, anosmia, dementia, and bladder disturbance.
• Toxin exposure (alcohol, phenytoin, organic mercury)
• Wilson’s disease: differs from the SCAs in that there is often accompanying parkinsonism, psychiatric manifestations, and hepatic dysfunction.
is usually later and parkinsonism, long tract signs, and orthostatic hypotension are ofte• Friedreich’s ataxia: differs from the SCAs in that inheritance is autosomal recessive, it almost always begins in childhood or adolescence, and it is associated with early lower limb areflexia.
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