Important metabolic causes of parkinsonism include hypothyroidism and parathyroid dysfunction. Patients with hyperparathyroidism have clinical presentation identical to that of idiopathic PD, but the syndrome is levodopa resistant. The symptoms, however, may be relieved after resolution of the parathyroid dysfunction by surgical removal of the parathyroid adenoma. Hypoparathyroidism may also cause levodopa unresponsive parkinsonism (69,70).
Bilateral striopallidodentate calcinosis, also known as Fahr's disease, is a rare disorder with calcium deposition in the subcortical nucleii and white matter bilaterally. Parkinsonism is reported in 57% of patients with this disorder; other movement disorders seen in Fahr's disease include chorea, tremor, dystonia, athetosis, and orofacial dyskinesias (71). Additional neurological manifestations include cognitive impairment, cerebellar signs, speech disorder, gait disorder, pyramidal signs, sensory symptoms, and psychiatric features (72). Patients have parkinsonism without evidence of parathyroid dysfunction in association with dementia and cerebellar signs. Lewy bodies may be found on autopsy. Response to levodopa is variable (72). No gene has yet been identified although linkage to chromosome 14 has been suggested (73).
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