Basal ganglia calcification: clinical manifestations and diagnostic evaluation

Physiological intracranial calcification occurs in about 0,3-1,5% of cases. It is asymptomatic and is detected incidentally by neuroimaging. Pathological basal ganglia calcification is due to various causes, such as: metabolic disorders, infectious and genetic diseases and other. Hypoparathyroidism and pseudohypoparathyroidism are the most common causes of pathological basal ganglia calcification. Besides tetany and seizures this condition is presented by parkinsonism and dementia. Such parkinsonism doesn't respond to drugs containing levodopha. Infections (toxoplasmosis, rubella, cytomegalovirus, cysticercosis, AIDS) give multiple and asymmetric intracranial calcification. Inherited and neurodegenerative diseases cause symmetrical, bilateral basal ganglia calcification which is not related to metabolic disorders (blood calcium level and other), those are: Cockayne syndrome, tuberous sclerosis, Fahr's syndrome, Down syndrome and other. We observed some cases of basal ganglia calcification and studied clinical manifestations and treatment tolerance of this pathological condition. Since adequate treatment of hypoparathyroidism may lead to marked clinical improvement, serum concentration of calcium, phosphorus, and parathyreoid hormone is suggested to be determined in all individuals with calcification of the basal ganglia to rule out hypoparathyroidism. Basal ganglia calcification in young patient with acute hepatitis may be result of Wilson disease.