[Extrapyramidal symptoms due to calcinosis cerebri in a patient with unknown primary hypoparathyroidism].

With a prevalence of up to 0.6% in the general population, cerebral calcifications are a common finding in neuroimaging tests, particularly in computed tomography (CT). This proportion increases in autopsy studies, in which microcalcifications are found in the globus pallidus and dentate nucleus in up to 70% of cases, as prevalence increases with age.1 Such calcifications are considered to be pathological when they are extensive or bilateral or occur in people under 40 years of age. When calcifications simultaneously involve the nucleus pallidus, the putamen, the dentate nucleus of the cerebellum, and hemispheric white matter (striatopallido-dentate calcinosis), the condition is known as Fahr syndrome.2 The most common causes of Fahr syndrome include, in addition to an idiopathic etiology and congenital infections (toxoplasmosis), changes in calcium metabolism, mainly primary hypoparathyroidism, either autoimmune or associated with a polyglandular syndrome, postoperative hypoparathyroidism or pseudohyperparathyroidism, which account for up to 80% of cases with calcifications in the basal ganglia.1--3 It is however an uncommon condition. Although Delacour in 1850 and Virchow five years later were the first to histologically describe bilateral calcifications in the basal ganglia, it was not until 1939 that Eaton related such calcifications to chronic hypoparathyroidism.3--5 The mechanism by which calcium becomes deposited in those areas has yet to be clearly elucidated. Various hypotheses have been suggested, including chronic changes in intracellular and extracellular calcium and phosphate levels in neuroglial structures, changes in the blood--brain barrier, or a decreased blood flow in the basal ganglia.2,3,6 As regards the clinical consequences, we also do not know why some individuals remain asymptomatic while