Calcification of the basal ganglia in chronic hypoparathyroidism.

An 80-yr-old man with a more than 60-yr history of postsurgical hypoparathyroidism was evaluated for hypocalcemia detected during hospitalization after a fall. The patient had long-standing intermittent paresthesias in his distal extremities, but denied muscle cramps, tetany, or seizures. His past medical history was remarkable for an episode of nephrolithiasis in his 20s. He had been taking up to 4000 mg calcium carbonate (oral, daily) before admission. On examination, Chvostek and Trousseau signs, tremor, and rigidity were absent. Laboratory studies included: 5.9 mg/dl serum calcium (normal range, 8.4–10.5), 0.78 mmol/liter ionized calcium (normal range, 1.13–1.32), 6.7 mg/dl phosphate (normal range, 2.7–4.5), 3.2 g/dl albumin (normal range, 3.5–5.3), and 1 pg/ml intact PTH (normal range, 10–65). In Fig. 1, brain computed tomography showed diffuse, symmetric parenchymal calcifications involving the dentate nuclei (A), thalami (B, curved arrow), globus palladi (B, arrowhead), caudate heads (B, straight arrow), and deep cerebral white matter (C). The patient was treated with 0.5 g calcitriol and 1000 mg calcium carbonate (oral, daily). After 1 week, his chronic paresthesias resolved and serum calcium rose to 9.2 mg/dl. Although Virchow (1) and Bamberger (2) independently described the histology of bilateral basal ganglia calcifications in 1855, it was not until 1939 that their association with chronic hypoparathyroidism was recognized by Eaton et al. (3). Microscopic colloid deposition around cerebral blood vessels is followed by calcification most commonly in the basal ganglia, but also in the thalami, dentate nuclei, cerebral cortex, centrum semiovale, and mesencephalic gray matter (4, 5). Patients may remain asymptomatic or develop Parkinsonian features.