Calcification of the Basal Ganglia in Chronic Hypoparathyroidism

Rita Rastogi, Norman J. Beauchamp and Paul W. Ladenson

Division of Endocrinology and Metabolism, Departments of Medicine (R.R., P.W.L.) and Radiology (N.J.B.), Johns Hopkins University, Baltimore, Maryland 21287-0003

Address all correspondence and requests for reprints to: Paul W. Ladenson, M.D., Department of Medicine, Division of Endocrinology and Metabolism, The Johns Hopkins University, 1830 East Monument Street, Suite 333, Baltimore, Maryland 21287-0003.

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. 1Go, 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 µg calcitriol and 1000 mg calcium carbonate (oral, daily). After 1 week, his chronic paresthesias resolved and serum calcium rose to 9.2 mg/dl.



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Figure 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).

 
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.

Received November 15, 2002.

Accepted January 6, 2003.

References

  1. Virchow R 1855 Kalk-Metastasen. Virchows Arch Pathol Anat 8:103–113
  2. Bamberger, cited by Von Rokitansky K 1856 Lehrbuch der pathologischen Anatomie, vol 2. Vienna: Wilhelm Braumuller
  3. Eaton LM, Camp JD, Love JG 1939 Symmetric cerebral calcification, particularly of the basal ganglia, demonstrable roentgenographically; calcification of the finer cerebral blood vessels. Arch Neurol Psychiatry 41:921–942
  4. Bennett JC, Maffly RH, Steinbach HL 1959 The significance of bilateral basal ganglia calcification. Radiology 72:368–378[Medline]
  5. Polverosi R, Zambelli C, Sbeghen R 1994 Calcification of the basal nuclei in hypoparathyroidism; the computed and magnetic resonance tomographic aspects. Radiol Med (Torino) 87:5–12




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