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Intracranial Calcification Due to Hypoparathyroidism

Computed tomography of the head showing bilateral and symmetrical calcifications in basal ganglia in the axial image (A), and in the cerebellum and at the gray-white junction in the sagittal image (B).

Computed tomography of the head showing bilateral and symmetrical calcifications in basal ganglia in the axial image (A), and in the cerebellum and at the gray-white junction in the sagittal image (B).

To the Editor:

A 70-year-old Japanese man with a history of idiopathic hypoparathyroidism presented to the Emergency Department of our hospital owing to weakness in his right leg. Although his primary care doctor had prescribed activated vitamin D analogues, his serum calcium level was slightly low at 8.0 mg/dL. Owing to suspicions of stroke, he underwent radiographic imaging of the head. Computed tomography revealed bilateral and symmetrical calcifications in the basal ganglia, cerebellum, and at the gray-white junction in the axial image and the sagittal image (Figure). These findings were consistent with those of long-term hypoparathyroidism. Diffusion-weighted magnetic resonance imaging revealed a high-intensity area in his left deep white matter of the brain, which was consistent with acute cerebral infarction. He received inpatient treatment for acute cerebral infarction and was discharged with functional recovery.

Hypoparathyroidism is an endocrine disorder caused by deficiency of parathyroid hormone, which results in decreased serum calcium and increased serum phosphorus levels.1 Chronic hypoparathyroidism can cause basal ganglia calcifications, as in this case, cataracts, dental abnormalities, or ectodermal manifestations.1 The mechanism of intracranial calcification in hypoparathyroidism has not been completely understood and may be related more to the duration of hypocalcemia and hyperphosphatemia than parathyroid hormone itself.2 Moreover, hyperphosphatemia increases ectopic calcification in brain tissue.2 The extent of calcification is variable and depends on the duration of metabolic abnormalities, stage of the disease, and volume of the calcium deposit.2Some patients with basal ganglia calcifications develop parkinsonism and other movement disorders including dystonia, hemiballismus, choreoathetosis, and dementia, while others remain asymptomatic.3Hypoparathyroidism-induced intracranial calcification can be incidentally noted on computed tomography as in this patient; however, it does not require further investigation or treatment beyond the management of appropriate serum calcium level.

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-Ko Harada, MD, Tatsuya Fujikawa, MD, PhD

This article originally appeared in the June issue  of The American Journal of Medicine.

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