Secondary Hypoparathyroidism and Intracranial Calcifications

Hypoparathyroidism is a well-known potential complication of total thyroidectomy and is permanent in 1-3% of cases. One rare complication of chronic hypocalcemia is intracranial calcification, most commonly affecting the basal ganglia. We present a patient with longstanding postsurgical hypoparathyroidism, extensive central nervous system (CNS) calcinosis, but only mild neurologic symptoms.

Case Description:

A 46-year-old male presented for evaluation of worsening dyspnea, orthopnea, palpitations, peripheral edema, and dizziness over four months. The patient underwent thyroidectomy at age 16 years for management of a goiter. Despite persistent hypocalcemia following surgery, he was only prescribed calcium carbonate 3,000 mg daily, and serum calcium levels before hospital admission were consistently < 6.5 mg/dL. Admission laboratories were notable for serum calcium 5.0 mg/dL (8.5-10.1) and intact PTH 6.3 pg/mL (18.4-80.1). Neither Chvostek’s nor Trousseau’s signs were elicited. Computed tomography (CT) of the head done to evaluate dizziness showed extensive calcification of the basal ganglia, thalamus, and cerebellar hemispheres. Adding calcitriol to the patient’s regimen for hypoparathyroidism improved serum calcium into the range of 8-9 mg/dL, though sevelamer was required to control hyperphosphatemia. The patient was also found to have heart failure with reduced ejection fraction. Despite appropriate management of heart failure and resolution of other symptoms, the patient’s dizziness persisted.

Discussion:

The mechanisms by which chronic hypocalcemia lead to CNS calcification are not entirely clear, but it is known that persistently low serum calcium level and calcium/phosphate ratio predisposes to calcification of arterial walls, the perivascular space, and eventually neurons. Most commonly affected sites are the basal ganglia, thalamus, dentate nucleus, cerebral cortex, and cerebellum. Progressive mineralization of CNS tissue appears to eventually compromise blood flow, leading to injury and loss of function in affected areas of brain. The patient’s persistent dizziness despite appropriate treatment of hypocalcemia and heart failure appears to be due to the effects of cerebellar calcification. This case illustrates the importance of recognizing permanent hypoparathyroidism after anterior neck surgery and appropriate management of hypocalcemia to prevent CNS calcification from occurring. Though significant CNS calcification takes many years to occur, the effects are permanent. CT to evaluate for CNS calcifications should be considered in patients with longstanding hypocalcemia and neurological complaints or examination findings.