# Brain Calcifications Secondary to Idiopathic Hyperthyroidism and Hypoparathyroidism

## TL;DR

A rare case of brain calcifications caused by combined hyperthyroidism and hypoparathyroidism is reported, showing how treating the hormonal imbalance resolved neurological symptoms.

## Contribution

This case report highlights hypoparathyroidism as a rare but treatable cause of brain calcifications and seizures.

## Key findings

- The patient's neurological symptoms improved after treatment with calcium, vitamin D, and antithyroid agents.
- Brain calcifications were observed in the basal ganglia and thalami via CT scan.
- The case emphasizes the importance of considering hypoparathyroidism in seizure differential diagnoses.

## Abstract

Background: Thyroid and parathyroid hormones are essential components of the metabolic system and its regulation. Concurrent hyperthyroidism with hypoparathyroidism is an extremely rare finding and is not considered a common etiology of brain calcifications seen on imaging. Brain calcifications can cause a range of neurologic symptoms, including movement disorders, cognitive impairment, and seizures. Prompt recognition and treatment of hypoparathyroidism are essential to prevent or minimize the development of brain calcifications and associated neurologic symptoms.

Case Report: A 39-year-old female presented to the emergency department in an unconscious state with generalized weakness and tonic-clonic seizures for 1 day. On clinical examination, she had jerky movements of her upper limbs, and her Glasgow Coma Scale score was 4/15. Supporting hypoparathyroidism, she had low levels of serum parathyroid hormone, calcium, and vitamin D and a high level of serum phosphorus. Her magnesium level was normal. Thyroid profile revealed hyperthyroidism. Noncontrast-enhanced computed tomography scan at the midbrain level showed multiple bilateral hyperintense areas in the basal ganglia and thalami suggestive of calcifications. The patient was treated with calcium and vitamin D supplements and antithyroid agents that successfully resolved her symptoms.

Conclusion: This case provides important documentation for including hypocalcemia as a result of hypoparathyroidism in the differential diagnosis of patients with seizures. The treatment approach used with our patient can be considered for managing seizures in cases where the underlying cause is challenging to identify. This case highlights the importance of a thorough evaluation and individualized treatment plan for patients with seizures.