Introduction: Fahr’s syndrome (FS) is a rare neurodegenerative disorder characterized by bilateral and symmetrical calcification of basal ganglia and other brain structures. In contrast to Fahr’s disease, FS is distinguished by the association of secondary etiology. The diagnosis is confirmed by neuroimaging studies such as a head computer tomography (CT) scan or magnetic resonance imaging, which displays the calcification of basal ganglia and other structures in a bilateral and symmetrical pattern. Case Report: A 63-year-old female with a previous history of total thyroidectomy and ischemic stroke presented to our hospital with altered mentation and recurrent generalized tonic-clonic seizures. Laboratory evaluation revealed hypocalcemia, hypokalemia, and hypoparathyroidism. Imaging with head CT was consistent with FS, demonstrating bilateral, symmetrical, and extensive calcification of basal ganglia, corona radiata, and cerebellar hemispheres with ventricular enlargement. Conclusion: Our case represents a long-term consequence of untreated post-surgical hypoparathyroidism, which led to secondary FS. Long-term hypocalcemia and low calcium/phosphate ratio are associated with basal ganglia calcification in patients with hypoparathyroidism. Maintenance of eucalcemic and euphosphatemic state is essential as the preventive measure for metastatic calcification. There is currently no definitive treatment for FS, with adjunctive symptomatic treatments to reduce the clinical manifestations.

Aim: To describe a rare case of Fahr’s syndrome (FS) associated with chronic post-surgical hypoparathyroidism and hypocalcemia. Case Presentation: A 63-year-old female with a previous history of total thyroidectomy and hemiplegia presented to our hospital with altered mentation and recurrent generalized tonic-clonic seizures. Laboratory evaluation revealed hypoparathyroidism, hypocalcemia, and hypokalemia. Head computed tomography (CT) scan was consistent with FS, demonstrating extensive, bilateral, and symmetrical calcified deposits in the brain, predominantly in basal ganglia, corona radiata, and cerebellar hemispheres. The association with post-surgical hypoparathyroidism and relevant biochemical indices determined the suspected etiology of the pathologic process of ectopic calcification. Discussion: FS is a rare, neurodegenerative disorder characterized by abnormal bilateral ectopic calcified deposits in the basal ganglia and other brain structures. FS presents with a wide variety of neurological and psychiatric manifestations. The diagnosis is confirmed by neuroimaging studies such as a head CT scan or magnetic resonance imaging, which displays the calcification of BG and other structures in a bilateral and symmetrical pattern. Biochemical analysis may adjunctively identify the underlying risk factor of the disease. Conclusion: Our case represents a long-term severe consequence of untreated post-surgical hypoparathyroidism, which has consequently led to irreversible secondary FS. Maintenance of eucalcemic and euphosphatemic states is essential to prevent the progression of ectopic cerebral calcification.