Fahr’s Syndrome Secondary to Hypoparathyroidism Presenting With Neurological and Cardiac Manifestations

Fahr's syndrome is characterised by bilateral intracranial calcifications secondary to systemic or metabolic disease. We report a 56-year-old man with Fahr's syndrome due to hypoparathyroidism who presented with collapse and seizure-like activity during alcohol consumption. Laboratory investigations demonstrated chronic hypocalcaemia with suppressed parathyroid hormone and hyperphosphataemia. Non-contrast CT revealed symmetrical calcifications of the basal ganglia and cerebellar dentate nuclei, confirming Fahr's syndrome. ECG on admission showed borderline QT prolongation (Bazett 479 ms; heart rate seventy-one beats per minute), consistent with repolarisation delay in hypocalcaemia. Lateral T-wave inversions were observed without chest pain, dynamic ST segment change, or troponin rise, and were interpreted as non-specific repolarisation abnormalities. Continuous telemetry captured several runs of non-sustained ventricular tachycardia (VT). Echocardiography demonstrated mildly reduced left ventricular systolic function with concomitant diastolic dysfunction. The patient received intravenous calcium gluconate followed by oral calcium carbonate and active vitamin D (alfacalcidol), with ongoing rhythm surveillance using a cardiac monitor. On follow-up, there were intermittent supraventricular and ventricular ectopics and brief Wenckebach, but no sustained ventricular arrhythmias. This case highlights the multi-system impact of chronic hypocalcaemia in hypoparathyroidism. While intracranial calcifications are irreversible, timely correction of calcium may ameliorate neurological symptoms and reduce arrhythmia risk. Clinicians should consider metabolic aetiologies in syncope with seizure-like activity and QT prolongation, and institute prompt biochemical correction alongside cardiac monitoring.