Objective:

To illustrate the role of metabolic evaluation in refractory seizures and demonstrate how enzyme-inducing antiseizure medications can exacerbate hypocalcemia in primary hypoparathyroidism.

Background:

Seizures are a common presentation to ED. Most of the chronic seizures are attributable to epilepsy or an underlying structural condition. Hypocalcemia, although a common cause of acute seizures, remains an undervalued etiology for long term seizures refractory to polytherapy. Chronic hypocalcemia, often due to hypoparathyroidism, can present with seizures and basal ganglia calcifications, as seen in Fahr’s syndrome. In addition, long-term use of enzyme-inducing antiepileptics such as phenytoin and carbamazepine may exacerbate hypocalcemia by accelerating vitamin D catabolism.

Design/Methods:

NA

Results:

We report the case of a 27-year-old male who presented with recurrent generalized tonic–clonic seizures for one week, accompanied by abnormal posturing and perioral paresthesias. He had a history of seizure disorder for five years and was on multiple antiepileptic drugs (Phenytoin, Valproate, Carbamazepine). Examination revealed positive Trousseau’s and Chvostek’s signs. Laboratory investigations demonstrated severe hypocalcemia (serum calcium 2.2 mg/dL; ionized calcium 0.55 mmol/L), low parathyroid hormone (1.82 pg/mL), hypomagnesemia, and hyperphosphatemia. CT head without contrast showed bilateral symmetrical basal ganglia calcifications, confirming the diagnosis of Fahr’s syndrome secondary to hypoparathyroidism. The patient was managed with intravenous calcium gluconate, magnesium sulfate, and levetiracetam (non-enzyme inducer), while previous enzyme inducing antiepileptic medications were discontinued. Over 24 hours, serum calcium normalized, and seizures subsided. He was discharged on oral calcium, calcitriol, and levetiracetam, with dietary counseling and regular follow-up.

Conclusions:

This case underscores the importance of considering hypocalcemia as a reversible cause of refractory seizures. Prompt recognition of metabolic etiologies can prevent unnecessary escalation of antiepileptic therapy and avoid iatrogenic complications. With correction of calcium levels and optimization of medications, our patient experienced significant improvement and reassurance. He remained seizure-free, adherent to treatment, and under regular endocrinology follow-up.