OBJECTIVE: Seizures following administration of potent bisphosphonates have been reported only sporadically in the medical literature. The rare cases described were often attributed to other precipitating factors such as hypoglycemia, acute infection, or predisposition to post-bisphosphonate hypocalcemia. We review the previous cases and present a new case of suspected seizure episode following zoledronic acid therapy. METHODS: We describe a case of a 63-year-old woman with a history of well-controlled epileptic disorder with no seizure activity in recent years. She was treated with intravenous zoledronic acid due to osteoporosis. Twelve hours after treatment, she suffered an episode of loss of consciousness with urinary incontinence suspected to be seizure-related. RESULTS: Unlike previously reported cases, our patient had a low risk for postinfusion hypocalcemia as her creati-nine, calcium, parathyroid hormone, and vitamin D were all within normal limits prior to the infusion. CONCLUSION: Our interpretation of the scenario described is based on clinical judgment and not supported by ancillary studies. Nevertheless, our case, along with the limitations described, joins other reports, and raises questions about possible interaction between a convulsion disorder and a potent bone resorption inhibition administration, leading to a relative hypocalcemia and possible seizure threshold reduction. This question should be further explored by other studies.
OBJECTIVE: Seizures following administration of potent bisphosphonates have been reported only sporadically in the medical literature. The rare cases described were often attributed to other precipitating factors such as hypoglycemia, acute infection, or predisposition to post-bisphosphonate hypocalcemia. We review the previous cases and present a new case of suspected seizure episode following zoledronic acid therapy. METHODS: We describe a case of a 63-year-old woman with a history of well-controlled epileptic disorder with no seizure activity in recent years. She was treated with intravenous zoledronic acid due to osteoporosis. Twelve hours after treatment, she suffered an episode of loss of consciousness with urinary incontinence suspected to be seizure-related. RESULTS: Unlike previously reported cases, our patient had a low risk for postinfusion hypocalcemia as her creati-nine, calcium, parathyroid hormone, and vitamin D were all within normal limits prior to the infusion. CONCLUSION: Our interpretation of the scenario described is based on clinical judgment and not supported by ancillary studies. Nevertheless, our case, along with the limitations described, joins other reports, and raises questions about possible interaction between a convulsion disorder and a potent bone resorption inhibition administration, leading to a relative hypocalcemia and possible seizure threshold reduction. This question should be further explored by other studies.