Weighing the Risk of Seizure Control: A Case of Levetiracetam-Induced Rhabdomyolysis

Abstract

Rhabdomyolysis, a severe condition marked by the breakdown of muscle tissue, leads to the release of intracellular contents into the bloodstream. This condition can be triggered by a range of factors, including intense physical activity, traumatic injuries, certain medications, and infections. Diagnosis typically involves detecting elevated creatine phosphokinase (CPK) levels alongside characteristic clinical symptoms. Levetiracetam-induced rhabdomyolysis is an exceptionally rare phenomenon, with only a few cases documented in the literature. In this report, we present a 47-year-old male patient in our intensive care unit who developed rhabdomyolysis after continuing his home dose of levetiracetam following a witnessed seizure. Despite four days of aggressive hydration, his CPK levels continued to rise, ultimately peaking at 46,671 U/L. With no other apparent causes, levetiracetam was suspected as the culprit and subsequently discontinued. Remarkably, the patient's condition improved quickly after stopping the medication, with CPK levels dropping within two days, allowing for a successful transition to lacosamide. Although rare, this case highlights the critical need to monitor CPK levels in patients who develop rhabdomyolysis symptoms after restarting levetiracetam therapy. We recommend considering discontinuation of levetiracetam if no other identifiable causes are found.

Keywords: creatine kinase; levetiracetam; rhabdomyolysis; seizure; seizure medications.

Figure 1. CPK trend

CPK: creatine phosphokinase; LEV: levetiracetam