Multifocal myoclonus secondary to levetiracetam toxicity and comatose state: case reportA 52-year-old woman developed multifocal myoclonus secondary to levetiracetam toxicity following treatment with levetiracetam for epileptic seizure. Additionally, she developed comatose state following treatment with propofol for non-convulsive status epilepticus [durations of treatments to reactions onsets not stated; not all dosages stated].The woman, who had medical history of chronic kidney disease (on haemodialysis), hypertension and hypothyroidism, was admitted at George Washington University Hospital in USA for cauterisation following heavy vaginal bleeding secondary to a loop electrosurgical excision surgery, which she underwent 17 days previously. Intraoperatively, she developed cardiac arrest with spontaneous return of circulation after 6 minutes of advanced cardiac life support. She remained intubated and sedated with propofol infusion and dexmedetomidine [dexmedetomidine-hydrochloride] in the ICU. After surgery, her extremities were moving spontaneously. On the following day, she developed facial twitching which was suggesting epileptic seizures. She was then treated with IV levetiracetam 1000mg and lorazepam. Neurological investigations on the same day revealed persistent uprolling of the eyes with occasional spontaneous blinks. Further investigations revealed non-convulsive status epilepticus. It ultimately resolved after up-titration of propofol at 60 µg/kg/min, levetiracetam 1500mg twice in a day, in addition to lacosamide. Thereafter, the neurological investigations revealed comatose state without any clinical evidence of seizures, which was presumably due to propofol.The woman's therapy with propofol was discontinued. Neurological examination revealed spontaneous blinks, spontaneous movements of all extremities and symmetric withdrawal of all limbs to noxious stimuli although she remained in a vegetative state. In the following days, her neurologic status worsened with episodes of multifocal myoclonic jerks that were noted only upon holding the propofol infusion. Her myoclonic twitching was noted as asynchronously affecting in the left shoulder, forehead, abdomen and extremities. The EEG revealed evidence of generalised dysfunction, in addition to muscle artifact, specifically in the right frontal and left occipital leads, suggestive of multifocal myoclonic activity, without an ictal correlate. She had concomitant renal disease. Therefore, it was considered that the accumulation of levetiracetam metabolites ultimately led to levatiracetam toxicity causing multifocal myoclonus. Therefore, the dose of levetiracetam was reduced to 500mg twice a day with addition of 500mg after each haemodialysis session. Valproic acid was then added to therapy. At that time levetiracetam levels were supra-therapeutic (49.8 mg/L). Subsequently, levetiracetam was discontinued. Consequently, myoclonus resolved and levetiracetam levels normalised over the following 4 days. She was on continuous EEG monitoring during that period with...
