A 49-year-old, right-handed man was diagnosed with relapsing-remitting MS in 2005. The diagnosis of MS was established by clinical, MRI, and CSF criteria. He was being treated with natalizumab since 2008. Eight months before admission, dalfampridine had been introduced, and he responded with improved walking speed. In June 2011, he was brought to the emergency department after his roommate witnessed several generalized tonic–clonic seizures. His outpatient medications included dalfampridine, natalizumab, morphine sulfate, and tizanidine. He had no previous history of seizures, CNS infections, head trauma, or renal insufficiency. There was no family history of epilepsy. He had a remote history of cocaine abuse 5 years earlier.
The status epilepticus was initially treated with lorazepam and fosphenytoin; but the seizures persisted, requiring that the patient be intubated for airway protection and placed on a propofol infusion, which led to clinical and electrographic cessation of seizures. Phenytoin was started for maintenance, and dalfampridine was withdrawn. MRI of the brain with gadolinium revealed extensive periventricular and juxtacortical white-matter lesions, but no new T2 hyperintense lesions or contrast-enhancing lesions. Serology including electrolytes and creatinine was within normal limits. Cerebrospinal fluid was also normal, and PCR for the JC virus was not detected.
Urine toxicology was positive for cocaine and cannabis, and the patient admitted to smoking marijuana laced with crack cocaine before presentation. Two consecutive EEGs showed bilateral fronto-central sharp waves within a disorganized background, so antiepileptic drug therapy was switched to levetiracetam. He was discharged to a rehabilitation facility. Two months after discharge a repeat EEG did not show epileptiform activity. He complained of irritability on the levetiracetam, so he was switched to lamotrigine. Six months later, he remains seizure-free and has continued to abstain from cocaine use.