Abstracts

Rationale: Periodic lateralized epileptiform discharges (PLEDs) are an electroencephalogram (EEG) pattern observed in acute destructive cerebral lesions. PLEDs are associated with partial seizure disorders, although they are generally, but controversially, not considered ictal. Presently, there are no prospective reports describing outcomes in patients acutely treated with antiepileptic medications (AEM) for PLEDs on EEG. We document the electroencephalographic and clinical courses of eleven patients after treatment of PLEDs with AEM. Methods: This is an ongoing prospective observational study of eleven patients from April 2008 to the present whom we acutely treated by starting AEM or by increasing doses after finding PLEDs on their EEGs. We excluded patients where PLEDs occurred after a post-anoxic cerebral injury. We followed their inpatient and outpatient electroencephalographic and clinical courses. Results: Eight patients had structural lesions to account for PLEDs; two had a non-structural PLEDs etiology. One had PLEDs after recent uncomplicated elective aneurysm clipping, and its etiology remains unclear. Nine of the 11 patients were discharged from the hospital at their baseline mental status, while two died in the hospital with subdural hematomas as their PLEDs etiology. Seven obtained inpatient follow-up EEGs after AEM treatment, two of which demonstrated severe diffuse cerebral dysfunction with burst suppression in one and delta slowing with periods of no electrical activity in the second. These two recordings belong to the patients who died. Four of the other follow-up EEGs showed slowing with resolution of PLEDs, and these patients were discharged home at their baseline. One follow-up EEG demonstrated triphasic waves throughout the recording. This patient was discharged in a persistent vegetative state, which was her baseline. Six of the surviving patients have remained seizure-free. Three were lost to follow-up. Eight are on maintenance AEM. Conclusions: The majority of patients in our study were discharged from the hospital at their baseline after AEM treatment for PLEDs on EEG. Structural versus non-structural PLEDs etiology made no difference in terms of the discharged patients’ outcome. Two patients who died had follow-up EEGs showing severe diffuse cerebral dysfunction while the discharged patients had milder abnormalities on follow-up EEG. Our study thus far suggests that a follow-up EEG after AEM treatment of PLEDs may correlate to a patient’s outcome. We would like to see if this trend continues in a larger cohort of patients.