Abstracts

Lupus cerebritis is a known complication of vasculitic disorders of autoimmune origin, and it is frequently characterized by alteration in mental status and seizures. We report the first known case of lupus cerebritis presenting with BIPLEDs on EEG that resolved with intravenous solumedrol therapy. A case review of the inpatient and outpatient medical records including chart documentation, EEGS with and without prolonged video monitoring, and laboratory tests, was performed in a 59 year old woman diagnosed with lupus cerebritis. A subsequent review of medical literature on EEG in vasculitis and periodic EEG patterns was also performed. A 59 year old female with a history of systemic lupus who presented to the emergency room in hypertensive emergency ( blood pressure [gt]220/110) with new onset and continuous convulsive seizures. For blood pressure management, the patient was refractory to numerous antihypertensive medications. For acute management of seizures the patient received a total of Ativan 10mg intravenously and was loaded with 20mg/kg of fosphenytoin. The patient was intubated and initiated on propofol infusion for treatment of refractory hypertension. CSF studies were normal. MRI of the brain showed abnormal high T2/flair signal in the subcortical and white matter of the bi-frontal and biparietal regions confirming a diagnosis of lupus cerebritis. Continous EEG monitoring was initiated for evaluation of non-convulsive seizures or status epilepticus. The EEG exhibited bilateral independent periodic lateralizing epileptiform discharges (BIPLEDS). Two Seizures characterized by evolution of the BIPLEDs were recorded in the first 12 hours. Doses of phenytoin and propofol remained unchanged. High dose intravenous Solumedrol therapy was initiated 36 hours after admission with clinical improvement in the patient and complete resolution of BIPLEDs on EEG within 24 hours. Bilateral independent periodic lateralizing epileptiform discharges (BIPLEDS) have been reported on EEG in association with CNS infection, anoxic encephalopathy, bilateral structural lesions, and metabolic abnormalities. Suggestion as to origin of the discharges in cerebral gray or white matter have also been raised to determine if cortical isolation is a critical mechanism in the pathogenesis of this phenomena. Mortality in patients with BIPLEDs is reported higher than other periodic EEG patterns. To date, no case of CNS vasculitis has been reported to exhibit this EEG pattern, nor are any reports present of resolution with treatment of the underlying pathology. Further prospective studies considering long term intensive care monitoring should be considered in comatose patients with CNS vasculitis and/or with periodic EEG patterns to assess responsiveness to treatment of the underlying pathology.