ABSTRACT
Burst-suppression pattern on electroencephalography (EEG) occurs upon dissociation of the cortex from underlying brain structures. Unless the pattern is a physiologic consequence of administered sedatives, this electroencephalographic pattern is indicative of a poor neurologic outcome and high mortality. We report a case of a 29-year-old female thought to be brain dead based on initial physical examination and EEG findings of burst-suppression, who was later found to have supratherapeutic serum levels of bupropion. This is the second documented case of burst-suppression pattern on EEG in a patient who overdosed on bupropion. We propose that burst-suppression in the setting of bupropion toxicity may revert with drug clearance.
Subject(s)
Bupropion/poisoning , Drug Overdose/complications , Pupil Disorders/chemically induced , Adult , Drug Overdose/therapy , Electroencephalography , Female , Humans , Nervous System Physiological Phenomena/drug effects , Pupil Disorders/etiology , Pupil Disorders/therapy , Treatment OutcomeABSTRACT
Porokeratosis is hypothesized to be an inherited autosomal dominant disorder with variable penetrance. It has been linked to ultraviolet (UV) radiation in genetically predisposed individuals, to antibody-related autoimmune disease treated with systemic steroids, and to other immunosuppressive states including chronic liver disease. The authors describe an unusual case of a patient with new-onset hepatitis of unclear etiology who developed concomitant erythematous annular plaques with atrophic centers and elevated scaling borders on the lower extremities. The histological features of these lesions were consistent with disseminated superficial porokeratosis (DSP). The authors present this patient and a review of the literature to support the direct pathological link between hepatitis and DSP, irrespective of the state of the immune system. Further research would be helpful in clarifying the pathogenesis of porokeratoses in patients with hepatic dysfunction.
