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        Bupropion overdose as a clinically significant confounder of the neurological examination

        Ranier Reyes,Stephen Figueroa 대한신경집중치료학회 2020 대한신경집중치료학회지 Vol.13 No.2

        Background: Bupropion is a selective dopamine and norepinephrine reuptake inhibitor utilized in the treatment of multiple neuropsychiatric conditions. It has been implicated as a brain death mimic due to its association with a comatose examination. Case Report: A 31-year-old man with depression and anxiety ingested bupropion as part of a multi-drug overdose in a suicide attempt. During his hospital course, he suffered two cardiopulmonary arrests approximately 24 hours after ingestion. Neurological examination was excessively poor relative to imaging studies and was notable for absent brainstem reflexes. He was treated with targeted temperature management and lipid emulsion therapy with rapid improvement. He was eventually discharged after making a complete neurological recovery. Conclusion: Bupropion is a unique clinical confounder and may be associated with a disproportionately poor neurological examination in the setting of intoxication. Many factors should be considered in the approach to evaluation, treatment, and prognostication of these patients.

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        Management of propofol-related infusion syndrome and discussion of <i>POLG</i> mitochondrial mutation: a case report

        Nguyen Brian,Figueroa Stephen 대한신경집중치료학회 2022 대한신경집중치료학회지 Vol.15 No.2

        Background: Propofol-related infusion syndrome (PRIS) is a known complication of long-term propofol infusion. Providers should be aware of PRIS risk, as early recognition is key to avoiding mortality, which can range from 30% to 60%. The underlying mechanism of PRIS is unknown, but some studies suggest that underlying mitochondrial dysfunction may predispose patients to developing PRIS. Case Report: We present a case of refractory adult-onset epilepsy that was challenging due to a paradoxical response to propofol with worsening brief ictal/interictal rhythmic discharges and complicated by development of PRIS. We aimed to discuss the clinical presentations of PRIS, along with a review of the mitochondrial POLG mutation found in our patient, which has also been described in other case reports of refractory adult-onset epilepsy. Conclusions: We discuss the treatment strategy utilized in hopes of raising awareness of the risks in managing patients with epilepsy who have a potential underlying mitochondrial disorder.

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