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• W2241449617 abstract "OBJECTIVEWe present a rare case of delayed post-hypoxic leukoencephalopathy (DPHL) developing two weeks after an unintentional narcotics overdose.BACKGROUNDDPHL is a demyelinating process occurring acutely, 1-4 weeks after an initial recovery from an extended hypoxic event such as carbon monoxide poisoning, respiratory suppression, or myocardial infarction. Presentation may vary but consists of deteriorating mental status accompanied by symptoms of frontal lobe and basal ganglia dysfunction. The diagnosis is frequently supported by MRI evidence of diffuse hemispheric demyelination sparing cerebellar and brainstem tracts or elevated CSF myelin basic protein.DESIGN/METHODSPatient was a 69 year old woman, initially admitted to a local Medical ICU for unintentional narcotic overdose leading to cardiac arrest, cardiogenic shock, multi-organ failure, and right parietal stroke with left-sided hemiparesis and neglect. After a week, she made a good recovery, returning nearly completely to her high-functioning pre-morbid mental status. She was transferred to Columbia University Neuro ICU for evaluation of several minutes-long episodes of apnea and unresponsiveness occurring two weeks after the initial event. These episodes of unresponsiveness occurred increasingly frequently but with interval resolution, progressing over days, however, to akinetic mutism with frontal release, flexor rigidity and tremor and, ultimately, coma. Continuous video EEG was without evidence of seizure activity. Non-contrast head CT showed multifocal hypodensities affecting right frontal-parietal and left occipital lobes and bilateral basal ganglia with patchy white matter involvement sparing the U fibers and internal capsule. CT angiography showed regular and patent vessels. Extensive cardio-embolic work-up resulted negative. MRI Brain could not be performed due to implanted pacemaker. Lumbar puncture demonstrated no inflammatory cells, but protein and myelin basic protein were markedly elevated (>200 and >400, respectively). Brain biopsy showed post-anoxic changes including patchy demyelination of white matter and activated oligodendrocytes without activated monocytes or evidence of small vessel inflammation, findings consistent with delayed post-hypoxic leukoencephalopathy.CONCLUSIONS: Clinical anticipation and recognition of DPHL should lead to earlier diagnosis and higher-value care. Disclosure: Dr. Doerner Rinaldi has nothing to disclose. Dr. Miller has nothing to disclose. Dr. Czeisler has nothing to disclose. Dr. Willey has nothing to disclose. Dr. John has nothing to disclose. Dr. Claassen has nothing to disclose. Dr. Mayer has received personal compensation for activities with Actelion, Baxter, Biogen Idec, Codman/Johnson & Johnson Company, CSL Behring, Cornerstone Therapeutics, CR Bard, Novartis, Orsan Technologies, Pfizer Inc, Sage Therapeutics, and Stryker. Dr. Mayer has received research support from Non-Invasive Medical Systems, Inc., and General Electric. Dr. Agarwal has nothing to disclose." @default.
• W2241449617 created "2016-06-24" @default.
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• W2241449617 date "2014-04-08" @default.
• W2241449617 modified "2023-10-03" @default.
• W2241449617 title "Akinetic Mutism And Parkinsonian Features Progressing To Coma Following A Hypoxic Event With Extended Lucid Interval: Manifestations Of Delayed Post-Hypoxic Leukoencephalopathy (P4.033)" @default.
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