• Title/Summary/Keyword: Leukoencephalopathies

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Delayed Anoxic Encephalopathy after Carbon Monoxide Poisoning: Evaluation of Therapeutic Effect by Serial Diffusion-Tensor Magnetic Resonance Imaging and Neurocognitive Test (일산화탄소중독 이후 발생한 지연무산소뇌병증: 확산텐서영상 및 신경인지기능검사를 이용한 치료 효과의 평가)

  • Ryu, Ho-Sung;Kim, Youngwook;Jung, Boo-Kyoung;Kim, Yong-Won
    • Journal of the Korean neurological association
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    • v.36 no.4
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    • pp.358-362
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    • 2018
  • Delayed anoxic encephalopathy after carbon monoxide (CO) poisoning is characterized by neurological deterioration that occurs after recovery from acute CO intoxication. There has been no established therapy. We report a patient recovered from acute CO intoxication developed various neurological symptoms. After the administration of high dose prednisolone and anticholinesterase inhibitor, the therapeutic effect was remarkable and confirmed by quantitative analysis of diffusion-tensor imaging (DTI). DTI could be used to evaluate the therapeutic effect for delayed anoxic encephalopathy after CO poisoning.

Delayed Post-Hypoxic Leukoencephalopathy Induced by an Overdose with Fentanyl Patches: A Case Report (펜타닐 첩포 남용으로 인한 지연성 저산소성 백색질뇌증: 증례 보고)

  • Jin Sol Choi;Eun Ae Yoo;Jin Ok Choi;Soo Jung Kim
    • Journal of the Korean Society of Radiology
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    • v.81 no.4
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    • pp.972-978
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    • 2020
  • Fentanyl intoxication has occasionally been reported since fentanyl patches became available for medical use. Delayed post-hypoxic leukoencephalopathy is a complication of hypoxia. However, its neuropsychiatric symptoms can be delayed, and it can progress to leukoencephalopathy even after full recovery from coma due to acute intoxication. Herein, we report a case of fentanyl intoxication in a 65-year-old man who was presented to the hospital because of unconsciousness for 13 hours after using ten fentanyl patches simultaneously. Initial brain CT findings were non-specific. Twenty days later, delayed neuropathologic symptoms manifested, and MRI showed bilaterally symmetrical, heterogeneous, confluent high signal intensities on T2-weighted/fluid attenuated inversion recovery MRI in the cerebral white matter with diffusion restriction. This was followed by rapid exacerbation of neuropathological symptoms with diffuse severe cerebral atrophy over 1 year.