Clinical neuropharmacology · 2026
Cytotoxic Lesion of the Corpus Callosum After Hospital-Administered Intravenous Fentanyl for Trigeminal Neuralgia: A Case Report and Focused Review.
СтатьяКлинический случайОбзорНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Benito-León Julián
Аннотация
OBJECTIVES: Fentanyl-associated neurotoxicity is increasingly recognized across illicit, inhalational, transdermal, pediatric, and delayed posthypoxic exposures, but isolated splenial CLOCC after hospital-administered intravenous fentanyl has not been well characterized.
METHODS: This is a single-patient case report with a focused review of fentanyl-associated neurotoxic syndromes and proposed mechanisms.
RESULTS: A 41-year-old woman with trigeminal neuralgia presented with severe facial pain. After droperidol, metoclopramide, and metamizole failed to control symptoms, intravenous fentanyl (75 μg) was administered. Soon afterward, she developed dizziness, nausea, vomiting, left-sided paresthesias, hypoesthesia, and mild weakness. Initial computed tomography was unrevealing, and cerebrospinal fluid findings were normal. Brain magnetic resonance imaging (MRI) obtained 8 days later showed a 6-mm midline splenial lesion that was hyperintense on T2-weighted and FLAIR sequences, restricted on diffusion-weighted imaging, and nonenhancing, consistent with CLOCC. Follow-up MRI showed complete radiologic resolution, but serial assessments documented persistent deficits in the left upper and lower extremities, including impaired fine motor control, dysdiadochokinesia, arm and leg weakness, foot drag, and gait imbalance; somatosensory-evoked potentials showed mild dysfunction of the left lower-extremity pathway. Review of comparable fentanyl-associated cases shows a spectrum ranging from isolated callosal injury to diffuse, cerebellar, and delayed leukoencephalopathic phenotypes.
CONCLUSIONS: This case expands the neuroimaging spectrum of fentanyl-associated brain injury and supports a toxic-metabolic pathogenesis in which splenial CLOCC may represent a focal manifestation of broader opioid-related white-matter vulnerability.
METHODS: This is a single-patient case report with a focused review of fentanyl-associated neurotoxic syndromes and proposed mechanisms.
RESULTS: A 41-year-old woman with trigeminal neuralgia presented with severe facial pain. After droperidol, metoclopramide, and metamizole failed to control symptoms, intravenous fentanyl (75 μg) was administered. Soon afterward, she developed dizziness, nausea, vomiting, left-sided paresthesias, hypoesthesia, and mild weakness. Initial computed tomography was unrevealing, and cerebrospinal fluid findings were normal. Brain magnetic resonance imaging (MRI) obtained 8 days later showed a 6-mm midline splenial lesion that was hyperintense on T2-weighted and FLAIR sequences, restricted on diffusion-weighted imaging, and nonenhancing, consistent with CLOCC. Follow-up MRI showed complete radiologic resolution, but serial assessments documented persistent deficits in the left upper and lower extremities, including impaired fine motor control, dysdiadochokinesia, arm and leg weakness, foot drag, and gait imbalance; somatosensory-evoked potentials showed mild dysfunction of the left lower-extremity pathway. Review of comparable fentanyl-associated cases shows a spectrum ranging from isolated callosal injury to diffuse, cerebellar, and delayed leukoencephalopathic phenotypes.
CONCLUSIONS: This case expands the neuroimaging spectrum of fentanyl-associated brain injury and supports a toxic-metabolic pathogenesis in which splenial CLOCC may represent a focal manifestation of broader opioid-related white-matter vulnerability.