Delayed leukoencephalopathy after acute carbon monoxide intoxication

Abstract

Delayed leukoencephalopathy is an uncommon complication of hypoxic-ischemic events of different etiologies, including carbon monoxide intoxication. We present a case of a 40-year-old male patient who was admitted with rapidly progressive neurocognitive and behavioral deficits. There was a history of accidental carbon monoxide intoxication one month before, presenting with loss of consciousness and short hospitalization, followed by a complete clinical recovery. The imaging studies in the delayed phase depicted confluent, symmetric supra-tentorial white matter lesions in keeping with diffuse demyelinization. Restricted diffusion and metabolite abnormalities in magnetic resonance proton spectroscopy were also seen. The diagnosis of CO-mediated delayed post-hypoxic leukoencephalopathy was assumed after exclusion of other mimickers. Hyperbaric oxygen therapy was tentatively performed and the patient had a favorable clinical and radiological evolution.

Effects of N-butylphthalide on the activation of Keap1/Nrf-2 signal pathway in rats after carbon monoxide poisoning

“…In recent decades, many scholars focused on the pathogenesis, including hypoxia, excitotoxicity, binding to intracellular proteins and disrupting cellular metabolism, lipid peroxidation, apoptosis and cerebral edema, but it is still poorly elucidated about acute brain injury and delayed encephalopathy following CO poisoning (Han et al, 2007;Geraldo et al, 2014). Thus new drugs can be identified and disease mechanisms better understood by establishment of well controlled animal model systems.…”

N-Butylphthalide Alleviates Blood–Brain Barrier Impairment in Rats Exposed to Carbon Monoxide

“…However, their pathogenesis is poorly understood (Hampson et al, 2009; Geraldo et al, 2014). Currently, there is no efficient treatment and prevention for the neurologic sequelae after CO exposure.…”

Rare anoxic brain injury sequela of delayed posthypoxic leukoencephalopathy due to recreational drug overdose with benzodiazepines

“…The patient's clinical course is consistent with DPHL, as she had an inciting event with acute encephalopathy and a lucid period for approximately 3 weeks when she was doing well at home. She subsequently had return of acute encephalopathy with psychosis 4 weeks after the initial event.…”

“…She subsequently had return of acute encephalopathy with psychosis 4 weeks after the initial event. There is some limitation though, as most patients return to baseline prior to the acute encephalopathy, with some patients returning to their work environments . This patient had not returned to baseline but did significantly improve after the inciting event, with short‐term memory loss as the major symptom.…”