Delayed post-hypoxic leukoencephalopathy: case report with a review of disease pathophysiology

Abstract

Delayed post-hypoxic leukoencephalopathy is a rare clinical phenomenon usually observed in a small number of carbon monoxide poisoning survivors. A similar phenomenon is reported here in a patient who successfully recovered from a large overdose of diazepam and methadone, but then abruptly declined 3 weeks after the initial event. Magnetic resnance revealed confluent white matter hyperintensity on fluid-attenuated inversion recovery and T2 weighted sequences, and spectroscopy revealed elevated peaks in choline, creatinine, and lactate. Analysis and review of the literature suggests this phenomenon occurs on average about 19 days after the initial event. Although the pathophysiology remains obscure, it is noted here that the mean lucid interval coincides approximately with the replacement half-life for myelin related lipids and proteins.

Delayed post‐hypoxic leukoencephalopathy with a peculiar autoantibody association

“…A possible explanation may relate to the half‐life of myelin‐related proteins, which has been estimated to be about 19 days in animal models. This duration is similar to the mean extent of the “lucid interval” described in patients with DPHLE . Our patient showed a marked dressing and limb apraxia as the dominant clinical feature in the very early stages of relapse.…”

“…This duration is similar to the mean extent of the "lucid interval" described in patients with DPHLE. 3 Our patient showed a marked dressing and limb apraxia as the dominant clinical feature in the very early stages of relapse. This is a rather peculiar aspect, not described in other reports of DPHLE.…”

Delayed posthypoxic leukoencephalopathy following alcohol and psychotropic drug overdose: a case report

“…Despite relatively minor changes on MRI, our patient experienced a poor outcome, as observed for many previous patients who have overdosed of benzodiazepines and alcohol [4][5][6][7][8][9][10]. The clinical presentation of our patient was complicated by mild chronic anemia (Hb 10-12 g/ dL), although he had no history of anemia.…”

“…2C, bottom panels). In many previously reported cases [4][5][6][7][8][9][10][11][12][13], changes that were observed in the more rostral regions were more dramatic than those in the periventricular region. However, in this case, the changes in the periventricular region were the most dramatic, and there were few changes in the more rostral regions, such as the centrum semiovale ( Fig.…”

Clinical Reasoning: A case of altered mental status, not otherwise specified

“…One explanation for the delay may relate to the fact that the mean lucid interval coincides approximately with the replacement half-life for myelin lipids and proteins. 7 Other suggested mechanisms include direct toxicity of carbon monoxide or heroin (heroin-associated delayed spongiform leukoencephalopathy) 8 to oligodendrocytes as well as disruption of myelin-producing pathways due to pseudodeficiency of arylsulfatase A. 9 The fact that a number of cases have shown significant recovery may relate to the ability of oligodendrocytes to repair their myelin sheaths, and oligodendrocyte progenitors to differentiate into mature myelinforming oligodendrocytes.…”