Delayed post-hypoxic leukoencephalopathy

Abstract

Delayed post-hypoxic leukoencephalopathy is a clinical syndrome caused by a lesion of the white matter of the brain with an acute onset developing several days after emerging from coma. The reason of delayed post-hypoxic leukoencephalopathy is prolonged cerebral hypooxygenation, it often results from carbon monoxide poisoning, less often it is associated with acute brain hypoxia caused by respiratory failure, an overdose of opiates. The leading role in the clinical picture of delayed post-hypoxic leukoencephalopathy is played by the duration and severity of cerebral anoxia in the acute period of the disease. The period of temporary well-being of a patient with an episode of acute hypoxia lasts 2 to 40days. Pathogenesis and pathophysiology have not been well studied. Its development after carbon monoxide poisoning is considered to be caused by direct myelinotoxic effect. Itis essential to collect a detailed history for diagnosing a case, neurovisualization is an informative method for investigation. Magnetic resonance imaging may detect the signs that are pathognomonic for delayed post-hypoxic leukoencephalopathy, that is diffuse hyperintensity of the white matter of the cerebral hemispheres in T2-mode, symmetry of the damage of both cerebral hemispheres, damage of the subcortical gray matter globus pallidus. The standards for the treatment of delayed post-hypoxic leukoencephalopathy have not been developed. The use of glucocorticoids has been described, perspective use of amantadine were shown in case of frontal-subcortical syndrome. There are recommendations on prescribing the following therapy for the patients with delayed post-hypoxic leukoencephalopathy: hyperbaric oxygenation, coenzymeQ10, vitaminE and groupB. We present a clinical observation that demonstrates the complexity of the clinical picture of delayed post-hypoxic leukoencephalopathy, the difficulty of its diagnosis without taking into account information about previous carbon monoxide poisoning. The results of magnetic resonance imaging at the onset of the disease are considered to be of utmost interest. The clinical observation of the patient presented in the article allows us to make an assumption about pathogenesis and contributes to search for means aimed at preventing the development of delayed post-hypoxic leukoencephalopathy in people with acute carbon monoxide poisoning.

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