Affiliations: [a] Department of Neurology, University of Utah, Salt Lake City, UT, USA | [b] Evergreen Neuroscience Institute, Kirkland, WA, USA | [x] Brain Injury Rehabilitation Unit, HealthONE Spalding Rehabilitation Hospital, Aurora, CO, USA | [y] Neurobehavioral Disorders Program, University of Colorado Denver, Aurora, CO, USA
Correspondence:
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Address for correspondence: David Shprecher, DO, Assistant Professor, Department of Neurology, University of Utah, 729 Arapeen Drive, Salt Lake City, UT 84108, USA. Tel.: +1 (801) 585 9386; E-mail: [email protected]
Abstract: Delayed post-hypoxic leukoencephalopathy (DPHL) is a demyelinating syndrome characterized by acute onset of neuropsychiatric symptoms days to weeks following apparent recovery from coma after a period of prolonged cerebral hypo-oxygenation. It is diagnosed, after excluding other potential causes of delirium, with a clinical history of carbon monoxide poisoning, narcotic overdose, myocardial infarction, or another global cerebral hypoxic event. The diagnosis can be supported by neuroimaging evidence of diffuse hemispheric demyelination sparing cerebellar and brainstem tracts, or by an elevated cerebrospinal fluid myelin basic protein. Standard or hyperbaric oxygen following CO poisoning may reduce the likelihood of DPHL or other neurologic sequelae. Bed rest and avoidance of stressful procedures for the first 10 days following any prolonged hypoxic event may also lower the risk. Gradual recovery over a 3 to 12 month period is common, but impaired attention or executive function, parkinsonism, or corticospinal tract signs can persist. Stimulants, amantadine or levodopa may be considered for lasting cognitive or parkinsonian symptoms. Anticipation and recognition of DPHL should lead to earlier and more appropriate utilization of health care services.
