Assessment of damage to cerebral white matter fiber in the subacute phase after carbon monoxide poisoning using fractional anisotropy in diffusion tensor imaging
- PMID: 20066405
- DOI: 10.1007/s00234-009-0649-x
Assessment of damage to cerebral white matter fiber in the subacute phase after carbon monoxide poisoning using fractional anisotropy in diffusion tensor imaging
Abstract
Introduction: Chronic neuropsychiatric symptoms after carbon monoxide (CO) poisoning are caused by demyelination of cerebral white matter fibers. We examined whether diffusion tensor imaging can sensitively represent damage to fibers of the centrum semiovale in the subacute phase after CO intoxication.
Methods: Subjects comprised 13 adult patients with CO poisoning, classified into three groups according to clinical behaviors: group A, patients with transit acute symptoms only; group P, patients with persistent neurological symptoms; and group D, patients with "delayed neuropsychiatric sequelae" occurring after a lucid interval. Median fractional anisotropy (FA) and apparent diffusion coefficient (ADC) of the centrum semiovale bilaterally at 2 weeks were compared between these groups and a control group of ten healthy volunteers. Myelin basic protein (MBP) concentration in cerebrospinal fluid was examined at 2 weeks to evaluate the degree of demyelination in patients.
Results: MBP concentration was abnormal or detectable for all group P and group D patients but was undetectable for all patients assigned to group A. Low FA values in groups P and D displaying chronic neurological symptoms clearly differed from those in controls and group A without chronic neurological symptoms, but ADC showed no significant differences between patient groups.
Conclusions: MBP concentration at 2 weeks after CO inhalation confirmed a certain extent of demyelination in the central nervous system of patients who would develop chronic neurological symptoms. In these patients, FA sensitively represented damage to white matter fibers in the centrum semiovale in the subacute phase after CO intoxication.
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