American Journal of Neuroradiology 20:1628-1635 (10 1999)
© 1999 American Society of Neuroradiology
ARTICLE
The Incidence of T2-Weighted MR Imaging Signal Abnormalities in the Brain of Cocaine-Dependent Patients Is Age-Related and Region-Specific
a From the Mental Health Service Line (G.B.), Central Arkansas Veterans Healthcare System, Little Rock, AR; the Department of Psychiatry (G.B., P.H.L.), University of Arkansas for Medical Sciences, Little Rock, AR; VA Greater Los Angeles Healthcare System (G.B., M.B., P.H.L., N.E., J.M.), West Los Angeles, CA; the Department of Psychiatry (G.B., I.B.G., M.B., D.S., J.M.), University of California, Los Angeles, CA; the Department of Radiology (D.B.H.), University of California, Los Angeles, CA; and the Medication Development Division (P.B.), National Institute on Drug Abuse, Rockville, MD.
BACKGROUND AND PURPOSE: Cocaine and its metabolites can produce vasospasm, and cocaine-dependent patients are at increased risk for stroke. Based on previous case reports, we hypothesized that the incidence of hyperintense brain lesions observed on T2-weighted MR images would also be increased in asymptomatic cocaine-dependent individuals.
METHODS: Sixty-two male "crack" (smoked) cocainedependent participants ranging in age from 25 to 66 years were compared with 116 normal male control participants ranging in age from 25 to 80 years. Those with histories of neurologic symptoms or illnesses were excluded. The severity of hyperintense lesions was rated on a 0- to 3-point scale, and ratings of 3 were used in the data analysis as an indicator of a probable pathologic process. Three regions were separately rated: the cerebral white matter, insular subcortex white matter, and subcortical gray matter (basal ganglia and thalamus region).
RESULTS: Significantly increased risk of severe lesions was observed in the two white matter regions of the cocaine-dependent group (odds ratio of 16.7 and 20.3) but not in the subcortial gray matter region (odds ratio of 1.4). In the insula subcortex white matter, the risk of lesions increased with age in the cocaine-dependant sample, but remained essentially absent among normal controls through the age of 80 years. In the cerebral white matter, the relationship of age and risk of lesion among normal participants was similar in shape to that in cocaine-dependent participants, but equivalent risk was seen 20 years earlier among cocaine-dependent participants.
CONCLUSIONS: Cocaine-dependent participants had a significantly increased age-related risk of white matter damage. The possible clinical implications of this damage are discussed.
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