Magnetic resonance imaging evidence of "silent" cerebrovascular toxicity in cocaine dependence

Background: Cocaine and its metabolites can produce vasospasm. Cocaine-dependent (CD) patients are at increased risk for stroke, and a high frequency of brain perfusion defects has been observed in clinically asymptomatic CD subjects, This is the first controlled magnetic resonance imaging (MRI) study of clinically asymptomatic CD subjects. Methods: Two age-matched groups of male subjects (61 CD and 57 control) participated in the study, Subjects with a history of neurologic symptoms or major medical or neurologic illness, such as hypertension, diabetes, or significant head trauma, were excluded The severity of hyperintense lesions observed on T2-weighted MRI images were rated on a O-3-point scale by an experienced radiologist who was blind to all clinical data. Ratings of 3 were felt to be significant indicators of a possible disease process and were used in the data analysis, three regions were separately rated: the cerebral white matter, subinsular white matter, and subcortical gray matter (basal ganglia and thalamus region). Results: Despite the exclusion criteria minimizing risk factors for cerebrovascular events, 17 of the 61 (27.9%) CD subjects and 4 of 57 (7%) of the control subjects had severe hyperintense lesions suggestive of subclinical or "silent" anoxic vascular events. Significant group differences were observed in the two white matter regions but not in the subcortical gray matter region. The risk of severe white matter lesions in the CD group increased with age, reaching 50% in the oldest age quartile (46-58 years), and this increase was not related to the number of years cocaine was used. Conclusions: The data suggest that asymptomatic CD patients are a heterogeneous population with a significantly increased age-related risk of white matter neuro-vascular toxicity, Premature neurovascular damage may impact treatment outcomes and, as the CD population ages, may manifest as an increased incidence of cognitive deficits, (C) 1999 Society of Biological Psychiatry.