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

Background: Cocaine and its metabolites can produce vasospasm. Cocaine-depe ndent (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) stu dy of clinically asymptomatic CD subjects. Methods: Two age-matched groups of male subjects (61 CD and 57 control) par ticipated in the study, Subjects with a history of neurologic symptoms or m ajor medical or neurologic illness, such as hypertension, diabetes, or sign ificant head trauma, were excluded The severity of hyperintense lesions obs erved on T2-weighted MRI images were rated on a O-3-point scale by an exper ienced radiologist who was blind to all clinical data. Ratings of 3 were fe lt to be significant indicators of a possible disease process and were used in the data analysis, three regions were separately rated: the cerebral wh ite matter, subinsular white matter, and subcortical gray matter (basal gan glia and thalamus region). Results: Despite the exclusion criteria minimizing risk factors for cerebro vascular events, 17 of the 61 (27.9%) CD subjects and 4 of 57 (7%) of the c ontrol subjects had severe hyperintense lesions suggestive of subclinical o r "silent" anoxic vascular events. Significant group differences were obser ved 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 w ith age, reaching 50% in the oldest age quartile (46-58 years), and this in crease was not related to the number of years cocaine was used. Conclusions: The data suggest that asymptomatic CD patients are a heterogen eous population with a significantly increased age-related risk of white ma tter neuro-vascular toxicity, Premature neurovascular damage may impact tre atment outcomes and, as the CD population ages, may manifest as an increase d incidence of cognitive deficits, (C) 1999 Society of Biological Psychiatr y.