Cerebrovascular changes in the basal ganglia with HIV dementia

Background: HIV dementia is a form of subcortical dementia. Clinical, radio logic, pathologic, and biochemical studies suggest a major contribution of basal ganglia dysfunction to the pathogenesis of this disorder. Many invest igators have proposed a contribution of a disrupted blood-brain barrier (BB B) to the pathogenesis of HnT dementia. Objective: To identify microvascula r abnormalities in vivo in basal ganglia or white matter of persons with HI V dementia. Methods: Time course of MRI postcontrast enhancement was determ ined in basal ganglia and white matter of HIV-infected persons without deme ntia (Memorial Sloan Kettering [MSK] score of 0; n = 4); HIV-infected perso ns with mild dementia (MSK score of 0.5; n = 2); and HIV-infected persons w ith moderate-to-severe dementia (MSK greater than or equal to 1.0; n = 6). Results: Increased basal ganglia enhancement was observed in individuals wi th moderate-to-severe dementia relative to nondemented individuals, both im mediately and 30 minutes after contrast administration. Decline of basal ga nglia enhancement was slower in the moderately to severely demented patient s and, when normalized to intravascular enhancement of sagittal sinus, sugg ested leakage of contrast agent, consistent with increased permeability of BBB. A significant correlation between the postcontrast fractional enhancem ent at 30 minutes (FE30) and the MSK score was noted. White matter showed n o significant differences in postcontrast enhancement among the three group s. Conclusion: Increased early enhancement in basal ganglia of the HIV deme ntia group is consistent with increased regional cerebral blood volume (rCB V). Increased late enhancement is strongly suggestive of BBB disruption. Si milar abnormalities were absent in the white matter adjacent to the caudate nucleus.