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Neuroimaging correlates of HIV-associated BBB compromise.

Avison MJ, Nath A, Greene-Avison R, Schmitt FA, Greenberg RN, Berger JR

Department of Neurology, University of Kentucky Medical Center,Lexington, KY, USA. calum.avison@vuiis.vanderbilt.edu

The mechanisms underlying blood-brain barrier (BBB) compromise in human immunodeficiency virus (HIV) infection and the ways in which BBB compromise might impair neurocognitive function remain poorly understood. This study had two aims: (1) to examine the relationship between BBB breakdown, measured using contrast-enhanced magnetic resonance imaging (CE-MRI), plasma viral load, and neurological status; and (2) to examine the influence of highly active antiretroviral therapy (HAART) on the relationship between neuroinflammation using myoinositol/creatine (mI/Cr), a surrogate marker of glial activation as measured by magnetic resonance spectroscopy (MRS), and BBB compromise determined by CE-MRI. In 25 HIV-infected patients, we found that: (1) the severity of neurocognitive impairment correlated with the degree of BBB breakdown in the basal ganglia; (2) for any given degree of BBB compromise, patients with high plasma viral load were more severely impaired; (3) BBB compromise correlated with mI/Cr in the basal ganglia; and (4) for any given level of mI/Cr, the severity of BBB compromise and the severity of neurocognitive impairment were significantly less in patients on HAART than in those who were HAART-naive. These results confirm a role for BBB compromise in the pathogenesis of HIV-associated neurocognitive impairment and suggest that elevated plasma viral load in the presence of BBB compromise may increase the risk for development of HIV-associated dementia (HAD). Additionally, they suggest a salutary effect of HAART on the incidence and severity of HAD, which may, in part, be due to protection of BBB integrity.

Published 6 December 2004 in J Neuroimmunol, 157(1): 140-6.
Full-text of this article is available online (may require subscription).

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