1. ¹Neuroscience Program, SRI International, Menlo Park, CA, USA
2. ²Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA, USA
3. ³Department of Electrical Engineering and Computer Science, MIT, Cambridge, MA, USA
4. ⁴Harvard-MIT Division of Health Sciences and Technology, MIT, Cambridge, MA, USA

Correspondence: Dr A Pfefferbaum, Neuroscience Program, SRI International, 333 Ravenswood Avenue, Menlo Park, CA 94025, USA. Tel: +1 650 859 2927; Fax: +1 650 859 2743; E-mail: dolf@synapse.sri.com

Received 22 November 2004; Revised 8 February 2005; Accepted 14 February 2005; Published online 6 April 2005.

Abstract

Alcoholism comorbidity is highly prevalent in individuals infected with human immunodeficiency virus (HIV). Each condition is known to affect brain structure, function, and metabolism, but the combined effects on the brain have only recently been considered. Single-voxel, proton MR spectroscopy (MRS) has yielded sensitive measures of early brain deterioration in the progression of HIV, but has limited coverage of neocortex, whereas MRS imaging (MRSI) can simultaneously interrogate large regions of cortex. Included were 15 men with HIV+alcoholism, nine men with HIV alone, eight men with alcoholism alone (abstinent for 3–17 months), and 23 controls. The two HIV groups were matched in T-cell count and were not demented; the two alcoholism groups were relatively matched in lifetime alcohol consumption. We used MRSI with a variable-density spiral sequence to quantify major proton metabolites—N-acetylaspartate (NAA), creatine (Cr), and choline (Cho)—in the superior parietal–occipital cortex. Metabolites were expressed in absolute units and as the NAA/Cr ratio. Significant group effects were present for NAA and Cr. Only the HIV+alcoholism group was significantly affected, exhibiting a 0.8 SD deficit in NAA and a 1.0 SD deficit in Cr. The deficits were not related to highly active antiretroviral therapy (HAART) status. Neither HIV infection nor alcoholism independently resulted in parietal–occipital cortical metabolite abnormalities, yet each disease carried a liability that put affected individuals at a heightened risk of neuronal compromise when the diseases were compounded. Further, the use of absolute measures revealed deficits in NAA and Cr that would have gone undetected if these metabolites were expressed as a ratio.