The relationship between subjective awareness and objective neuropsychological status in HIV-1 infection remains unclear. Forty-six HIV-1 seropositive males were administered a battery of neuropsychological measures assessing episodic memory, metacognition, and depression. Results of ANOVA revealed a dissociation between subjects' self-complaint of neuropsychological impairment and objective performance, with subjects who denied cognitive impairment performing worse on memory testing. Three subgroups were identified: A group whose self-reported cognitive impairment exceeded deficits demonstrated on memory testing (37% of subjects); a group who denied impairment but evidenced deficits on memory testing (26% of subjects); and a group whose self-appraisal was consistent with performance (37% of subjects). These data suggest that self-report of cognitive dysfunction among HIV-1 infected subjects is frequently at variance with objective neuropsychological testing and that diminished awareness of decline among medically symptomatic HIV-1 infected subjects can be identified.

Our study investigates the nature of elevated depression scores on the MMPI-168 in human-immunodeficiency-virus- (HIV-)infected individuals. Comparison of MMPI scales, factor scores, and individual depression item endorsement rates were made between three groups of homosexual/bisexual men: asymptomatic HIV-1 seropositives (n = 156), symptomatic HIV-1 seropositives (n = 156), and a comparison group of HIV-1 seronegatives (n = 117). Elevated scores were found on the MMPI depression scale for all three groups, with HIV infection and the presence of symptoms being associated with significant elevations in depression. Analyses of these elevated scores through the use of factor scores and individual item analyses strongly suggest that endorsement of items related to physical symptoms and neuropsychological complaints accounted for much of the difference in overall depression scores between samples. Implications are discussed for measurement and diagnosis of depression in HIV populations.

Positron-emission tomography was coupled with neurological and neuropsychological evaluation to study regional cerebral activity and neurologic status in two groups. Seventeen patients with full-blown AIDS and 14 seronegative control subjects were studied using [18F]2-fluoro-2-deoxy-D-glucose in a resting state. The AIDS group had relative regional hypermetabolism in the basal ganglia and thalamus; stepwise multiple-regression analyses revealed a significant relationship for the AIDS group between temporal lobe metabolism and severity of dementia on the AIDS Dementia Complex Rating Scale. These results suggest that the basal ganglia, thalamus, and temporal lobes are differentially affected in AIDS.

The relationship of self-reported cognitive, motor, and affective complaints to actual neuropsychological functioning was explored in a cohort of predominantly symptomatic HIV-1 seropositive individuals. Ninety-two symptomatic HIV-1 infected subjects were questioned about complaints common in HIV infection and were assessed with a comprehensive neuropsychological test battery. No relationship was found between subjective complaints and cognitive functioning, yet a significant relationship was found between self-reported difficulties and formal measures of affect and mood. Failure to show a relationship between self-reported cognitive status and actual neuropsychological functioning in this cohort suggests that complaints of cognitive decline may be attributable to emotional factors.

The authors studied the relationship between brain metabolic activity and quantitative electroencephalographic power in AIDS. Basal ganglia and thalamic metabolic activity, measured with positron emission tomography, correlated positively with EEG power in the 6-10-Hz band across most head regions. Metabolic activity of anatomically defined cortical regions did not correlate with EEG power recorded over each region. These results support previously reported associations between abnormalities in subcortical metabolic activity and EEG activity. The lack of correlation between cortical metabolic activity and EEG activity suggests that previously observed abnormalities in EEG activity are primarily subcortical in origin.