Background:
Cognitive impairment in patients with human immunodeficiency virus (HIV) is associated with higher morbidity. The prevalence of and the metabolite changes in the brain associated with cognitive impairment in anti-retroviral therapy naïve
patients with HIV is unknown.
Objective:
To estimate the prevalence of, and the neurometabolites associated with cognitive impairment in antiretroviral therapy
(ART) naïve patients with HIV.
Methods:
We conducted a cross-sectional study among ART naïve patients with HIV aged 18-50 years in a tertiary care center in
India. Cognition was tested using the Post Graduate Institute battery of brain dysfunction across five domains; memory, attentioninformation processing, abstraction executive, complex perceptual, and simple motor skills. We assessed the total N-acetyl aspartyl
(tNAA), creatine (tCr) and glutamate + glutamine (Glx) using 3T magnetic resonance spectroscopy. Cognitive impairment was defined as an impairment in ≥2 domains.
Results:
Among 43 patients eligible for this study, the median age was 32 years (IQR 29, 40) and 30% were women. Median CD4
count and viral load were 317 cells/µL (IQR 157, 456) and 9.3 copies/ µL (IQR 1.4, 38), respectively. Impairment in at least one
cognitive domain was present in 32 patients (74.4%). Impairment in simple motor skills and memory was present in 46.5% and 44%
of patients, respectively. Cognitive impairment, defined by impairment in ≥2 domains, was found in 22 (51.2%) patients. There was
a trend towards higher concentration of tNAA (7.3 vs. 7.0 mmol/kg), tGlx (9.1 vs. 8.2 mmol/kg), and tCr (5.5 vs. 5.2 mmol/kg) in the
frontal lobe of patients with cognitive impairment vs. without cognitive impairment but it did not reach statistical significance (p>0.05
for all). There was no difference in the concentration of these metabolites in the two groups in the basal ganglia.
Conclusions:
There is a high prevalence of cognitive impairment in ART naïve patients with HIV. There is no difference in metabolites in patients with or without cognitive impairment. Further studies, with longitudinal follow-up, are required to understand the
underlying pathophysiological mechanisms.
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