Background: Cognitive impairment in patients with human immunodeficiency virus
(HIV) is associated with higher morbidity. The prevalence of 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 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, attention-information 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.
Conclusion: 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