The anatomical changes in the brain that may
contribute to impaired cognitive function in people with HIV are not well
understood.
Ryan Sanford of the Montreal Neurological Institute at
McGill University and colleagues longitudinally assessed brain volume in 46
HIV-positive people with well-controlled virus and 31 demographically matched
HIV-negative individuals. About half were men, the average age was
approximately 50 years and they had 14 years of education on average. In the
HIV-positive group the current and nadir CD4 counts were 641 and 200 cells/mm3,
respectively.
Participants
completed two sessions of neuroimaging and neuropsychological testing done approximately
two years apart. The assessment covered six cognitive domains with eight
standard tests. Standardised Z-scores were calculated for each test, as well as
an overall neuropsychological summary score (NPZ-8).
At both visits
HIV-positive participants had significantly worse cognitive performance than
HIV-negative people, with lower scores for NPZ-8 and the executive function,
attention, working memory and processing speed components.
However, there
was no significant changes in NPZ-8 score over time in either group, nor a
difference in rates of change between the two groups. The HIV-positive group
saw a greater improvement in memory and a trend toward a larger decline in
executive function.
Likewise,
tensor-based morphometry revealed significantly reduced subcortical volume in
the thalamus, caudate, putamen, globus pallidus and mid-brain in HIV-positive
people at both visits. But no major changes in brain volume were observed over
time in any region in either group, nor different rates of change between the
groups. Lower nadir CD4 count had a weak correlation with smaller brain
volumes.
"No
evidence of on-going brain injury or overall cognitive decline were
detected," the researchers concluded. "These findings support the
hypothesis that cognitive and structural brain differences in HIV-positive
patients most likely occur during the period of untreated infection, suggesting
a possible neurocognitive benefit from early combination ART initiation."
Finally, Dominique
Costagliola of the Sorbonne and INSERM in Paris and colleagues looked
at the prevalence of cerebral small vessel disease (CSVD) in people living with HIV
compared to HIV-negative people age 50 and older.
CSVD – defined by
abnormalities in white matter, silent brain infarction (obstructed blood
supply) or micro-bleeds – is a major cause of future vascular events such as
stroke, cognitive impairment, frailty and poor survival, the researchers noted
as background.
This analysis included 456 HIV-positive people in the
French ANRS EP51 MICROBREAK cohort and 154 HIV-negative people. About 80% were
men and the median age was about 56 years. Participants in the HIV-positive
group were on ART with suppressed viral load for at least a year. The median
and nadir CD4 counts were 655 and 195 cells/mm3; they did not have
HCV co-infection. Most cardiovascular risk factors were seen more often among
people with HIV, including hypertension and abnormal blood lipid levels, as was
regular alcohol use; more than 40% in both groups smoked.
In this cross-sectional study each participant
received a single MRI, and results were analysed by two experienced
neuroradiologists who were blinded to their HIV status.
CSVD was detected in 52% of
HIV-positive and 36% of HIV-negative participants, a significant difference
(adjusted odds ratio [OR] 2.3). Severe CSVD was observed in 19% and 14%,
respectively (adjusted OR 1.6).
But the impact of HIV differed according to age.
HIV-positive people under age 54 were about five times more likely, and those
in the 54-60 age group were nearly four times more likely, to develop CSVD
compared to HIV-negative people; however, for people over age 60 there was
essentially no difference (adjusted OR 5.3, 3.7 and 1.2, respectively).
In addition to HIV, being aged over 60, hypertension and
nadir CD4 count below 200 cells/mm3 were also associated with
greater risk of CSVD, the researchers reported.