Abstract
While the arrival of combination antiretroviral therapy significantly decreased the prevalence of HIV-associated dementia, between 35 and 70% of all infected adults continue to develop some form of cognitive impairment. These deficits appears to affect multiple neural subsystems, but the mechanisms and extent of damage are not fully understood. In the current study, we utilized magnetoencephalography (MEG), advanced oscillatory analysis methods, and a paired-pulse somatosensory stimulation paradigm to interrogate pre-attentive inhibitory processing in 43 HIV-infected adults and 28 demographically-matched uninfected controls. MEG responses were imaged using a beamformer, and time series data were extracted from the peak voxel in grand-averaged functional brain images to quantify the dynamics of sensory gating, oscillatory power, spontaneous power, and other neural indices. We found a significantly weakened response to the second stimulation compared to the first across groups, indicating significant sensory gating irrespective of HIV-infection. Interestingly, HIV-infected participants exhibited reduced neural responses in the 20–75 Hz gamma range to each somatosensory stimulation compared to uninfected controls, and exhibited significant alterations in peak gamma frequency in response to the second stimulation. Finally, HIV-infected participants also had significantly stronger spontaneous activity in the gamma range (i.e., 20–75 Hz) during the baseline period before stimulation onset. In conclusion, while HIV-infected participants had the capacity to efficiently gate somatosensory input, their overall oscillatory responses were weaker, spontaneous baseline activity was stronger, and their response to the second stimulation had an altered peak gamma frequency. We propose that this pattern of deficits suggests dysfunction in the somatosensory cortices, which is potentially secondary to accelerated aging.
Highlights
Since the advent of combination antiretroviral therapy, the prevalence of HIV-associated dementia (HAD) has significantly decreased, while that of other forms of HIV-associated neurocognitive disorders (HAND) has remained largely the same or even increased (Antinori et al, 2007; Cysique and Brew, 2009; Heaton et al, 2010; Heaton et al, 2011; Robertson et al, 2007)
A study of resting cerebral blood flow revealed diminished rCBF within the lenticular nuclei and visual cortex for HIV-infected participants compared to uninfected controls
While participants with HIV did not differ in their gating of repetitive stimuli, other somatosensory indices were significantly altered
Summary
Since the advent of combination antiretroviral therapy (cART), the prevalence of HIV-associated dementia (HAD) has significantly decreased, while that of other forms of HIV-associated neurocognitive disorders (HAND) has remained largely the same or even increased (Antinori et al, 2007; Cysique and Brew, 2009; Heaton et al, 2010; Heaton et al, 2011; Robertson et al, 2007). 35–70% of all HIV-infected individuals continue to develop at least some form of cognitive impairment, and this has a major economic and societal impact on the United States and worldwide (Heaton et al, 2010; Heaton et al, 2011; Robertson et al, 2007; Simioni et al, 2010). A study of resting cerebral blood flow (rCBF) revealed diminished rCBF within the lenticular nuclei and visual cortex for HIV-infected participants compared to uninfected controls. This reduction in rCBF was shown in both impaired and unimpaired participants with HIV compared to controls, suggesting that at least some neurobiological changes in blood flow precede neuropsychological deficit (Ances et al, 2009). A similar study using fMRI but focusing on the interaction between age and HIV-
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