ObjectiveHere we tested the effect of combined antiretroviral therapy (cART) on deviant electroencephalographic (EEG) source activity in treatment-naïve HIV individuals.MethodsResting state eyes-closed EEG data were recorded before and after 5 months of cART in 48 male HIV subjects, who were naïve at the study start. The EEG data were also recorded in 59 age- and sex-matched healthy subjects as a control group. Frequency bands of interest included delta, theta, alpha1, alpha2 and alpha3, based on alpha frequency peak specific to each individual. They also included beta1 (13–20 Hz) and beta2 (20–30 Hz). Low-resolution brain electromagnetic tomography (LORETA) estimated EEG cortical source activity in frontal, central, temporal, parietal, and occipital regions.ResultsBefore the therapy, the HIV group showed greater parietal delta source activity and lower spatially diffuse alpha source activity compared to the control group. Thus, the ratio of parietal delta and alpha3 source activity served as an EEG marker. The z-score showed a statistically deviant EEG marker (EEG +) in 50% of the HIV individuals before therapy (p < 0.05). After 5 months of cART, delta source activity decreased, and alpha3 source activity increased in the HIV subjects with EEG + (about 50% of them showed a normalized EEG marker).ConclusionsThis procedure detected a deviant EEG marker before therapy and its post-therapy normalization in naïve HIV single individuals.SignificanceThe parietal delta/alpha3 EEG marker may be used to monitor cART effects on brain function in such individuals.
Background Motor impairment after stroke is due not only to direct tissue loss but also to disrupted connectivity within the motor network. Mixed results from studies attempting to enhance motor recovery with Transcranial Magnetic Stimulation (TMS) highlight the need for a better understanding of both connectivity after stroke and the impact of TMS on this connectivity. This study used TMS-EEG to map the causal information flow in the motor network of healthy adult subjects and define how stroke alters these circuits. Methods Fourteen stroke patients and 12 controls received TMS to two sites (bilateral primary motor cortices) during two motor tasks (paretic/dominant hand movement vs. rest) while EEG measured the cortical response to TMS pulses. TMS-EEG based connectivity measurements were derived for each hemisphere and the change in connectivity (ΔC) between the two motor tasks was calculated. We analyzed if ΔC for each hemisphere differed between the stroke and control groups or across TMS sites, and whether ΔC correlated with arm function in stroke patients. Results Right hand movement increased connectivity in the left compared to the right hemisphere in controls, while hand movement did not significantly change connectivity in either hemisphere in stroke. Stroke patients with the largest increase in healthy hemisphere connectivity during paretic hand movement had the best arm function. Conclusions TMS-EEG measurements are sensitive to movement-induced changes in brain connectivity. These measurements may characterize clinically meaningful changes in circuit dynamics after stroke, thus providing specific targets for trials of TMS in post-stroke rehabilitation.
Introduction: Stroke produces profound local and systemic immune responses that engage all major innate and adaptive immune compartments. The aim of this study was to characterize the systemic immune response to stroke and to determine if it contributes to long-term cognitive disability. Methods: We included 24 consecutive subjects with ischemic stroke and excluded patients for autoimmune disorders, use of immunosuppressant drugs, or life expectancy <90 days. Blood samples were collected for up to 9 timepoints after stroke (days 1, 2, 3, 5, 7, 14, 30, 90, and 365). Change in cognitive function between days 90 and 365 was assessed using the Montreal Cognitive Assessment (MoCA). Control samples were from a cohort of 24 sex- and age-matched patients prior to hip replacement surgery. We used mass cytometry to acquire 240 immune features from each sample, representing 20 immune cell subtypes, their frequency, cell surface markers, and activation states. Elastic Net (EN) regularized regression modeling was used to characterize phases of the immune response and to correlate stages of the immune response with change in cognitive function. Results: The EN model identified three distinct phases of the systemic immune response to ischemic stroke: The acute phase (day 2) was characterized by increased STAT3 (signal transducer and activator of transcription 3) signaling responses in innate immune cell types. The intermediate phase (day 5) was characterized by increased CREB (cAMP response element-binding protein) signaling responses in adaptive immune cell types. The late phase (day 90) was characterized by persistent elevation of neutrophils and IgM+ B cells. By day 365 there was a return to baseline immune responses, comparable to the controls. A decline in MoCA scores between day 90 and day 365 after stroke correlated with a stronger inflammatory response in the acute phase (r = -0.692, Bonferroni-corrected p = 0.04). Conclusions: The results demonstrate three distinct phases of the peripheral immune response that occur after stroke, spanning from days 2 to day 90. The acute phase immune response predicts post-stroke cognitive decline, suggesting that therapies aimed at optimizing this response could lead to preservation of cognitive functioning post-stroke.
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