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Thapa, T.

Publications and source records attributed to Thapa, T..

3 recordsLinked to original sources

Task-related changes in aperiodic activity are related to visual working memory capacity independent of event-related potentials and alpha oscillations

Research using electroencephalography (EEG) has shown that individual differences in visual working memory capacity are related to slow-wave event-related potentials (ERPs) and suppression of alpha-band oscillatory power during the delay period of memory tasks. However, recent evidence suggests that changes in non-oscillatory (aperiodic) features of the EEG signal are related to working memory performance. We assessed several features of task-related changes in aperiodic activity including its spatial distribution, the effect of memory load, and the relationships between aperiodic activity, memory capacity, slow-wave ERPs, and alpha suppression. Eighty-four healthy individuals performed a continuous recall working memory (WM) task consisting of 2, 4 or 6 coloured squares while EEG was recorded. Aperiodic activity during a baseline and WM delay period was quantified by fitting a model to the background of the EEG power spectra, which returned parameters describing the slope (exponent) and broadband offset of the spectra. The aperiodic exponent decreased (i.e., slope flattened) in lateral parieto-occipital electrodes but increased (i.e., slope steepened) in fronto-central electrodes during the WM delay period, whereas the offset decreased over parieto-occipital electrodes. These task-related changes in aperiodic activity did not differ between memory loads. Larger increases in the aperiodic exponent were associated with higher working memory capacity measured from both the WM task and a separate battery of complex span tasks, a relationship that was independent of slow-wave ERPs and alpha suppression. Our findings suggest that WM task-related changes in aperiodic activity are region specific and reflect an independent neural mechanism that is important for general working memory ability.

neuroscience↗

No evidence for changes in GABA concentration, functional connectivity, or working memory following continuous theta burst stimulation over dorsolateral prefrontal cortex

Continuous theta burst stimulation (cTBS) is thought to reduce cortical excitability and modulate functional connectivity, possibly by altering cortical inhibition at the site of stimulation. However, most evidence comes from the motor cortex and it remains unclear whether similar effects occur following stimulation over other brain regions. We assessed whether cTBS over left dorsolateral prefrontal cortex altered gamma aminobutyric acid (GABA) concentration, functional connectivity and brain dynamics at rest, and brain activation and memory performance during a working memory task. Seventeen healthy individuals participated in a randomised, sham-controlled, cross-over experiment. Before and after either real or sham cTBS, magnetic resonance spectroscopy was obtained at rest to measure GABA concentrations. Functional magnetic resonance imaging (fMRI) was also recorded at rest and during an n-back working memory task to measure functional connectivity, regional brain activity (low-frequency fluctuations), and task-related patterns of brain activity. We could not find evidence for changes in GABA concentration (P=0.66, Bayes factor [BF10]=0.07), resting-state functional connectivity (P(FWE)>0.05), resting-state low-frequency fluctuations (P=0.88, BF10=0.04), blood-oxygen level dependent activity during the n-back task (P(FWE) >0.05), or working memory performance (P=0.13, BF10=0.05) following real or sham cTBS. Our findings add to a growing body of literature suggesting the effects of cTBS are highly variable between individuals and question the notion that cTBS is a universal inhibitory paradigm.

neuroscience↗

Slow peak alpha frequency and corticomotor depression linked to high pain susceptibility in transition to sustained pain

Mechanisms that predict an individuals susceptibility to pain, before pain is present or in the first few days following pain onset, are unknown. We utilised a clinically-relevant human transitional pain model (intramuscular injections of nerve growth factor) to examine brain mechanisms that predict pain susceptibility. Resting state EEG and corticomotor excitability measured by TMS were evaluated longitudinally in healthy individuals as pain developed and resolved over 21 days. Whereas pre-pain central peak alpha frequency (PAF) correlated with peak pain occurring 4-6 days later, altered corticomotor excitability developed several days after pain onset and showed two distinct patterns (facilitation, depression). Individuals with combined slow PAF and corticomotor depression developed more severe pain. These data provide the first evidence of the temporal profile of key brain mechanisms as pain progressively develops. PAF and corticomotor excitability could represent biomarkers for susceptibility to high pain severity and subsequently, the development of chronic pain.

neuroscience↗