Biology subjects

Sulcova, D.

Publications and source records attributed to Sulcova, D..

3 recordsLinked to original sources

bioRxiv2024

Stimulation parameters shape effective connectivity pathways: insights from microstate analysis on TMS-evoked potentials

Transcranial magnetic stimulation (TMS)-evoked potentials (TEPs) represent an innovative measure for examining brain connectivity and developing biomarkers of psychiatric conditions. Minimising TEP variability across studies and participants, which may stem from methodological choices, is therefore vital. By combining classic peak analysis and microstate investigation, we tested how TMS pulse waveform and current direction may affect effective connectivity when targeting the primary motor cortex (M1). We aim to disentangle whether changing these parameters affects the degree of activation of the same neural circuitry or may lead to changes in the pathways through which the induced activation spreads. Thirty-two healthy participants underwent a TMS-EEG experiment in which the pulse waveform (monophasic, biphasic) and current direction (posterior-anterior, anterior-posterior, latero-medial) were manipulated. We assessed the latency and amplitude of M1-TEP components and employed microstate analyses to test differences in topographies. Results revealed that TMS parameters strongly influenced M1-TEP components amplitude but had a weaker role over their latencies. Importantly, microstate analysis showed that the current direction in monophasic stimulations changed the pattern of evoked microstates at the early TEP latencies, as well as their duration and the overall amount of activated brain resources associated. This study shows that the current direction of monophasic pulses may modulate cortical sources contributing to TEP signals, activating neural populations and cortico-cortical paths more selectively. Biphasic stimulation reduces the variability associated with current direction and may be better suited when TMS targeting is blind to anatomical information.

neuroscience↗

bioRxiv2022

Exploring the properties of the left angular gyrus using TMS-evoked potentials

The angular gyrus (AG) is involved in multiple cognitive processes and its structural alterations are commonly observed in many neuropsychiatric syndromes. Since changes in excitability may precede structural changes and clinical symptoms, there is a need for diagnostic tools assessing the functional state of hub brain regions like the AG. The combination of transcranial magnetic stimulation (TMS) and electroencephalography (EEG) can provide such functional readouts by probing the brain response to direct stimulation. This study aimed to characterize TMS-evoked potentials (TEP) elicited by AG stimulation, determine optimal stimulation parameters, and identify TEP biomarkers of AG function. We recorded AG-TEPs in 19 subjects using four TMS orientations and three intensities and compared TEP spatiotemporal features using topographic dissimilarity and microstate analyses. Additionally, we explored the relationship between AG-TEP topography and TMS-evoked muscular activity. Our results showed topographic variability in AG-TEP components P25, N45, and N75. The P25 topography was sensitive to TMS orientation, while the topography of N45 and N75 was highly dependent on both coil orientation and intensity. Interestingly, we found that TMS-evoked muscular activity was also dependent on both these parameters and strongly related to the occurrence of a specific topographic pattern, which therefore possibly corresponds to the somatosensory brain response to muscle contraction. We conclude that the early AG-TEP component P25 likely reflects neural processes triggered by direct AG activation and could provide an index of local excitability. Later components N45 and N75 must be interpreted with caution as they may primarily reflect peripherally evoked activity.

neuroscience↗

bioRxiv2022

Evaluation of GABAAR-mediated inhibition in the human brain using TMS-evoked potentials

GABAA receptor (GABAAR) - mediated inhibition participates in the control of cortical excitability, and its impairment likely contributes to the pathologic excitability changes that have been associated with multiple neurological disorders. Therefore, there is a need for its direct evaluation in the human brain, and the combination of transcranial magnetic stimulation (TMS) and electroencephalography (EEG) might represent the optimal tool. TMS-evoked brain potentials (TEPs) capture the spread of activity across the stimulated brain network, and since this process at least partially depends on the GABAAR-mediated inhibition, TEPs may constitute relevant biomarkers of local GABAAergic function. Here, we aimed to assess the effect of GABAARs activation using TEPs, and to identify TEP components that are sensitive to the state of GABAAergic inhibition. In 20 healthy subjects, we recorded TEPs evoked by sub- and supra-threshold stimulation of the primary motor cortex (M1), motor-evoked potentials (MEPs) and resting-state EEG (RS-EEG). GABAARs were activated (1) pharmacologically by oral administration of alprazolam compared to placebo within each subject, and (2) physiologically using a sub-threshold conditioning stimulus to characterize the effect of short-latency intracortical inhibition (SICI). In supra-threshold TEPs, alprazolam suppressed the amplitude of components N17, N100 and P180, and increased component N45. The pharmacological modulation of N17 correlated with the change observed in MEPs and with the alprazolam-induced increase of lower {beta}-band RS-EEG. Only a reduction of N100 and P180 was found in sub-threshold TEPs. TEP SICI manifested as a reduction of N17, P60 and N100, and its effect on N17 correlated with the alprazolam-induced N17 suppression and {beta} increase. Our results indicate that N17 of supra-threshold TEPs could serve as a non-invasive biomarker of local cortical excitability reflecting the state of GABAAR-mediated inhibition in the sensorimotor network. Furthermore, the alprazolam-induced increase of {beta}-band oscillations possibly corresponds to the increased inhibitory neurotransmission within this network.

neuroscience↗