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Khalili-Ardali, M.

Publications and source records attributed to Khalili-Ardali, M..

3 recordsLinked to original sources

Electrophysiological Signature of Stroke Recovery: Investigating EEG Biomarkers for Prognostic Insights

Stroke is a leading cause of long-term disability, often resulting in persistent motor impairments reflecting disruptions in large-scale brain networks. While electroencephalography (EEG) has long been used to monitor neurophysiological changes following stroke, an integrated framework capturing spatiotemporal dynamics would help understand changes over time. In this study, we analysed resting-state EEG from stroke patients at one week (Session 1) and three months (Session 2) post-stroke to investigate electrophysiological biomarkers of motor recovery, indexed by changes in the Fugl-Meyer scale ({Delta}FM ). We quantified spectral properties, focusing on the relative alpha band power, microstate metrics such as mean duration, complexity, and transition probabilities, and measures of metastability and synchrony derived from the Kuramoto Order Parameter. Among all the EEG measures, the longitudinal change in relative alpha power emerged as the strongest single correlate of motor improvement, accounting for the largest proportion of variance among the examined EEG measures. Although metastability and synchrony alone did not reach statistical significance, they showed moderate positive correlations with {Delta}FM, particularly in the alpha and theta ranges, and once combined with alpha power, added 26% in explaining the variance in {Delta}FM . Microstate parameters did not explain additional variance in recovery once alpha power and network-level dynamics were considered. A hierarchical model combining alpha power, metastability/synchrony, and microstates explained over 78% of the variance in {Delta}FM, indicating that stroke recovery involves restoring balanced alpha oscillations and flexible large-scale brain coordination. Future research with larger samples and more frequent longitudinal assessments is required to confirm the prognostic utility of integrated EEG biomarkers for guiding personalised stroke rehabilitation strategies.

neuroscience↗

Neural Activity dynamic in Primate Cortex Across Consciousness Levels: Insights from High-Density Neuropixel Recording

This study investigates the anesthesia mechanisms induced by sevoflurane and how it modulates neural activity in the posterior parietal cortex (PPC) and prefrontal cortex (PFC) in Non Human Primates (NHPs) using high density Neuropixel probes. Spiking and local field potentials (LFPs) were recorded in two macaque monkeys under going four sevoflurane concentrations (2%, 3%, 4%, and 6%). We aimed to (i) quantify the emergence of anesthesia-induced Up/Down state dynamics, (ii) track changes in oscillatory power and inter-regional synchrony, and (iii) determine whether frontal and parietal areas exhibit differential sensitivity to rising and falling anesthetic depth. Across different anesthetic levels, we observed characteristic slow oscillations in delta range in both PFC and PPC, with neurons transitioning between high-firing "Up" states and near-silent "Down" states. Deeper anesthesia extended Down states, suppressed mean firing rates, and reduced the frequency and duration of Up states. In M1, no single units were detected in PFC, and only a few were recorded in M2. We suspect misalignment of the probe with PFC pyramidal cells and extensive suppression in PFC as the main reasons. Recurrent Neural Networks (RNN) was used to extract Up/Down states from LFP activities, based one the pattern observed in the PPC. The PPC [->] PFC information flow observed in Transfer Entropy analysis suggests that even under anesthesia, some level of feedforward-like interactions may persist. Up states originate in deep cortical layers and propagate toward superficial layers, following a bottom-up progression, indicating that deep-layer pyramidal neurons, which receive strong thalamic input, may be the primary drivers of Up states. The short Up states under deep anesthesia might represent a failed ignition attempt, where the brain momentarily tries to reactivate but cannot sustain functional activity due to global inhibition. LFP analyses revealed that although the absolute delta power remains high at different anesthetic levels, the relative delta band power is anti correlated with anesthetic depth, due to sporadic short (20ms to 40ms) burst in gamma (30-100 Hz) that appeared transient in nature. Lower sensitivity to anesthesia dose changes were observed in PFC as compared to PPC. This could explain why anesthesia first impairs cognitive function before affecting basic sensory responses. These results indicates that the traditional Up/Down state models might oversimplify anesthetic brain dynamics. While anesthesia is often described as a state of simple global slow-wave oscillations, the observed Up/Down state durations are not uniform, they fluctuate, follow non-trivial transition patterns, and differ between PFC and PPC.

neuroscience↗

Anaesthesia disrupts mesoscale signal propagation in spite of enhanced responsivity in frontal but not in parietal cortex

Loss of consciousness under anaesthesia is accompanied by widespread silencing of neurons, and disruption of cortical dynamics. Yet, how this affects mesoscale signal propagation within higher-order associative areas, crucially implicated in theories of consciousness, remains poorly understood. Here we combined intracortical microstimulation, and simultaneous multielectrode recordings in the ventrolateral prefrontal cortex (vlPFC) and the posterior parietal cortex (PPC) of macaques across wakefulness, and graded depths of anaesthesia. Spiking responses revealed distinct regimes: in the PFC, higher-amplitude stimulation elicited a delayed single rebound after sustained inhibition, whereas in the PPC, a faster and double-rebound profile emerged. Despite enhanced local spiking and LFP responsivity under anaesthesia, we found a strong and selective suppression of lateral signal propagation in the PFC - a breakdown strikingly absent in the PPC. This dissociation suggests that anaesthesia disrupts consciousness not merely by silencing cortical populations, but by impairing mesoscale integrative processes critical for neuronal dynamics at multiple scales. Our findings demonstrate in a causal and spatially-resolved manner, that lateral signal spread within higher-order cortex is a key mechanism underlying conscious awareness, and its loss under anaesthesia.

neuroscience↗