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Obaid, S.

Publications and source records attributed to Obaid, S..

5 recordsLinked to original sources

Connectome-wide mega-analysis identifies a reproducible functional network signature of temporal lobe epilepsy

Resting-state functional magnetic resonance imaging (MRI) studies have reported abnormal intrinsic functional connectivity (FC) across distributed circuits in patients with temporal lobe epilepsy (TLE), indicating a system-level impact of the disorder. However, findings remain inconsistent due to limited sample sizes and methodological heterogeneity, leaving the structural determinants and clinical relevance of FC alterations unresolved. To identify a robust and reproducible FC signature, we conducted a data-driven, connectome-wide mega-analysis in a large multicentre cohort of 652 participants (297 TLE, 73 disease controls, and 282 healthy controls) with multimodal 3T MRI and deep clinical phenotyping. We identified convergent FC reconfigurations at both group and individual levels that preferentially involved densely connected hubs, manifesting as hyperconnectivity in frontoparietal association systems and hypoconnectivity in temporal and paralimbic systems. Integrating structural cortical wiring features further revealed that these extensive alterations were constrained by corticocortical proximity, microstructural similarity, and white matter connectivity. Clinically, the FC phenotype tracked symptom burden and disease progression, informed postsurgical seizure outcome, and distinguished TLE from other focal epilepsies. Collectively, these findings systematically delineate a neurobiologically grounded, hub-centric pattern of intrinsic network disruption in TLE, anchored in temporolimbic and adjacent transmodal systems, with potential utility for individualized phenotypic stratification and outcome prognostication.

neuroscience↗

Precision mapping and molecular contextualization of surgical outcome epicenters in temporal lobe epilepsy

AO_SCPLOWBSTRACTC_SCPLOWTemporal lobe epilepsy is the most common drug-resistant epilepsy, with surgical resection offering the primary path to seizure freedom. Despite standardized approaches, a substantial proportion of patients experience seizure recurrence, and the neurobiological substrates underlying these divergent outcomes remain unclear. We applied an individualized normative modeling framework to multimodal preoperative MRI data in a group that subsequently underwent surgical resection, to characterize patient-specific structural deviations and identify disease epicenters. Patients who became seizure-free exhibited spatially coherent abnormalities localized to the hippocampus and ipsilateral association regions, anchored in agranular limbic territories and enriched for genes linked to calcium-dependent signaling. Non-seizure-free patients, on the other hand, showed a more heterogeneous and distributed pattern of deviations, consistent with a "temporal-plus" network organization, and broader neuromodulatory dysregulation. Crucially, overlap between resected tissue and network-defined epicenters was closely associated with seizure freedom, independent of total resection volume. These findings provide a multiscale framework for precision surgical planning, shifting the focus from standardized tissue removal to targeted disconnection of patient-specific pathological hubs.

neuroscience↗

Beta bursts mediate amygdala gating of hippocampal emotional encoding

The amygdala and hippocampus are key structures in emotional processing, yet the transient neural dynamics coordinating their interaction remain poorly understood. We simultaneously recorded single-neuron activity and local field potentials from these regions in epilepsy patients performing an emotional image-rating task. Neurons in both areas exhibited firing rate changes predictive of subjective emotional valence. While conventional spectral analysis revealed no valence-specific patterns, beta bursts (13-30 Hz)--transient, high-power events-were uniquely modified by task features. In both regions, beta bursts were associated with increased gamma amplitude and enhanced phase coherence, with beta-gamma phase-amplitude coupling capturing emotion-related dynamics. Critically, amygdala beta bursts were associated with strong suppression of hippocampal firing, coinciding with interneuron activation, during negative valence/highest arousal processing, whereas hippocampal bursts showed no reciprocal influence. These findings suggest that beta bursts may represent a temporally precise neural correlate of emotional appraisal and a candidate mechanism for targeted neuromodulation in mood disorders.

neuroscience↗

Statistical learning in epilepsy: Behavioral, anatomical, and causal mechanisms in the human brain

Statistical learning, the fundamental cognitive ability of humans to extract regularities across experiences over time, engages the medial temporal lobe in the healthy brain. This leads to the hypothesis that statistical learning may be impaired in epilepsy patients, and that this impairment could contribute to their varied memory deficits. In turn, epilepsy patients provide a platform to advance basic understanding of statistical learning by helping to evaluate the necessity of medial temporal lobe circuitry through disease and causal perturbations. We implemented behavioral testing, volumetric analysis of the medial temporal lobe substructures, and direct electrical brain stimulation to examine statistical learning across a cohort of 61 epilepsy patients and 28 healthy controls. Behavioral performance in a statistical learning task was negatively associated with seizure frequency, irrespective of where seizures originated in the brain. The volume of hippocampal subfields CA1 and CA2/3 correlated with statistical learning performance, suggesting a more specific role of the hippocampus. Indeed, transient direct electrical stimulation of the hippocampus disrupted statistical learning. Furthermore, the relationship between statistical learning and seizure frequency was selective: behavioral performance in an episodic memory task was impacted by structural lesions in the medial temporal lobe and by antiseizure medications, but not by seizure frequency. Overall, these results suggest that statistical learning may be hippocampally dependent and that this task could serve as a clinically useful behavioral assay of seizure frequency distinct from existing neuropsychological tests. Simple and short statistical learning tasks may thus provide patient-centered endpoints for evaluating the efficacy of novel treatments in epilepsy.

neuroscience↗

Graphene Biointerface for Cardiac Arrhythmia Diagnosis and Treatment

Heart rhythm disorders, known as arrhythmias, cause significant morbidity and are one of the leading causes of mortality. Cardiac arrhythmias are primarily treated by implantable devices, such as pacemakers and defibrillators, or by ablation therapy guided by electroanatomical mapping. Pharmacological treatments are mostly ineffective. Both implantable and ablation therapies require sophisticated biointerfaces for electrophysiological measurements of electrograms and delivery of therapeutic stimulation or ablation energy. In this work, we report for the first time on graphene biointerface for in vivo cardiac electrophysiology. Leveraging sub-micrometer thick tissue-conformable graphene arrays, we demonstrate sensing and stimulation of the open mammalian heart both in vitro and in vivo. Furthermore, we demonstrate graphene pacemaker treatment of a pharmacologically-induced arrhythmia, AV block. The arrays show effective electrochemical properties, namely interface impedance down to 40 Ohmxcm2 at 1kHz, charge storage capacity up to 63.7 mC/cm2, and charge injection capacity up to 704 C/cm2. Transparency of the graphene structures allows for simultaneous optical mapping of cardiac action potentials and optogenetic stimulation while performing electrical measurements and stimulation. Our report presents evidence of the significant potential of graphene biointerfaces for the future clinical device- and catheter-based cardiac arrhythmias therapies.

bioengineering↗