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Thalamic neuromodulation is an established treatment option for drug-resistant epilepsy (DRE), yet how thalamic input reshapes cortico-cortical interactions on the sub-second timescale remains poorly defined.1 Deep brain stimulation (DBS) of the anterior thalamic nucleus (AN) reduces seizures with benefit in focal DRE,1 and for multifocal or generalized phenotypes, DBS and brain-responsive neurostimulation (RNS) targeting the centromedian nucleus (CM) likewise demonstrate seizure reduction.2,3 DBS typically uses continuous high-frequency stimulation; still, single-pulse electrical stimulation (SPES) during stereo-EEG (SEEG) provides a complementary perturbational assay to quantify immediate thalamic network engagement and derive pulse-locked biomarkers for subsequent testing under therapeutic stimulation paradigms.
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Kanai et al. (2026) studied this question.
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