Abstract Number: Esoc2026ys282 Functional Connectivity in Perihaemorrhagic Edema for Predicting Recovery in Neurorehabilitation for Intracerebral Haemorrhage

Abstract Background and aims Intracerebral haemorrhage (ICH) is associated with high mortality and morbidity. While primary haemorrhage-related injury seems irreversible, the perihaemorrhagic edema (PHE) is a modifiable driver of secondary injury and an outcome predictor. However, no effective treatment of PHE exists and mechanisms linking it to functional impairment remain unclear. We aim to quantify functional connectivity (FC) between PHE and unaffected brain areas to determine if this interregional synchronization of neuronal oscillations serves as a predictive biomarker for recovery, establishing PHE as therapeutic target. Methods This single-center prospective exploratory study will enroll 30 patients with supratentorial ICH (10-80mL volume) with lobar involvement undergoing inpatient neurorehabilitation. Exclusion criteria include prior stroke, traumatic brain injury, epilepsy, or surgical bone removal. We plan 4 study Visits aligned with PHE evolution (Figure 1). High-density EEG and MRI for FC computation, alongside clinical assessments are performed at Visit 1, 2, and 4. A telephone Visit 3 and Visit 4 assess functional outcomes. The primary endpoint is clinical recovery defined as Extended Barthel Index change between Visits 1-2. Secondary endpoints include functional outcome, quality of life, and motor/ cognitive scores. Multivariable models, adjusted for clinical covariates, will be used for analyses. Results Independent funding is secured; recruitment is planned for Q2/2026. We expect FC in the PHE region to be reduced compared to the contralesional site and anticipate this will predict recovery. By clarifying this network-level interplay, this project provides the scientific foundation for future transcranial direct current stimulation interventions paving the way for active therapeutic options to improve ICH recovery. Conflict of interest G. Sökeland: supported by a National MD-PhD Fellowship from the Swiss Academy of Medical Sciences (SAMW). B. Savic: nothing to disclose in regards to the project. B. Siepen: nothing to disclose in regards to the project. M. Goedlin: nothing to disclose in regards to the project. J. Rauch: nothing to disclose in regards to the project. J. Lippert: nothing to disclose in regards to the project. F. Schuler: nothing to disclose in regards to the project. D. Seiffge: nothing to disclose in regards to the project. S. Jung: nothing to disclose in regards to the project. B. Volbers: reports personal fees from Ipsen Pharma, personal fees from CSL Behring, personal fees from AstraZeneca, non-financial support from AbbVie, personal fees from Boehringer Ingelheim GmbH, personal fees from AbbVie, grants from Bangerter Rhyner Foundation, personal fees from Athersys, Inc., personal fees from Sivantos GmbH, personal fees from Bristol-Myers Squibb GmbH & Co. KGaA, personal fees from University of Bern, outside the submitted work. Table 1 - belongs to Methods