A6 Chronic subdural hematoma and cognitive impairment: a theory on angio-senescence and lymphatic/glymphatic impairment with potential implications in endovascular treatment

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Background/Introduction The impact of chronic subdural hematoma (CSDH) on the underlying brain has barely been explored. The higher prevalence of cognitive impairment suggests induced secondary brain injury potentially mediated by senile angiogenic dysfunction, decreased meningeal lymphatic and glymphatic clearance, leading to perpetuation of subdural collection and accumulation of neuron metabolism produces waste. Under this theory, endovascular treatment of inflammatory dys-angiogenic neo-membranes could potentially reverse cognitive decline. Objective/Purpose To assess secondary brain injury in patients with CSDH and determine the impact of middle meningeal artery embolization (MMAe). Methods/Case Description Preliminary series (n = 10) of patients with CSDH treated with MMAe and comprehensively evaluated with advanced neuroimaging and neuropsychological testing. MRI including DCE and DTI-ALPS was performed before and 6 weeks after treatment, to assess blood-brain barrier (BBB) permeability, microstructural integrity and glymphatic clearance. Results/Findings BBB permeability (Ktrans) showed higher values at baseline than 6 weeks after treatment. Glymphatic showed improved clearance after treatment. Changes in BBB and glymphatic were more evident in the ipsilateral hemisphere. No changes were observed in white matter structure during the follow-up period. Scoring in neuropsychological and functional tests improved after treatment. Discussion/Conclusions/Learning Points This small series suggests CSDH induces neuro-vascular and glymphatic impairment in the subjacent brain. While these seem to ameliorate after embolization of subdural neo-membranes, improvement in cognitive function seems to follow. These preliminary results warrant further exploration; yet these observations support a novel hypothesis on the effects of CSDH on brain clearance pathways and its implications in endovascular treatment.

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