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As pointed out [60], it has to be the counteraction of the reduced capillary perfusion pressure, increased cerebral blood volume, venous flow obstruction, increased intracranial pressure and blood-brain barrier disruption, resulting in a decreased cerebral blood flow [60]

This exceptional clinical aggression is consistent with the tumors high proliferative index (Ki-67 50%) and the R2 resection status, suggesting early dissemination of gross or microscopic residual disease along the neuraxis, potentially via perineural spread or CSF-mediated seeding