Aims

Stroke is a frequent and devastating disease. The majority of survivors remains disabled, despite significant progress in acute treatment. Self healing mechanisms of the brain exist and could open treatment avenues for those who survive with brain injury. However, knowledge about these mechanisms is still incomplete. We hypothesize that hypoperfusion in the acute phase of ischemic stroke is the trigger for self healing mechanisms, specifically for plasticity in intact brain surrounding the injury. Through a collaboration between neurology, neuroradiology, neurosurgery and neuropathology we test this hypothesis in parallel research in humans and animal models.