A common, life-threatening complication of stroke is cerebral oedema (brain swelling) and subsequent elevated intracranial pressure (ICP). Stroke patients suffering this condition are more likely to die or be left permanently disabled as a result. Despite this, current treatments for cerebral oedema and elevated ICP are largely ineffective in treating this life threatening condition, given that they simply treat the symptoms rather than address the cause of the swelling. Pharmacological treatments aim to pull water out of the brain to decrease the swelling whilst decompressive surgery aims to accommodate the swollen brain and although life saving, it is highly invasive and potentially risky. As a result, alternate treatments for brain swelling that address the cause of the swelling and stop it in its tracks are urgently required in order to improve survival and long-term outcomes for stroke patients.
To address this the Neurological Diseases laboratory at the University of Adelaide has identified a novel therapy to treat brain swelling following stroke that targets the action of substance P and blocks its receptor (NK1 tachykinin receptor). Levels of substance P are increased in the brain following stroke, causing an increase in the permeability of blood vessels, movement of water into the brain, cerebral oedema and poor outcomes. Results to date show that NK1 tachykinin receptor antagonist treatment completely prevents blood vessel permeability changes, brain swelling, elevated ICP and mortality following stroke. The next stage is to assess long-term efficacy, as it is essential that patients not only survive an episode of brain swelling but also have meaningful function. Using a novel pre-clinical stroke model that we have developed we will determine the long-term effects of NK1 tachykinin receptor antagonist treatment on functional outcome following stroke. Results from these studies provide compelling evidence for the use of NK1 tachykinin receptor antagonists for the treatment of brain swelling following stroke.