Young stroke

Subarachnoid haemorrhage (SAH) is a type of stroke caused by a bleed in the subarachnoid space located between the brain and the skull. Secondary brain damage that occurs as a consequence of SAH is responsible for a large proportion of SAH patients suffering with long-term disability. Around a quarter of the SAH patient population are under the age of 45. Young adults initially tend to recover better following a SAH compared to older patients, however their life expectancy is dramatically reduced, losing on average 21 years. Interestingly, some of the changes that occur in the brain following SAH are very similar to those that are observed during ageing and in Alzheimer’s disease, a type of dementia. This could explain why younger SAH survivors are at an increased risk of developing dementia.

Cerebrospinal fluid (CSF) is a clear, colourless liquid found around the brain and in the interconnecting cavities (ventricles) within the brain. CSF flows through these ventricles and out into the subarachnoid space. From here, CSF can move into and out of the brain along channels adjacent to the blood vessels within the brain, known as the glymphatics pathway. CSF then drains into the bloodstream and lymphatic system. CSF has an important role in maintaining brain function, protecting the brain from impacting on the skull and regulating pressure within the skull. It also removes waste products and moves nutrients and hormones around the brain.

The dynamic nature of the CSF system means CSF is constantly being replaced, therefore disruption of this system can be detrimental to brain health. SAH has a big impact on the CSF dynamics system. The bleed increases volume within the skull leading to an increase in brain pressure, which in turn reduces blood supply to the brain. In addition, blood products are released into the CSF which damage the CSF dynamics system. One area affected by SAH is the glymphatics pathway, resulting in reduced clearance of CSF from the brain and the build-up of toxic waste products, damaging the brain. Reduced CSF clearance from the brain is also observed with ageing and in Alzheimer’s disease, therefore SAH may prematurely age the CSF dynamics system in the brain.

Dr Botfield’s work will aim to determine whether SAH in young adults accelerates brain ageing through its effects on the CSF dynamics system.

This work will provide further fundamental understanding of the age-related changes that occur in the brain following SAH. It will advance our knowledge about scarring processes in the brain, and also provide information about a potential therapeutic strategy for improving CSF clearance from the brain. This could reverse the damage after SAH that leads to age-related conditions such as dementia in young SAH survivors.