Vitamin C concentrations following aneurysmal subarachnoid haemorrhage
- Research Opportunity
- Honours students
- Number of Honour Places Available
- Department / Centre
- Medicine and Radiology
- Royal Melbourne Hospital
|Associate Professor Adam Deaneemail@example.com,au||0431967560||Personal web page|
|Dr Mark Plummerfirstname.lastname@example.org||0419708399|
|Dr Yasmine Ali Abdelhamidemail@example.com||0416186874|
Summary A prospective interventional study to understand whether vitamin C concentrations in plasma and CSF are reduced following aneurysmal subarachnoid haemorrhage.
Subarachnoid haemorrhage (SAH) occurs when a weakened blood vessel in the brain (cerebral aneurysm) ruptures. This form of stroke affects approximately 2,500 Australians each year and has devastating consequences. Outcomes for patients after this type of stroke (aneurysmal subarachnoid haemorrhage, aSAH) are generally poor, with a high level of death and disability. Moreover, aSAH affects a younger demographic compared to other stroke subtypes leading to increased loss of productive years.
Vasospasm is the leading modifiable cause of poor outcome following aSAH. The term 'vasospasm' implies the constriction or uncontrolled spasm of blood vessels in the brain. Cerebral vasospasm develops in approximately two-thirds of patients following SAH, which may progress to further permanent brain injury, i.e. secondary stroke due to vasospasm. Accordingly, prevention of vasospasm and these secondary strokes remains the key target for novel treatments following aSAH.
At present, the only treatment that reduces secondary stokes is a blood pressure drug, nimodipine. This drug is now routinely administered to patients with aSAH.
Vitamin C is safe and inexpensive and when administered in pharmacological doses it dilates blood vessels and protects brain cells. However, these effects have never been assessed in patients following aSAH.
Given the paucity of interventions to prevent vasospasm and the neuroprotective properties of vitamin C we wish to conduct an interventional study to evaluate whether vitamin C levels in the blood and brain are associated with vasospasm. If this study demonstrates that endogenous concentrations are reduced this would provide a rationale to trial intravenous supplementation of vitamin C in this patient population.
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