Aneurysm / Subarachnoid hemorrhage
Aneurysmal subarachnoid hemorrhage (aSAH) is the second most common type of hemorrhagic stroke, and results from rupture of a basal cerebral artery aneurysm. The blood leaves the cerebral circulation and accumulates in the subarachnoid space covering the brain surface. Mortality and disability rates of individuals reaching medical care are 30% and 30%, respectively. Among survivors, only 60% are able to resume their previous lifestyles. Delayed cerebral ischemia (DCI) is the most prominent in-hospital complication after aSAH and is presumably caused by breakdown of erythrocyte products in the subarachnoid space (Vergouwen et al 2010).
The clinical signs of DCI are global and focal neurological deficits which lead to significant deterioration in functional outcome (Vergouwen et al 2011). In electrocorticographic (ECoG) recordings, clusters of recurrent spreading depolarizations (SDs) with prolonged depression of the spontaneous activity indicate the occurrence of DCI (Dreier et al 2006).
DCI represents a model disease for hypoxic-ischemic injury for two reasons (Dreier 2011). First, it occurs with a peak incidence around day seven after the initial hemorrhage while the patient is already on the intensive care unit. In animal experiments, neuroprotectants have been found to be most effective either when given within minutes after the onset of acute neuronal injury or when they have been preadministered. Thus, DCI allows us to treat patients with a neuroprotectant before the possible insult or very shortly thereafter to prove or disprove the neuroprotective concept. Second, neurosurgical procedures are indicated in patients early after the initial hemorrhage, allowing implantation of invasive probes. This provides the unique option to invasively monitor the whole period of ischemic stroke development in patients, to perform early treatment stratification according to the presence or absence of biomarkers such as SDs sensed in real time by neuromonitoring devices, and then record the parenchymal response to the neuroprotectant.
- Dreier JP, Woitzik J, Fabricius M, Bhatia R, Major S, Drenckhahn C, Lehmann TN, Sarrafzadeh A, Willumsen L, Hartings JA, Sakowitz OW, Seemann JH, Thieme A, Lauritzen M, Strong AJ (2006) Delayed ischaemic neurological deficits after subarachnoid haemorrhage are associated with clusters of spreading depolarizations. Brain 129:3224-37
- Dreier JP (2011) The role of spreading depression, spreading depolarization and spreading ischemia in neurological disease. Nat Med 17:439-47
- Vergouwen MD, Vermeulen M, van Gijn J, Rinkel GJ, Wijdicks EF, Muizelaar JP, Mendelow AD, Juvela S, Yonas H, Terbrugge KG, Macdonald RL, Diringer MN, Broderick JP, Dreier JP, Roos YB (2010) Definition of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage as an outcome event in clinical trials and observational studies: proposal of a multidisciplinary research group. Stroke 41:2391-5
- Vergouwen MD, Etminan N, Ilodigwe D, Macdonald RL (2011) Lower incidence of cerebral infarction correlates with improved functional outcome after aneurysmal subarachnoid hemorrhage. J Cereb Blood Flow Metab 31:1545-53