Abstract
Aneurysmal subarachnoid hemorrhage (SAH) is a sub-type of hemorrhagic stroke associated with the highest rates of mortality and long-term neurological disabilities. Despite the improvement in the management of SAH patients and the reduction in case fatality in the last decades, disability and mortality remain high in this population. Brain injury can occur immediately and in the first days after SAH. This early brain injury can be due to physical effects on the brain such as increased intracranial pressure, herniations, intracerebral, intraventricular hemorrhage, and hydrocephalus. After the first 3 days, angiographic cerebral vasospasm (ACV) is a common neurological complication that in severe cases can lead to delayed cerebral ischemia and cerebral infarction. Consequently, the prevention and treatment of ACV continue to be a major goal. However, most treatments for ACV are vasodilators since ACV is due to arterial vasoconstriction. Other targets also have included those directed at the underlying biochemical mechanisms of brain injury such as inflammation and either independently or as a consequence, cerebral microthrombosis, cortical spreading ischemia, blood–brain barrier breakdown, and cerebral ischemia. Unfortunately, no pharmacologic treatment directed at these processes has yet shown efficacy in SAH. Enteral nimodipine and the endovascular treatment of the culprit aneurysm, remain the only treatment options supported by evidence from randomized clinical trials to improve patients’ outcome. Currently, there is no intervention directly developed and approved to target neuroinflammation after SAH. The goal of this review is to provide an overview on anti-inflammatory drugs tested after aneurysmal SAH.
Highlights
Aneurysmal subarachnoid hemorrhage (SAH) is a complex cerebrovascular disease with profound systemic complications [1,2,3]
Angiographic vasospasm occurs in approximately 70% of patients during the first 2 weeks after SAH, but the incidence of delayed cerebral ischemia (DCI) is only around 30% [7]
CycA proved safe to use but failed to prevent the development of cerebral vasospasm or delayed ischemic deficits in patients considered at high risk
Summary
Aneurysmal subarachnoid hemorrhage (SAH) is a complex cerebrovascular disease with profound systemic complications [1,2,3]. Because of the failure of several pharmacological trials and the dissociation between vasospasm-related morbidity and functional outcomes, other possible mechanisms, such as early brain injury, cortical spreading ischemia, microthrombosis, cerebral autoregulation impairment, and capillary transit time heterogeneity, are thought to play a role in the pathophysiology of DCI and DCI-related cerebral infarction [1, 3, 19, 20] These additional mechanisms tend to be more difficult to assess clinically and the dissociation mentioned above could be due to drug toxicity and off-target effects, effects of rescue therapy, inadequate trial sample size and other trial design problems, and testing of only one dose and dose regimen. The risk of DCI is increased by the amount of subarachnoid blood (i.e., the volume, density, and persistence of blood in the subarachnoid space) [43,44,45]; Table 1 | Summary of medication with anti-inflammatory activity tested in SAH
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