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A cerebral (brain) aneurysm refers to the localized ballooning of a cerebral artery, typically affecting
2-5% of the global population[1] . It first arises due to a focal weakening in the artery. Over many years, compounding hemodynamic forces will act on this weakened region, resulting in an intracranial aneurysm[2] . Eventually, the wall may thin to the point that the aneurysm spontaneously ruptures. The most common outcome of such an event is a subarachnoid hemorrhage (SAH), the bleeding into the subarachnoid space.

An intracranial aneurysm may arise from a myriad of risk factors, including hypertension, female sex, smoking, arteriosclerosis, and familial history[3] . Various techniques exist to diagnose an unruptured aneurysm, including magnetic resonance imaging, computed tomography scan, angiography (CT, MR, catherer) or a combination[4] . However, an aneurysm is mostly asymptomatic, and not typically diagnosed until a rupture occurs. At point of rupture, the bleeding must first be stopped, by either microsurgical clipping or endovascular coiling. If diagnosed before rupture, these techniques may also be employed to remove an aneurysm.

Unfortunately, even after stopping bleeding, the prognosis of aneurismal SAH patients remains poor. Most notably, many patients will develop delayed neurological deficits, leading to poor outcome and perhaps death[5] . Various pathophysiological mechanisms to account for the delayed neurological decline have been suggested, with most revolving around changes to the cerebral vasculature. Traditionally, cerebral vasospasm has been touted as the main contributor to poor outcome, though some series are now suggesting this is not the case [6] . More contemporary hypotheses include microvascular constriction, microembolism, cortical spreading depression[5].

In terms of post-surgical treatment, most target the reversal of cerebral perfusion deficits after cerebral vasospasm, though none have been particular successful[5]. More efforts are underway to investigate other possible avenues to prevent neurological decline, including anti-inflammatory[7] and anti-coagulatory drugs[8] .

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Pathogenesis and Treatments (Filza N)
      1.1 Etiology
            1.1.1 Internal Elastic Laminae Degeneration and Arterial Wall Bulging
            1.1.2 Myointimal Hyperplasia
            1.1.3 Inflammation, Macrophage Infiltration and Arterial Wall Bulging
      2.1 Risk factors
            2.1.1 Hypertension
            2.1.2 Smoking
            2.1.3 Gender
      3.1 Types of Intracranial Cerebral Aneurysm
            3.1.1 Saccular
            3.1.2 Fusiform
            3.1.3 Mycotic
            3.1.4 Dissecting
      4.1 Diagnosing Intracranial Cerebral Aneurysm
            4.1.1 Arteriography
            4.1.2 Computed Tomography Angiogram
            4.1.3 Magnetic Resonance Angiogram
     5.1 Surgical Interventions
           5.1.1 Microsurgical Clipping
           5.1.2 Endovascular Coiling
Rupture (Hoyee W)
      Clinical presentation
            4.1 Neurological symptoms
            4.2 Grading scales
      Delayed cerebral ischemia
            5.1 Defining criterion
            5.2 Pathogenesis
                  5.2.1 Cerebral vasospasm
                  5.2.2 Microvascular constriction
                  5.2.3 Cortical spreading depression
                  5.2.4 Microembolism
      Treatment
            6.1 Vasospasm
                  6.1.1 Pharmacological
                  6.1.2 Non-pharmacological Treatment
            6.2 Clinical trials


References
  1. ^ Rinkel, G.J., Djibuti, M., Algra, A., & van, G.J. Prevalence and risk of rupture of intracranial aneurysms: a systematic review. Stroke 29, 251-256 (1998).
  2. ^ Watton, P.N., Raberger, N.B., Holzapfel, G.A., & Ventikos, Y. Coupling the hemodynamic environment to the evolution of cerebral aneurysms: computational framework and numerical examples. J Biomech. Eng 131, 101003 (2009).
  3. ^ Yasuno, K. et al. Common variant near the endothelin receptor type A (EDNRA) gene is associated with intracranial aneurysm risk. Proc. Natl. Acad. Sci. U. S. A 108, 19707-19712 (2011).
  4. ^ Macdonald, R.L. Evidence-based treatment of subarachnoid hemorrhage: current status and future possibilities. Clin Neurosurg 53, 257-266 (2006).
  5. ^ Macdonald, R.L., Pluta, R.M., & Zhang, J.H. Cerebral vasospasm after subarachnoid hemorrhage: the emerging revolution. Nat Clin Pract. Neurol 3, 256-263 (2007).
  6. ^ Vergouwen,M.D. et al. 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, 2391-2395 (2010).
  7. ^ Provencio, J.J. & Vora, N. Subarachnoid hemorrhage and inflammation: bench to bedside and back. Semin. Neurol 25, 435-444 (2005).
  8. ^ Sabri, M. & Macdonald, R.L. Statins: a potential therapeutic addition to treatment for aneurysmal subarachnoid hemorrhage? World Neurosurg 73, 646-653 (2010).