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Topic: The Role of Inflammation in Cerebral Aneurysm
The role of inflammation in cerebral aneurysms
Ali H. Turkmani , Nancy J. Edwards , Peng R. Chen 1
1,2
1
1 Department of Neurosurgery, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
2 Department of Neurology, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
ABSTRA CT
The natural history of unruptured intracranial aneurysms (IAs) is poorly understood. At present, risk factors for aneurysm rupture
are limited to demographics and rudimentary anatomic features of the aneurysm. The first sign of aneurysm destabilization and
rupture may be subarachnoid hemorrhage, a potentially devastating brain injury with high morbidity and mortality. An emerging body
of literature suggests a complex inflammatory cascade likely promotes aneurysm wall remodeling and progressive ballooning of
the arterial wall, ultimately terminating in aneurysm rupture. These events likely begin with hemodynamic, flow-related endothelial
injury; the injured endothelium stimulates inflammation, including the recruitment and transmigration of inflammatory cells, particularly
macrophages. Various proteases are secreted by the inflammatory infiltrate, resulting in degradation of the extracellular matrix and
the structural changes unique to IAs. Detailed understanding of these inflammatory processes may result in (1) early identification
of patients at high risk for aneurysm rupture, perhaps via arterial wall imaging, and (2) targeted, noninvasive therapies to treat or
even prevent cerebral aneurysms.
Key words: Aneurysms, atherosclerosis, inflammation, intracranial
INTRODUCTION In order to appropriately tailor treatment decisions,
further understanding of the pathophysiology behind
Subarachnoid hemorrhage due to intracranial aneurysm growth and rupture is needed. In recent years,
aneurysm (IA) rupture is a devastating disease. a growing body of literature has identified inflammation
Initial mortality may be as high as 40-50%, and of as a key player in the pathogenesis of intracranial
those who survive, one-third to one-half are left aneurysms (IAs), from aneurysmogenesis and vascular
[1]
with permanent neurologic deficits. When an remodeling to aneurysm destabilization and rupture.
unruptured aneurysm is discovered in a patient, Here, we will review the pathology of IAs along with
current therapeutic options to prevent aneurysm the literature supporting a role for inflammation in this
rupture include invasive endovascular occlusion pathology; we will also examine potential inflammatory
versus surgical therapy, or close radiologic follow-up targets for noninvasive treatment of IAs.
with intervention when the risk of rupture is deemed
high enough. That being said, risk stratification of STRUCTURAL CHARACTERISTICS OF
patients with an unruptured IA is based on a limited INTRACRANIAL ANEURYSMS
understanding of natural history, size appears to
[2]
contribute to aneurysm destabilization, but there Intracranial aneurysms are believed to be acquired
are likely other, poorly understood factors at play. vascular lesions; they are exceedingly rare in children
And as demonstrated in the International Study of and their incidence increases with age. [4,5] As IAs
Unruptured Intracranial Aneurysms (ISUIA), invasive are preferentially located at bifurcations and sharp
endovascular or surgical treatments are associated curves, hemodynamics (e.g. various shear stressors)
with an overall 1-year morbidity/mortality of 10%. [3] are believed to trigger aneurysmogenesis. From
a structural perspective, compared to extracranial
Access this article online vessels, intracranial vessels have less elastic fiber in
Quick Response Code: the tunica media and adventitia, less smooth muscle
Website: in the media, and a thinner adventitia. At vessel
[6]
www.nnjournal.net
bifurcations, the apical portion of the intracranial
DOI: vessel lacks smooth muscle cells (SMCs), a gap referred
10.4103/2347-8659.153982 to as the “medial raphe”. During the initiation of
[7]
aneurysms, the luminal surface of the vessel becomes
Corresponding Author: Dr. Peng R. Chen, Department of Neurosurgery, University of Texas Health Science at Houston, 7000
Fannin, Suite 1200, Houston, TX 77030, USA. E‑mail: Peng.R.Chen@uth.tmc.edu
102 Neuroimmunol Neuroinflammation | Volume 2 | Issue 2 | April 15, 2015