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Topic: The Role of Inflammation in Cerebral Aneurysm

Hemodynamics, inflammation, vascular

remodeling, and the development and rupture

of intracranial aneurysms: a review

Francesco Signorelli , Benjamin Gory , Roberto Riva , Paul‑Emile Labeyrie , Isabelle Pelissou‑Guyotat ,
1
3
1,2
3
3
Francis Turjman 3
1 Service of Neurosurgery D, Civil Hospitals of Lyon, 59, Boulevard Pinel, 69500 Bron‑Lyon, France.
2 Department of Experimental and Clinical Medicine, University “Magna Graecia” of Catanzaro, 88100 Catanzaro, Italy.
3 Service of Interventional Neuroradiology, Civil Hospitals of Lyon, 59, Boulevard Pinel, 69500 Bron‑Lyon, France.
ABSTRA CT

The central nervous system is an immunologically active environment where several components of the immune and inflammatory
response interact among them and with the constituents of nervous tissue and vasculature in a critically orchestrated manner,
influencing physiologic and pathologic processes. In particular, inflammation takes a central role in the pathogenesis of intracranial
aneurysms (IAs). The common pathway for aneurysm formation involves endothelial dysfunction and injury, a mounting inflammatory
response, vascular smooth muscle cells (VSMCs) phenotypic modulation, extracellular matrix remodeling, and subsequent cell
death and vessel wall degeneration. We conducted a literature review (1980-2014) by Medline and EMBASE databases using the
searching terms “IA” and “cerebral aneurysm” and further search was performed to link the search terms with the following key words:
inflammation, hemodynamic(s), remodeling, macrophages, neutrophils, lymphocytes, complement, VSMCs, mast cells, cytokines,
and inflammatory biomarkers. The aim of this review was to summarize the most recent and pertinent evidences regarding the
articulated processes of aneurysms formation, growth, and rupture. Knowledge of these processes may guide the diagnosis and
treatment of these vascular malformations, the most common cause of subarachnoid hemorrhage, which prognosis remains dismal.

Key words: Inflammation, hemodynamics, vascular remodeling, intracranial aneurysms

INTRODUCTION However, the majority of IAs diagnosed following
their rupture is small and located on the anterior
Saccular intracranial aneurysms (IAs) are the most circulation, [8,9] which indicates that the statistical
frequent cause of subarachnoid hemorrhage (SAH), approach does not allow individualizing the risk of
the stroke type with the higher morbidity and rupture. Elucidating the pathogenic pathways inherent
mortality. [1,2] A precise evaluation of their rupture to the development and rupture of IAs may allow
risk is crucial to orient treatment of unruptured IAs identifying more reliable markers of rupture-prone IAs.
relatively to the risk of endovascular or surgical A growing body of evidence supports the correlation
treatment. [2-7] Statistic studies involved patients between modification of hemodynamic factors and
suffering from aneurysm rupture found that cigarette arterial wall alteration leading to IAs development
smoking, arterial hypertension, ethnic origin, age, and rupture. [10-13] Particularly, wall shear stress (WSS)
previous SAH, size ≥ 7 mm, localization of IAs at the gradient might be an important factor of vascular
posterior circulation and aneurysm’s shape are the remodeling through multiple mechanisms involving
most important variables regarding the rupture risk. [2-7] endothelial cells (ECs) and vascular smooth muscle
cells (VSMCs) modification of gene expression
Access this article online triggered by local inflammatory reaction and leading to
Quick Response Code: degenerative changes of arterial wall. [14] In this article,
Website: we summarize the existing data, extracted from a review
www.nnjournal.net
of the pertinent literature, regarding inflammation and
DOI: hemodynamic stress in the pathogenesis of IAs. Our
10.4103/2347-8659.154885 endeavor is to explore the causative relationships
that may link hemodynamics, inflammation, vascular

Corresponding Author: Prof. Francesco Signorelli, Service of Neurosurgery D, Civil Hospitals of Lyon, 59, Boulevard Pinel,
69500 Bron‑Lyon, France. E‑mail: signorelli2007@gmail.com

Neuroimmunol Neuroinflammation | Volume 2 | Issue 2 | April 15, 2015 59