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Topic: The Role of Inflammation in Cerebral Aneurysm

Inflammation in human cerebral aneurysms:

pathogenesis, diagnostic imaging, genetics, and

therapeutics

Sarah A. Dooley , Joseph S. Hudson , David M. Hasan 3
1
2

1 Department of Neurosurgery, University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA.
2 Department of Neurosurgery, University of Iowa, Iowa City, IA 52242, USA.
3 Department of Neurosurgery, University of Iowa Hospital and Clinics, Iowa City, IA 52240, USA.

ABSTRA CT
Intracranial aneurysms are a life-threatening cerebrovascular pathology with a probability of spontaneous rupture. Current intervention
techniques carry inherent risk. Recent investigation has reinforced inflammation’s role in the pathophysiological process of cerebral
aneurysms. These data suggest alternative diagnostic and noninvasive therapeutic strategies. Furthermore, novel characteristics
of the underlying disease have been elucidated through distinct bioinformatic and gene expression profile analyses. This article will
emphasize the most recent investigation, highlighting findings of clinical significance and etiological relevance.

Key words: Diagnostic imaging, genetics, intracranial aneurysms, pathogenesis, therapeutics

INTRODUCTION as it pertains to IA pathogenesis, with a focus on
the most recent investigation. Furthermore, it will
Intracranial aneurysms (IAs) are a common offer a review of recent genetic and bioinformatic
multifactorial cerebrovascular disease. While having analyses, highlighting findings of pathological
a 3.2% prevalence rate in the general population significance and methodological diversity. The final
and 1.1% annual rupture risk, aneurysms remain sections will further illuminate both innovations in
lethal upon rupture in 40% of cases. [1-3] Risk for diagnostic imaging of aneurysmal inflammation and
aneurysmal subarachnoid hemorrhage (SAH) is higher experimentally efficacious noninvasive attempts at IA
in hypertensive patients, smokers, heavy drinkers, and prevention and regression.
females. [2,4] The current interventional techniques,
surgical clippings and endovascular occlusions, PATHOGENESIS
remain invasive despite advancements in technology.
Although SAH risk factors are known, a more complete Hemodynamic insult is considered to be one of the
understanding of the complex pathophysiology first steps in activating the cerebral vessel wall’s
underlying IA formation, progression, and rupture inflammatory response. There is a continuous balance
[7]
is needed. The majority of evidence from intensive between hemodynamic stress and the integrity of the
[5]
investigation has implicated a mounting inflammatory vessel wall. Upon the hemodynamic insult, this
response during the aneurysm pathogenesis. [5,6] balance is perturbed, leading to vessel wall weakening.
This data ultimately provides promising targets Dilation results, as extracellular matrix is degraded by
for in vivo molecular imaging and noninvasive IA increased levels of matrix metalloproteinases (MMP)
therapeutics. This article will discuss inflammation compounded by concomitant apoptotic death of
vascular smooth muscle cells (VSMCs). Initially, the
[7]
Access this article online vessel wall is highly organized. Integral disturbances
Quick Response Code: lead to less organization within the aneurysm wall
Website: and fewer distinct layers. Simultaneously, MMP
[5]
www.nnjournal.net
activation has been found to facilitate flow-induced
[8]
DOI: internal elastic lamina (IEL) fragmentation. Similar
10.4103/2347-8659.154433 IEL fragmentation is a feature commonly observed in
atherosclerotic lesions. [9]

Corresponding Author: Dr. David M. Hasan, Department of Neurosurgery, University of Iowa Hospital and Clinics, 200 Hawkins
Drive, Iowa City, IA 52240, USA. E‑mail: david‑hasan@uiowa.edu

Neuroimmunol Neuroinflammation | Volume 2 | Issue 2 | April 15, 2015 77