Intracranial aneurysm calcification - A narrative review

Abstract

Calcification of intracranial aneurysms is a well-known phenomenon. Whether microsurgical or endovascular techniques are used, calcifications may increase the difficulty of treatment. However, the implications of calcification on aneurysm biology and stability have received little attention. We review both investigational and clinical methods that are used to detect aneurysmal calcification. We also discuss the pathophysiology of aneurysm calcification, specifically the role that inflammation and smooth muscle cells play. We finally turn our attention to the clinical implications of aneurysm calcification including rupture risk and treatment considerations. Calcification may represent an important feature in the life cycle of an aneurysm and as imaging methods continue to improve, we may yet discover a biomarker for this process.

Keywords: Aneurysm calcification; Atherosclerotic calcification; Bone morphogenic protein; Msh Homeobox 2; Multiphoton microscopy; Optical coherence tomography; Runt-Related Transcription Factor 2; Vascular smooth muscle cells; micro-CT.

Figure 1.

Example of a giant anterior communicating artery aneurysm after craniotomy for treatment with neck and concentric calcifications (red arrows). Simple clip occlusion was not possible due to this therefore the patient underwent clip occlusion of the proximal A1 with A3-A3 side to side bypass and right M2 to A2 bypass with radial artery graft. A) Non-contrasted head CT in the axial plane showing concentric calcification. B) Sagittal plane CT angiogram showing calcification at the neck, a thin rim of calcification around the aneurysm, and forward deformation of the A2s. C) Coronal CT angiogram showing thin egg-shell calcification of the aneurysm.

Figure 2.

Summary of methods of detection of intracranial aneurysm calcification. (OCT=optical coherence tomography; MPM= Multiphoton microscopy; H&E= hematoxalin and eosin; VVG= Verhoeff-Van Gieson; CBP= calcium binding protein)

Figure 3.

The role of smooth muscle cells in the arterial calcification process. BMP through MSX-2/RUNX-2 and NF-kB act as the major drivers of the gene products involved in the calcification of the extra-cellular matrix. OPN, ON, OC have all been shown to inhibit calcification of the HA matrix outside of cells. MGP, through vitamin K is also responsible for inhibiting calcification of the matrix. (BMP= bone morphogenic protein; MSX-2= Msh Homeobox 2; RUNX-2= Runt-Related Transcription Factor 2; NF-κB= Nuclear Factor Kappa B; MGP= Matrix Gla Protein; PiT-1= Sodium-dependent phosphate transporter 1; Vit K= vitamin K; Ca= calcium; Pi= inorganic phosphate; Na= sodium; OPN= osteopontin; ON= osteonectin; OC= osteocalcin; HA= hydroxyapatite).