Growth-driven mechanical buckling as a mechanism of age-related tortuosity in human cerebral arteries

Human cerebral arteries tend to become increasingly winding with age, but the reason behind this phenomenon is not fully understood. In order to investigate how arterial bends form and what factors influence their spacing, researchers modeled a cerebral artery as a slender elastic vessel supported by surrounding tissue. The length of the vessel remains constant, and it can only bend in a plane tangent to the brain surface.

As the natural length of the vessel increases through aging, axial compression builds up within the vessel until it reaches a point where the vessel buckles.

The bending of the vessel partially relieves the compression, leading to the growth of bending waves whose amplitude increases as the elongation continues. Factors such as arterial bending stiffness and tissue support play a crucial role in determining the wavelength of these bending waves, which is found to be much larger than and directly proportional to the vessel diameter. Other parameters have a comparatively weak influence on the wavelength.

To validate these predictions, numerical simulations were conducted, capturing a pre-buckling phase, rapid amplification of waves, and slow post-buckling growth during continued elongation. These results were then compared with three-dimensional centerlines of cerebral arteries reconstructed from magnetic resonance angiography in healthy adults. The study found that older age was associated with greater arterial length and an excess-length ratio, supporting the model's predictions.

Furthermore, for arterial waves that are mostly parallel to the brain surface, the wavelength was found to increase with vessel diameter, which aligns with the model's predictions. However, there was no significant association between wave amplitude and age. Overall, the combination of modeling and imaging results suggests that growth-driven buckling and post-buckling deformation under spatial constraints provide a plausible mechanical explanation for age-related cerebral arterial tortuosity.

This framework establishes a link between vascular aging and growth-driven instability and pattern formation, with potential applications to understanding blood vessels in diseased states beyond the brain.