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Abstract
Rationale The role of hypertension in cerebral small vessel disease is poorly understood. At the base of the brain (the ‘vascular centrencephalon’), short straight arteries transmit blood pressure directly to small resistance vessels; the cerebral convexity is supplied by long arteries with many branches, resulting in a drop in blood pressure. Hypertensive small vessel disease (lipohyalinosis) causes the classically described lacunar infarctions at the base of the brain; however, periventricular white matter intensities (WMIs) seen on MRI and WMI in subcortical areas over the convexity, which are often also called ‘lacunes’, probably have different aetiologies.
Objectives We studied pressure gradients from proximal to distal regions of the cerebral vasculature by mathematical modelling.
Methods and results Blood flow/pressure equations were solved in an Anatomically Detailed Arterial Network (ADAN) model, considering a normotensive and a hypertensive case. Model parameters were suitably modified to account for structural changes in arterial vessels in the hypertensive scenario. Computations predict a marked drop in blood pressure from large and medium-sized cerebral vessels to cerebral peripheral beds. When blood pressure in the brachial artery is 192/113 mm Hg, the pressure in the small arterioles of the posterior parietal artery bed would be only 117/68 mm Hg. In the normotensive case, with blood pressure in the brachial artery of 117/75 mm Hg, the pressure in small parietal arterioles would be only 59/38 mm Hg.
Conclusion These findings have important implications for understanding small vessel disease. The marked pressure gradient across cerebral arteries should be taken into account when evaluating the pathogenesis of small WMIs on MRI. Hypertensive small vessel disease, affecting the arterioles at the base of the brain should be distinguished from small vessel disease in subcortical regions of the convexity and venous disease in the periventricular white matter.
- Small vessel disease
- lacunar
- lobar
- amyloid
- blood pressure
- mathematicalmodelling
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Footnotes
Contributors JDS: conceived the study and wrote the first and subsequent drafts; PJB and LOM: performed the calculations, created the images and contributed to revisions.
Competing interests None declared.
Provenance and peer review Not commissioned; internally peer reviewed.
Data sharing statement All relevant data are within the paper. ADAN model description is fully available in Refs. 10 and 11. ADAN model parameters are fully available (as indicated in Ref. 11) in the repository . Numerical methodology is described in detail in Ref. 17 (and references therein). Regarding the generation of CCO networks we employed algorithms already documented in Refs. 16 and 18. The geometry of CCO networks to perform simulations as well as the mean blood pressure in all peripheral segments is available as a Supplementary Data File (CCO_LsA_N.vtk and CCO_LsA_H.vtk for lenticulostriate artery and CCO_PPB_MCA_N.vtk and CCO_PPB_MCA_H.vtk for the posterior parietal branch of the middle cerebral artery, N: normotensive, H: hypertensive).
Correction notice This paper has been amended since it was published Online First. Owing to a scripting error, some of the publisher names in the references were replaced with ’BMJ Publishing Group'. This only affected the full text version, not the PDF. We have since corrected these errors and the correct publishers have been inserted into the references.