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Intracranial Pulsatility

Bilateral compression of the jugular veins has also been shown to increase pulsatility in the pial arteries [87], suggesting that the functional compliance of the cortical veins not only influences the CSF dynamics but also blood flow in the cerebral vascular bed

[88]. In healthy young adults, the flow of blood through the cerebral capillaries is constant and non-pulsatile [70]. However, if the compliance of the veins that traverse the SAS is impaired, say through constriction or partial occlusion of the extracranial cerebral venous drainage pathways, then this will tend to decrease intracranial compliance, leading to larger pressure pulsatility in the cerebral vasculature [88].

As individuals age, their arteries become less compliant, causing the intracranial windkessel mechanism to become less efficient, with the result that blood flow entering the cerebral vascular bed becomes more pulsatile [70, 89]. Stiffening of the aorta has also been linked to the transmission of excessive flow pulsatility into the brain [90, 91], something that will increase endothelial shear stresses and has been linked with microstructural WM changes in healthy older individuals [92]. Tarumi et al. [90] demonstrated that arterial stiffness in ageing is positively correlated with cerebral vascular pulsatility and that this in turn is associated with a greater volume of WM hyperintensities. Excessive intracranial cardiac-related pulsatility has also been associated with brain atrophy among elderly individuals [93]. Microstructural changes associated with increased cerebral pulsatility may therefore represent early-stage alterations in the structural organisation of the WM, likely to precede the emergence of leukoaraiosis [92].

Ageing of the brain in healthy individuals is characterised by atrophy and WM signal abnormality changes, typically detected as leukoaraiosis [94]. Leukoaraiosis is known to be associated with hypertension. Given that hypertension is associated with reduced vascular compliance [95], particularly in smaller arterial vessels [96], it is therefore perhaps not surprising that leukoaraiosis has been shown to be characterised by increased arterial and sinus pulsatility [70]. Likewise, patients with normal pressure hydrocephalus (NPH), a condition frequently linked with leukoaraiosis, appear to exhibit increased pulsatility in the blood flow through the cerebral vascular bed [70]. While the mechanisms linking these conditions with vascular pulsatility in the brain are poorly understood, it has been shown that advancing age is associated with higher pulsatility of CBF, which in turn is accompanied by a reduction in total CBF [90]. Given that higher pulsatility of CBF has been associated with microstructural WM damage [92] and greater WM hyperintensities [90] in older adults, this suggests that ischemic stress, arising from reduced CBF, may be involved in promoting WM damage - something that others have suggested [43, 44, 54, 56].

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