Cerebral blood flow (CBF) is the amount of arterial blood delivered to brain tissue per unit of time. It is most commonly measured as millilitres of blood per 100 g of tissue per minute. Characteristic values for grey matter are 60 ml/min/100 g and 15 ml/min/100 g for white matter. CBF control is via control of the diameter of the feeding arterioles.
CBF is the primary rate constant controlling the supply of nutrients and removal of waste products from the brain. Below a threshold level, duration multiplied by the absolute CBF level can predict tissue infarction .
While CBV measurement with intravascular tracers is relatively straightforward, the measurement of CBF is more challenging [7, 46], as it requires delicate de-convolution methods.
In particular, one method tries to deconvolve the effects of a bolus of finite width (as estimated from the arterial signal near a large feeding vessel, such as the anterior communicating artery). This arterial input function is taken to represent the profile of the bolus at its point of entry into each individual voxel based on the assumption that every voxel has the same arterial input function. This is clearly an oversimplification, and un certainties about regional changes in the profile and timing of the bolus can cause significant errors in CBF evaluation [7, 47].
Good absolute CBF correlation with H215O PET has been shown in anaesthetized healthy pigs  and an excellent relative CBF correlation has been reported in an experimental model of ischaemia . However, in diseased brain, where collateral pathways are more common, intravascular tracer CBF measurements that do not account for variations in bolus delay (caused by arterial stenoses and occlusions) and dispersion are inaccurate [7, 46, 59].
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