In the brain, CBF varies directly with cerebral perfusion pressure (CPP; defined as the difference between mean arterial pressure and intracranial pressure) and inversely with cerebrovascular resistance (which is the sum of the resistance to flow generated by the vasculature, particularly at the level of the small pial arteries and penetrating pre-capillary arterioles). In general, the contribution of any given cerebral vessel to overall CBF is defined by factors such as its radius and length, and the viscosity and pressure of blood flowing through it.
The average rate of blood flow in the brain is approximately 50-55 ml/100 g/min. In pathological states, this global flow rate may decrease, leading to rate-dependent neurological manifestations. The link between flow rate and electrophysiological and clinical findings underlies the concept of "flow thresholds". Remarkably, clinical evidence for a neurological deficit may not appear until average flow has fallen to 50% or below of normal levels (i.e. to approximately 25-30 ml/100 g/min). At this threshold, global neurological impairment is noted and, below this, the margin between reversible and irreversible ischemic damage becomes narrow. Brain "electrical failure" begins at rates of about 16-18 ml/100 g/min, while cytotoxic edema from failure of ionic pumps, particularly Na+K+ATPases, develops at 10-12 ml/100 g/min. Finally, metabolic failure with gross disturbance of cellular energy homeostasis occur at rates of less than 10 ml/100 g/min.
In 1783, Alexander Monro proposed that the incompressibility of the cranial vault mandated a relatively constant intracranial blood volume at all times - a notion supported by George Kellie at the turn of the century. However, this proposal was later challenged by Sir George Burrows, who postulated that any variation in the volume of one of the three principal intracranial contents, namely brain parenchyma (1200-1600 ml), blood (100-150 ml) and cerebrospinal fluid (CSF, 100-150 ml), was accompanied by a compensatory change in the volume of the other two. In fact, this latter notion forms the basis of the relationship between intracranial pressure and cerebral blood volume (CBV). This pressure-volume relationship implies that in order to maintain a constant intracranial pressure in the face of rising CSF volume, blood volume must fall and when this can no longer occur, the brain will herniate caudally. Importantly, as intracranial pressure rises there is a fall in CBF in association with reduced CBV, most likely from structural compression of the vasculature.
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