The brain comprises around 2% of total body weight, yet it receives 15-20% of the total cardiac output. This is because the brain has a relatively high metabolic demand, due to being largely reliant on oxidative metabolism. Loss of consciousness occurs within 10 seconds of the interruption of arterial blood supply to the brain and irreparable damage to brain tissue occurs after only a few minutes. ¹
The Monro-Kellie hypothesis
The cranium, enclosing the brain, forms a fixed space comprising three components: blood, cerebrospinal fluid, and brain tissue. These components remain in a state of dynamic equilibrium, therefore any decrease in any one of them results in an increase of the other two. 2
Cerebral perfusion pressure
Cerebral perfusion pressure (CPP) drives oxygen and nutrient supply to brain tissues. The brain can autoregulate blood flow in order to ensure constant flow that is isolated from fluctuations in systemic blood pressure. This microcirculation is regulated by cerebral vessel constriction and dilatation. Most of the blood within the cranial cavity is contained within the low-pressure venous system. Venous compression is the main method of displacing blood volume in the aforementioned mechanism. This is the mechanism that is frequently lost secondary to head trauma, leading to cerebral ischaemia and neuronal death (secondary brain injury). CPP can be calculated using the following formula3:
CPP = MAP – ICP
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Arterial Blood Supply to the Brain
The arterial blood supply to the brain can be divided into the anterior and posteriorcirculation. The former is derived from the left and right internalcarotidarteries, and the latter is derived from the left and right vertebralarteries.
The anteriorcirculation is responsible for supplying the:
Internal Carotid Arteries
Course and branches
The left and right commoncarotidarteriesbifurcate at the level of C3/C4 to give off the internalcarotidarteries (ICA) within the carotid sheath.
The internal carotid arteries then proceed through the respective carotidcanal, within the petrous portion of the temporalbone.
Once in the cranial cavity, the internal carotid arteries pass anteriorly through the cavernoussinus.
Once the internal carotid arteries are distal to the cavernous sinus, each gives rise to the following branches:
Ophthalmic artery: Supplies all the structures in the orbit as well as some structures in the nose, face and meninges.
Posterior communicating artery:
Anteriorly connects to the internal carotid artery prior to the terminal bifurcation of the ICA into the anterior cerebral artery and middle cerebral artery.
Posteriorly, it communicates with the posterior cerebral artery.
Anterior cerebral artery: Supplies oxygenated blood to most midline portions of the frontal lobes and superior medial parietal lobes.
The internal carotid arteries then continue as the middlecerebralarteries. The middle cerebral arteries supply the lateral cerebral cortex, in addition to the anterior temporal lobes and the insular cortices.
Bouthillier classification of ICA segments
This system breaks the ICA down into seven segments, which can be useful when describing pathology such as stenosis or aneurysms: 5
C1 – Cervical
C2 – Petrous
C3 – Lacerum
C4 – Cavernous
C5 – Clinoid
C6 – Ophthalmic (supraclinoid)
C7 – Communicating (terminal)
The posteriorcirculation is responsible for supplying the:
Course and branches
The left and right vertebralarteries arise from their respective subclavianarteries, on the posterosuperior aspect.
The vertebralarteries then proceed to enter the transverseforamina of the spine at level C6 and continue superiorly.
After passing through the transverseforamen of C1, the arteries traverse the foramenmagnum.
Once inside the cranialvault, the vertebral arteries give off the following branches:
Posterior inferior cerebellar artery (PICA) – this is the largest branch of the vertebral artery and is one of three main arteries supplying the cerebellum
Anterior and posterior meningeal arteries – supply the dura mater
Anterior and posterior spinal arteries – supply the spinal cord along its entire length
The vertebralarteries then converge to form the basilarartery at the base of the pons, inside the cranium.
The vertebralartery is generally divided into foursegments: 6
V1 – preforaminal
V2 – foraminal
V3 – atlantic, extradural, or extraspinal
V4 – intradural, intracranial
Course and branches
The basilarartery runs superiorly within the central groove of the pons, giving off a number of branches including the pontinearteries, which supply the pons.
The basilar artery eventually anastomoses with the circleofWillis via the posteriorcerebralarteries and posteriorcommunicatingarteries.
Clinical relevance: Locked-in syndrome
Pontineinfarcts cause an interruption in the myriad of neuronal pathways enabling communication between the cerebrum, cerebellum and spinal cord. This can result in completeparalysis of all voluntarymusclegroups, sparing those controlling the eyes. Individuals suffering from damage to the pons are fullyconscious and cognitivelyintact. 7
Circle of Willis
Anatomy of the Circle of Willis
As outlined above, the terminalbranches of the anterior and posteriorcirculation form an anastomosis to create a ring-like vascular structure known as the circle of Willis, within the base of the cranium (highlighted in pink below).
The left and right internalcarotidarteries continue as the middlecerebralarteries (MCA), after each giving off a branch to supply the anteriorcerebralarteries (ACA). The anteriorcommunicatingartery links the two anterior cerebral arteries together.
The internalcarotidarteries also give off the posteriorcommunicatingarteries (PCoA), linking the middlecerebralarteries (MCA) with the posteriorcerebralarteries (PCA). 8
Clinical relevance: Aneurysms
Saccular or ‘berry‘, aneurysms occur most frequently within the circle of Willis vasculature and are the most common cause of non-traumatic subarachnoidhaemorrhage. Treatment involves urgent neurosurgical referral and subsequent endovascularcoiling or inserting a surgicalclip to occlude flow to an aneurysm. 9
Clinical relevance: Third cranial nerve palsy
The thirdcranialnerve is commonly affected by aneurysms in the circleofWillis, particularly those involving the posteriorcommunicatingartery (PoCA) due to its close anatomical relationship.
Clinically, “surgical” third nerve palsy can be differentiated from “medical” third nerve palsy by evidence of pupillary involvement. External compression of the third nerve affects parasympathetic fibres surrounding the outermost region of the third nerve. This compression results in an inability to constrict the pupil, making it appear fixed and dilated (often referred to as a ‘blown pupil’).
“Medical” third nerve palsy results from involvement of the vaso vasorum, which is involved in supplying the central area of the third cranial nerve. This results in pupillary involvement arising much later. Common causes of “medical” third nerve palsy include those affecting microvasculature, such as diabetes and atherosclerosis. ²
The anteriorcerebralarteries, middlecerebralarteries and posteriorcerebralarteries each supply a territory of the brain (see the image below).
Each region of the brain has specific associated functions, enabling clinicians to discern the site of pathology through history and neurological examination of the patient.
As discussed earlier, the brain is extremely vulnerable to stress in the form of depleted blood supply. A cerebrovascular event (stroke) is a clinical syndrome caused by disruption of blood supply to the brain, characterised by rapidly developing signs of focal or global disturbance of cerebral functions, lasting for more than 24 hours or leading to death.
Strokes can be classified into two major categories: 10
Ischaemic stroke (87%)
Haemorrhagic stroke (13%)
Ischaemic strokes occur when the blood supply to an area of the brain is reduced, resulting in tissue hypoperfusion.
There are several mechanisms which can result in an ischaemic stroke including:
Embolism: An embolus from somewhere else in the body (e.g. the heart, commonly secondary to atrial fibrillation) causes obstruction of a cerebral vessel, resulting in hypoperfusion to the area of brain the vessel supplies.
Thrombosis: A blood clot forms locally within a cerebral vessel (e.g. due to atherosclerotic plaque rupture).
Systemic hypoperfusion: Reduced blood supply to the entire brain secondary to systemic hypotension (e.g. cardiac arrest).
Cerebral venous sinus thrombosis: Blood clots form in the veins that drain the brain, resulting in venous congestion and hypoxia which damages brain tissue.
Fitzgerland, M.T.J., Gruener, G., Mtui, E. (2012) Clinical Neuroanatomy and Neuroscience. 6 edn. United States: Saunders.
Van Beek, A.H., Claassen, J.A., Rikkert, M.G. and Jansen, R.W. (2008) ‘Cerebral autoregulation: an overview of current concepts and methodology with special focus on the elderly’, Journal of Cerebral Blood Flow & Metabolism, 28(6), 1071-85.
Crossman, A.R., Neary, D. (2014) Neuroanatomy: an Illustrated Colour Text. 5 edn. London: Churchill Livingstone.
Alpers, B.J., Berry, R.G. and Paddison, R.M. (1959) ‘Anatomical studies of the circle of Willis in normal brain’, A. M. A. Archives of Neurology & Psychiatry, 81(4), 409-18.
Van der Schaaf, I., Algra, A., Wermer, M., Molyneux, A., Clarke, M., van Gijn, J. and Rinkel, G. (2005) ‘Endovascular coiling versus neurosurgical clipping for patients with aneurysmal subarachnoid haemorrhage’, Cochrane Database of Systematic Reviews, (4), CD003085.
Donnan GA, Fisher M, Macleod M, Davis SM (May 2008). “Stroke”. Lancet. 371 (9624): 1612–23. doi:10.1016/S0140-6736(08)60694-7. PMID 18468545.
Figure 1: Melissa Gough, 2018
Figure 2: Internal Carotid Artery. By OpenStax College [CC BY 3.0], via Wikimedia Commons