Learning objectives.
By reading this article, you should be able to:
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Describe the anatomy of cerebral circulation.
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Discuss the significance and importance of the circle of Willis.
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Identify the conditions that affect the cerebral arterial circulation and where it occurs commonly.
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Explain why the cerebral venous circulation is unique and how it is protective.
Key points.
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The brain uses 20% of the body's oxygen requirements, cardiac output and glucose usage.
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Neuronal death occurs after 5 min of circulatory arrest.
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Seventy percent of ischaemic strokes occur in the anterior circulation; 90% of these occur in the middle cerebral artery.
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Cerebral aneurysms are commonly found at bifurcations; 85% are in the anterior circulation.
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The cavernous sinus is the only place in the body where an artery passes through a venous structure.
The brain is the most energy-hungry organ in the body. Although the brain constitutes only 2% of the total body mass, it consumes 20% of the body's glucose-derived energy, oxygen requirements and cardiac output.1 This article describes the relationship between embryological development and cerebral anatomy, and the consequent neurological manifestations of diseases of the cerebral arterial supply and venous drainage.
The unique features of the cerebral circulation are relevant to all anaesthetists because we need to understand the risk of perioperative stroke, and have strategies to manage patients with a history of stroke or other abnormalities of the cerebral circulation.
Development
The development of the cerebral circulation occurs in two main stages: vasculogenesis and angiogenesis. This development occurs even before the heart starts beating. Vasculogenesis is the de novo creation of blood vessels where previously none existed. Angiogenesis is driven by hypoxia within the fetus and is the production of new capillaries from existing blood vessels.
The circulatory system develops from the six pairs of branchial arch arteries. The third pair of branchial arch arteries and the distal segment of the paired dorsal aortae become the internal carotid arteries (ICAs). The anterior division of the ICA goes on to form the primitive olfactory artery, which becomes the middle (MCA) and anterior cerebral arteries (ACA), whilst a posterior division eventually becomes the posterior cerebral artery (PCA). Initially, the posterior circulation relies on anastomoses from the anterior circulation to the basilar artery before the development of the vertebral arteries and the loss of the anastomoses.2
Arterial circulation
The blood supply to the brain is through the two ICAs and the vertebrobasilar system, which provide 70% and 30% of the flow, respectively. The vertebral arteries originate from the subclavian arteries and join to form the basilar artery. This basilar artery then divides again to form the PCAs that anastomose with the ICAs to form a system at the base of the brain called the circle of Willis. The ICAs also continue on to form the MCAs and join anteriorly to form two ACAs (Fig. 1). The anterior cerebral circulation, made up of the ACAs and MCAs, also includes the anterior choroidal artery, which can be significant in disease. It usually arises from proximal to the bifurcation of the ACAs and MCAs, although there are a number of variations.
Fig 1.
Contrast-enhanced magnetic resonance angiography (MRA) showing cerebral arterial circulation. A1, A2, segments of anterior cerebral artery; AICA, anterior inferior cerebellar artery; basilar, basilar artery; LICA, left internal carotid artery; M1, M2, M3, M4, segments of middle cerebral artery; P1, segment of posterior cerebral artery; RICA, right internal carotid artery; RVA, right vertebral artery.
The ACAs supply most of the medial part of the cerebral hemispheres; the MCAs supply the lateral sides of the hemispheres, and the PCAs supply the occipital and inferior parts of the temporal lobes.
Anterior cerebral arteries
The ACAs supply all of the medial surfaces of the frontal and parietal lobe, the majority of the corpus callosum and the frontobasal cerebral cortex. These areas include the frontal, prefrontal, primary motor, primary sensory and supplemental motor cortices (which contain Broca's speech area). The main motor and sensory functions relate to the lower limbs and speech motor production.
The ACA is split into five segments: A1–5. These segments denote the distance of the vessel from the origin of the ACA, and supply distinct anatomical areas (Fig 2; Table 1).1
Fig 2.
Sagittal view of non-contrast CT scan of the brain with a diagram of the course of anterior cerebral artery superimposed on it. A, anterior cerebral artery; A1, pre-communicating segment of the anterior cerebral artery; A2, post-communicating infracallosal segment of the anterior cerebral artery; A3, precallosal segment of the anterior cerebral artery; A4, supracallosal segment of the anterior cerebral artery; A5, postcallosal segment of the anterior cerebral artery; B, orbitofrontal artery; C, frontopolar artery; D, callosomarginal artery; E, pericallosal artery; F, posterior internal frontal artery; G, superior parietal artery; H, inferior parietal artery.
Table 1.
Segment, anatomy, cerebral area supplied and deficit if the cerebral artery is occluded
| Artery | Segment | Anatomy | Areas supplied | Deficit |
|---|---|---|---|---|
| Anterior cerebral artery | A1 (pre-communicating) | Originating from the terminal bifurcation of the internal carotid artery, extending ∼14 mm in length and terminating at the anterior communicating artery | Caudate nucleus and anterior limb of internal capsule, anterior hypothalamus, septum pellucidum, anterior commissure, fornix and anterior striatum |
|
| A2 (post-communicating, infracallosal) | From the anterior communicating artery to the lamina terminalis and along the rostrum of the corpus callosum, terminating either at the genu of the corpus callosum or at the origin of the callosomarginal artery | Anterior caudate nucleus, internal capsule and inferior and inferomedial surfaces of the frontal lobe | ||
| A3 (precallosal) | From the corpus callosum or the callosomarginal artery, terminating directly posterior above the corpus callosum | Corpus callosum, superior frontal gyrus, precuneus and medial aspect of the hemisphere | ||
| A4 (supra-callosal) | Above the body of the corpus callosum anterior to the plane of the coronal suture | Corpus callosum | ||
| A5 (postcallosal) | Above the body of the corpus callosum posterior to the plane of the coronal suture | Corpus callosum | ||
| Middle cerebral artery | M1 (horizontal) | Sphenoidal segment and runs within the Sylvian fissure parallel to the sphenoid ridge before becoming M2 segment | Head and body of caudate nucleus, parts of the internal capsule, putamen, lateral pallidum and anterior temporal lobe |
|
| M2 (insular) | From the limen insulae to the circular sulcus of the insular | Parts of the parietal lobes | ||
| M3 (opercular) | Run to the superficial border of the Sylvian fissure before becoming the cortical M4 segment | Frontal, parietal and temporal opercula | ||
| M4 (cortical) | Extends over the cortical surface of the cerebral hemisphere | Hemispheric surface of frontal and parietal lobes | ||
| Posterior cerebral artery | P1 (pre-communicating) | From the termination of the basilar artery to the posterior communicating artery within the interpeduncular cistern | Paramedian parts of the upper midbrain and thalamus |
|
| P2 (post-communicating) | Around the midbrain through the crural and ambient cisterns | Ventrolateral thalamus, geniculate body, posterior thalamus and hippocampus | ||
| P3 (quadrigeminal) | Quadrigeminal cistern to the entrance of the occipital lobe | Inferotemporal areas | ||
| P4 (cortical) | Cortical surface of the occipital lobe | Occipital cortex | ||
| Anterior choroidal artery | — | From the internal carotid artery, runs along the optic tract to the choroidal fissure | Hippocampus, amygdala, posterior limb internal capsule, midbrain, thalamus and geniculate nucleus |
|
Middle cerebral arteries
The MCA is the largest of the intracerebral vessels. It supplies a large area of the lateral surface of the brain, including the cerebral cortex of the lateral frontal, parietal and temporal lobes; part of the basal ganglia; and the internal capsule. The basal ganglia are involved in motor control, learning and executive function along with emotions. The motor and sensory areas supplied are mainly those of the face and upper limbs.
The MCA is split into segments M1–4. It arises from the ICA and continues into the lateral sulcus where it divides further and supplies the lateral cerebral cortex (Fig. 3; Table 1).1
Fig 3.
Coronal view of noncontrast CT scan of the brain with a diagram of the course of middle cerebral artery superimposed on it. ACA, anterior communicating artery; ICA, internal carotid artery; M1, horizontal segment of the middle cerebral artery; M2, insular segment of the middle cerebral artery; M3, opercular segment of the middle cerebral artery; M4, cortical segments of the middle cerebral artery.
Posterior cerebral arteries
The PCAs are the terminal branches of the basilar artery. They supply the occipital lobe, which includes the visual areas and the lower portion of the temporal lobe. It also supplies the thalamus, which relays sensory and motor signals, deep structures of the brain and part of the internal capsule, which contains the descending parts of the lateral and anterior corticospinal tracts.
The PCA is split into four segments P1–4. It arises from the basilar artery and projects towards the occiput and over the tentorium cerebelli to the occipital lobe (Fig. 4; Table 1).1
Fig 4.
Sagittal view of noncontrast CT scan of the brain with a diagram of the course of posterior cerebral artery superimposed on it. A, basilar artery; B, internal carotid artery; C, posterior cerebral artery; D, medial posterior choroidal artery; E, lateral posterior choroidal artery; F, splenial artery; G, posterior temporal artery; H, posterior temporal artery; I, occipital artery; P1, precommunicating segment of the posterior cerebral artery; P2, post-communicating segment of the posterior cerebral artery; P3, quadrigeminal segment of the posterior cerebral artery; P4, cortical segment of the posterior cerebral artery.
Conditions affecting the cerebral arterial circulation
Vessel occlusion
Stroke is the fourth biggest cause of mortality in the UK. Eighty-five percent of all strokes are ischaemic, and there are around 100,000 strokes in the UK every year. Almost two thirds of stroke survivors leave hospital with a disability, with high costs to society.3
Ischaemic strokes are caused by blockages to the blood supply to parts of the brain. The effect and disability depend on where the blockage occurs (Table 1).
The majority of ischaemic strokes (70%) occur in the anterior circulation, that is, from the ICA, ACA or MCA. Pure ACA infarcts are uncommon (2%), as there is good collateral blood supply. The most common sites of ICA occlusion are the proximal 2 cm and the carotid siphon. These sites can be silent, owing to the fact that there is extensive collateral supply. Middle cerebral artery occlusion is the most common of the anterior circulation strokes accounting for 90% of infarcts and generally occurs in M1 or M2 (Fig. 5). Thirty-three percent of these strokes are in the deep MCA territory and 50% superficial.4
Fig 5.
Angiogram showing M1 occlusion located at A (left). Scan showing a decreased blood vessel density in the area shaded with red (right).
The large vessel occlusions of the proximal anterior and posterior circulations have historically caused long-term morbidity and mortality, as they are commonly refractory to thrombolysis. These occlusions account for 24–46% of ischaemic strokes, although it is hoped that with the advent of mechanical thrombectomy, this will improve.5 The cerebral arterial circulation is unique in that the circle of Willis allows collateral blood flow to occur if a main artery is completely occluded on one side. It is important to maintain the mean arterial pressure in patients with an acute ischaemic stroke in the hope that the collateral circulation will perfuse the ischaemic areas to some extent before mechanical thrombectomy can be performed.
Cerebral aneurysm
Cerebral aneurysm (CA) is an abnormal bulging weakness in a cerebral artery wall that becomes thin and has the potential to rupture. The estimated worldwide prevalence of CA is 3.2%.6 The rate of rupture is about 10 per 100,000. Most CAs are saccular (berry), but there are a small percentage of fusiform and mycotic aneurysms. Cerebral aneurysms are commonly found at bifurcations in major cerebral arteries, where there is most haemodynamic stress in a vessel. Eighty-five percent of berry aneurysms are located in the anterior circulation. The three most common areas are the anterior communicating artery (30%), followed by the posterior communicating artery (25%) and the MCA (20%).7
Fusiform aneurysms tend to occur in the posterior circulation. Ten percent of all CAs are on the basilar artery, particularly on the basilar tip, and 5% are on the vertebral artery.7 Cerebral aneurysms are found incidentally, but symptoms can range from headaches to unconsciousness and death. Rupture of the CAs can cause intracranial and subarachnoid haemorrhage. Treatment can be with surgical clipping of aneurysm or endovascular coiling.
Arteriovenous malformation and collateral vessels
Arteriovenous malformations (AVMs) are arteriovenous shunts. The lack of an intertwining capillary bed results in pulsatile high flow and medium-to high-pressure channels more liable to rupture. Arteriovenous malformations are thought to be hereditary with a prevalence of 0.14% and a lifelong risk of bleeding of 2–4%.8 Patients usually present with haemorrhage or seizures. Diagnosis is via cerebral angiogram. Treatment is by surgical excision, stereotactic radiosurgery and embolisation.
Moyamoya disease is a rare progressive congenital condition, in which the ICAs are narrowed, limiting the flow to the brain. The brain compensates for the decreased blood supply by developing tiny collateral vessels to the oxygen-deprived areas. This appearance on imaging earns it the name, which is Japanese for ‘puff of smoke’. Moyamoya disease is more common in the East Asian population and is associated with some diseases, such as Down syndrome, neurofibromatosis type 1 and sickle cell disease. The incidence is one in 1,000,000 in Western populations with two peaks of presentation: one in childhood (from 5 to 15 yrs) and another in adulthood (in their 40s).9 The initial presentation can be with a transient ischaemic attack or ischaemic or haemorrhagic stroke. The most common symptoms are headaches, weakness or numbness in limbs, paralysis and dysphasia. The gold standard for diagnosis is an angiogram. Treatment can be medical or surgical. Medical treatment includes aspirin, which may reduce the risk of strokes. Surgical treatments aim to restore blood flow to the deprived areas of the brain by direct or indirect bypass procedures. Direct bypass procedures, such as extracranial to intracranial bypass, are preferred in older children and adults. Indirect bypass procedures, such as pial synangiosis, encephaloduroarteriosynangiosis and dural inversion, are used in children aged <10 yrs.
Venous circulation
The cerebral venous circulation (Fig. 6) has a wide variability between people and even between the two hemispheres compared with the arterial system. They differ from other veins in the body, as they do not follow the pathway of the associated cerebral arteries and do not have valves. This makes the venous circulation bidirectional, which is essential in intracranial pressure (ICP) regulation in relation to posture and cerebral venous outflow. These qualities make the cerebral venous circulation unique and protect against several clinical conditions of the brain.
Fig 6.
Angiogram showing anterior communicating artery (ACOM) aneurysm: anteroposterior view (left) and lateral view (right). A, basilar artery; B, anterior cerebral artery; C, ACOM aneurysm; D, middle cerebral artery.
Venous circulation of the cerebrum consists of deep and superficial cerebral veins, which drain into the dural venous sinuses located in between the periosteal and meningeal layers of the dura mater, and eventually drain into the internal jugular vein (IJV).
Deep cerebral veins
The deep cerebral veins are closely associated with the thalamus originating at the foramen of Munro, and run posteriorly within the roof of the third ventricle. The two veins anastomose to form the great vein of Galen (GV). The basal vein of Rosenthal drains the midbrain structures and into the GV, which drains into the straight sinus.
Superficial cerebral veins
These veins comprise the superior cerebral veins and the Sylvian vein. The superior cerebral veins extend on the lateral surface of the brain superiorly to drain into the superior sagittal sinus, which is within the falx cerebri. The Sylvian vein lies in the Sylvian fissure and drains into three different sinuses. It drains in the superior sagittal sinus via the superior anastomotic vein of Trolard, transverse sinus via the inferior anastomotic vein of Labbe and anteriorly into the cavernous sinus. The cavernous sinus is located in the middle cranial fossa next to the sella turcica and pituitary gland, and is the only place in the body that an artery passes inside a venous structure. This sinus contains important structures, such as the ICA, carotid plexus and cranial nerves (oculomotor, trochlear, ophthalmic, maxillary and abducens nerves).
The falx cerebri contains the superior sagittal, inferior sagittal and straight sinus. These anastomose at the confluence of sinuses located at the internal occipital protuberance. This becomes the transverse sinus, which emerges as the sigmoid sinus and drains into the IJV together with the cavernous sinus carrying deoxygenated blood back to the heart. The IJV is able to drain 100% of the cerebral venous outflow, but there is a second venous system; the vertebral venous plexus (VVP) can drain up to 30% of the venous outflow from the brain. The majority of veins in the posterior fossa drain into the inferior petrosal sinus. This sinus is a connection between IJV and VVP.
Clinical conditions affecting the cerebral venous circulation
Cerebral venous sinus thrombosis (CVST) is uncommon, accounting for 0.5–1% of strokes, as there are substantial compensations in the cerebral venous systems. This is because cerebral veins and sinuses have no valves and no tunica muscularis layer. Symptoms of CVST vary according to the location of thrombus, but are commonly headaches, blurred vision, focal deficits, seizures and coma. The most common area affected is the superior sagittal sinus and the lateral sinuses.10 They are often unrecognised initially. Anticoagulation is the first line of treatment.
Infections of the brain can occur as dural sinuses are in communication with extracranial venous systems via many emissary veins. The absence of valves allows retrograde flow of blood from superficial structures into the brain and can be a site of entry of infection.
The cerebral venous drainage may also be affected by postural changes. Excessive neck flexion and neck rotation may result in kinking and obstruction of the IJV, which may in turn lead to an increase in ICP. The VVP can compensate for such changes to some extent in normal life.11 This may not be true during surgery and anaesthesia.
Conclusions
The cerebral circulation is complex, and if interrupted or affected, it can produce a number of clinical syndromes dependent on the area of the brain affected; these are then modified, depending on the extent of collateral blood flow present. The anatomy of the circle of Willis allows extensive protection and continued flow in the presence of a large vessel occlusion.
Anaesthetists and intensivists should have a working knowledge of cerebral vascular anatomy to help diagnose patients and guide anaesthesia and resuscitation. Maintenance of cerebral perfusion pressures is especially important in patients with ischaemic stroke undergoing mechanical thrombectomy to maintain collateral flow and improve outcomes. Patients should be positioned carefully to avoid kinking the IJV and potentially increasing intracranial pressures.
MCQs
The associated MCQs (to support CME/CPD activity) are accessible at www.bjaed.org/cme/home for subscribers to BJA Education.
Declaration of interests
The authors declare that they have no conflicts of interest.
Biographies
Audrey TanFRCA is a consultant anaesthetist at St George's University Hospitals NHS Foundation Trust and a senior lecturer at St George's, University of London. Her main interests are anaesthesia for neurosurgery.
Daniel Roberts BSc (Hons)FRCA is a consultant anaesthetist at St George's University Hospitals NHS Foundation Trust and a senior lecturer at St George's, University of London. His main interests are anaesthesia for trauma and neurosurgery.
Matrix codes: 1A01, 2F01, 3F00
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