# Lecture 14: Cerebral Blood Supply ## Unit 2.5: Neuroscience --- ## Learning Objectives By the end of this lecture, students will be able to: 1. Describe the arterial supply to the brain including the internal carotid and vertebrobasilar systems 2. Explain the anatomy and clinical significance of the Circle of Willis 3. Describe the vascular territories of the major cerebral arteries 4. Explain the clinical presentations of major arterial territory strokes 5. Describe the venous drainage of the brain including dural sinuses 6. Apply understanding of cerebrovascular anatomy to clinical stroke localization --- ## Lecture Outline ### I. Overview of Cerebral Circulation The brain represents approximately 2% of body weight yet receives 15-20% of cardiac output, reflecting its extraordinarily high metabolic demands. Cerebral blood flow averages 50-55 mL per 100 grams of brain tissue per minute, totaling approximately 750 mL per minute. The brain has virtually no capacity for anaerobic metabolism and minimal energy stores, making it exquisitely vulnerable to interruption of blood supply. Cessation of cerebral blood flow leads to loss of consciousness within seconds and irreversible neuronal injury within minutes. The brain receives its arterial supply from two paired systems: the internal carotid arteries anteriorly and the vertebral arteries posteriorly. These systems anastomose at the base of the brain to form the Circle of Willis, providing potential collateral pathways if one vessel becomes occluded. However, the Circle of Willis is complete in only about 25% of individuals, and even when anatomically complete, collateral capacity varies considerably. The internal carotid system supplies approximately 80% of cerebral blood flow, including the majority of the cerebral hemispheres. The vertebrobasilar system supplies the posterior cerebral hemispheres, cerebellum, and brainstem. Regulation of cerebral blood flow involves several mechanisms. Autoregulation maintains constant cerebral blood flow across a range of mean arterial pressures (approximately 60-150 mmHg) through myogenic responses of cerebral arterioles. Below the lower autoregulatory limit, blood flow becomes pressure-dependent and the brain becomes vulnerable to ischemia. Above the upper limit, hyperperfusion can cause edema and hemorrhage. Carbon dioxide is a potent regulator of cerebral blood flow, with hypercapnia causing vasodilation and hypocapnia causing vasoconstriction. Metabolic coupling matches local blood flow to neuronal activity through neurovascular signaling mechanisms. Cerebral circulation overview: Panel 1 - Anterior view of the brain showing internal carotid arteries entering skull through carotid canals and vertebral arteries entering through foramen magnum, with approximate percentage of blood flow contribution labeled. Panel 2 - Graph demonstrating autoregulation curve with cerebral blood flow on y-axis and mean arterial pressure on x-axis, showing plateau region and pressure-dependent zones. Panel 3 - Diagram of CO2 reactivity showing vasodilation with hypercapnia and vasoconstriction with hypocapnia. Panel 4 - Neurovascular coupling illustration showing active neurons releasing signals that dilate local arterioles to increase blood flow. --- ### II. Internal Carotid Artery System The internal carotid artery (ICA) originates from the common carotid artery bifurcation at approximately the C4 vertebral level in the neck. The carotid bifurcation contains the carotid sinus, a baroreceptor-rich dilation at the ICA origin, and the carotid body, a chemoreceptor located at the bifurcation. The ICA ascends without branches in the neck, enters the skull through the carotid canal in the petrous temporal bone, and follows an S-shaped course through the cavernous sinus (the carotid siphon) before penetrating the dura medial to the anterior clinoid process. The segments of the internal carotid artery are classified by the Bouthillier system. The C1 (cervical) segment extends from the bifurcation to the skull base. The C2 (petrous) segment traverses the petrous temporal bone. The C3 (lacerum) segment crosses over the foramen lacerum. The C4 (cavernous) segment courses through the cavernous sinus, in close proximity to cranial nerves III, IV, V1, V2, and VI. The C5 (clinoid) segment is at the anterior clinoid process. The C6 (ophthalmic) segment gives rise to the ophthalmic artery. The C7 (communicating) segment terminates at the ICA bifurcation. The major branches of the internal carotid artery include the ophthalmic artery, the first major branch, which supplies the retina and orbit and is clinically important because retinal artery occlusion causes sudden painless vision loss. The posterior communicating artery connects to the posterior cerebral artery, forming part of the Circle of Willis. The anterior choroidal artery supplies the optic tract, cerebral peduncle, posterior limb of internal capsule, and choroid plexus. The internal carotid artery terminates by bifurcating into the anterior cerebral artery (ACA) and middle cerebral artery (MCA), the largest terminal branch. Internal carotid artery: Panel 1 - Lateral view showing ICA origin at common carotid bifurcation with carotid sinus and body labeled, cervical segment ascending without branches. Panel 2 - Skull base view showing ICA entering carotid canal, traversing petrous bone, and S-shaped course through cavernous sinus with segments labeled C1-C7. Panel 3 - Close-up of cavernous sinus showing ICA surrounded by cranial nerves III, IV, V1, V2, VI with anatomical relationships. Panel 4 - ICA termination showing bifurcation into ACA and MCA, with posterior communicating and anterior choroidal branches labeled. --- ### III. Anterior Cerebral Artery The anterior cerebral artery (ACA) is the smaller terminal branch of the internal carotid artery, coursing medially above the optic nerve and chiasm to reach the interhemispheric fissure. The two anterior cerebral arteries are connected near the midline by the anterior communicating artery (AComm), which is the most common site of intracranial aneurysms. The ACA then curves around the genu of the corpus callosum and continues posteriorly along the medial surface of the hemisphere. The ACA is divided into three segments. The A1 (horizontal or precommunicating) segment extends from the ICA bifurcation to the anterior communicating artery. Hypoplasia or absence of one A1 segment is common and can affect collateral capacity. The A2 (vertical or postcommunicating) segment extends from the AComm to the junction of the rostrum and genu of corpus callosum. The A3 (precallosal) segment curves around the genu. Major named branches include the medial lenticulostriate arteries (from A1) supplying deep structures, the orbitofrontal artery, the frontopolar artery, and the pericallosal and callosomarginal arteries coursing along the corpus callosum. The ACA territory includes the medial surfaces of the frontal and parietal lobes, from the frontal pole to the parietal-occipital sulcus. This encompasses the leg and foot portions of the primary motor and sensory cortices on the medial paracentral lobule, as well as the supplementary motor area and anterior cingulate cortex. The corpus callosum receives its blood supply from ACA branches. Occlusion of the ACA produces contralateral leg-predominant weakness and sensory loss, with relative sparing of face and arm (supplied by MCA). Bilateral ACA infarction, which can occur with AComm aneurysm rupture or vasospasm, may cause akinetic mutism from damage to the cingulate gyri and supplementary motor areas bilaterally, along with personality changes and urinary incontinence. Anterior cerebral artery: Panel 1 - Basal view showing A1 segments coursing medially above optic chiasm to join at anterior communicating artery, then ascending in interhemispheric fissure. Panel 2 - Midsagittal view showing ACA curving around corpus callosum genu with pericallosal and callosomarginal branches labeled along medial hemisphere surface. Panel 3 - Medial surface with ACA territory shaded showing motor and sensory areas for leg/foot on paracentral lobule. Panel 4 - Clinical presentation of ACA stroke showing contralateral leg weakness with preserved arm and face, foot drop during walking. --- ### IV. Middle Cerebral Artery The middle cerebral artery (MCA) is the largest terminal branch of the internal carotid artery and the most common site of ischemic stroke. It courses laterally in the Sylvian (lateral) fissure and supplies the majority of the lateral cerebral hemisphere convexity. The MCA territory includes critical language areas (Broca's and Wernicke's areas in the dominant hemisphere), motor and sensory cortices for the face and upper extremity, and frontal eye fields. The MCA is divided into four segments. The M1 (horizontal or sphenoidal) segment extends from the ICA bifurcation to the Sylvian fissure and gives rise to the lateral lenticulostriate arteries, which are critical perforating branches supplying the basal ganglia, internal capsule, and adjacent white matter. The M2 (insular) segment courses over the insula in the depths of the Sylvian fissure. The M3 (opercular) segment loops over the opercula. The M4 (cortical) segments are the terminal branches over the lateral cortical surface. Major cortical branches include the orbitofrontal, prefrontal, precentral, central, postcentral, posterior parietal, angular, posterior temporal, and anterior temporal arteries. MCA occlusion produces the most clinically recognizable stroke syndrome. Proximal M1 occlusion affects both deep perforator territory and cortical branches, producing contralateral hemiparesis (face and arm greater than leg), contralateral hemisensory loss, homonymous hemianopia (from optic radiation involvement), and eyes deviated toward the lesion side. In the dominant hemisphere, global aphasia occurs. In the non-dominant hemisphere, hemispatial neglect and anosognosia develop. Superior division MCA strokes primarily cause Broca's aphasia with hemiparesis, while inferior division strokes cause Wernicke's aphasia with hemianopia and less motor deficit. Lenticulostriate artery occlusion produces pure motor hemiparesis from internal capsule lacunar infarction. Middle cerebral artery: Panel 1 - Basal view showing MCA originating from ICA bifurcation, M1 segment coursing laterally with lenticulostriate perforators, entering Sylvian fissure. Panel 2 - Lateral view showing MCA branching pattern over lateral hemisphere with major cortical branches labeled (precentral, central, angular, temporal). Panel 3 - Lateral convexity with MCA territory shaded in red, showing motor/sensory strip for face and arm, Broca's and Wernicke's areas. Panel 4 - Clinical presentation grid comparing proximal MCA, superior division, inferior division, and lenticulostriate strokes with characteristic deficits. --- ### V. Vertebrobasilar System The vertebral arteries arise from the subclavian arteries and ascend through the transverse foramina of cervical vertebrae C6 through C1. They enter the skull through the foramen magnum, course along the anterolateral medulla, and join at the pontomedullary junction to form the basilar artery. The vertebral arteries supply the medulla, posterior inferior cerebellum, and contribute to spinal cord blood supply. The basilar artery ascends along the ventral pons and terminates at the pontomesencephalic junction by bifurcating into the two posterior cerebral arteries. Major branches of the vertebral arteries include the posterior inferior cerebellar artery (PICA), which is the largest vertebral branch and supplies the lateral medulla and posterior inferior cerebellum. Occlusion of PICA or the vertebral artery causes the lateral medullary (Wallenberg) syndrome. The anterior spinal artery arises from the vertebral arteries near their junction and descends along the anterior spinal cord. The posterior spinal arteries may arise from the vertebral arteries or PICA. The basilar artery gives rise to several important branches. The anterior inferior cerebellar artery (AICA) supplies the lateral pons and anterior inferior cerebellum. The superior cerebellar artery (SCA) arises just before the basilar bifurcation and supplies the superior cerebellum and parts of the midbrain and pons. Numerous pontine perforating branches supply the basis pontis. The labyrinthine (internal auditory) artery usually arises from AICA and supplies the inner ear. Basilar artery occlusion is a neurological emergency causing quadriplegia, bilateral cranial nerve deficits, and potentially "locked-in syndrome" where the patient is awake but can only communicate through vertical eye movements. Vertebrobasilar system: Panel 1 - Posterior view showing vertebral arteries arising from subclavian, ascending through transverse foramina C6-C1, entering foramen magnum, and joining to form basilar artery. Panel 2 - Ventral brainstem view showing basilar artery on pons with labeled branches: AICA, pontine perforators, SCA, and terminal bifurcation into PCAs. Panel 3 - Cerebellar arterial territories in posteroinferior view: PICA (green), AICA (blue), SCA (red) territories with watershed zones. Panel 4 - Locked-in syndrome illustration showing patient aware but paralyzed, only able to move eyes vertically, with basilar artery occlusion on MRA. --- ### VI. Posterior Cerebral Artery and Circle of Willis The posterior cerebral artery (PCA) is the terminal branch of the basilar artery, curving around the midbrain in the ambient cistern to supply the medial and inferior temporal lobe, occipital lobe, and posterior thalamus. The PCA is connected to the internal carotid system by the posterior communicating artery (PComm). In approximately 20-30% of individuals, one PCA arises directly from the ICA (fetal PCA configuration), which has implications for stroke when the ICA is occluded. The PCA is divided into four segments. The P1 (precommunicating) segment extends from the basilar bifurcation to the PComm junction and gives rise to perforating branches to the midbrain and thalamus. The P2 (ambient) segment courses around the midbrain in the ambient cistern. The P3 (quadrigeminal) segment is in the quadrigeminal cistern. The P4 represents the terminal cortical branches. Major branches include the thalamoperforating arteries, the posterior choroidal arteries supplying the choroid plexus, and cortical branches to the temporal and occipital lobes including the calcarine artery. The Circle of Willis is an arterial anastomosis at the base of the brain connecting the anterior and posterior circulations. It comprises the two ACAs connected by the AComm, the two PCAs connected to the ICAs by the PComms, and the proximal ICA segments. The Circle provides potential collateral pathways when one supplying artery is occluded. However, the Circle is complete and functional in only 25-50% of individuals; common variants include hypoplastic or absent A1, P1, or communicating segments. When collateral capacity is limited, carotid or vertebral occlusion is more likely to cause stroke. Posterior cerebral artery and Circle of Willis: Panel 1 - Basal view of complete Circle of Willis with all components labeled: AComm connecting ACAs, A1 segments, ICAs, PComms connecting to P1 segments, PCAs, and basilar artery. Panel 2 - Lateral view showing PCA segments P1-P4 curving around midbrain with perforating branches to thalamus and cortical branches to occipital and temporal lobes. Panel 3 - Common Circle of Willis variants: hypoplastic A1, absent PComm, fetal PCA configuration (arising from ICA). Panel 4 - Medial and inferior surface showing PCA territory including calcarine cortex, medial occipital, and inferior temporal with visual cortex highlighted. --- ### VII. Cerebral Arterial Territories Understanding cerebral arterial territories is essential for stroke localization. The anterior cerebral artery supplies the medial surfaces of the frontal and parietal lobes from the frontal pole to the parietal-occipital sulcus. This includes the paracentral lobule containing motor and sensory cortex for the leg and foot, the supplementary motor area, and the anterior two-thirds of the corpus callosum. The ACA also supplies a small strip of the superior frontal and parietal convexity. The middle cerebral artery has the largest territory, encompassing most of the lateral cerebral convexity. The superficial territory includes the lateral frontal lobe (including Broca's area in the dominant hemisphere), the lateral parietal lobe, the superior temporal gyrus (including Wernicke's area), and the insular cortex. The motor and sensory cortices for the face and arm lie within MCA territory. The deep territory, supplied by lenticulostriate perforators, includes the putamen, globus pallidus, caudate head, and the anterior limb and genu of the internal capsule. The posterior cerebral artery supplies the occipital lobe including the primary visual cortex along the calcarine fissure, the medial and inferior temporal lobe including the hippocampus, and the splenium of the corpus callosum. Deep PCA territory includes the thalamus (posterior and lateral portions via thalamoperforating and thalamogeniculate branches) and the midbrain. Watershed zones, at the borders between arterial territories, are vulnerable to hypoperfusion during systemic hypotension because they are furthest from the feeding arteries. Cerebral arterial territories: Panel 1 - Lateral view of hemisphere with color-coded territories: ACA (blue) superior strip, MCA (red) majority of lateral surface, PCA (green) occipital pole, showing watershed zones at borders. Panel 2 - Medial view with ACA (blue) medial frontal and parietal, PCA (green) medial occipital and temporal, with paracentral lobule and calcarine cortex highlighted. Panel 3 - Coronal section showing deep territories: MCA lenticulostriate territory (basal ganglia, internal capsule), ACA territory (caudate head), PCA thalamic territory. Panel 4 - Axial MRI slices showing infarcts in each arterial territory with characteristic patterns and clinical correlations. --- ### VIII. Cerebral Venous Drainage Cerebral venous drainage differs fundamentally from arterial supply in that veins do not follow the arteries and drain into valveless dural venous sinuses. The superficial venous system drains the cortical surface through cortical veins that empty into the nearest sinus. Important superficial veins include the vein of Trolard (superior anastomotic vein) connecting Sylvian veins to the superior sagittal sinus, and the vein of Labbé (inferior anastomotic vein) connecting to the transverse sinus. The superficial middle cerebral vein courses along the Sylvian fissure to the cavernous sinus. The deep venous system drains the deep white matter, basal ganglia, and thalamus. The internal cerebral veins course in the roof of the third ventricle, receiving the thalamostriate and choroidal veins. The two internal cerebral veins join the basal veins of Rosenthal (which drain the midbrain and basal structures) to form the great vein of Galen (great cerebral vein) in the quadrigeminal cistern. The vein of Galen drains into the straight sinus. The dural venous sinuses are formed by separations of the dural layers and are lined by endothelium but lack valves and muscular walls. The superior sagittal sinus runs in the attached border of the falx cerebri from the crista galli to the confluens of sinuses at the internal occipital protuberance. It receives cortical veins and arachnoid granulations for CSF absorption. The inferior sagittal sinus runs in the free edge of the falx and joins the great vein of Galen to form the straight sinus. The transverse sinuses course from the confluens along the tentorium to become the sigmoid sinuses, which exit the skull as the internal jugular veins. The cavernous sinuses flank the sella turcica and receive blood from orbital and superficial facial veins. Cerebral venous drainage: Panel 1 - Lateral view showing superficial veins (Trolard, Labbé, superficial middle cerebral) draining into dural sinuses with direction of flow indicated. Panel 2 - Midsagittal view showing deep venous system: internal cerebral veins joining vein of Galen, draining to straight sinus. Panel 3 - Superior view of dural sinuses: superior sagittal receiving cortical veins, confluens of sinuses, transverse sinuses coursing to sigmoid sinuses and jugular veins. Panel 4 - Coronal section at level of cavernous sinus showing its relationship to pituitary gland, with cranial nerves in lateral wall and ICA traversing the sinus. --- ### IX. Vascular Pathology and Stroke Syndromes Stroke results from interruption of blood supply (ischemic) or rupture of a blood vessel (hemorrhagic). Ischemic stroke accounts for approximately 85% of strokes and can result from large vessel atherosclerosis, cardioembolism, small vessel disease (lacunar), or other causes including dissection and vasculitis. The clinical presentation depends on which vascular territory is affected, allowing localization based on the pattern of deficits. Large vessel anterior circulation strokes produce recognizable syndromes. MCA territory stroke, as discussed previously, causes contralateral hemiparesis (face and arm greater than leg), hemisensory loss, homonymous hemianopia, and either aphasia (dominant hemisphere) or neglect (non-dominant). ACA territory stroke causes contralateral leg-predominant weakness and sensory loss with relative sparing of face and arm. Internal carotid artery occlusion may cause massive hemispheric infarction with MCA and ACA involvement, or may be asymptomatic if collateral circulation is adequate. Posterior circulation strokes produce distinct syndromes. PCA territory stroke causes contralateral homonymous hemianopia with macular sparing (due to dual blood supply of the macular cortex) and may affect memory if the medial temporal lobe is involved. Thalamic strokes cause sensory loss and may produce thalamic pain syndrome (Dejerine-Roussy). Brainstem strokes produce crossed findings with ipsilateral cranial nerve deficits and contralateral long tract signs. Cerebellar strokes cause ipsilateral ataxia, vertigo, and nystagmus, with risk of brainstem compression from edema. Lacunar strokes from small vessel disease produce pure motor, pure sensory, ataxic hemiparesis, or sensorimotor syndromes without cortical signs. Stroke syndromes: Panel 1 - Comparison table of MCA, ACA, and PCA stroke presentations with characteristic findings for each territory. Panel 2 - Lateral medullary syndrome (Wallenberg) diagram showing crossed sensory findings: ipsilateral face (trigeminal nucleus), contralateral body (spinothalamic tract) with additional features labeled. Panel 3 - Lacunar stroke locations in the internal capsule, thalamus, and pons with corresponding clinical syndromes. Panel 4 - CT and MRI appearance of acute infarcts in different territories: hypodense on CT, restricted diffusion on DWI MRI. --- ### X. Clinical Evaluation and Vascular Imaging Clinical stroke evaluation begins with rapid assessment using standardized tools such as the NIH Stroke Scale (NIHSS), which quantifies deficits in consciousness, gaze, visual fields, facial movement, limb strength, ataxia, sensation, language, dysarthria, and neglect. The score guides treatment decisions and predicts outcome. Time of symptom onset is critical for determining eligibility for thrombolysis (within 4.5 hours) or thrombectomy (up to 24 hours for selected patients with favorable imaging). Neuroimaging is essential for stroke evaluation. Non-contrast CT of the head is the initial imaging study, performed to exclude hemorrhage before considering thrombolysis. Ischemic changes may be subtle or absent in the first few hours. CT angiography (CTA) demonstrates the vascular anatomy and identifies large vessel occlusions amenable to thrombectomy. CT perfusion (CTP) can distinguish the ischemic core (irreversibly damaged tissue) from penumbra (at-risk but potentially salvageable tissue). MRI with diffusion-weighted imaging (DWI) is highly sensitive for acute ischemia within minutes of onset, and can be combined with perfusion imaging to identify penumbra. Vascular imaging modalities assess the cerebral circulation. Carotid duplex ultrasonography evaluates the cervical carotid arteries for stenosis and plaque. Transcranial Doppler can assess intracranial vessels including detection of vasospasm after subarachnoid hemorrhage. MR angiography (MRA) provides non-invasive imaging of intracranial and extracranial vessels, though it may overestimate stenosis. CT angiography offers rapid, detailed vascular imaging. Conventional catheter angiography remains the gold standard for vascular detail and is required for endovascular interventions. Vessel wall imaging with high-resolution MRI can detect vasculitis, dissection, and intracranial atherosclerotic plaque. Vascular imaging: Panel 1 - CT sequence in acute stroke: non-contrast (to exclude hemorrhage) → CTA (to identify occlusion) → CTP (to assess penumbra), with sample images showing each modality. Panel 2 - MRI diffusion-weighted imaging (DWI) showing hyperintense acute infarct with corresponding ADC map showing dark restricted diffusion. Panel 3 - MRA and CTA comparison showing Circle of Willis anatomy with example of MCA occlusion visible on both modalities. Panel 4 - Carotid duplex ultrasound showing normal vs stenotic internal carotid artery with spectral Doppler waveforms indicating high-grade stenosis. --- ## Summary - Cerebral blood supply derives from paired internal carotid arteries (anterior circulation, ~80%) and vertebral arteries (posterior circulation, ~20%) - The internal carotid artery terminates as the ACA and MCA; the vertebral arteries join to form the basilar artery, which terminates as the PCAs - The Circle of Willis connects anterior and posterior circulations, providing potential collateral pathways, but is complete in only ~25-50% of individuals - ACA supplies the medial frontal and parietal surfaces; ACA stroke causes contralateral leg weakness greater than arm - MCA has the largest territory (lateral convexity); MCA stroke causes contralateral face/arm weakness, aphasia (dominant) or neglect (non-dominant) - PCA supplies the occipital lobe and medial temporal lobe; PCA stroke causes contralateral homonymous hemianopia - Vertebrobasilar strokes cause brainstem syndromes with crossed findings (ipsilateral cranial nerve, contralateral motor/sensory) - Venous drainage is through superficial and deep systems into valveless dural sinuses, ultimately reaching the internal jugular veins - Stroke localization requires correlation of clinical deficits with arterial territories - Acute stroke imaging includes non-contrast CT, CTA/CTP, and DWI MRI for treatment decision-making --- ## Key Terms | Term | Definition | |------|------------| | Circle of Willis | Arterial anastomosis at skull base connecting anterior and posterior circulations | | Internal carotid artery | Major anterior circulation vessel supplying the anterior brain | | Middle cerebral artery | Largest ICA branch supplying lateral hemisphere; most common stroke site | | Anterior cerebral artery | Supplies medial frontal and parietal surfaces; leg motor/sensory cortex | | Posterior cerebral artery | Terminal basilar branch supplying occipital lobe and visual cortex | | Lenticulostriate arteries | MCA perforators supplying basal ganglia and internal capsule | | Watershed zone | Border territory between arterial territories vulnerable to hypoperfusion | | Dural venous sinus | Venous channel between dural layers draining cerebral veins | --- *This content is subject to the [MIT License](https://opensource.org/licenses/MIT). © 2024–2026 Hibbert School of Medicine.*