Cerebral Blood Supply & Circle of Willis

The brain is perfused by two paired arterial systems — the internal carotid (anterior) circulation and the vertebrobasilar (posterior) circulation — anastomosing at the base of the brain through the Circle of Willis. This single topic stitches together pure anatomy MCQs (branches, communicating arteries, aneurysm sites) and applied neurology (stroke territory localisation, watershed infarcts). Master the territory maps and you can answer a "lesion-to-deficit" question without memorising tables.

Overview: the two arterial systems

The brain receives roughly 15–20% of cardiac output and consumes ~20% of total body oxygen despite being only ~2% of body weight — hence its exquisite sensitivity to ischaemia.

Feature	Anterior (carotid) system	Posterior (vertebrobasilar) system
Origin	Internal carotid artery (ICA)	Vertebral arteries (from subclavian)
Supplies	Most of cerebral hemispheres, eye, basal ganglia, internal capsule	Brainstem, cerebellum, occipital lobe, inferomedial temporal lobe, thalamus
Main terminal branches	ACA + MCA	Two PCAs (from basilar tip)
Proportion of cerebral flow	~80%	~20%

High-yield: The ICA has no branches in the neck — the first branch is the ophthalmic artery, given off intracranially after the artery emerges from the cavernous sinus. A neck branch should make you suspect the external carotid.

Internal carotid artery — segments and branches

The classic surgical/Bouthillier nomenclature divides the ICA into seven segments (C1 cervical → C7 communicating). For exams, remember the four branches and four terminal branches:

• Ophthalmic artery — first major intracranial branch; supplies the retina via the central artery of the retina (an end-artery → its occlusion causes amaurosis fugax / sudden monocular blindness).
• Posterior communicating artery (PComm) — links ICA to PCA.
• Anterior choroidal artery — supplies the posterior limb of internal capsule, optic tract, choroid plexus, parts of midbrain. Occlusion → contralateral hemiplegia, hemianaesthesia, homonymous hemianopia (the classic triad).
• Terminal bifurcation → anterior cerebral artery (ACA) and middle cerebral artery (MCA).

The Circle of Willis — anatomy

An arterial polygon in the interpeduncular fossa / suprasellar cistern, encircling the optic chiasma, infundibulum, and structures of the interpeduncular fossa. It equalises pressure between the two carotids and provides collateral circulation.

Constituent vessels (flow direction):

1. Two anterior cerebral arteries (ACAs) — connected anteriorly by the single
2. Anterior communicating artery (AComm)
3. Two internal carotid arteries (contributing at the bifurcation)
4. Two posterior communicating arteries (PComm) — connecting ICA to
5. Two posterior cerebral arteries (PCAs) — connected posteriorly to the
6. Basilar artery (single, formed by the union of the two vertebral arteries)

So the circle is completed: AComm → ACA → ICA → PComm → PCA → basilar → (back to PCA).

High-yield: The Circle of Willis is complete and "textbook normal" in only ~20–40% of individuals. Anatomical variants are the rule, not the exception.

Mnemonic for the circle's arteries (anterior to posterior): "A Big Pizza Pie, Apple Pie" → AComm, Basilar contribution, PComm, PCA, ACA, ICA — but more reliably just learn the polygon visually.

Common anatomical variants

Variant	Description	Significance
Fetal-type PCA	PCA supplied mainly by PComm from ICA rather than basilar (PComm large, P1 hypoplastic)	Carotid disease can cause occipital/PCA-territory stroke; ~20–30%
Hypoplastic/absent PComm	One or both PComm tiny	Poor posterior collateral
Hypoplastic A1 segment	One ACA proximal segment small	Both ACAs may fill from one ICA via AComm
Azygos ACA	Single midline ACA trunk	Bilateral ACA infarct if occluded
Persistent trigeminal artery	Embryonic carotid-basilar anastomosis persists	Most common persistent fetal carotid–vertebrobasilar anastomosis

High-yield: A hypoplastic A1 plus an AComm aneurysm is a classic high-flow setup — the AComm carries cross-flow, predisposing to aneurysm.

Cortical arterial territories

Knowing the three cerebral arteries' cortical maps lets you reverse-engineer the artery from a deficit.

Anterior cerebral artery (ACA)

• Supplies the medial surface of the frontal and parietal lobes (up to the parieto-occipital sulcus) and the leg area of the motor/sensory homunculus (paracentral lobule).
• Occlusion → contralateral leg > arm/face weakness and sensory loss, urinary incontinence, abulia, and (if anterior) frontal release signs / grasp reflex.

Middle cerebral artery (MCA)

• The largest terminal branch of the ICA and the most commonly occluded cerebral vessel; supplies the lateral convexity of the hemisphere and (via lenticulostriate branches) deep structures.
• Occlusion (main stem) → contralateral face & arm > leg weakness and sensory loss, homonymous hemianopia, gaze deviation towards the lesion, and aphasia (dominant) or hemineglect (non-dominant).

High-yield ACA vs MCA rule: Leg = ACA, Face/Arm = MCA. The homunculus medial→leg, lateral→face/arm.

Posterior cerebral artery (PCA)

• Supplies the occipital lobe (visual cortex), inferomedial temporal lobe, and (via deep branches) thalamus and midbrain.
• Occlusion → contralateral homonymous hemianopia with macular sparing (dual supply of occipital pole by MCA), alexia without agraphia (dominant), visual agnosia. Bilateral PCA → cortical blindness (Anton syndrome if denial).

Deep perforators (lacunar territory)

• Lenticulostriate arteries (from MCA M1) supply the internal capsule, basal ganglia — classic site of hypertensive haemorrhage (putamen) and lacunar infarcts (pure motor stroke = posterior limb internal capsule).
• Recurrent artery of Heubner (from ACA, near AComm) supplies the head of caudate and anterior internal capsule.
• Artery of Percheron — a single trunk from one PCA (P1) supplying bilateral paramedian thalami ± midbrain; occlusion → bilateral thalamic infarct with altered consciousness.

Stroke territory localisation — flow approach

A practical stepwise approach to "given a deficit, name the artery":

Step 1: Cortical signs (aphasia, neglect, hemianopia) present? → cortical (large vessel) stroke. Pure motor/sensory only? → lacunar (deep perforator).

Step 2: Pattern of weakness → Face/arm > leg → MCA | Leg > arm → ACA | Crossed (ipsilateral face, contralateral body) → brainstem (vertebrobasilar).

Step 3: Visual field cut with macular sparing → PCA (occipital).

Step 4: Brainstem signs (vertigo, diplopia, dysphagia, crossed findings) → posterior circulation.

So: deficit pattern → cortical vs deep → anterior vs posterior → specific artery.

High-yield: Lateral medullary (Wallenberg) syndrome = occlusion of PICA / vertebral artery. Features: ipsilateral facial sensory loss, Horner syndrome, ataxia, palatal/vocal cord palsy (dysphagia, hoarseness) + contralateral body pain/temperature loss — a classic crossed sensory pattern. Medial medullary = anterior spinal artery → contralateral hemiplegia + ipsilateral tongue weakness (CN XII) + contralateral position/vibration loss.

Watershed (border-zone) infarcts

Occur at the junction between two arterial territories, where perfusion pressure is lowest. Caused by global hypoperfusion (hypotension, cardiac arrest, severe carotid stenosis) rather than embolism.

Watershed zone	Location	Clinical picture
Cortical (external) border zone	Between ACA–MCA and MCA–PCA	Proximal arm/shoulder weakness — "man-in-a-barrel" syndrome; transcortical aphasia
Internal (subcortical) border zone	Between deep & superficial MCA perforators (corona radiata/centrum semiovale)	"Rosary-bead" / linear infarcts; worse prognosis, often progressive

High-yield: The man-in-the-barrel syndrome (bilateral proximal upper limb weakness with spared distal/lower limbs) localises to bilateral ACA–MCA cortical watershed infarction after a hypotensive insult.

Berry (saccular) aneurysms

Arise at arterial bifurcations of the Circle of Willis, where the media is congenitally deficient. ~85% occur in the anterior circulation.

Frequency of sites (descending):

1. Anterior communicating artery (AComm) — most common site overall (~30–35%).
2. Posterior communicating artery (PComm) / ICA–PComm junction (~25%).
3. MCA bifurcation (~20%).
4. ICA terminus / basilar tip / PICA — posterior circulation aneurysms.

High-yield: A PComm aneurysm classically causes a painful third nerve (CN III) palsy with a fixed, dilated pupil (pupil-involving, because the superficial parasympathetic fibres are compressed). A pupil-sparing CN III palsy suggests ischaemic/diabetic microvascular cause.

• Rupture → subarachnoid haemorrhage (SAH) — "thunderclap headache", worst of life, neck stiffness.
• Investigation of choice for SAH: non-contrast CT head (sensitivity highest within 6 h); if negative but suspicion high → lumbar puncture for xanthochromia (peaks 12 h, may need 6–12 h after onset).
• Definitive vascular imaging: CT angiography / DSA (gold standard).
• Associations: autosomal dominant polycystic kidney disease (ADPKD), Ehlers-Danlos type IV, coarctation of aorta, fibromuscular dysplasia.

Charcot–Bouchard microaneurysms (distinct from berry) are tiny aneurysms of lenticulostriate perforators in chronic hypertension → cause intracerebral (not subarachnoid) haemorrhage, typically in the basal ganglia/putamen.

Venous drainage (briefly, exam-relevant)

Cerebral veins → dural venous sinuses → internal jugular vein. Key facts:

• Superior sagittal sinus — thrombosis causes parasagittal (bilateral leg) infarcts; common in dehydration, pregnancy, prothrombotic states.
• Cavernous sinus contents: CN III, IV, V1, V2, and VI plus the ICA. CN VI lies most medial (next to ICA) → first affected in cavernous sinus thrombosis.
• Great cerebral vein of Galen → straight sinus.

Diagnosis & investigation of choice

Scenario	Investigation of choice
Acute stroke (rule out bleed)	Non-contrast CT head (first-line)
Early ischaemic stroke / posterior fossa	Diffusion-weighted MRI (DWI) — most sensitive for early infarct
Vessel occlusion / LVO before thrombectomy	CT angiography
Subarachnoid haemorrhage	Non-contrast CT, then LP if negative
Aneurysm/AVM definitive map	Digital subtraction angiography (DSA) — gold standard
Carotid stenosis screen	Carotid Doppler ultrasound

Management / drug of choice (overview)

• Acute ischaemic stroke: IV alteplase (rt-PA) within 4.5 hours of onset (after excluding haemorrhage); mechanical thrombectomy for large-vessel occlusion up to 24 h in selected patients.
• Acute antiplatelet: aspirin 300 mg once thrombolysis excluded/completed.
• Secondary prevention: antiplatelet (aspirin/clopidogrel), statin, BP and glycaemic control; anticoagulation if cardioembolic (AF).
• Aneurysmal SAH: secure aneurysm by endovascular coiling (preferred) or surgical clipping; oral nimodipine to prevent vasospasm-related delayed cerebral ischaemia.

High-yield: Nimodipine (a calcium-channel blocker) is the drug of choice to reduce delayed ischaemic deficit after aneurysmal SAH — it improves neurological outcome, not by preventing radiographic vasospasm per se.

Complications

• Vasospasm & delayed cerebral ischaemia (peak day 4–14 post-SAH).
• Hydrocephalus (communicating, from blood in subarachnoid space).
• Rebleeding (highest risk in first 24 h if aneurysm unsecured).
• Haemorrhagic transformation of an ischaemic infarct, especially after thrombolysis.
• Malignant MCA infarction with cerebral oedema → may need decompressive hemicraniectomy.
• Cerebral salt wasting / SIADH causing hyponatraemia after SAH.

Key differentials

• Ischaemic vs haemorrhagic stroke — clinically indistinguishable; CT mandatory before thrombolysis.
• SAH vs migraine vs meningitis — thunderclap headache + neck stiffness needs CT/LP.
• Lacunar vs cortical stroke — absence of cortical signs (aphasia, neglect, visual field loss) favours lacunar.
• Wallenberg (PICA) vs medial medullary (ASA) — crossed sensory vs hemiplegia + tongue.
• Berry vs Charcot–Bouchard aneurysm — subarachnoid vs intraparenchymal (basal ganglia) bleed.

Recently asked / exam angle

• "Most common site of berry aneurysm" → anterior communicating artery.
• A diagram-based MCA/ACA/PCA territory map with an arrow → name the artery / expected deficit.
• "Painful CN III palsy with dilated pupil" → PComm aneurysm.
• "Sudden monocular blindness" → central retinal / ophthalmic artery (branch of ICA).
• "Bilateral proximal arm weakness after cardiac arrest" → watershed (ACA–MCA) infarct, man-in-a-barrel.
• Lateral medullary syndrome features and the vessel (PICA/vertebral).
• "First branch of internal carotid artery" → ophthalmic artery (no cervical branches).
• "Artery supplying posterior limb of internal capsule" → anterior choroidal artery.
• Investigation of choice for SAH (CT → LP) and for early infarct (DWI-MRI).
• ADPKD association with berry aneurysm/SAH.

Rapid revision

1. ICA gives no branches in the neck; first branch = ophthalmic artery.
2. Circle of Willis is anatomically complete in only ~20–40% of people.
3. AComm = commonest berry aneurysm site; ~85% of aneurysms are anterior circulation.
4. PComm aneurysm → painful, pupil-involving CN III palsy.
5. Leg weakness = ACA; face/arm = MCA; hemianopia with macular sparing = PCA.
6. MCA is the most commonly occluded cerebral artery.
7. Lenticulostriate (MCA) perforators → internal capsule lacunes & hypertensive putaminal bleed.
8. Anterior choroidal artery → posterior limb internal capsule, optic tract (triad of hemiplegia, hemianaesthesia, hemianopia).
9. Wallenberg = PICA/vertebral; crossed sensory + Horner + dysphagia.
10. Watershed infarcts follow global hypoperfusion; man-in-a-barrel = ACA–MCA border zone.
11. Charcot–Bouchard microaneurysms cause intracerebral (basal ganglia) haemorrhage, not SAH.
12. Nimodipine prevents delayed ischaemia after SAH; alteplase ≤4.5 h for acute ischaemic stroke.