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Anatomy

Circle of Willis: Anatomy, Variants, and Significance in Stroke

WhiteCoat Pro Editorial BoardApril 11, 2026Updated September 16, 20265 min read
Contents · 13 sections
  1. 1. Constituent arteries
  2. 2. Source of cerebral blood supply
  3. 3. Anterior cerebral artery (ACA)
  4. 4. Middle cerebral artery (MCA)
  5. 5. Posterior cerebral artery (PCA)
  6. 6. Communicating arteries
  7. 7. Variants and anomalies
  8. 8. Clinical syndromes of occlusion
  9. 9. Collateral circulation
  10. 10. Aneurysms
  11. 11. Neuroimaging
  12. 12. Surgical and endovascular interventions
  13. 13. FAQ

In a nutshell. The circle of Willis is an anastomotic ring at the base of the brain connecting the carotid and vertebrobasilar systems. Components: two anterior cerebral arteries (ACAs) and one anterior communicating artery (AComA), two internal carotid arteries, two posterior communicating arteries (PComAs), two posterior cerebral arteries (PCAs), basilar artery. A complete circle is present in only 20–50% of people. It allows compensation for the occlusion of a single main trunk, but in cases of hypoplasia (ACA A1 segment, PCA P1 segment, PComA), collateralization is limited. MCA syndrome is a typical "stroke" with contralateral hemiparesis; PCA causes homonymous hemianopia; ACA causes leg paresis and abulia.

1. Constituent arteries

  • Anterior: two ACAs + AComA.
  • Lateral: two internal carotid arteries (ICAs).
  • Communicating: two PComAs between the ICA and PCA.
  • Posterior: two PCAs + basilar artery.
  • The anterior part is the ICA territory, and the posterior part is the vertebrobasilar system.

2. Source of cerebral blood supply

  • Anterior circulation (internal carotid arteries, ~75%): ACA, MCA, anterior choroidal, ophthalmic.
  • Posterior circulation (vertebral + basilar, ~25%): PCA, cerebellar arteries (PICA, AICA, SCA), brainstem branches.
  • The circle provides a potential "bridge" between vascular territories.

3. Anterior cerebral artery (ACA)

  • Branches off the ICA, courses medially toward the longitudinal cerebral fissure.
  • Segments: A1 (from ICA to AComA), A2 (distal to AComA, anterior to the genu of the corpus callosum), A3, A4, A5.
  • A1 gives off branches — lenticulostriate (recurrent artery of Heubach), supplies basal ganglia and anterior optic chiasm.
  • Supply area: medial surface of the frontal and parietal lobes, cingulate gyrus, anterior corpus callosum.

4. Middle cerebral artery (MCA)

  • The largest terminal branch of the ICA.
  • Segments: M1 (horizontal, up to bifurcation), M2 (in the Sylvian fissure), M3, M4.
  • M1 gives off lenticulostriate branches to the basal ganglia and internal capsule.
  • Supply area: lateral surface of the frontal, parietal, and temporal lobes, insula, lateral part of the lentiform nucleus, caudate nucleus, internal capsule.

5. Posterior cerebral artery (PCA)

  • Arises from the basilar artery (in 70–80%); in 10–20% of cases — from the PComA (fetal PCA).
  • Segments: P1 (to PComA), P2 (winds around the cerebral peduncle from PComA), P3 (in the occipitotemporal sulcus), P4.
  • Branches to the thalamus (paramedian, thalamoperforating, thalamogeniculate).
  • Supply area: occipital lobe, medial surface of the temporal lobe, thalamus, midbrain, choroid plexus of the lateral ventricle.

6. Communicating arteries

AComA

  • Short (≤ 4 mm), connects the two ACAs.
  • Gives off small branches to the hypothalamus and optic chiasm.
  • Most frequent site for aneurysms (30–35% of intracranial aneurysms).

PComA

  • Connects the ICA and PCA.
  • Close proximity to the III cranial nerve — PCoA aneurysm → n. oculomotorius palsy.
  • Branches to the thalamus and cerebral peduncle.

7. Variants and anomalies

  • A complete classical circle is present in only 20–50% of people.
  • Hypoplasia/agenesis of the ACA A1 segment — 10%.
  • PComA hypoplasia — up to 30%.
  • Fetal PCA (arising from the PComA rather than the basilar) — 10–20%.
  • Azygos ACA (single median trunk of both ACAs) — rare.
  • ICA trifurcation (ACA + MCA + PCA originating from a single ICA).
  • Significance: determines collateralization during occlusion and stroke patterns in vascular insufficiency.

8. Clinical syndromes of occlusion

ArteryClinical Practice
ACAContralateral leg paresis (greater), aspontaneity, incontinence, abulia
MCA (M1)Contralateral hemiparesis (face and arm), hemihypesthesia, aphasia (dominant), hemianopia, gaze palsy
LenticulostriateLacunar syndromes: pure motor, pure sensory, sensorimotor, ataxic hemiparesis, dysarthria-clumsy hand
PCAHomonymous hemianopia (with macular sparing), alexia without agraphia (dominant), prosopagnosia
Thalamic branchesDejerine-Roussy syndrome (hypesthesia + pain), impaired consciousness in bilateral paramedian occlusion
BasilarLocked-in syndrome, quadriparesis, dysarthria, impaired consciousness
Vertebral / PICAWallenberg syndrome (lateral medullary)

9. Collateral circulation

  • Via the circle of Willis — the main pathway during ICA or basilar occlusion.
  • Extra-/intracranial anastomoses: ophthalmic artery (collateral flow from the external carotid during ICA occlusion), leptomeningeal anastomoses between MCA/ACA/PCA.
  • Efficacy depends on the completeness of the circle and the rate of occlusion development (acute is worse, chronic allows collaterals to form).

10. Aneurysms

  • 80–90% of intracranial aneurysms are located in the circle of Willis and its branches.
  • Locations: ACoA (30–35%), PCoA (30%), MCA bifurcation (20%), basilar apex (10%).
  • Rupture causes subarachnoid hemorrhage (SAH) with severe headache, nuchal rigidity, and impaired consciousness.
  • Diagnostics: CT (95% sensitivity in the first 6 h), CT angiography, LP if CT is negative.
  • Treatment: clipping or endovascular coiling; choice of method depends on location and anatomy.

11. Neuroimaging

  • CT angiography (CTA) — rapid method, good detail, standard for suspected occlusion/aneurysm.
  • MR angiography (MRA, TOF) — non-contrast, suitable for elective screening.
  • Digital subtraction angiography (DSA) — gold standard for detailed evaluation and simultaneous treatment.
  • TCD — real-time blood flow assessment, spasm after SAH.

12. Surgical and endovascular interventions

  • Aneurysm clipping — open neurosurgery.
  • Endovascular coiling with/without stent or flow-diverter.
  • Carotid endarterectomy — for stenosis > 70% (symptomatic) or > 60% (asymptomatic in men).
  • Carotid stenting — alternative to endarterectomy.
  • Thrombectomy for acute ischemic stroke in the M1/ICA territory — 6-hour window (up to 24 h with perfusion imaging).

13. FAQ

Why is the circle of Willis often "incomplete"?
Embryonic development is variable: hypoplasia and asymmetry are normal. It is clinically significant only when collateralization is required — during occlusions or surgical interventions.

Why are ACoA aneurysms more common?
Turbulence and hemodynamic stress on the vessel wall occur at the bifurcation and flow inflection point. The ACoA is short and experiences the highest pressure.

What is "top of the basilar syndrome"?
Occlusion of the distal basilar artery and both P1 segments of the PCA — bilateral thalamic and occipital infarction: impaired consciousness, pupillary defects, blindness, hallucinations.

How to identify a fetal PCA and why is it important?
The PCA originates from the PCoA due to P1 hypoplasia; in ICA occlusion, the PCA is also affected. This is important when planning carotid surgery.

What is the HINTS test?
Head impulse, Nystagmus type, Test of Skew — in patients with acute dizziness: helps detect posterior circulation stroke despite a normal CT; sensitivity is higher than early MRI.

See also: Stroke · SAH · Aorta · CSF · Anatomy Catalog

This material is educational in nature and does not replace a doctor's consultation. Verify treatment regimens and dosages with current clinical guidelines.

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