Cerebrovascular Anatomy

1. Two Vascular Territories

The brain is supplied by four arteries — two internal carotids and two vertebrals — that fuse, branch, and irrigate everything from the olfactory bulbs to the spinomedullary junction. They divide into two great functional systems:

The two systems anastomose anteriorly and posteriorly through the Circle of Willis, which provides the brain’s main collateral reserve. Outside the Circle, the cortical pial network and a handful of meningeal anastomoses are the only redundancy — which is why occlusions of distal cortical branches are usually unforgiving.

2. The Internal Carotid System

The internal carotid artery (ICA) arises from the common carotid bifurcation at the upper border of the thyroid cartilage (C3–C4 vertebral level), ascends without branching through the neck, enters the carotid canal of the petrous temporal bone, traverses the cavernous sinus in a sigmoid bend, and pierces the dura just medial to the anterior clinoid process to enter the subarachnoid space. Bouthillier’s classification divides it into seven segments:

Four branches emerge before the terminal bifurcation, each with a stroke phenotype of its own:

• Ophthalmic artery — the first intradural branch. Embolus here causes amaurosis fugax or central retinal artery occlusion (Hollenhorst plaque). A retinal TIA is a carotid TIA until proven otherwise — ipsilateral ICA imaging is mandatory.
• Posterior communicating artery (PCom) — runs posteriorly to anastomose with the P1 segment of the PCA, closing the posterior half of the Circle of Willis. PCom aneurysms classically compress CN III — presenting with painful, pupil-involving third-nerve palsy.
• Anterior choroidal artery (AChA) — small but mighty. Supplies the posterior limb of the internal capsule, medial globus pallidus, optic tract, lateral geniculate (lower part), and hippocampal/uncal cortex. Occlusion produces a classic triad of contralateral hemiplegia, hemianaesthesia, and homonymous hemianopia (the “triad of Foix”).
• Terminal bifurcation into ACA (medial hemisphere) and MCA (lateral hemisphere). The ICA terminus or “T-occlusion” is one of the most devastating large-vessel occlusions, infarcting both ACA and MCA territories simultaneously.

3. The Vertebrobasilar System

The vertebral arteries arise from the subclavians, ascend through the foramina transversaria of C6–C1, hook over the atlas in the suboccipital triangle, pierce the atlanto-occipital membrane and dura, and enter the posterior fossa to fuse at the pontomedullary junction into the basilar artery. The vertebrals (V1–V4) are uniquely vulnerable to dissection at V3 (the most mobile, atlantal segment) — chiropractic manipulation, sports trauma, or simply rotating the neck to back a car can shear the intima. Posterior-circulation stroke in patients under 45 is dissection until proven otherwise.

The vertebrobasilar tree, with each branch's territory:

Top-of-the-basilar syndrome (Caplan 1980) is the cataclysmic version: an embolus lodges at the basilar tip and infarcts both PCA territories, the rostral midbrain and bilateral thalami, producing coma, vertical gaze palsy, pupillary abnormalities, and cortical blindness. The “basilar artery occlusion” (BAO) carries ~80% mortality untreated — recanalisation is the only effective therapy.

Wallenberg’s lateral medullary syndrome (Adolf Wallenberg 1895) is the textbook case study in functional neuroanatomy: PICA occlusion infarcts the lateral medulla, cutting the spinothalamic tract (contralateral body pain/temperature loss), the spinal trigeminal nucleus (ipsilateral facial pain/temp loss), the descending sympathetic fibres (ipsilateral Horner), the vestibular nuclei (vertigo, nystagmus), the inferior cerebellar peduncle (ipsilateral ataxia), and nucleus ambiguus (dysphagia, hoarseness, ipsilateral palatal/vocal cord paralysis). A single lesion explains seven findings.

4. The Circle of Willis

The arterial polygon at the base of the brain — described by Thomas Willis in Cerebri Anatome (1664) and engraved by Christopher Wren — is the brain’s great anastomotic ring. Its component vessels:

• Two A1 segments of the ACAs, joined anteriorly by the anterior communicating artery (ACom).
• Two ICA termini, each giving off a posterior communicating artery (PCom).
• Two P1 segments of the PCAs, fed by the basilar tip.

In principle this allows blood to reach any hemisphere from any of the four feeding arteries. In practice, only ~40–50% of people have a textbook complete Circle. The remainder have one or more hypoplastic / absent segments — most commonly an absent or thread-like PCom or A1 — which dramatically affects collateral capacity when an upstream vessel occludes.

Common anatomical variants:

• Hypoplastic / absent A1 (~10%) — both ACAs fed by one ICA via ACom. ACom occlusion in this configuration infarcts both medial frontal lobes.
• Hypoplastic / absent PCom (~25%) — isolates the carotid and vertebrobasilar systems; no anterior–posterior collateral.
• Fetal-type PCA (~20%) — PCA arises from ICA via a dominant PCom, with hypoplastic P1; occipital infarct from a carotid occlusion.
• Azygos ACA — a single, unpaired ACA supplies both medial hemispheres.
• Persistent trigeminal artery / hypoglossal artery — embryonic remnants connecting carotid to basilar; usually incidental.

Functionally, the Circle is a conditional collateral — vessels open up only when a pressure gradient develops across them. In a slow-progression carotid stenosis, the contralateral ICA reverses flow through the ACom and recruits the ipsilateral ACom and PCom; in an acute occlusion the same anatomy may not be functional quickly enough to save the penumbra.

5. MCA Territory

The middle cerebral artery is the largest branch of the ICA and supplies the bulk of the lateral cerebral hemisphere — ~two-thirds of one cerebral hemisphere by volume. It is the most common site of large-vessel occlusion (LVO) and the workhorse vessel of stroke practice. Its segmental anatomy:

At the M1–M2 junction, the MCA classically bifurcates into a superior and an inferior division (occasionally trifurcates). The two divisions drape over opposite banks of the Sylvian fissure and supply distinct cortical territories:

An M1 occlusion proximal to the bifurcation kills both divisions plus the lenticulostriate perforators, producing a malignant complete-MCA syndrome with dense hemiplegia, hemisensory loss, hemianopia, global aphasia (dominant) or profound neglect (non-dominant), and forced gaze deviation toward the side of the lesion. Edema after large MCA infarcts can become life-threatening (“malignant MCA syndrome”) by day 2–5, an indication for hemicraniectomy in selected younger patients.

6. ACA Territory

The anterior cerebral artery courses medially from the ICA terminus, meets its mate at the ACom, then turns dorsally over the genu of the corpus callosum and runs posteriorly along its dorsal surface as the pericallosal artery. Its segmental anatomy (A1 precommunicating; A2 infracallosal; A3 precallosal; A4 supracallosal; A5 postcallosal) maps to a stable cortical territory: the medial surface of the frontal and parietal lobes from the orbital cortex to the precuneus, plus the anterior 4/5 of the corpus callosum.

Key cortical functions in this territory:

• Primary motor & sensory cortex for the lower limb (paracentral lobule) — this is the ACA's signature deficit: contralateral leg weakness with relatively spared face and arm.
• Supplementary motor area (SMA) — lesion produces transcortical motor aphasia (dominant) or akinetic mutism (large bilateral lesions).
• Cingulate gyrus — bilateral cingulate damage causes akinetic mutism: the patient is awake, follows with the eyes, but does not speak or move spontaneously.
• Medial prefrontal & orbitofrontal cortex — disinhibition, abulia, primitive reflexes (grasp, root, palmomental), urinary incontinence (bilateral medial frontal cortex contains a continence centre).
• Corpus callosum — large strokes produce a callosal disconnection syndrome: ideomotor apraxia of the left hand, alien-hand phenomenon, anomia for objects in the left visual field.

ACA infarcts are uncommon (~3% of ischaemic strokes); when they occur in isolation, the source is usually embolic from cardiac or carotid origin, or stenosis of the A1 segment. Bilateral ACA infarcts can occur from a single ACom region embolism in patients with an azygos ACA or hypoplastic A1.

7. PCA Territory

The posterior cerebral arteries arise from the basilar bifurcation, course laterally around the cerebral peduncles, and sweep over the medial temporal and occipital surfaces. Segments: P1 (precommunicating, between basilar and PCom), P2 (ambient cistern, around the midbrain), P3 (quadrigeminal), P4 (calcarine).

PCA territory is functionally tripartite:

Alexia without agraphia (Déjérine 1892) is the classic left PCA syndrome: an infarct of the left occipital cortex plus the splenium of the corpus callosum disconnects the right (intact) visual cortex from the left language cortex. The patient cannot read but can write — and then cannot read what she has just written. A single elegant lesion confirms left-hemispheric dominance for language and the corpus callosum's role in interhemispheric transfer.

Artery of Percheron. A normal anatomical variant in ~7% of brains: a single thalamoperforator arises from one P1 and supplies both paramedian thalami. Its occlusion produces bilateral paramedian thalamic infarcts with abrupt coma, vertical gaze palsy, and amnesia — and frequently tricks the radiology reader because the territory is bilateral and looks like an encephalitis or metabolic insult.

8. Perforating & Penetrating Arteries

The perforators are the terminal end-arteries of the brain — tiny (~100–400 μm), unbranched vessels that arise at right angles from the proximal great arteries and bury straight down into deep grey matter and white matter. They have no collaterals. They are the substrate of small-vessel disease, and small-vessel disease drives ~25% of ischaemic strokes, the great majority of vascular cognitive impairment, and (when their walls weaken under chronic hypertension and burst) the bulk of deep ICH. They deserve a chapter of their own.

The four major perforator pools:

8.1 Lacunar syndromes — the perforator alphabet

Fisher (1965, 1978, 1982) catalogued the small deep infarcts of the cerebral hemispheres and brainstem — lacunes — and showed that despite the small lesion size (< 1.5 cm), they cluster into a handful of stereotyped clinical syndromes. Recognising a lacunar syndrome at the bedside has practical consequences: large-vessel occlusion is unlikely, thrombectomy is not indicated, and the underlying biology is hypertensive small-vessel disease (lipohyalinosis, microatheroma) rather than embolism. The classic five:

Lipohyalinosis (Fisher) is the small-vessel biology behind these lesions: chronic hypertension drives plasma protein insudation into the wall of perforators, replacing smooth muscle with a glassy fibrinoid; the lumen narrows and eventually thromboses, producing a small infarct, or the wall ruptures, producing deep hypertensive ICH (basal ganglia, thalamus, pons, cerebellum). Charcot and Bouchard described microaneurysms on these same vessels in 1868 — the proximate haemorrhagic lesion.

9. Watershed Zones

At the boundaries between major arterial territories, perfusion is supplied by the most distal pial branches of two adjacent arteries — tissue at the “end of the line” from both sides. These watershed (border-zone) regions have the lowest baseline perfusion pressure of any brain region. When systemic blood pressure drops or a proximal stenosis limits inflow, they are the first to fail. Watershed infarcts are therefore the signature of low-flow / haemodynamic ischaemia — a different physiology from embolism or thrombotic occlusion.

Three classic watershed zones:

Mechanism. Cerebral autoregulation (Lassen) maintains constant CBF over a wide range of mean arterial pressures (~60–160 mmHg) by myogenic adjustment of arteriolar tone. When inflow is limited proximally — severe carotid stenosis, hypotensive crisis, cardiac arrest with prolonged hypoperfusion — the watershed is the first to cross below the ischaemic threshold because it has the highest resistive distance from the feeding artery. The CBF–CPP relation is approximately \(\text{CBF} = \text{CPP} / \text{CVR}\), and during failed autoregulation CBF tracks CPP linearly — the watershed is where the line first crosses the ~20 mL/100 g/min infarction threshold.

Imaging signature: bilateral or unilateral DWI hyperintensities in a wedge along the parasagittal frontoparietal cortex, in a deep linear/string pattern in the corona radiata, or both. Their presence on MRI demands a search for proximal stenosis (carotid duplex, CTA) and global hypoperfusion (cardiac arrest, sepsis, peri-operative hypotension, profound anaemia).

10. Venous Anatomy & Cerebral Venous Sinus Thrombosis

Cerebral venous drainage is a two-tier system: superficial cortical veins drain the cortex into the dural venous sinuses, and deep cerebral veins drain the subcortical grey and white matter into the great vein of Galen and the straight sinus. The dural sinuses are valveless venous channels enclosed between layers of dura mater — they cannot collapse, but they can occlude.

• Superior sagittal sinus (SSS) — runs along the upper margin of the falx, drains both cerebral hemispheres' superolateral surfaces. Receives CSF from arachnoid villi. Thrombosis: bilateral parasagittal infarcts/haemorrhages, raised ICP from CSF reabsorption failure (papilloedema, headache, seizure).
• Transverse / sigmoid sinuses — from the confluence of sinuses (torcula) laterally to the jugular bulb. Often asymmetric; the right side is dominant in most. Thrombosis: temporal lobe infarction, ipsilateral mastoid pain.
• Cavernous sinuses — lateral to the sella turcica, traversed by the ICA and CN III, IV, V₁, V₂, VI. Thrombosis (often septic, from facial / sphenoidal infections): proptosis, chemosis, painful ophthalmoplegia, sensory loss in V₁/V₂; bilateral involvement typical because the two cavernous sinuses communicate.
• Straight sinus / vein of Galen — drains deep structures (basal ganglia, thalami, deep white matter). Thrombosis is among the most lethal: bilateral thalamic / basal ganglionic oedema, depressed consciousness.
• Cortical veins — bridging veins traverse the subdural space to reach the SSS. Their tearing produces subdural haematoma after acceleration trauma in the elderly; their thrombosis produces focal cortical infarct/haemorrhage.

Cerebral venous sinus thrombosis (CVST) is an under-recognised stroke mimic. Hallmark features:

• Younger patients, female predominance (3:1) — pregnancy, puerperium, oral contraceptives, hereditary thrombophilia, dehydration, malignancy, infection (mastoiditis, sinusitis), and post-vaccinal syndromes (vaccine-induced thrombotic thrombocytopenia, VITT).
• Subacute headache (~90%) — the most common presentation; often the only feature for days.
• Seizures (~40%) — far more common than in arterial stroke.
• Focal deficits that cross arterial territories — e.g. bilateral parasagittal weakness from SSS thrombosis.
• Raised ICP picture (papilloedema, sixth-nerve palsy).
• Imaging: empty-delta sign on contrast CT (filling defect in SSS), absent flow on MR/CT venogram — the diagnostic confirmation.

Treatment is anticoagulation (heparin acutely, transitioning to warfarin or DOAC) even in the presence of associated haemorrhagic infarction — the haemorrhage is venous in origin and continued clot propagation is the dominant threat. Endovascular thrombectomy is reserved for clinical deterioration despite anticoagulation.