Vascular Territories & Stroke Syndromes

Few exercises reward the localizing neurologist as reliably as the acute stroke. The arterial supply of the brain is orderly, and each major vessel feeds a predictable patch of cortex, white matter, or brainstem. Because the homunculus, the visual pathways, and the language network sit in fixed locations, the pattern of deficits at the bedside frequently names the occluded artery before the scanner confirms it. Master a handful of templates and you can localize most strokes from the history and exam alone.

The Two Circulations

The brain receives blood from two paired systems that join at the circle of Willis:

• Anterior circulation — the internal carotid arteries and their branches (anterior cerebral and middle cerebral arteries). Supplies most of the cerebral hemispheres: frontal, parietal, and lateral temporal lobes, plus the deep gray and internal capsule. Clinically dominated by hemispheric signs — hemiparesis, hemisensory loss, aphasia, neglect, and visual field cuts.
• Posterior circulation — the paired vertebral arteries unite to form the basilar artery, which gives rise to the posterior cerebral arteries. Supplies the brainstem, cerebellum, thalamus, and occipital (and inferomedial temporal) lobes. Clinically dominated by the "D" symptoms — dizziness, diplopia, dysarthria, dysphagia — together with crossed signs and visual field loss.

A practical bedside rule: cortical signs (aphasia, neglect, hemianopia) point to the carotid/MCA–ACA system; crossed signs (ipsilateral cranial nerve plus contralateral long tract) and prominent ataxia, vertigo, or diplopia point to the vertebrobasilar system.

Anterior Cerebral Artery (ACA)

The ACA sweeps over the corpus callosum to supply the medial frontal and parasagittal cortex — the territory that contains the leg area of the motor and sensory homunculus, folded down onto the interhemispheric surface. The signature is therefore weakness and sensory loss that are worse in the contralateral leg than in the arm or face, the mirror image of the MCA pattern.

• Contralateral leg-predominant weakness and sensory loss (foot and proximal leg most affected; face usually spared).
• Abulia — reduced spontaneity of speech, thought, and movement from medial frontal (supplementary motor / cingulate) involvement; bilateral ACA infarction (a risk with a shared "azygos" ACA or anterior communicating artery aneurysm clipping) can produce akinetic mutism.
• Urinary incontinence from involvement of the paracentral lobule (medial cortical micturition area).
• Transcortical motor aphasia with dominant-hemisphere lesions — sparse, effortful output with strikingly preserved repetition.
• Other medial-frontal release phenomena may appear, including a contralateral grasp reflex.

Middle Cerebral Artery (MCA)

The MCA is the largest cerebral artery and the most common site of large-vessel occlusion. It supplies the lateral convexity of the hemisphere — the face and arm regions of the homunculus, the optic radiations, and, in the dominant hemisphere, the perisylvian language network. The hallmark is contralateral weakness and sensory loss affecting the face and arm more than the leg.

• Contralateral face- and arm-predominant weakness and sensory loss (leg relatively spared).
• Contralateral homonymous hemianopia from optic radiation involvement.
• Conjugate eye deviation toward the lesion in large strokes — the intact contralateral frontal eye field drives the eyes "away from the weak side."

Dominant hemisphere (usually left): aphasia. The MCA's two main cortical divisions map roughly onto the two classic language syndromes:

• Superior division (frontal opercular branches) → predominantly Broca-type (non-fluent, expressive) aphasia, often with face/arm weakness.
• Inferior division (temporoparietal branches) → predominantly Wernicke-type (fluent, receptive) aphasia, often with a superior visual field cut and little or no weakness.
• Occlusion of the MCA stem proximal to the bifurcation can cause a global aphasia with dense hemiplegia.

Non-dominant hemisphere (usually right): neglect syndromes — contralateral (typically left) hemispatial neglect, anosognosia (denial of deficit), extinction to double simultaneous stimulation, and dressing/constructional apraxia. Aprosodia (loss of emotional speech intonation) parallels the dominant-side language deficits.

Posterior Cerebral Artery (PCA)

The PCA supplies the occipital lobe (primary visual cortex) and the inferomedial temporal lobe, and its proximal perforators feed parts of the thalamus and midbrain.

• Contralateral homonymous hemianopia — typically with macular sparing, because the occipital pole (which represents the macula) often receives collateral supply from MCA branches.
• Alexia without agraphia with dominant (usually left) PCA infarction that damages the left occipital cortex and the splenium of the corpus callosum — patients can write but cannot read what they have written (a classic disconnection syndrome).
• Thalamic involvement (from PCA perforators) → contralateral hemisensory loss and the delayed, burning thalamic (Dejerine–Roussy) pain syndrome.
• Bilateral PCA / occipital infarction can produce cortical blindness, sometimes with denial of the deficit (Anton syndrome).

Lacunar Syndromes

Lacunes are small infarcts (classically <15 mm) in the territory of a single deep penetrating artery — the lenticulostriate branches of the MCA, thalamoperforators, and pontine perforators of the basilar — usually from lipohyalinosis driven by chronic hypertension and diabetes. Because these vessels feed deep structures (internal capsule, basal ganglia, thalamus, pons) and not the cortex, the defining feature is the absence of higher cortical signs: no aphasia, no neglect, no loss of consciousness. A homonymous field cut is not itself a cortical sign — it is a retrochiasmal visual-pathway sign (optic tract, optic radiations, thalamic/LGN, or occipital cortex) — but the small deep penetrator territories of classic lacunes do not include that pathway, so a field cut is characteristically absent and its presence argues against a pure lacune. The five classic syndromes are:

• Pure motor hemiparesis — the most common; face, arm, and leg equally weak without sensory or cortical signs. Localizes to the posterior limb of the internal capsule or the basis pontis.
• Pure sensory stroke — contralateral hemisensory loss alone, classically from a ventral posterolateral thalamic lacune.
• Ataxic hemiparesis — weakness and cerebellar-type ataxia on the same side of the body (usually contralateral to a supratentorial lesion), with the ataxia out of proportion to the weakness (pons or internal capsule).
• Dysarthria–clumsy hand — facial weakness, dysarthria, and clumsiness of the hand (basis pontis or internal capsule/corona radiata).
• Mixed sensorimotor stroke — combined hemiparesis and hemisensory loss without cortical signs (thalamus plus adjacent internal capsule).

Posterior Circulation: Brainstem & Cerebellum

Brainstem strokes produce crossed syndromes — an ipsilateral cranial-nerve deficit with contralateral long-tract findings. The cranial-nerve loss is ipsilateral because the nucleus or fascicle is struck before the nerve exits, whereas the body findings are contralateral because the corticospinal tract is still above the pyramidal (medullary) decussation and the body's spinothalamic fibers have already crossed in the spinal cord before ascending through the brainstem.

• PICA (posterior inferior cerebellar artery) → lateral medullary (Wallenberg) syndrome: ipsilateral facial pain/temperature loss (CN V spinal nucleus), ipsilateral Horner syndrome, ataxia, dysphagia and hoarseness (nucleus ambiguus), vertigo and nystagmus, with contralateral pain/temperature loss over the body (spinothalamic tract). Note the crossed sensory pattern — face on one side, body on the other.
• AICA (anterior inferior cerebellar artery) → lateral pontine syndrome, resembling Wallenberg but distinguished by ipsilateral hearing loss and facial weakness, because AICA supplies the inner ear (via the labyrinthine artery) and the facial nerve nucleus (CN VII, CN VIII).
• Basilar artery → infarction of the ventral pons can produce the locked-in syndrome: quadriplegia and lower cranial-nerve palsy with preserved consciousness and vertical eye movements/blinking as the only means of communication. Basilar occlusion is a neurologic emergency with high mortality.
• "Top of the basilar" syndrome — embolic occlusion of the rostral basilar compromising the midbrain, thalamus, and occipital/temporal lobes, producing visual (hemianopia, cortical blindness), oculomotor, and behavioral disturbances (somnolence, confusion, peduncular hallucinosis) often without major limb weakness.
• Vertebrobasilar TIAs classically present with the "D's": dizziness, diplopia, dysarthria, dysphagia, and drop attacks — and should not be dismissed as benign, as they may herald basilar thrombosis.

Watershed (Borderzone) Infarcts

Watershed zones lie at the borders between major arterial territories, where perfusion pressure is lowest and most vulnerable to a global drop in flow (severe hypotension, cardiac arrest, or critical carotid stenosis). Two patterns are recognized:

• Cortical (external) borderzones — between ACA–MCA and MCA–PCA territories. The ACA–MCA borderzone serves the proximal arm and shoulder region of the homunculus, producing the striking "man in a barrel" picture of bilateral proximal arm weakness with relatively preserved hand and leg strength.
• Internal borderzones — deep white matter between the deep penetrators and the superficial pial supply, typically a marker of hemodynamic compromise from large-artery stenosis.

The presence of bilateral or borderzone-pattern infarction should prompt a search for global hypoperfusion or a flow-limiting proximal stenosis rather than a single embolic source.

Quick Reference: Artery, Territory & Hallmark

Pearl. Two exam findings instantly separate cortical from deep strokes: cortical involvement is announced by aphasia, neglect, or a homonymous visual field cut, whereas a clean hemiparesis with none of those features should raise the question of a lacune in the internal capsule or pons. The first question after "which side?" is therefore "are there cortical signs?"