Stroke: arterial territories and syndromes

1. The circle of Willis

Two internal carotid and two vertebral arteries feed the brain. The vertebral arteries join to form the basilar artery, which divides into the posterior cerebral arteries; the circle of Willis links front and back through the anterior and posterior communicating arteries. Each internal carotid ends as the anterior and middle cerebral arteries.

Surgeon’s corner: Only a minority of people have a complete, symmetrical circle. Aneurysms sit at its branch points, most often the anterior communicating artery; a posterior communicating aneurysm can compress the oculomotor nerve (painful third nerve palsy with a dilated pupil).

2. Three territories

Green, the anterior cerebral artery: the medial surface of the frontal and parietal lobes and a strip along the top. Orange, the middle cerebral artery: almost the whole lateral surface and the insula — and, through its lenticulostriate branches, most of the putamen, the body of the caudate and the upper internal capsule (the anterior choroidal artery and the recurrent artery of Heubner supply the rest). Blue, the posterior cerebral artery: the occipital lobe, the underside of the temporal lobe and, through perforators, the thalamus. Turn the brain to see each one.

Surgeon’s corner: The borders between territories are watershed zones: severe hypotension or a tight carotid stenosis can infarct them, typically giving proximal arm and shoulder weakness ("man in a barrel") when both sides are affected.

3. Middle cerebral artery: the classic stroke

A proximal (M1) occlusion of the left middle cerebral artery: right face and arm weakness more than the leg, right-sided sensory loss, right homonymous hemianopia, eyes deviated to the left — and, in the dominant hemisphere, aphasia. In the right hemisphere the same picture comes with left neglect instead of aphasia.

Surgeon’s corner: Face and arm more than leg points to the MCA; leg more than arm to the ACA. A large MCA infarct swells over 2–5 days (malignant MCA infarction): decompressive hemicraniectomy within 48 hours saves lives (strongest evidence up to age 60; considered in selected older patients).

4. MCA divisions: Broca or Wernicke

Beyond M1 the MCA usually splits. The superior division (orange) feeds the frontal operculum and the face–arm part of the motor and sensory strips: Broca aphasia with right face and arm weakness and sensory loss. The inferior division (pink) feeds the temporal and inferior parietal lobes: Wernicke aphasia and a right homonymous hemianopia or upper quadrantanopia, often without weakness — easily mistaken for confusion.

Surgeon’s corner: A patient suddenly "confused" who speaks fluently but makes no sense: think of a left inferior-division MCA stroke and test language and fields before blaming delirium.

5. Small vessels: lacunar strokes

The lenticulostriate arteries leave the M1 at right angles and run straight up into the basal ganglia and internal capsule. Hypertension and diabetes damage their walls: they block (recent small subcortical infarcts, under 20 mm on diffusion MRI, which later leave small cavities called lacunes) or burst (deep haemorrhage). In the posterior limb of the internal capsule the motor fibres are packed together, so a tiny lesion weakens face, arm and leg equally.

Surgeon’s corner: Classic lacunar syndromes: pure motor, pure sensory (thalamus), sensorimotor, ataxic hemiparesis, dysarthria–clumsy hand. Cortical signs (aphasia, neglect, hemianopia) argue against a lacune.

6. Anterior cerebral artery: the leg

The ACA runs over the corpus callosum and supplies the medial frontal and parietal lobes, including the leg area of the motor and sensory strips. Occlusion: weakness and sensory loss of the opposite leg more than the arm, urinary incontinence and — with frontal damage — abulia, a striking lack of initiative.

Surgeon’s corner: Bilateral ACA infarcts (both supplied from one A1 segment, or vasospasm after an anterior communicating aneurysm bleed) can leave a patient mute and immobile (akinetic mutism) with both legs weak.

7. Posterior cerebral artery: vision and the thalamus

The PCA wraps round the midbrain to the occipital lobe and the underside of the temporal lobe; its perforating branches feed the thalamus and midbrain. Occipital infarct: opposite homonymous hemianopia, often sparing the macula. Thalamic infarct: opposite sensory loss, sometimes followed months later by burning thalamic pain.

Surgeon’s corner: Left PCA infarct including the splenium of the corpus callosum: alexia without agraphia — the patient can write but not read it back. Medial temporal involvement adds memory loss.

8. Basilar artery: the brainstem

The basilar artery runs up the front of the pons and gives branches to the brainstem and cerebellum before dividing into the posterior cerebral arteries. Occlusion can be devastating: fluctuating weakness on both sides, double vision, slurred speech, drowsiness, then coma. A ventral pontine infarct can leave a patient conscious but paralysed except for vertical eye movements and blinking: locked-in syndrome.

Surgeon’s corner: Think of basilar occlusion in any sudden coma, or bilateral signs with eye-movement problems: CT angiography at once — thrombectomy is effective up to 24 hours after onset in moderate to severe deficits.

9. Vertebral artery and PICA: the lateral medullary syndrome

The intracranial vertebral artery (most often) or its branch, the posterior inferior cerebellar artery, supplies the lateral medulla; PICA also supplies the underside of the cerebellum. Lateral medullary infarct: vertigo and nystagmus, loss of pain and temperature on the same side of the face and the opposite side of the body, ipsilateral Horner syndrome, dysphagia and hoarseness (nucleus ambiguus) and ipsilateral ataxia — usually without weakness.

Surgeon’s corner: Often caused by vertebral artery dissection: neck pain or recent neck trauma before the stroke. Large cerebellar infarcts swell and compress the brainstem and fourth ventricle: watch consciousness closely; posterior fossa decompression can save the patient.

10. Time is brain: the first hour

In a large vessel occlusion, about two million neurons die every minute. Establish when the patient was last seen well, measure the deficit (NIHSS) and image at once: CT excludes haemorrhage, CT angiography finds the occlusion, perfusion imaging shows tissue that can still be saved.

Surgeon’s corner: Current European (ESO) guidance: intravenous thrombolysis (alteplase, or tenecteplase) within 4.5 h of the time last known well, and in selected patients up to 9 h or after waking with a stroke when MRI or perfusion imaging shows salvageable tissue. Mechanical thrombectomy for anterior-circulation large vessel occlusion within 6 h, and from 6 to 24 h when imaging shows salvageable tissue; selected large-core infarcts also benefit. Basilar occlusion: thrombectomy up to 24 h. Never delay thrombectomy to wait for thrombolysis to work. Check glucose, blood pressure and swallowing early.