Blood supply of the brain

Arterial inflow

• Internal carotid arteries (anterior circulation, about 80% of flow) give the ophthalmic, posterior communicating and anterior choroidal arteries, then divide into the anterior and middle cerebral arteries.
• Vertebral arteries arise from the subclavians, ascend through the foramina transversaria of C6–C1, enter the foramen magnum and give the PICA and the anterior spinal artery. They join at the lower border of the pons to form the basilar artery, which gives AICA, pontine branches, the labyrinthine artery and the superior cerebellar arteries before dividing into the two posterior cerebral arteries.
• So the PCA is normally a branch of the basilar, joined to the carotid system by the posterior communicating artery.

Circle of Willis and aneurysms

• The ring is formed by the two ACAs joined by the anterior communicating artery, the terminal ICAs, the two posterior communicating arteries and the two PCAs. It shares flow when one inflow narrows slowly, but it is complete in only a minority of people.
• Berry (saccular) aneurysms form at branch points where the tunica media and internal elastic lamina are deficient. Commonest at the anterior communicating artery, then the PCom and the MCA bifurcation. Associations: ADPKD, Ehlers–Danlos, coarctation, smoking, hypertension. A PCom aneurysm causes a painful pupil-involving III palsy.
• Charcot–Bouchard microaneurysms are tiny (under 1 mm) dilatations of the penetrating lenticulostriate arterioles in chronic hypertension; their rupture causes deep haemorrhage (putamen, thalamus, pons, cerebellum). Lipohyalinosis of the same vessels causes lacunar infarcts.

Territories and stroke syndromes

• Macular sparing in PCA stroke: the occipital pole (macular cortex) also receives MCA collaterals.
• Locked-in syndrome: basilar occlusion infarcts the ventral pons, destroying corticospinal and corticobulbar tracts bilaterally. The tegmentum (reticular activating system) and the midbrain vertical gaze centres are spared, so the patient is conscious and communicates by blinking and vertical eye movements.
• Hemiballismus after a small stroke points to the contralateral subthalamic nucleus.

Border zones and other mechanisms

• Watershed infarcts occur at the edges between territories during profound hypotension (cardiac surgery, arrest). The ACA–MCA border zone holds the shoulder and upper arm area, giving bilateral proximal arm weakness with face, hands and legs spared ("man in a barrel").
• Cerebral amyloid angiopathy: beta-amyloid in cortical and leptomeningeal vessel walls of the elderly causes lobar (cortical) haemorrhages in normotensive patients, often with memory decline and multiple old cortical microbleeds on MRI. Avoid anticoagulation where possible.
• Vertebral artery dissection after neck manipulation or trauma: neck pain followed by posterior circulation stroke, often lateral medullary syndrome. Carotid dissection gives neck pain, Horner syndrome and anterior circulation signs.
• Commonest site of embolic and thrombotic infarction overall: the MCA territory.

Pathology of infarction

• Brain infarcts undergo liquefactive necrosis (high lipid content, few connective tissue elements, many lysosomal enzymes). Macrophages (microglia) clear debris over weeks and repair is by gliosis (astrocyte proliferation), leaving a cyst.
• Red (haemorrhagic) infarcts follow embolism with reperfusion; pale infarcts follow thrombosis.

Acute stroke and TIA care

Venous drainage

• Superficial cerebral veins drain to the superior sagittal sinus; deep veins form the internal cerebral veins and the great cerebral vein (of Galen), which joins the inferior sagittal sinus to form the straight sinus. The cerebellar vermis lies against the straight sinus region in the posterior fossa.
• Cerebral venous sinus thrombosis: headache, seizures, papilloedema, venous haemorrhage; risk with pregnancy, oral contraceptives and dehydration. Deep venous thrombosis can mimic bilateral thalamic infarction.

Cerebral blood flow

• About 50 mL/100 g/min (about 15% of cardiac output), held constant by autoregulation over a mean arterial pressure of roughly 60–150 mmHg.
• Carbon dioxide is the most powerful local regulator: hypercapnia (and H⁺, adenosine) dilates cerebral vessels and increases perfusion; hyperventilation constricts them.

Remember ACA is the leg, MCA is face, arm and speech, PCA is vision with the macula spared; basilar in the ventral pons locks the patient in.

Exam trap A Heubner artery infarct weakens the face and arm, not the leg, even though it is an ACA branch.

Exam trap Lobar haemorrhage in an elderly normotensive patient with microbleeds is amyloid angiopathy, not hypertensive.

How FCPS asks about this

• Conscious, quadriplegic, only blinks and moves eyes vertically: ventral pons, basilar artery.
• Fluent jargon, poor comprehension, upper quadrant field loss, no weakness: inferior division of the left MCA.
• Bilateral proximal arm weakness after cardiac surgery hypotension: ACA–MCA border zone infarcts.
• Saccular dilatations on lenticulostriate arterioles: Charcot–Bouchard microaneurysms.
• TIA resolved, CT normal: aspirin 300 mg and urgent TIA clinic.
• Stroke at 2 hours, CT clear: intravenous alteplase.
• Necrosis type in brain infarct: liquefactive; healed by gliosis.