| Segment | Location | Key Points |
|---|---|---|
| Cervical | Carotid bifurcation → skull base | No major branches; common site for atherosclerosis |
| Petrous | Carotid canal (temporal bone) | Protected; small branches to petrous bone & middle ear |
| Cavernous | Within cavernous sinus | Close to CN III, IV, V1, V2, VI → cavernous sinus pathology |
| Supraclinoid (Terminal) | After exiting cavernous sinus | Gives off: Ophthalmic, PCom, Anterior Choroidal, ACA, MCA |
“Carotid T” = terminal ICA occlusion at the carotid bifurcation into ACA & MCA → massive MCA ± ACA syndrome + often poor collaterals.
Key branches:
| Pattern | Clinical Features | Key Clues / Localization |
|---|---|---|
| M1 Proximal (before lenticulostriates) |
• Dense contralateral hemiplegia (face, arm, leg) • Contralateral hemisensory loss • Gaze deviation toward lesion • Aphasia (dominant) or neglect (non-dominant) • Often early edema, mass effect |
Cortical + deep signs. Internal capsule + cortex involved. Very severe deficit at onset (“devastating MCA stroke”). |
| M1 Distal (after lenticulostriates) |
• Cortical signs prominent (aphasia/neglect, field cut) • Weakness typically less dense (internal capsule spared) • May have mild–moderate face/arm > leg weakness |
Cortical signs without profound dense hemiplegia. Think more distal M1 or large M2 branch occlusion. |
| Superior Division (M2) |
• Face & arm weakness prominent • Little or no visual field deficit • Dominant: Broca’s aphasia (nonfluent, good comprehension) • Non-dominant: Mild neglect, motor apraxia |
Motor + Broca’s = superior division (dominant). Visual field often spared or mild. |
| Inferior Division (M2) |
• Prominent visual field deficit (HH or quadrantanopia) • Little or no weakness • Dominant: Wernicke’s aphasia (fluent, poor comprehension) • Non-dominant: Severe neglect, anosognosia |
Fluent aphasia + HH with minimal weakness = inferior division (dominant). Non-dominant: “classic neglect” pattern. |
Dense hemiplegia + aphasia/neglect → think proximal M1 (cortex + internal capsule).
Fluent aphasia + HH but NO weakness → inferior division MCA.
Course: From ICA → A1 segment → ACom → A2 pericallosal/callosomarginal branches.
Territory:
ACA Stroke Syndrome:
Origin: Supraclinoid ICA (classically) – small but high-yield vessel.
Structures supplied:
Classic AChA Stroke Triad:
Often incomplete in real-life, but exam loves the triad.
Origin: First major branch of supraclinoid ICA; enters optic canal with optic nerve.
Supplies: Retina, optic nerve head, orbit.
Clinical:
The Circle of Willis is the most important arterial anastomosis in the body, connecting the anterior and posterior circulations at the base of the brain.
| Segment | Vessel | Connects |
|---|---|---|
| Anterior | Anterior communicating artery (ACom) | Right ACA ↔ Left ACA |
| Anterolateral | A1 segment of ACA (bilateral) | ICA → ACom |
| Lateral | Internal carotid arteries (bilateral) | Anterior ↔ Posterior via PCom |
| Posterolateral | Posterior communicating arteries (PCom, bilateral) | ICA ↔ PCA |
| Posterior | P1 segment of PCA (bilateral) | Basilar → PCom |
Complete circle (textbook): 2 ACAs + ACom + 2 ICAs + 2 PComs + 2 PCAs (P1). This provides collateral flow if one major vessel is occluded.
A “complete” Circle of Willis is found in only ~25-50% of the population. Common variants significantly affect stroke risk and collateral capacity.
| Variant | Prevalence | Clinical Significance |
|---|---|---|
| Hypoplastic or absent PCom | ~30% | ↓ Anterior-posterior collateral; higher stroke risk with ICA occlusion |
| Hypoplastic or absent A1 | ~10% | Bilateral ACA territory at risk if remaining A1/ACom occluded |
| Fetal PCA (PCA from ICA via PCom) | ~15-30% | PCA territory depends on ICA (not basilar); ICA occlusion → PCA stroke |
| Absent ACom | ~5% | No cross-flow between ACAs |
| Infundibular dilation (at PCom origin) | Common | Can mimic aneurysm on imaging; usually benign (<3mm funnel shape) |
| Location | % of Intracranial Aneurysms | Classic Presentation |
|---|---|---|
| ACom | ~30% (most common) | Worst headache of life; may cause bilateral ACA ischemia, abulia, memory loss |
| PCom | ~25% | CN III palsy (pupil-involving) + headache = until proven otherwise an aneurysm. “Down and out” with dilated pupil |
| MCA bifurcation | ~20% | Contralateral weakness/aphasia if rupture; temporal hematoma |
| Basilar tip | ~5-10% | Devastating SAH; may compress brainstem |
| ICA (cavernous/paraclinoid) | ~5% | May be incidental; cavernous = lower rupture risk |
PCom aneurysm = CN III palsy with pupil involvement (dilated, “down and out”). ACom aneurysm = most common overall. Fetal PCA variant (~20%) means PCA territory depends on ICA, not basilar → changes stroke risk profile and surgical planning.
Vertebral arteries: Join to form basilar at pontomedullary junction.
Key branches:
Origin: Terminal branches of basilar artery.
Territory:
PCA Stroke Syndrome:
| Syndrome | Artery | Localization & Key Features |
|---|---|---|
| Lateral Medullary (Wallenberg) | PICA (usually vertebral/PICA) |
• Vertigo, nystagmus, nausea • Ipsilateral facial pain/temp loss (trigeminal nucleus) • Contralateral body pain/temp loss (spinothalamic) • Dysphagia, hoarseness, diminished gag (nucleus ambiguus) – “Don’t PICA horse” • Ipsilateral Horner’s, ataxia |
| Lateral Pontine | AICA (anterior inferior cerebellar) |
• Similar to PICA but more facial nucleus involvement • Ipsilateral facial paralysis, ↓ lacrimation, salivation, taste (ant 2/3) • Vertigo, nystagmus • Ipsilateral ataxia • “Facial droop means AICA’s pooped” |
| Medial Medullary | Anterior spinal (branch of vertebral) |
Triad: • Contralateral hemiparesis (corticospinal) • Contralateral dorsal column loss (proprioception/vibration) • Ipsilateral tongue weakness (CN XII) – tongue deviates toward lesion |
| Locked-in Syndrome | Basilar ventral pons |
• Quadriplegia, anarthria • Preserved consciousness & vertical eye movements • Result of bilateral corticospinal & corticobulbar tract involvement |
| Weber Syndrome | Paramedian midbrain (PCA branches) |
• Ipsilateral CN III palsy • Contralateral hemiparesis • Classic midbrain “alternating” hemiplegia |
| Superior Cerebellar Artery (SCA) stroke | SCA |
• Ipsilateral limb ataxia, dysmetria • Nausea, vomiting, nystagmus • Contralateral pain/temp loss (body) • Facial pain/temp may be spared (vs PICA/AICA) |
Posterior circulation strokes often give “crossed findings” – ipsilateral cranial nerve signs with contralateral motor/sensory deficits.
Key venous patterns:
• Elderly fall + gradual confusion = subdural (bridging veins).
• Young woman + headache + papilledema + seizure = suspect venous sinus thrombosis.
| Clinical Finding | Most Likely Vessel | Localization Clue |
|---|---|---|
| Leg > arm weakness, abulia | ACA | Medial frontal/parietal, anterior cingulate |
| Face/arm > leg weakness, aphasia | Dominant MCA | Lateral frontal/parietal, perisylvian |
| Neglect, left-sided inattention | Right MCA (inferior division) | Non-dominant parietal/temporal |
| HH with macular sparing | PCA | Occipital cortex (dual supply) |
| HH + dense hemiparesis (face, arm, leg) | Proximal M1 or ICA | Cortex + internal capsule |
| HH + hemiparesis + hemisensory loss | Anterior choroidal | Posterior limb IC + optic tract |
| Vertigo + ipsilateral face pain/T loss + contralateral body pain/T loss + dysphagia | PICA | Lateral medulla (Wallenberg) |
| Painful ophthalmoplegia + proptosis | Cavernous sinus (venous) | CN III, IV, V1, V2, VI involvement |
Think artery = pattern of deficit; think vein/sinus = headache, ↑ICP, seizures, multifocal deficits.
