Cerebrovascular Anatomy
Cerebrovascular Anatomy
What Do You Need to Know?
- Anterior vs. posterior circulation anatomy and key branches
- ICA segments (Bouthillier C1–C7) and their clinical significance
- Circle of Willis components and clinically significant normal variants
- Vascular territory stroke syndromes for each major artery
- Localization: cortical vs. subcortical, anterior vs. posterior, lateral vs. medial
- Blood supply of key structures (internal capsule, thalamus, brainstem)
- Watershed (border zone) infarct patterns and mechanisms
- Intracranial aneurysm sites and their classic presentations
Anterior Circulation
Common Carotid Artery (CCA)
Anatomy
- Right CCA: from brachiocephalic (innominate) artery; Left CCA: directly from aortic arch
- Bifurcates at ~C4 level (angle of jaw) into ECA and ICA
- Carotid body (at bifurcation): chemoreceptor (O2, CO2, pH); innervated by CN IX
- Carotid sinus (proximal ICA): baroreceptor; innervated by CN IX (Hering nerve)
Clinical Significance
- Carotid bifurcation = most common site of cerebral atherosclerosis (62%), followed by vertebral artery origin (15%), MCA origin (10%)
- Carotid sinus hypersensitivity → syncope with head turning or tight collars
- Carotid body tumor (paraganglioma) → painless pulsatile neck mass at angle of jaw
External Carotid Artery (ECA)
Key Branches
- Internal maxillary → middle meningeal artery: enters via foramen spinosum; rupture → epidural hematoma (lens-shaped, temporal)
- Superficial temporal artery: STA-MCA bypass in Moyamoya; biopsied in giant cell arteritis
- Ascending pharyngeal: Supplies CN IX, X, XI at jugular foramen; can be source of embolism during embolization procedures
- Facial artery: ECA-ICA collateral pathway (via angular artery ↔ ophthalmic artery)
- Occipital artery: ECA-vertebral collateral pathway
Clinical Significance
- ECA branches form collateral pathways to ICA and vertebral territories — can rescue flow in chronic ICA occlusion
- ECA feeders are commonly recruited by dural arteriovenous fistulas and meningiomas
Internal Carotid Artery (ICA)
Segments (Bouthillier C1–C7)
| Segment | Name | Key Branches | Clinical Significance |
|---|---|---|---|
| C1 | Cervical | None | Most common site for atherosclerosis and dissection; no branches = distinguishes from ECA on angiography |
| C2 | Petrous | Caroticotympanic, vidian | Through carotid canal in temporal bone; vulnerable in skull base fractures |
| C3 | Lacerum | None (small periosteal) | Short segment over foramen lacerum; transition zone |
| C4 | Cavernous | Meningohypophyseal trunk, inferolateral trunk | Within cavernous sinus; adjacent to CN III, IV, V1, V2, VI; aneurysm → CCF with proptosis, chemosis, CN VI palsy |
| C5 | Clinoid | None | Short transition; enters subarachnoid space through dural ring |
| C6 | Ophthalmic | Ophthalmic artery, superior hypophyseal | Ophthalmic a. = first major intradural branch → retina + optic nerve; superior hypophyseal → pituitary stalk (Sheehan syndrome) |
| C7 | Communicating | PCom, AChA | Terminates as ACA + MCA at the “carotid T”; PCom aneurysm → CN III palsy |
Syndromes
- “Carotid T” occlusion: Terminal ICA at ACA/MCA bifurcation → devastating combined ACA + MCA syndrome
- Ipsilateral monocular blindness + contralateral hemiparesis = ICA localization
- “Man-in-a-barrel”: Bilateral arm weakness with spared legs — bilateral ACA/MCA watershed from bilateral ICA disease or cardiac arrest
🧪 ICA Dissection
- Important cause of young stroke; trauma, neck manipulation, or spontaneous (connective tissue disorders: Ehlers-Danlos type IV, Marfan, fibromuscular dysplasia)
- Classic triad: Ipsilateral headache/neck pain + partial Horner’s (miosis + ptosis WITHOUT anhidrosis — sympathetics on ICA wall, sudomotor fibers follow ECA) + delayed ischemic symptoms
- Imaging: CTA/MRA “flame-shaped” tapering; fat-sat MRI shows crescent sign (intramural hematoma)
- Can also cause ipsilateral CN XII palsy (ICA in close proximity to hypoglossal nerve in upper cervical space)
Ophthalmic Artery
Anatomy
- First major intradural branch of ICA (C6); enters orbit via optic canal alongside CN II
- Key branches: Central retinal artery (end artery → retina), posterior ciliary arteries (optic nerve head, choroid), lacrimal artery
Syndromes
- Amaurosis fugax: Transient monocular vision loss (“curtain coming down”) — hallmark of ICA disease; Hollenhorst plaques (cholesterol emboli) on fundoscopy
- CRAO: Sudden painless monocular blindness; pale retina with “cherry red spot” (fovea perfused by choroidal circulation); in elderly consider GCA
Anterior Ischemic Optic Neuropathy (AION)
| Feature | Arteritic (A-AION / GCA) | Non-Arteritic (NA-AION) |
|---|---|---|
| Age | Typically >70 | Typically 50–70 |
| Mechanism | Giant cell arteritis → posterior ciliary artery inflammation | Hypoperfusion of posterior ciliary arteries; nocturnal hypotension |
| Disc appearance | Pallid (chalky white) disc edema | Hyperemic disc edema; “disc at risk” (small crowded disc, no cup) |
| Visual field | Severe vision loss; altitudinal defect | Altitudinal defect (usually inferior); less severe |
| Systemic clues | Jaw claudication, scalp tenderness, elevated ESR/CRP, PMR | Vascular risk factors (HTN, DM, OSA) |
| Key action | Emergent steroids before biopsy to prevent fellow eye involvement | No proven treatment; control risk factors |
| Fellow eye risk | Very high without treatment (days–weeks) | ~15% over 5 years |
Anterior Choroidal Artery (AChA)
Anatomy
- From supraclinoid ICA (C7) just distal to PCom — long, narrow, highly vulnerable end artery
- Territory: Posterior 2/3 of posterior limb of IC, internal globus pallidus, optic tract, lateral geniculate body, medial temporal lobe (hippocampus), amygdala
Syndromes
- Classic AChA triad: Contralateral hemiparesis + hemisensory loss + homonymous hemianopia WITHOUT cortical signs
- Absence of aphasia/neglect distinguishes AChA from MCA stroke — key board differentiator
- Variable presentation due to rich anastomotic network; can present as an isolated lacunar-like syndrome
Middle Cerebral Artery (MCA)
Segments
- M1 (horizontal/sphenoidal): Gives off lenticulostriate arteries (6–12 deep penetrators → basal ganglia, posterior limb IC, corona radiata)
- M2 (insular): Bifurcates (or trifurcates) into superior and inferior divisions in Sylvian fissure
- M3 (opercular): Over the opercula
- M4 (cortical): Terminal cortical branches
Territory
- Lateral frontal (motor cortex for face/arm, frontal eye fields, Broca’s area)
- Parietal (sensory cortex, angular and supramarginal gyri)
- Superior temporal (Wernicke’s area) and insula
- Deep: putamen, outer globus pallidus, posterior limb IC, corona radiata
Variants
- Early bifurcation: M1 bifurcates near its origin — can mimic M2 occlusion on angiography
- Accessory MCA: Arises from A1 or ACA — provides additional supply to MCA territory
Syndromes
- Complete MCA (M1): Face/arm > leg weakness, hemisensory loss, homonymous hemianopia, aphasia (dominant) or neglect (nondominant), gaze deviation toward lesion
- Superior division: Face/arm weakness + Broca’s aphasia (dominant); contralateral lower facial droop
- Inferior division: Wernicke’s aphasia or hemispatial neglect, homonymous hemianopia (or superior quadrantanopia), minimal motor deficit
- Gerstmann syndrome (dominant angular gyrus — inferior division): Finger agnosia + acalculia + right-left disorientation + agraphia
Lenticulostriate Arteries
- Arise from M1 — “arteries of stroke” (Chârcot)
- End arteries (no collaterals) → occlusion = lacunar infarcts; rupture = putaminal hemorrhage (most common hypertensive ICH)
- Lateral lenticulostriates (from M1) vs. medial lenticulostriates (from A1/ACA — Heubner’s territory)
💎 Board Pearl
MCA is the most commonly affected vessel in ischemic stroke. M1 occlusion with good leptomeningeal collaterals may present with cortical signs (aphasia/neglect) without dense hemiplegia — collaterals rescue cortex but lenticulostriates have no collaterals. Gerstmann syndrome = dominant angular gyrus (inferior MCA division).
Anterior Cerebral Artery (ACA)
Segments
- A1: ICA → ACom (gives off medial lenticulostriates)
- A2: ACom → pericallosal/callosomarginal bifurcation; gives off recurrent artery of Heubner
- A3–A5: Distal cortical branches (pericallosal, callosomarginal)
Territory
- Anterior 3/4 of medial hemisphere (leg/foot motor and sensory cortex)
- Medial-orbital frontal lobe, anterior cingulate gyrus
- Anterior 4/5 of corpus callosum
- Heubner’s artery: Head of caudate, anterior limb IC, anterior putamen
Variants
- Azygos ACA: Single midline A2 supplies both hemispheres — occlusion → bilateral ACA syndrome
- Bihemispheric ACA: One A2 supplies both medial hemispheres (if contralateral A1 hypoplastic)
Syndromes
- A1 occlusion: Usually well tolerated (ACom cross-flow). If both ACAs from single A1 or azygos ACA → bilateral ACA infarcts with paraplegia, abulia, akinetic mutism
- A2 occlusion: Contralateral leg >> arm/face weakness and sensory loss, urinary incontinence, abulia, alien limb phenomenon, grasp reflex, transcortical motor aphasia (dominant)
- Heubner’s occlusion: Contralateral face/arm weakness (caudate head → abulia + behavioral changes)
Posterior Circulation
Vertebral Artery
Anatomy
- First branch of subclavian artery; through transverse foramina C6–C1; enters cranium via foramen magnum
- Both vertebrals join at pontomedullary junction → basilar artery
- Left VA dominant in ~50%; significant asymmetry in ~25%
Key Branches
- PICA: Lateral medulla + inferior cerebellum
- Anterior spinal artery: Medial medulla; joins contralateral ASA to form single midline vessel down spinal cord
- Posterior spinal artery
Syndromes
- Subclavian steal: Proximal subclavian stenosis → retrograde flow in ipsilateral VA during arm exercise → vertebrobasilar symptoms (vertigo, diplopia, ataxia) with arm use
- Bow hunter syndrome: Dynamic VA compression during head rotation → posterior circulation ischemia
🧪 Vertebral Artery Dissection
- Important cause of posterior circulation stroke in young patients; neck trauma, chiropractic manipulation, or spontaneous
- Presentation: Posterior neck pain / occipital headache + lateral medullary syndrome (Wallenberg)
- Most commonly at V3 segment (atlas loop — C1-C2, where VA is most mobile and vulnerable)
- Imaging: CTA/MRA shows VA narrowing or occlusion; fat-sat MRI shows intramural hematoma
- Can cause SAH if dissection extends intracranially (intradural V4 segment)
Basilar Artery
Anatomy
- Ascends along ventral pons from pontomedullary junction to interpeduncular fossa
- Branches: Paramedian penetrators (medial pons), short circumferential (lateral pons), AICA, SCA
- Terminates by bifurcating into bilateral PCAs
Variants
- Persistent trigeminal artery (0.1–0.6%): Most common persistent carotid-basilar anastomosis; connects cavernous ICA to mid-basilar; associated with aneurysms and TN
- Persistent hypoglossal artery (0.02–0.1%): Connects cervical ICA to basilar via hypoglossal canal; may cause CN XII palsy; associated with aneurysms
- Persistent otic artery: Rarest; ICA to basilar through internal auditory canal
- Basilar fenestration: Partial duplication; most common at proximal basilar; associated with aneurysm risk
Syndromes
- Basilar occlusion: Neurological emergency; quadriplegia, bulbar dysfunction, coma; high mortality without recanalization
- Locked-in syndrome: Ventral pons bilateral infarct → quadriplegia + anarthria with preserved consciousness and vertical eye movements only
- “Top of the basilar”: Rostral brainstem + bilateral PCA territory → coma, cortical blindness, amnesia, behavioral changes, CN III palsy
Cerebellar Arteries (PICA, AICA, SCA)
| Artery | Origin | Territory | Key Syndrome |
|---|---|---|---|
| PICA | Vertebral | Lateral medulla, inferior cerebellum (tonsil, inferior vermis) | Wallenberg: Vertigo/nystagmus, ipsi face + contra body pain/temp, dysphagia/hoarseness (nucleus ambiguus), ipsilateral Horner’s, ipsilateral ataxia. NO motor weakness (pyramid spared) |
| AICA | Proximal basilar | Lateral pons, MCP, inner ear (via labyrinthine artery) | Lateral inferior pontine: Ipsilateral hearing loss + tinnitus, facial weakness (CN VII), facial numbness (CN V), vertigo, ataxia + contra pain/temp loss |
| SCA | Distal basilar | Superior cerebellum, SCP, dorsolateral pons/midbrain | Ipsilateral ataxia (SCP), contralateral pain/temp loss, ipsilateral Horner’s; CN IV palsy possible |
Posterior Circulation Red Flags
- “Crossed findings” = ipsilateral CN signs + contralateral motor/sensory → localizes to brainstem
- AICA is the only cerebellar artery that causes hearing loss (labyrinthine artery) — vertigo + hearing loss + facial weakness = AICA
- Wallenberg spares motor function — if hemiparesis is present, think medial or hemimedullary syndrome
- Cerebellar infarcts can swell and compress brainstem → rapid deterioration; may require emergent suboccipital decompressive craniectomy
Posterior Cerebral Artery (PCA)
Anatomy
- From basilar bifurcation (~70%) or ICA via PCom in fetal variant (~25%)
- P1 segment: Basilar tip → PCom junction; gives off thalamoperforating arteries (paramedian midbrain, medial thalamus)
- P2 segment: Around midbrain; gives off thalamogeniculate arteries (posterior/lateral thalamus, LGN), posterior choroidal arteries
- P3–P4: Cortical branches to inferomedial temporal lobe and medial occipital lobe (V1)
Variants
- Artery of Percheron: Single artery from one P1 supplies bilateral medial thalami — occlusion → bilateral paramedian thalamic infarcts
Syndromes
- Cortical PCA: Contralateral homonymous hemianopia with macular sparing (dual MCA/PCA supply to occipital pole)
- Left PCA + splenium: Alexia without agraphia (right visual cortex intact but disconnected from left language areas)
- Bilateral PCA (“top of the basilar”): Cortical blindness + Anton syndrome (denial of blindness), Balint syndrome (simultanagnosia + oculomotor apraxia + optic ataxia), amnesia
- Thalamic (Dejerine-Roussy): Contralateral hemisensory loss → delayed central thalamic pain with allodynia and hyperpathia
- Artery of Percheron occlusion: Coma/hypersomnia + vertical gaze palsy + amnesia; pathognomonic “butterfly” pattern on DWI
- Prosopagnosia: Bilateral inferomedial temporal (fusiform gyri) → inability to recognize faces
💎 Board Pearl
Artery of Percheron = anatomic variant where a single artery from one P1 supplies both medial thalami. Occlusion → bilateral paramedian thalamic infarcts with coma/hypersomnia + vertical gaze palsy + amnesia. Pathognomonic “butterfly” pattern on DWI. Always think of it with bilateral thalamic lesions in a vascular pattern.
Circle of Willis & Aneurysms
- Connects anterior and posterior circulations at base of brain
- Components: ACom, bilateral A1, bilateral ICA (terminal), bilateral PCom, bilateral P1, basilar tip
- Complete circle found in only 25–50% of individuals — variants have major clinical implications
Clinically Significant Variants
- Fetal PCA (20–30%): PCA from ICA via PCom instead of basilar → ICA occlusion can cause both anterior AND posterior territory infarcts; basilar occlusion spares PCA territory
- Hypoplastic/absent PCom (~30%): Poor anterior-posterior collateral; higher stroke risk with ICA or basilar occlusion
- Hypoplastic/absent A1 (~10%): Both ACA territories dependent on a single A1
- Fenestration: Duplicated arterial segment with intervening septum; associated with increased aneurysm risk at fenestration site
Intracranial Aneurysm Sites
| Location | Frequency | Classic Presentation |
|---|---|---|
| ACom | ~30% | Most common overall; SAH with bilateral ACA ischemia, memory impairment (septal/fornix) |
| PCom | ~25% | CN III palsy (pupil-involving) — ptosis, “down and out,” dilated pupil |
| MCA bifurcation | ~20% | Contralateral weakness/aphasia; Sylvian fissure/temporal hematoma |
| Basilar tip | 5–10% | Devastating SAH; brainstem compression; CN III palsy |
| ICA (cavernous) | 3–5% | CCF, CN III/IV/VI palsy, retro-orbital pain; extradural → does NOT cause SAH |
💎 Board Pearl
PCom aneurysm = CN III palsy with dilated pupil. Painful pupil-involving CN III palsy is an aneurysm until proven otherwise — get CTA/MRA urgently. Microvascular CN III (diabetes) typically spares the pupil because pupillary fibers travel superficially on CN III and are compressed first by aneurysm but spared by ischemia of the nerve’s interior.
Blood Supply of Key Structures
| Structure | Blood Supply | Infarction Syndrome |
|---|---|---|
| Anterior limb of IC | Recurrent artery of Heubner (ACA), medial lenticulostriates (A1) | Contralateral face/arm weakness, abulia, behavioral changes |
| Genu of IC | Direct ICA perforators, Heubner’s, medial lenticulostriates | Contralateral face/tongue weakness (corticobulbar fibers), dysarthria |
| Posterior limb of IC | Lateral lenticulostriates (MCA), AChA | Pure motor hemiparesis (most common lacunar syndrome); dense contralateral motor deficit |
| Caudate head | Recurrent artery of Heubner (ACA) | Abulia, behavioral changes, contralateral neglect (if right caudate) |
| Putamen | Lateral lenticulostriates (MCA) | Most common site of hypertensive ICH; contralateral hemiparesis |
| Globus pallidus | AChA (internal GP), lenticulostriates (external GP) | Movement disorders; internal GP infarct can mimic AChA syndrome |
| Anterior thalamus | Tuberothalamic artery (polar artery; from PCom) | Amnesia (mammillothalamic tract), personality changes, apathy |
| Medial thalamus | Thalamoperforating arteries (P1 — or artery of Percheron) | Decreased consciousness, vertical gaze palsy, amnesia |
| Lateral/posterior thalamus (VPL/VPM) | Thalamogeniculate arteries (P2) | Dejerine-Roussy: Hemisensory loss → thalamic pain; pure sensory stroke |
| Lateral geniculate body | AChA + thalamogeniculate (dual supply) | Sectoranopia (wedge-shaped visual field loss); spared central vision |
| Corona radiata | Lenticulostriates (deep MCA), ACA cortical branches (superficial) | Lacunar syndromes; variable motor/sensory deficits depending on fibers affected |
| Corpus callosum | Pericallosal artery (ACA); splenium = posterior choroidal (PCA) | Alien limb, callosal disconnection syndromes, alexia without agraphia (splenium) |
| Hippocampus | AChA + PCA (posterior choroidal) | Amnesia; bilateral involvement → anterograde memory loss |
| Basis pontis | Basilar paramedian penetrators | Bilateral → locked-in syndrome; unilateral → pure motor hemiparesis or ataxic hemiparesis |
| Spinal cord | Anterior spinal artery (anterior 2/3), posterior spinal arteries (posterior 1/3) | ASA syndrome: Bilateral motor paralysis + pain/temp loss with preserved dorsal column (proprioception, vibration) |
💎 Board Pearl
Internal capsule has a triple blood supply: anterior limb = Heubner’s (ACA); posterior limb = lenticulostriates (MCA) + AChA. This is why posterior limb IC infarcts are the most common lacunar location — lenticulostriates are vulnerable end arteries. Thalamus has 4 arterial territories (tuberothalamic, thalamoperforating, thalamogeniculate, posterior choroidal) — each produces a distinct syndrome.
Stroke Localization
Cortical vs. Subcortical
- Cortical signs (present = cortical stroke): Aphasia, neglect, hemianopia, agnosia, apraxia, gaze preference, seizures at onset
- Subcortical (lacunar) (cortical signs ABSENT): Pure motor, pure sensory, or sensorimotor deficit without aphasia, neglect, or visual field cut
- Subcortical strokes are typically small (<1.5 cm), in basal ganglia, thalamus, internal capsule, or pons
Cortical: Lateral (MCA) vs. Medial (ACA)
- Lateral (MCA): Face/arm > leg weakness; aphasia (dominant) or neglect (nondominant); gaze deviation toward lesion
- Medial (ACA): Leg >> arm/face weakness; abulia, incontinence, alien limb, grasp reflex
- Key: Distribution of weakness — MCA = upper > lower; ACA = lower > upper
Anterior vs. Posterior Circulation
- Anterior (ICA/MCA/ACA): Lateralized cortical signs — aphasia, neglect, unilateral motor/sensory, monocular visual symptoms
- Posterior (vertebrobasilar/PCA): Crossed findings, vertigo, diplopia, ataxia, bilateral motor/sensory, homonymous hemianopia, altered consciousness
- Key: Vertigo + ataxia + CN signs + crossed deficits = posterior. Aphasia/neglect + face/arm weakness = anterior
Large Vessel vs. Small Vessel
- LVO: Cortical signs present, large territory, high NIHSS, proximal vessel occlusion on CTA
- Small vessel (lacunar): Classic lacunar syndrome, no cortical signs, NIHSS ≤5, normal CTA
- 5 classic lacunar syndromes: Pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis, dysarthria-clumsy hand
💎 Board Pearl
Quick localization: Cortical signs (aphasia, neglect, hemianopia) = cortical. No cortical signs = subcortical/lacunar. Face/arm > leg = MCA. Leg > arm = ACA. Crossed findings (ipsilateral CN + contralateral body) = brainstem. Isolated hemianopia without weakness = PCA. Hemiparesis + hemianopia + hemisensory WITHOUT aphasia/neglect = AChA.
Watershed (Border Zone) Territories
| Type | Location | Mechanism | Clinical Features | DWI Pattern |
|---|---|---|---|---|
| Anterior cortical | ACA/MCA border (parasagittal frontal-parietal) | Bilateral ICA disease, cardiac arrest, severe hypotension | Proximal arm/leg weakness > distal; bilateral → “man-in-a-barrel” | Parasagittal linear infarcts |
| Posterior cortical | MCA/PCA border (temporo-occipital) | Same as above | Visual field defects; transcortical aphasia (preserved repetition — perisylvian spared) | Occipitotemporal border zone infarcts |
| Internal (deep) | Between lenticulostriate and cortical MCA branches | Unilateral ICA stenosis/occlusion with hemodynamic failure | Can mimic lacunar syndrome; variable motor/sensory deficits | “String of pearls” — rosary-like chain of small infarcts |
- Think watershed when: Post-cardiac arrest, post-cardiac surgery, severe bilateral carotid disease, hypotensive episodes, proximal > distal weakness
- Watershed infarcts result from hypoperfusion, NOT embolism
💎 Board Pearl
Transcortical aphasias (preserved repetition) localize to watershed zones because the perisylvian language cortex is spared. Transcortical motor = anterior watershed (ACA/MCA). Transcortical sensory = posterior watershed (MCA/PCA). Bilateral watershed after cardiac arrest → “man-in-a-barrel.”
Quick Reference: Vascular Territories
| Vessel | Key Territory | Classic Deficit |
|---|---|---|
| ICA | MCA ± ACA | Ipsilateral monocular blindness + contralateral hemiparesis |
| MCA (M1) | Lateral hemisphere, BG, IC | Face/arm > leg weakness, aphasia (L) or neglect (R), gaze deviation |
| MCA superior div. | Frontal-parietal | Face/arm weakness + Broca’s aphasia |
| MCA inferior div. | Temporal-parietal | Wernicke’s aphasia or neglect; hemianopia; minimal weakness |
| Lenticulostriate | BG, posterior limb IC | Pure motor hemiparesis (most common lacunar) |
| ACA | Medial frontal/parietal | Leg > arm weakness, abulia, incontinence, alien limb |
| AChA | Posterior limb IC, optic tract | Hemiparesis + hemisensory + hemianopia (no cortical signs) |
| PCA (cortical) | Occipital, inferomedial temporal | Homonymous hemianopia with macular sparing; alexia without agraphia (L) |
| PCA (thalamic) | Posterior thalamus | Dejerine-Roussy: sensory loss → thalamic pain |
| Artery of Percheron | Bilateral medial thalami | Coma + vertical gaze palsy + amnesia |
| PICA | Lateral medulla | Wallenberg: vertigo, ipsi face + contra body pain/temp, dysphagia, Horner’s |
| AICA | Lateral pons, inner ear | Facial weakness, hearing loss, vertigo, ataxia |
| SCA | Superior cerebellum, SCP | Ipsilateral ataxia, contralateral pain/temp loss |
| Basilar | Bilateral basis pontis | Locked-in: quadriplegia, anarthria, preserved vertical gaze |
| Watershed | Border zones | Proximal > distal weakness; bilateral → “man-in-a-barrel” |
References
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- Lazzaro NA, Wright B, Castillo M, et al. Artery of Percheron infarction: imaging patterns and clinical spectrum. AJNR Am J Neuroradiol. 2010;31(7):1283-1289.
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