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Vascular Anatomy

Anatomy

🩸 Anterior Circulation – Internal Carotid & Branches

Internal Carotid Artery (ICA) – Segments & Key Branches

ICA Segments (high-yield)

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

ICA Stroke – Clinical Pattern

  • Often = MCA ± ACA territory (if poor collateral flow via ACom/PCom)
  • Carotid T occlusion: Severe deficit – dense contralateral hemiplegia, hemisensory loss, gaze deviation, aphasia (dominant) or neglect (non-dominant), homonymous hemianopia
  • Retinal ischemia: Amaurosis fugax or monocular vision loss (ophthalmic artery)
  • Clue: Ipsilateral monocular blindness + contralateral hemiparesis → think ICA
💎 Board Pearl

“Carotid T” = terminal ICA occlusion at the carotid bifurcation into ACA & MCA → massive MCA ± ACA syndrome + often poor collaterals.

🧠 Middle Cerebral Artery (MCA) & Divisions

MCA Anatomy & Territories

MCA Segments

  • M1: Horizontal/sphenoidal segment – from origin to bifurcation/trifurcation
  • M2: Insular segments (superior & inferior divisions)
  • M3/M4: Opercular & cortical branches over convexity

Key branches:

  • Lenticulostriate arteries (from M1): Supply basal ganglia & posterior limb of internal capsule (“arteries of stroke”)
  • Cortical branches: Lateral frontal, parietal, temporal lobes

Typical MCA Territory Deficit

  • Contralateral face & arm weakness > leg
  • Contralateral hemisensory loss (face/arm > leg)
  • Contralateral homonymous hemianopia (optic radiations)
  • Dominant hemisphere: Aphasia (Broca/Wernicke/global)
  • Non-dominant hemisphere: Hemispatial neglect, anosognosia, constructional apraxia
  • Eyes often deviate toward the lesion in acute phase

MCA Syndromes – M1 Proximal vs Distal vs Divisions

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.
💎 Board Pearl

Dense hemiplegia + aphasia/neglect → think proximal M1 (cortex + internal capsule).
Fluent aphasia + HH but NO weakness → inferior division MCA.

🧍 Anterior Cerebral, Anterior Choroidal & Ophthalmic Arteries

Anterior Cerebral Artery (ACA)

Course: From ICA → A1 segment → ACom → A2 pericallosal/callosomarginal branches.

Territory:

  • Medial frontal & parietal lobes
  • Leg area of motor & sensory cortex
  • Anterior corpus callosum & cingulate

ACA Stroke Syndrome:

  • Contralateral leg weakness > arm/face
  • Contralateral leg sensory loss
  • Urinary incontinence
  • Abulia, akinetic mutism (medial frontal/anterior cingulate)
  • Frontal release signs (grasp reflex)
  • Alien limb phenomena (medial frontal/callosal)
Anterior Choroidal Artery (AChA)

Origin: Supraclinoid ICA (classically) – small but high-yield vessel.

Structures supplied:

  • Posterior limb of internal capsule
  • Optic tract & lateral geniculate body
  • Medial temporal lobe (hippocampus)
  • Globus pallidus

Classic AChA Stroke Triad:

  • Contralateral hemiparesis (posterior limb IC)
  • Contralateral hemisensory loss
  • Contralateral homonymous hemianopia (optic tract/LGN)

Often incomplete in real-life, but exam loves the triad.

Ophthalmic Artery

Origin: First major branch of supraclinoid ICA; enters optic canal with optic nerve.

Supplies: Retina, optic nerve head, orbit.

Clinical:

  • Amaurosis fugax: Transient monocular vision loss (“curtain coming down”) from retinal ischemia due to carotid disease.
  • Retinal artery occlusion: Sudden painless monocular blindness; cherry red spot.

🔄 Posterior Circulation – Vertebrobasilar & PCA

Vertebral & Basilar Arteries – Overview

Vertebral arteries: Join to form basilar at pontomedullary junction.

Key branches:

  • PICA – posterior inferior cerebellar artery
  • Anterior spinal artery
  • AICA – anterior inferior cerebellar artery
  • SCA – superior cerebellar artery
  • Paramedian & circumferential branches to brainstem
Posterior Cerebral Artery (PCA)

Origin: Terminal branches of basilar artery.

Territory:

  • Occipital lobe (primary visual cortex)
  • Inferomedial temporal lobes
  • Posterior thalamus
  • Splenium of corpus callosum

PCA Stroke Syndrome:

  • Contralateral homonymous hemianopia ± macular sparing
  • Alexia without agraphia (left PCA + splenium)
  • Visual agnosia, prosopagnosia (ventral occipitotemporal)
  • Thalamic pain syndrome (Dejerine–Roussy) if thalamus involved
  • Bilateral PCA → cortical blindness ± Anton syndrome

🧲 Brainstem & Cerebellar Stroke Syndromes (Pattern Recognition)

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)
💎 Board Pearl

Posterior circulation strokes often give “crossed findings” – ipsilateral cranial nerve signs with contralateral motor/sensory deficits.

🩻 Cerebral Venous System – Superficial, Deep & Dural Sinuses

Superficial & Deep Cerebral Veins

Superficial Veins

  • Drain cerebral cortex and subcortical white matter
  • Empty mainly into superior sagittal sinus, transverse sinus
  • Bridging veins traverse subdural space → rupture → subdural hematoma, especially with atrophy/trauma

Deep Venous System

  • Internal cerebral veins: Drain deep structures (thalamus, basal ganglia, deep white matter)
  • Join to form the vein of Galen
  • Vein of Galen → straight sinus → transverse sinus
Dural Venous Sinuses & Clinical Correlates

Major Dural Sinuses

  • Superior sagittal sinus: Along falx; drains superficial hemispheric veins
  • Inferior sagittal sinus → straight sinus: Deep midline structures
  • Transverse & sigmoid sinuses: Exit skull via jugular foramen → internal jugular vein
  • Cavernous sinus: On either side of sella; ICA + CN III, IV, V1, V2, VI inside/along walls

Cerebral Venous Sinus Thrombosis (CVST)

  • Risk factors: Hypercoagulable states, pregnancy/postpartum, OCPs, infection
  • Symptoms: Headache, papilledema, seizures, focal deficits
  • Superior sagittal sinus thrombosis: Bilateral parasagittal weakness, seizures, ↑ ICP
  • Lateral (transverse/sigmoid) sinus: Headache, cerebellar signs, raised ICP

Cavernous Sinus Thrombosis

  • Etiology: Often from facial/sinus infections
  • Clinical:
    • Painful ophthalmoplegia (CN III, IV, VI involvement)
    • Decreased corneal reflex (V1)
    • Periorbital edema, proptosis
    • Often bilateral due to intercavernous connections
💎 Board Pearl

Key venous patterns: • Elderly fall + gradual confusion = subdural (bridging veins).
• Young woman + headache + papilledema + seizure = suspect venous sinus thrombosis.

📊 Vascular Anatomy & Stroke – Quick Reference

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
💎 Board Pearl

Think artery = pattern of deficit; think vein/sinus = headache, ↑ICP, seizures, multifocal deficits.