Overview

• The ICA is the major arterial supply to the anterior two-thirds of the cerebral hemisphere, including the frontal, parietal, and lateral temporal lobes
• Origin: CCA bifurcation at approximately the C3–C4 vertebral level (upper border of thyroid cartilage)
• The ICA lies posterolateral to the ECA at the bifurcation and has no branches in the neck (important distinguishing feature from ECA on angiography)
• Carotid body — chemoreceptor at the bifurcation (senses O₂, CO₂, pH; innervated by CN IX)
• Carotid sinus — baroreceptor in the proximal ICA wall (innervated by CN IX via Hering nerve)

ICA Segments — Bouthillier Classification (C1–C7)

ICA Stroke Syndromes

• ICA occlusion may be clinically silent if Circle of Willis collaterals are adequate (cross-filling via ACom and PCom)
• When symptomatic, ICA occlusion mimics a large MCA territory stroke (face/arm > leg weakness, hemisensory loss, aphasia or neglect)
• Ophthalmic artery involvement → ipsilateral monocular visual loss (amaurosis fugax if transient, central retinal artery occlusion if permanent)
• Combination of ipsilateral eye + contralateral body deficits (optico-pyramidal syndrome) is highly suggestive of ICA pathology

Carotid T Occlusion

• Definition: Occlusion at the ICA terminal bifurcation (the "T"), blocking flow to both ACA and MCA origins
• Clinical presentation: Devastating combined ACA + MCA territory infarction — dense hemiplegia (face, arm, and leg), hemisensory loss, hemianopia, global aphasia (dominant) or severe neglect (non-dominant)
• Often presents with impaired consciousness due to massive territory involvement
• Poor prognosis: Large-volume infarct with high risk of malignant edema and herniation
• Thrombectomy consideration: ICA-T occlusions are an important indication for endovascular thrombectomy, though outcomes are worse than isolated MCA occlusion

Overview

• The largest terminal branch of the ICA and essentially its direct continuation
• Supplies the lateral surface of the frontal, parietal, and temporal lobes — the largest cortical vascular territory
• The most common artery involved in ischemic stroke

MCA Segments (M1–M4)

Lenticulostriate Arteries

• Origin: Lateral group from M1 segment; medial group from A1 segment
• Supply: Putamen, caudate head, globus pallidus, anterior limb and genu of internal capsule, superior portion of posterior limb of internal capsule
• Called "arteries of stroke" (Charcot) — most common site of hypertensive intracerebral hemorrhage and lacunar infarction
• End arteries with no significant anastomoses → extremely vulnerable to occlusion
• Hypertensive lipohyalinosis and Charcot-Bouchard microaneurysms form in these vessels → putaminal hemorrhage

MCA Cortical Branches

Superior Division

• Orbitofrontal, prefrontal, precentral, and central arteries
• Supplies: lateral frontal lobe, including Broca area (dominant hemisphere), primary motor cortex (face and upper extremity), premotor cortex

Inferior Division

• Posterior parietal, angular, temporo-occipital, posterior and middle temporal arteries
• Supplies: lateral temporal and inferior parietal lobes, including Wernicke area (dominant hemisphere), angular gyrus, supramarginal gyrus

MCA Stroke Syndromes

Dominant vs. Non-Dominant Hemisphere MCA Stroke

ACA Segments (A1–A2)

Anterior Communicating Artery (ACom)

• Short connecting segment between the two A1 segments, completing the anterior Circle of Willis
• Most common site of intracranial aneurysm (~30% of all intracranial aneurysms)
• ACom aneurysm rupture → SAH, often with blood in the interhemispheric fissure
• ACom aneurysms are more common with A1 asymmetry (increased hemodynamic stress at the ACom)
• Surgical clipping of ACom aneurysms puts the recurrent artery of Heubner and hypothalamus at risk

Recurrent Artery of Heubner

• Origin: Proximal A2 (most commonly) or at the A1–ACom junction
• Course: Doubles back (recurs) along A1 to enter the anterior perforated substance
• Supplies: Caudate head, anterior limb of internal capsule, anterior putamen, nucleus accumbens, parts of the septal nuclei
• Largest perforating branch of the ACA
• Clinical significance: Vulnerable during ACom aneurysm clipping; occlusion → contralateral face and arm weakness (mimics MCA stroke) + behavioral changes (abulia, personality change)

ACA Stroke Syndrome

• Contralateral leg weakness (greater than arm or face) — because the leg motor cortex lies on the medial surface of the hemisphere in the ACA territory
• Contralateral leg sensory loss (same reasoning — medial somatosensory cortex)
• Abulia (akinetic mutism in bilateral ACA infarcts) — loss of motivation, apathy, reduced spontaneous speech; due to medial frontal/cingulate damage
• Alien limb phenomenon — involuntary purposeful movements of the contralateral arm; due to SMA and anterior corpus callosum (callosal disconnection) damage
• Transcortical motor aphasia (dominant hemisphere) — reduced speech output with preserved repetition; due to SMA or prefrontal damage
• Urinary incontinence — due to damage to the medial frontal micturition center (paracentral lobule)
• Grasp reflex and other frontal release signs with medial frontal damage
• Callosal disconnection syndromes — left-hand apraxia (inability of left hand to follow verbal commands) from anterior corpus callosum damage

Anatomy

• Origin: Arises from the C7 (communicating) segment of the ICA, just distal to the PCom origin and just proximal to the ICA bifurcation
• Course: Courses posterolaterally through the crural cistern, along the optic tract, enters the temporal horn of the lateral ventricle via the choroidal fissure
• Despite its small caliber, it supplies a disproportionately large and critical territory

Territory Supplied

• Posterior limb of the internal capsule (inferior/ventral portion) — corticospinal and corticobulbar tracts
• Optic tract
• Lateral geniculate nucleus (LGN)
• Medial temporal lobe — hippocampus, amygdala (partial)
• Medial globus pallidus
• Posterior portion of the thalamus (ventral posterolateral nucleus, partial)
• Choroid plexus of the temporal horn
• Cerebral peduncle (lateral portion)

Classic AChA Syndrome (AChA Triad)

• The classic AChA triad consists of:
  1. Contralateral hemiplegia — from posterior limb of internal capsule infarction
  2. Contralateral hemianopia (homonymous) — from lateral geniculate nucleus and/or optic tract involvement
  3. Contralateral hemisensory loss — from thalamic (VPL) or internal capsule involvement
• The full triad is uncommon in practice due to rich collateral supply; partial syndromes are more frequent
• AChA infarction can mimic a lacunar infarct of the internal capsule

Complete Anatomy

• An arterial anastomotic ring at the base of the brain in the interpeduncular and suprasellar cisterns
• Anterior components: bilateral A1 segments + anterior communicating artery (ACom)
• Lateral components: bilateral ICA (supraclinoid portion, C6–C7)
• Posterior components: bilateral posterior communicating arteries (PCom) + bilateral P1 segments
• Function: Provides collateral flow between anterior and posterior circulations, and between the two hemispheres
• A complete, textbook Circle of Willis is present in only ~25–50% of the population

Common Variants

Common Aneurysm Sites

Vertebral Artery — Four Segments (V1–V4)

Vertebral Artery Asymmetry

• Left VA is dominant (larger) in ~50%; right dominant in ~25%; codominant in ~25%
• A hypoplastic VA is present in ~15–25% of the population
• Occlusion of the dominant VA carries significantly higher stroke risk than occlusion of a hypoplastic VA

Posterior Inferior Cerebellar Artery (PICA)

• Origin: Most commonly from V4 (intracranial VA); occasionally extracranial origin
• Course: Wraps around the lateral medulla and inferior cerebellar peduncle
• Supplies: Lateral medulla (via perforating branches), inferior cerebellar vermis, tonsil, inferior cerebellar hemisphere, choroid plexus of 4th ventricle
• PICA occlusion (or more commonly the VA supplying it) → lateral medullary (Wallenberg) syndrome
• PICA absent in ~15–20% (territory supplied by AICA instead) — PICA–AICA dominance is a spectrum

Anterior Spinal Artery

• Origin: Two branches from the V4 segments that merge into a single midline vessel
• Course: Descends along the anterior median fissure of the medulla and entire spinal cord
• At the medullary level, supplies the medial medulla (pyramid, medial lemniscus, CN XII nucleus)
• Occlusion → medial medullary syndrome (Dejerine syndrome)

Basilar Artery

• Formation: Junction of both VAs at the pontomedullary junction
• Course: Ascends in the basilar sulcus on the ventral pons
• Termination: Bifurcates into the two posterior cerebral arteries (PCAs) at the midbrain level

Basilar Artery Branches

Anterior Inferior Cerebellar Artery (AICA)

• Origin: Lower third of basilar artery
• Supplies: Anteroinferior cerebellum, lateral lower pons, middle cerebellar peduncle
• Labyrinthine artery (internal auditory artery) — usually branches from AICA; supplies cochlea and vestibular apparatus
• AICA occlusion → lateral pontine syndrome: ipsilateral hearing loss, vertigo, facial weakness (CN VII), facial sensory loss (CN V), Horner syndrome, cerebellar ataxia, and contralateral pain/temperature loss

Superior Cerebellar Artery (SCA)

• Origin: Distal basilar, just before PCA takeoff
• Course: Wraps around the midbrain, parallels CN III, separated by the tentorial edge
• Key anatomic relation: CN IV (trochlear) passes between PCA and SCA
• Supplies: Superior cerebellar surface, dentate nucleus, superior cerebellar peduncle, upper lateral pons
• SCA syndrome: Ipsilateral cerebellar ataxia, ipsilateral Horner syndrome, contralateral pain/temperature loss (spinothalamic tract), possible CN IV palsy

PCA Segments (P1–P4)

Thalamoperforating Arteries (P1 Perforators)

• Arise from the P1 segment and basilar tip
• Supply: Medial thalamus, posterior hypothalamus, subthalamic nucleus, paramedian midbrain (including CN III nucleus, red nucleus)
• Artery of Percheron — rare variant (~4–12%) where a single thalamoperforating artery from one P1 supplies both medial thalami
• Artery of Percheron occlusion → bilateral paramedian thalamic infarction → hypersomnolence, vertical gaze palsy, memory deficits; MRI shows characteristic "butterfly" pattern on DWI

Thalamogeniculate Arteries (P2 Perforators)

• Arise from the P2 segment
• Supply: Posterolateral thalamus (ventral posterolateral nucleus [VPL], ventral posteromedial nucleus [VPM], pulvinar, lateral geniculate body)
• Occlusion → Dejerine-Roussy syndrome (thalamic pain syndrome)

PCA Stroke Syndromes

General Principles

• Brainstem strokes produce "crossed" findings — ipsilateral cranial nerve deficits + contralateral long-tract signs (motor/sensory)
• The level of the lesion is determined by which cranial nerve is affected
• Medial structures are supplied by paramedian perforators (from ASA or basilar); lateral structures are supplied by circumferential branches (PICA, AICA, SCA)
• Mnemonic for medial brainstem structures (the "4 Ms"): Motor pathway (corticospinal tract), Medial lemniscus, Medial longitudinal fasciculus (MLF), Motor nucleus of cranial nerves (CN III in midbrain, CN VI/VII in pons, CN XII in medulla)

Lateral Medullary Syndrome (Wallenberg Syndrome)

• Artery: PICA or (more commonly) the intracranial vertebral artery (V4)
• Affected structures and clinical findings:
  • Inferior cerebellar peduncle → ipsilateral cerebellar ataxia (limb and gait)
  • Vestibular nuclei → vertigo, nystagmus, nausea/vomiting
  • Nucleus ambiguus (CN IX, X) → ipsilateral palatal weakness, hoarseness, dysphagia, loss of gag reflex
  • Descending sympathetic tract → ipsilateral Horner syndrome (ptosis, miosis, anhidrosis)
  • Spinal trigeminal nucleus and tract (CN V) → ipsilateral facial pain/temperature loss
  • Spinothalamic tract → contralateral body pain/temperature loss
• Key feature: "Crossed" sensory loss — ipsilateral face + contralateral body (pain/temperature)
• Spared structures: Corticospinal tract (NO motor weakness), medial lemniscus (proprioception/vibration intact)
• Most common brainstem stroke syndrome

Medial Medullary Syndrome (Dejerine Syndrome)

• Artery: Anterior spinal artery or vertebral artery paramedian branches
• Affected structures and clinical findings:
  • Pyramid (corticospinal tract) → contralateral hemiparesis (spares the face)
  • Medial lemniscus → contralateral loss of proprioception and vibration (body)
  • CN XII nucleus/fibers → ipsilateral tongue weakness (tongue deviates toward the lesion)
• Much rarer than lateral medullary syndrome

Lateral Pontine Syndrome (AICA Syndrome)

• Artery: Anterior inferior cerebellar artery (AICA)
• Affected structures and clinical findings:
  • CN VII (facial nucleus/fibers) → ipsilateral facial weakness (LMN-type)
  • CN VIII (cochlear/vestibular) → ipsilateral hearing loss, vertigo, nystagmus
  • CN V (spinal trigeminal nucleus) → ipsilateral facial sensory loss (pain/temperature)
  • Descending sympathetic tract → ipsilateral Horner syndrome
  • Spinothalamic tract → contralateral body pain/temperature loss
  • Middle cerebellar peduncle / cerebellum → ipsilateral cerebellar ataxia
• Distinguishing feature from Wallenberg: Hearing loss and facial weakness point to the pons (AICA), not the medulla (PICA)

Locked-In Syndrome

• Artery: Basilar artery (bilateral paramedian perforator occlusion or basilar thrombosis)
• Lesion: Bilateral ventral pons (basis pontis)
• Clinical features:
  • Quadriplegia (bilateral corticospinal tracts destroyed)
  • Anarthria (bilateral corticobulbar tracts destroyed)
  • Preserved consciousness and cognition (reticular activating system in the tegmentum is spared)
  • Preserved vertical eye movements and blinking (CN III nucleus is in the midbrain, above the lesion)
  • Patient can only communicate via vertical eye movements and blinks
• Must be distinguished from coma — patient is fully awake and aware but cannot move
• EEG shows normal or near-normal waking pattern (confirms consciousness)

Weber Syndrome (Ventral Midbrain)

• Artery: Paramedian perforating branches of PCA (P1) or basilar tip
• Lesion: Ventral midbrain (cerebral peduncle + CN III fascicle)
• Clinical findings:
  • Ipsilateral CN III palsy (ptosis, "down and out" eye, dilated pupil)
  • Contralateral hemiparesis (face, arm, leg — from cerebral peduncle involvement)

Benedikt Syndrome (Tegmental Midbrain)

• Artery: Paramedian perforating branches of PCA (P1)
• Lesion: Midbrain tegmentum (red nucleus + CN III fascicle)
• Clinical findings:
  • Ipsilateral CN III palsy
  • Contralateral tremor/involuntary movements (rubral/Holmes tremor from red nucleus involvement)
  • Contralateral hemisensory loss may be present (medial lemniscus)
• Distinguishing feature from Weber: Involuntary movements (tremor/chorea) instead of/in addition to hemiparesis

Claude Syndrome

• Artery: Paramedian perforating branches of PCA (P1)
• Lesion: Dorsal midbrain tegmentum (red nucleus + superior cerebellar peduncle + CN III)
• Clinical findings:
  • Ipsilateral CN III palsy
  • Contralateral cerebellar ataxia (from superior cerebellar peduncle involvement)
• Distinguishing feature: Ataxia rather than tremor (as in Benedikt) or hemiparesis (as in Weber)

Top of the Basilar Syndrome

• Artery: Occlusion at the basilar tip (rostral basilar artery), affecting the PCA branches, thalamoperforating arteries, and SCA
• Clinical features:
  • Visual field deficits — bilateral hemianopia or cortical blindness (bilateral PCA territory)
  • Altered consciousness — from thalamic and midbrain reticular formation ischemia
  • Vertical gaze palsy — from midbrain (rostral interstitial nucleus of the MLF)
  • Pupillary abnormalities — unreactive or poorly reactive pupils (CN III nucleus)
  • Memory impairment — from bilateral medial thalamic or hippocampal ischemia
  • Behavioral changes — agitation, hallucinations (peduncular hallucinosis — vivid visual hallucinations from midbrain/thalamic ischemia)
• Often due to embolism to the basilar tip (cardiac or artery-to-artery)

Overview

• Cerebral veins are valveless — blood can flow in either direction depending on pressure gradients
• Venous drainage follows a different pattern than arterial supply — arterial territories do not neatly predict venous drainage territories
• Two main systems: superficial (cortical veins → dural sinuses) and deep (subependymal veins → internal cerebral veins → vein of Galen → straight sinus)

Superficial Cerebral Veins

• Drain the cortical surface and subcortical white matter
• Travel across the subarachnoid space, then traverse the subdural space as bridging veins to reach the dural sinuses
• Bridging veins are vulnerable to shearing forces (acceleration/deceleration injury) → subdural hematoma
• Bridging veins are especially vulnerable in the elderly (brain atrophy stretches these veins)

Key Named Superficial Veins

Deep Cerebral Veins

Dural Venous Sinuses

Cerebral Venous Sinus Thrombosis (CVST)

• Risk factors: Oral contraceptives, pregnancy/postpartum, dehydration, hypercoagulable states (Factor V Leiden, prothrombin gene mutation, antiphospholipid syndrome), infection (mastoiditis, sinusitis), malignancy
• Clinical presentation:
  • Headache (most common symptom; ~90%; often progressive, worst-ever, or thunderclap)
  • Elevated ICP — papilledema, nausea/vomiting, CN VI palsy (false localizing sign)
  • Seizures (more common than in arterial stroke; ~40%)
  • Focal deficits — depend on location (parasagittal = leg weakness from SSS; temporal lobe = aphasia from transverse sinus)
  • Venous infarcts may be hemorrhagic (venous infarcts are more likely to bleed than arterial infarcts)
• Imaging:
  • CT: "Dense triangle" sign (hyperdense thrombus in SSS), "empty delta" sign (on contrast CT — enhancing dural walls around non-enhancing thrombus)
  • MRI/MRV: Loss of flow void on T2; thrombus signal depends on age (T1 hyperintense in subacute phase); MRV shows absent flow
  • CT venography or MR venography — best diagnostic studies
• Treatment: Anticoagulation with heparin (even in the presence of hemorrhagic infarction), followed by warfarin or DOAC for 3–12 months depending on underlying etiology

Anterior Spinal Artery (ASA)

• Origin: Two branches from the intracranial V4 segments that merge into a single midline vessel on the ventral spinal cord
• Course: Descends along the anterior median fissure of the entire spinal cord
• Supplies: Anterior two-thirds of the spinal cord — corticospinal tracts (lateral), spinothalamic tracts, anterior horns (motor neurons), central gray matter
• Sulcal (central) arteries branch alternately left and right from the ASA to penetrate the anterior median fissure
• Despite running the entire length of the cord, the ASA is not a continuous conduit — it requires reinforcement from radiculomedullary arteries

Posterior Spinal Arteries (PSA)

• Origin: Paired arteries from V4 segments or sometimes from PICA
• Course: Run along the posterolateral sulci, flanking the dorsal root entry zone
• Supply: Posterior one-third of the spinal cord — dorsal columns (fasciculus gracilis, fasciculus cuneatus), dorsal horns
• Form a pial arterial plexus (vasocorona) on the cord surface
• The posterior spinal arteries have a more robust anastomotic network than the ASA → isolated posterior spinal artery syndrome is rare

Artery of Adamkiewicz (Arteria Radicularis Magna)

• The largest and most important radiculomedullary artery — critical for blood supply to the lower two-thirds of the spinal cord
• Origin: Arises from the left side in ~75–80% of cases; from an intercostal or lumbar artery between T9 and T12 (range T8–L2)
• Course: Enters the spinal canal through an intervertebral foramen, travels with the nerve root, makes a characteristic "hairpin turn" (ascending limb then descending limb) to join the ASA
• Clinical significance: Interruption during aortic surgery, aortic cross-clamping, aortic dissection, or thoracic/lumbar spine surgery → anterior spinal artery syndrome of the thoracolumbar cord
• Preoperative identification by CTA or MRA is performed before thoracoabdominal aortic surgery to plan cross-clamp levels

Radicular and Segmental Arteries

• Radicular arteries enter the spinal canal through intervertebral foramina and reinforce the ASA and PSA
• Only 6–8 major radiculomedullary arteries actually reach the ASA (most radicular arteries supply only the nerve roots)
• Cervical cord: Supplied by vertebral arteries, ascending cervical arteries, and deep cervical arteries — relatively rich blood supply
• Thoracic cord (T4–T8): A watershed zone with the fewest radicular contributors — most vulnerable to hypoperfusion

Spinal Cord Watershed Zones

• Upper thoracic cord (T4–T8) — between cervical arterial supply and the artery of Adamkiewicz territory; most vulnerable to systemic hypotension, aortic pathology
• Central gray matter / anterior horns — watershed between ASA sulcal branches (centrally) and pial vasocorona (peripherally); explains preferential motor neuron vulnerability

Anterior Spinal Artery Syndrome (Beck Syndrome)

• Pathophysiology: Infarction of the anterior two-thirds of the spinal cord (ASA territory)
• Clinical features:
  • Bilateral motor paralysis below the level of the lesion (corticospinal tracts)
  • Bilateral loss of pain and temperature sensation below the level (spinothalamic tracts)
  • Bowel and bladder dysfunction (autonomic pathways)
  • Preserved proprioception and vibration (posterior columns are in the PSA territory — spared)
• Most common causes:
  • Aortic surgery or aortic cross-clamping (artery of Adamkiewicz compromise)
  • Aortic dissection
  • Severe hypotension (systemic hypoperfusion)
  • Atherosclerosis of segmental arteries
  • Fibrocartilaginous embolism (disc herniation material entering spinal arteries)
• Acute onset with back pain is typical; deficit develops over minutes to hours
• MRI: T2 hyperintensity in the anterior cord ("owl eye" pattern on axial DWI from bilateral anterior horn involvement)