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 at the carotid bulb (bifurcation); innervated by the carotid sinus nerve of Hering (a branch of CN IX)

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 lenticulostriates from the M1 segment of MCA; medial lenticulostriates from the A1 segment of ACA (do NOT call A1 perforators "Heubner" — Heubner is a separate, larger A2/AComm-junction perforator; see Heubner section)
• Lateral lenticulostriate (M1) supply: Putamen, lateral globus pallidus (GPe), body of the caudate, superior portion of the posterior limb of the internal capsule, and adjacent corona radiata
• Medial lenticulostriate (A1) supply: anterior hypothalamus, optic chiasm/optic tract, septal region, anterior commissure region — NOT the caudate head or anterior limb of the internal capsule (those are Heubner territory). Note: territory conventions vary by source — some texts group Heubner as the largest medial LSA and include the caudate head and anterior IC within a combined medial-LSA territory.
• Called "arteries of stroke" (Charcot) — lateral LSAs are the most common site of lacunar infarction and of hypertensive (putaminal) intracerebral hemorrhage
• 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 common) or at the A1–ACom junction — it is the largest medial lenticulostriate / largest perforating branch of the ACA
• Course: Doubles back ("recurs") along A1 to enter the anterior perforated substance
• Supplies: Head of the caudate + anterior limb of the internal capsule + anterior putamen + nucleus accumbens + parts of the septal nuclei (this is the territory often mis-attributed to "A1 medial lenticulostriates" — it is Heubner)
• Clinical significance: Vulnerable during ACom aneurysm clipping; occlusion classically → contralateral face/arm-predominant weakness (leg fibers of the corticospinal tract sit in the posterior limb of the IC, which is AChA territory, so the leg tends to be relatively spared; leg weakness suggests ACA cortical/A2 territory or broader injury) + dysarthria + behavioral changes (abulia, personality change from caudate involvement) — clinically mimics a small MCA stroke

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) — carries corticospinal and corticobulbar tracts (this is the source of the dense hemiplegia)
• Optic tract + lateral geniculate nucleus (LGN) — source of the homonymous hemianopia (often with sectoranopia from LGN involvement)
• Medial temporal lobe — uncus, hippocampus, amygdala (partial)
• Medial globus pallidus (GPi) — NOT lateral GP (that's lateral lenticulostriate territory)
• Posterior portion of the thalamus (ventral posterolateral nucleus, partial)
• Choroid plexus of the temporal horn (the artery's namesake)
• Cerebral peduncle (medial portion containing the corticospinal tract)

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 from PCA by the tentorial edge
• Key anatomic relation: CN III (oculomotor) passes between PCA (above) and SCA (below) at the basilar apex. This anatomy explains CN III palsy with basilar tip aneurysm and PCom aneurysm (PCom is the medial border and SCA is the lateral border, with CN III sandwiched between). CN IV (trochlear) runs along the tentorium below SCA — below, not between PCA and SCA.
• Supplies: Superior cerebellar surface, dentate nucleus, superior cerebellar peduncle, upper lateral pons
• SCA syndrome: Ipsilateral cerebellar ataxia (limb & gait), ipsilateral Horner syndrome (descending sympathetics), contralateral pain/temperature loss (spinothalamic tract), ipsilateral hearing impairment (lateral lemniscus, variable), contralateral CN IV palsy or vertical/torsional eye-movement findings (trochlear nucleus / decussation involvement, variable). CN IV palsy is not a core feature of SCA stroke and should not be listed as a defining sign.

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 commonly named/recognized brainstem stroke syndrome (small pontine lacunar infarcts are actually more numerous in clinical practice, but Wallenberg is the classically described eponymic syndrome)
• Wallenberg "5 D's" mnemonic: Dysphagia (nucleus ambiguus), Dysphonia/hoarseness (nucleus ambiguus), Dysmetria/cerebellar ataxia (inferior cerebellar peduncle), Dizziness/vertigo (vestibular nuclei), and Diplopia from skew deviation (vestibular-ocular pathway involvement). (The mnemonic is heterogeneous in the literature; corticobulbar tracts are spared so true dysarthria is not classical, though hoarseness/dysphonia from nucleus ambiguus is universal.)

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 (variable — less consistent than in Wallenberg; the descending sympathetics run laterally throughout the brainstem so AICA can produce Horner, but it is not invariably present)
  • 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)

Overview

• 10-point CT scoring system for early ischemic change in the MCA territory on non-contrast CT
• Designed to operationalize the extent of early MCA infarct in a reproducible way for thrombectomy decision-making
• Assessed on two standardized axial CT slices: one at the level of the basal ganglia/thalamus (caudate, lentiform, IC, insula, M1–M3) and one at the supraganglionic level / corona radiata (M4–M6)

The 10 ASPECTS Regions

Scoring & Clinical Use

• 10 = normal CT; 0 = diffuse early infarction throughout the MCA territory
• One point is deducted for each region showing early ischemic change (loss of gray-white differentiation, sulcal effacement, hypoattenuation)
• ASPECTS ≤ 6 → large established infarct; generally a poor candidate for thrombectomy in the standard 0–6 h window (per HERMES pooled analysis & AHA/ASA guidelines)
• ASPECTS ≥ 6 + LVO (ICA terminus, M1, proximal M2) + early presentation → strong indication for endovascular thrombectomy
• In the extended (6–24 h) window (DAWN, DEFUSE-3), perfusion imaging (penumbra/core mismatch) dominates over raw ASPECTS
• Recent trials (SELECT2, RESCUE-Japan LIMIT, ANGEL-ASPECT) have extended thrombectomy benefit to low-ASPECTS (3–5) large core infarcts in selected patients — the threshold is no longer absolute

Overview

• TICI = Thrombolysis in Cerebral Infarction
• mTICI = modified TICI — introduced to refine the original 2 category (which lumped any partial reperfusion together) and is now the standard endovascular endpoint
• Assigned at the final post-thrombectomy angiogram by the interventionalist

mTICI Grades

Clinical Significance

• mTICI 2b–3 = "successful reperfusion" — the primary technical endpoint in HERMES and every positive endovascular thrombectomy trial
• Higher grade reperfusion (2c/3 vs. 2b) is associated with better 90-day functional outcome (mRS 0–2)
• Number of passes matters: "first-pass effect" (mTICI 2c/3 on a single pass) is associated with the best outcomes

Hunt & Hess (Clinical, 1–5)

WFNS (World Federation of Neurosurgical Societies)

Based on GCS + presence of major motor deficit — more reproducible than Hunt & Hess.

Modified Fisher (Radiographic — Predicts Vasospasm)

• Higher modified Fisher → higher risk of symptomatic vasospasm / delayed cerebral ischemia
• Grades 3 and 4 carry the greatest vasospasm risk and warrant aggressive TCD monitoring

Onset & Mechanism

• Onset: Day 3–14 post-SAH, peak day 7–10
• Mechanism: Blood breakdown products (oxyhemoglobin, endothelin-1) → smooth muscle contraction + endothelial dysfunction + cortical spreading depolarizations + microthrombosis
• Delayed cerebral ischemia (DCI) is the broader clinical syndrome of new focal deficit or decline ≥ 1 hour not explained by other causes — only partially overlaps angiographic vasospasm (cortical spreading depolarization and microcirculatory failure also contribute)

Monitoring

• Transcranial Doppler (TCD) — daily MCA mean velocities; rising velocities precede clinical DCI
  • MCA mean velocity > 120 cm/s = mild vasospasm; > 200 cm/s = severe
  • Lindegaard ratio = MCA mean velocity / extracranial ICA mean velocity
    • > 3 = vasospasm
    • > 6 = severe vasospasm
    • Distinguishes true vasospasm from generalized hyperdynamic flow
• CTA / CT perfusion or DSA for confirmation when TCD or clinical exam suggests DCI
• Clinical exam (neuro checks) remains the most sensitive tool in awake patients

Prevention & Treatment

• Nimodipine 60 mg PO q4h × 21 days — the only proven prophylaxis. Improves outcome independent of vasodilation (likely neuroprotective; angiographic vasospasm is not actually reduced). Hold dose if it drops BP.
• Euvolemic hypertension — the modern replacement for "triple-H" therapy (hypertensive, hypervolemic, hemodilution). Aggressive hypervolemia has been abandoned (no benefit, increased pulmonary edema/cardiac complications).
• Endovascular rescue for symptomatic refractory vasospasm: intra-arterial calcium channel blocker (verapamil, nicardipine) infusion; balloon angioplasty for proximal large-artery spasm
• Maintain euvolemia, normonatremia, normoglycemia; avoid statin discontinuation

Overview

• Lacunar infarct = small (≤ 15 mm) subcortical infarct in the territory of a single deep perforator (lenticulostriate, thalamoperforator, paramedian pontine, etc.)
• Typical locations: basal ganglia, internal capsule, thalamus, basis pontis, cerebellum
• Mechanism: lipohyalinosis / microatheroma of small penetrating arteries (NOT cardioembolic); main risk factors are chronic HTN, DM, age, smoking
• No cortical signs (no aphasia, neglect, visual field deficit, or cortical sensory loss) — this is a defining feature
• C. Miller Fisher described the original five classic syndromes; ~20 distinct lacunar syndromes are now recognized but five are tested

The Five Classic Fisher Lacunar Syndromes

Hypertensive ICH (Charcot-Bouchard Microaneurysms of Small Perforators)

Cerebral Amyloid Angiopathy (CAA)

• Disease of the elderly (typically > 65 y); leading cause of spontaneous lobar ICH in this age group
• Pathology: β-amyloid (Aβ) deposition in the walls of leptomeningeal and cortical small arteries/arterioles → vessel wall fragility, microaneurysm formation, and bleeding
• Hemorrhage pattern: Recurrent lobar (cortical / corticosubcortical) hemorrhages — typically occipital, parietal, or frontal; spares the deep gray matter and pons (which is the hypertensive ICH territory)
• Imaging (SWI/GRE):
  • Multiple lobar microbleeds (cortical/juxtacortical)
  • Cortical superficial siderosis (highly specific)
  • Convexity SAH (focal)
  • White-matter hyperintensities
• Boston criteria 2.0 (2022) — current diagnostic framework integrating hemorrhagic and non-hemorrhagic MRI markers
• "Amyloid spells" (transient focal neurologic episodes) — brief, recurrent, stereotyped sensory / motor symptoms; important stroke / TIA mimic; thought to reflect cortical spreading depolarization over siderosis — antiplatelet therapy in this setting may increase ICH risk
• Often co-exists with Alzheimer disease pathology; CAA accelerates cognitive decline
• Anticoagulation is generally contraindicated in established CAA; antiplatelet use requires individualized risk discussion

Overview

• Infarcts in the borderzone between two arterial territories — the region most vulnerable to hypoperfusion because it sits at the distal end of both vessels' supply
• Mechanisms: systemic hypotension (cardiac arrest, septic shock, surgical hypotension), severe ICA stenosis/occlusion with hypoperfusion, microemboli with impaired washout, severe anemia
• Two distinct anatomic patterns: external (cortical) and internal (subcortical)

External (Cortical) Watershed

Internal (Subcortical) Watershed

• Located in the corona radiata / centrum semiovale at the junction of deep perforator supply (lenticulostriates) and superficial pial-penetrating supply (medullary arteries from MCA cortical branches)
• Classic imaging pattern: "rosary bead" or "string of pearls" — multiple small confluent lesions in a linear paraventricular distribution on DWI
• Strongly associated with chronic high-grade ipsilateral ICA stenosis / occlusion + hemodynamic compromise — an important clue to look for upstream large-vessel disease

Epidemiology

• Most common identifiable cause of ischemic stroke in young adults (< 45 y) — accounts for ~15–20% of strokes in this age group
• Annual incidence: ICA dissection ~3/100,000; VA dissection ~1–1.5/100,000
• Triggers:
  • Trauma — often minor: chiropractic manipulation, cough/sneeze, heavy lifting, sports (martial arts, gymnastics), MVA
  • Connective tissue disorders — fibromuscular dysplasia (FMD), Ehlers-Danlos type IV (vascular), Marfan, osteogenesis imperfecta
  • Recent URI, migraine

ICA Dissection — Clinical Features

• Ipsilateral face / neck / orbital pain or headache (often first symptom; may precede stroke by days)
• Partial Horner syndrome: ptosis + miosis WITHOUT anhidrosis
  • Sympathetic oculomotor fibers run on the ICA → affected by ICA dissection
  • Sympathetic sudomotor (sweat) fibers travel with ECA branches to the face → spared in ICA dissection (hence the absence of anhidrosis on the face)
• Ipsilateral pulsatile tinnitus
• Lower cranial neuropathy (CN IX–XII palsy) if the false lumen compresses the carotid sheath nerves — particularly CN XII palsy
• Delayed cerebral ischemia (TIA or stroke) over hours to weeks — usually embolic from the dissection flap, not hemodynamic

VA Dissection — Clinical Features

• Posterior neck / occipital pain (most common presenting symptom)
• Posterior circulation stroke — classically Wallenberg syndrome from V4 dissection extending into PICA territory
• SAH if V4 (intradural) is involved

Imaging

• CTA / MRA — first-line; demonstrates the dissection flap, false lumen, tapered stenosis ("flame" sign), or pseudoaneurysm
• T1 fat-saturated axial MRI of the neck — "crescent sign" from intramural hematoma (high T1 signal of methemoglobin) within the vessel wall (highly specific)
• Catheter angiography rarely required (reserved for diagnostic uncertainty)

Treatment

• Antiplatelet therapy and anticoagulation are equivalent for stroke prevention — CADISS (Lancet Neurology 2015) and TREAT-CAD (Lancet Neurology 2021) trials showed no difference in stroke recurrence
• Choice is individualized: antiplatelet is generally preferred for simplicity; anticoagulation is sometimes selected for patients with high-burden mobile thrombus or severe luminal stenosis
• Duration: typically 3–6 months, then imaging follow-up; many dissections heal/remodel
• IV thrombolysis is not contraindicated for extracranial dissection (safe in CADISS / observational data)
• Stenting or surgical repair reserved for refractory ischemia or expanding pseudoaneurysm

Normal Aortic Arch

• Three great vessels arise (right to left): brachiocephalic (innominate) artery, left CCA, left subclavian artery
• The innominate trunk bifurcates into the right CCA and right subclavian

Common Variants

Overview

• During embryologic development, the carotid (anterior) and vertebrobasilar (posterior) circulations are connected by four transient pre-segmental arteries that normally involute. Persistence into adulthood is uncommon but high-yield for both vascular imaging and endovascular planning.
• From rostral to caudal: trigeminal → otic → hypoglossal → proatlantal

The Four Persistent Carotid-Basilar Anastomoses

Clinical Significance

• Alters the expected collateral pathways — an ICA occlusion in a patient with a PTA can compromise the posterior circulation
• Important to recognize during neurointervention to avoid inadvertent vessel injury or unexpected non-target embolization
• May be associated with intracranial aneurysms (especially at the proximal/distal junctions)

Definition

• Progressive stenosis/occlusion of the supraclinoid ICA, ICA terminus, and proximal ACA/MCA with development of fragile lenticulostriate / leptomeningeal collateral networks
• "Moyamoya" = Japanese for "puff of smoke" — describing the angiographic appearance of the hypertrophied basal collaterals
• Moyamoya disease = idiopathic, bilateral, often genetic (RNF213 mutation in East Asian populations)
• Moyamoya syndrome = same angiographic pattern in the setting of an underlying disorder — sickle cell disease, Down syndrome, NF1, prior cranial radiation, atherosclerosis, autoimmune disease

Epidemiology & Presentation

• Bimodal age distribution:
  • Children (peak ~5–10 y) → ischemic strokes / TIAs (often triggered by hyperventilation, crying, or hot food — vasoconstriction lowers an already marginal perfusion)
  • Adults (peak ~30–40 y) → hemorrhagic strokes from rupture of fragile dilated lenticulostriate collaterals (IVH or basal ganglia ICH)
• Higher prevalence in East Asian populations (Japan, Korea, China); familial cases ~10%
• May present with seizure, movement disorder (chorea), or cognitive decline

Imaging

• MRA / CTA / DSA: bilateral stenosis or occlusion of the supraclinoid ICA / ICA terminus + hypertrophied lenticulostriate collateral network ("puff of smoke")
• MRI: chronic ischemic lesions in watershed and deep gray matter
• "Ivy sign" on FLAIR — leptomeningeal hyperintensity from slow collateral flow
• Suzuki staging (1–6) describes angiographic progression

Treatment

• Surgical revascularization is mainstay for symptomatic ischemic disease:
  • Direct bypass: STA-MCA bypass (superficial temporal → M3/M4)
  • Indirect bypass: EDAS (encephaloduroarteriosynangiosis), EDAMS, omental transposition — especially favored in children
• Aspirin for ischemic moyamoya; avoid anticoagulation (bleeding risk from fragile collaterals)
• Avoid hyperventilation / hypocapnia (induces vasoconstriction → ischemia)

Genetics & Pathology

• Autosomal dominant
• NOTCH3 mutation on chromosome 19p13
• Pathology: degenerative non-amyloid, non-atherosclerotic arteriopathy of small and medium penetrating cerebral arteries; accumulation of granular osmiophilic material (GOM) in the vessel media — pathognomonic on skin biopsy electron microscopy
• Most common hereditary cause of stroke and vascular dementia in adults

Clinical Features

• Migraine with aura — often the earliest symptom (third decade); can include atypical or prolonged aura
• Recurrent subcortical lacunar infarcts and TIAs beginning in the fourth or fifth decade
• Mood disorder — depression, apathy
• Progressive vascular cognitive impairment / subcortical dementia
• Pseudobulbar palsy and gait disorder in later stages
• Death typically 2–3 decades after onset of strokes

Imaging (T2 / FLAIR MRI)

• Diffuse, confluent subcortical/periventricular white matter hyperintensity
• Anterior temporal pole T2/FLAIR hyperintensity — highly specific for CADASIL (sensitivity ~90%, specificity ~86–95% depending on series; O'Sullivan 2001 original cohort cited specificity ~86%)
• External capsule and corona radiata white matter changes
• Subcortical lacunar infarcts in basal ganglia, thalamus, brainstem
• Microbleeds on SWI

Diagnosis & Management

• Confirmed by NOTCH3 genetic testing; skin biopsy with EM shows GOM (less commonly used today)
• No disease-modifying therapy. Manage vascular risk factors (BP, lipids), aspirin for stroke prevention (debated; bleeding risk from microbleeds), migraine prophylaxis (avoid triptans/vasoconstrictors in those with strokes), antidepressants
• IV tPA is generally avoided in known CADASIL with extensive microbleeds (bleeding risk); decision is individualized

Reversible Cerebral Vasoconstriction Syndrome (RCVS) — "Call-Fleming Syndrome"

• Hallmark: Recurrent thunderclap headaches (often the only symptom) over days to weeks, accompanied by reversible multifocal segmental vasoconstriction of cerebral arteries
• May be complicated by:
  • Convexity (sulcal) SAH (small, non-aneurysmal — the most common bleeding pattern)
  • Ischemic stroke (often borderzone)
  • Lobar ICH
  • PRES-like vasogenic edema (overlap with PRES)
  • Seizures
• Triggers / associations:
  • Postpartum (especially with sympathomimetic drug exposure)
  • Vasoactive drugs: cannabis, cocaine, amphetamines, MDMA, SSRIs, SNRIs, triptans, nasal decongestants (pseudoephedrine), bromocriptine
  • Sexual activity, exertion, Valsalva, bathing in hot water
• Imaging:
  • "String of beads" — multifocal segmental vasoconstriction on MRA/CTA/DSA
  • Findings typically resolve in 1–3 months — defining feature
  • Initial vascular imaging can be normal; repeat at 1–2 weeks if suspicion is high
• Differential: primary CNS vasculitis (PACNS) — RCVS has no CSF inflammation, normal ESR/CRP, and resolves; PACNS has inflammatory CSF and persists/progresses without immunosuppression
• Treatment:
  • Remove the trigger; avoid further vasoconstrictors
  • Calcium channel blockers (nimodipine, verapamil) — symptomatic for headache; debated impact on stroke outcomes
  • Steroids are NOT indicated and may worsen outcomes — an important distinction from vasculitis

Posterior Reversible Encephalopathy Syndrome (PRES)

• Hallmark: Acute / subacute vasogenic edema in the parieto-occipital lobes bilaterally and symmetrically (cortex and subcortical white matter)
• Clinical: encephalopathy, seizures, headache, cortical visual disturbance / cortical blindness, focal deficit; can include status epilepticus
• Pathophysiology: failure of cerebral autoregulation under acute BP surge OR endothelial injury (cytotoxic agents) → vasogenic edema, preferentially affecting the relatively sympathetically denervated posterior circulation
• Triggers:
  • Severe / rapidly rising hypertension (hypertensive emergency)
  • Eclampsia / preeclampsia
  • Calcineurin inhibitors (cyclosporine, tacrolimus), other cytotoxic chemotherapy (cisplatin, bevacizumab)
  • Sepsis
  • Autoimmune disease (SLE, scleroderma renal crisis), TTP, renal failure
• Imaging:
  • Bilateral parieto-occipital T2/FLAIR hyperintensity, vasogenic edema pattern (high ADC on DWI)
  • Atypical PRES can involve brainstem, cerebellum, basal ganglia, frontal lobes — do not exclude PRES based on non-classical distribution
  • ~15% have associated SAH, ICH, or restricted diffusion (worse prognosis)
• Treatment: Aggressive BP control (target reduction of MAP ~20–25% in the first hour), remove offending agent, treat seizures, deliver fetus if eclampsia. Usually fully reversible; persistent edema or ICH worsens prognosis.

MMA Anatomy

• Branch of the maxillary artery (which is a terminal branch of the external carotid artery)
• Enters the cranium through the foramen spinosum
• Runs in the epidural space, deeply grooved into the inner table of the temporal bone (especially in the pterion region)
• Divides into anterior (frontal) and posterior (parietal) branches that supply the dura, periosteum, and outer cranial vault
• Has dangerous anastomoses with the ophthalmic artery (recurrent meningeal branch) — relevant for embolization (risk of non-target embolization to the eye)

Epidural Hematoma (EDH)

• Mechanism: Temporal bone fracture tears the MMA → arterial bleeding into the potential epidural space, stripping dura from inner table
• Classic clinical course:
  • Initial loss of consciousness from the head trauma
  • "Lucid interval" (~30% of patients) — minutes to hours of relative recovery
  • Rapid neurologic deterioration: progressive depression of consciousness, contralateral hemiparesis, ipsilateral blown pupil (uncal herniation compressing CN III)
• Imaging (CT):
  • Biconvex / lens-shaped (lentiform) hyperdense extra-axial collection
  • Does NOT cross suture lines (dural attachment limits spread) — in contrast to subdural hematoma, which crosses sutures but not midline
  • Typically does NOT cross the midline (dura is firmly adherent at the superior sagittal sinus); rare exception is a venous EDH from a torn dural sinus, which may cross the falx or tentorium
• Treatment: Surgical evacuation (craniotomy) for symptomatic / expanding EDH; small asymptomatic EDH can be observed

MMA Embolization for Chronic Subdural Hematoma

• Multiple recent RCTs (EMBOLISE, MEMBRANE, STEM, EMPROTECT) have shown that MMA embolization (with particles or liquid embolic) reduces recurrence and rescue surgery rates after burr-hole drainage of chronic SDH, particularly in the elderly
• Mechanism: MMA supplies the neovascular outer membrane of a chronic SDH; embolization devascularizes the source of recurrent bleeding
• Now considered an adjunctive option for recurrent / high-risk chronic SDH

Overview

• The cerebral vasculature maintains a constant cerebral blood flow (CBF) over a range of mean arterial pressures via myogenic + metabolic + neurogenic + endothelial mechanisms
• Normal autoregulatory range: MAP ~ 60–160 mmHg (CBF ~ 50 mL/100 g/min)
• Outside this range, CBF becomes pressure-passive — falls with hypotension, rises with hypertension
• The curve is shifted rightward in chronic hypertension — chronically hypertensive patients require higher MAP to maintain adequate perfusion and are at risk for hypoperfusion at "normal" pressures
• Autoregulation is impaired or lost in:
  • Acute ischemic stroke (in and around the penumbra)
  • Hemorrhagic stroke / ICH / SAH
  • Traumatic brain injury
  • Sepsis
  • Hepatic encephalopathy

Clinical BP Targets in Stroke & Brain Injury