---

Stroke: Causes & Detailed Comparison

---

What Is a Stroke?

---

PART 1 — Causes of Stroke (All Types)

A. Causes of Ischemic Stroke (~85% of all strokes)

1. Thrombotic (Large-Vessel Disease)

• Atherosclerosis — the most common cause; plaque buildup in carotid or intracranial arteries narrows the lumen, causing in-situ thrombosis
• Carotid artery stenosis — plaques at the carotid bifurcation are a major source
• Intracranial atherosclerosis — more prevalent in Asian, African, and Hispanic populations
• Arterial dissection — spontaneous or traumatic tearing of the arterial wall (carotid or vertebral), forming an intramural hematoma that occludes flow; common in young adults

2. Embolic

• Cardioembolic — clots form in the heart and travel to the brain:
  • Atrial fibrillation (AF) — #1 cardiac cause; left atrial appendage thrombus
  • Acute myocardial infarction with mural thrombus
  • Dilated cardiomyopathy
  • Valvular disease (rheumatic mitral stenosis, prosthetic valves, infective endocarditis)
  • Patent foramen ovale (PFO) — paradoxical embolism from venous clot
• Artery-to-artery embolism — fragments from atherosclerotic plaques in proximal vessels

3. Small-Vessel Disease (Lacunar Stroke)

• Lipohyalinosis — hypertension causes degenerative changes in small perforating arteries
• Microatheroma — small plaque in perforating arteries
• Results in small (<15 mm) deep infarcts in the basal ganglia, thalamus, internal capsule, pons

4. Other / Less Common Causes

---

B. Causes of Hemorrhagic Stroke (~15% of all strokes)

1. Intracerebral Hemorrhage (ICH) — Bleeding INTO Brain Tissue

2. Subarachnoid Hemorrhage (SAH) — Bleeding into the Subarachnoid Space

---

C. Shared / Common Risk Factors for All Strokes

---

PART 2 — Ischemic vs Hemorrhagic Stroke: Detailed Comparison

---

1. Basic Overview

---

2. Pathophysiology

---

3. Clinical Presentation

---

4. Neurological Deficits by Territory

---

5. Diagnosis

---

6. Management

Ischemic Stroke

Hemorrhagic Stroke (ICH)

Subarachnoid Hemorrhage (SAH)

---

7. Complications

---

8. Prognosis

---

Summary Table

---

• Harrison's Principles of Internal Medicine, 21st Edition (p. 12128)
• Reporting Standards for Type B Aortic Dissections (p. 16)
• AHA/ASA Guidelines for Early Management of Acute Ischemic Stroke (2019/2022 updates)
• AHA/ASA Guidelines for Management of Spontaneous ICH (2022)

---

Transient Ischemic Attack (TIA) & Acute Stroke Management

---

PART 1 — TRANSIENT ISCHEMIC ATTACK (TIA)

Definition

"A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction." (Adult Patients With Suspected TIA in the Emergency Department, p. 2)

• The old definition used 24 hours as the cutoff — if symptoms resolved within 24 hours, it was called a TIA
• This was abandoned because ~1/3 of all TIAs show evidence of infarction on MRI despite symptom resolution
• Most TIAs last fewer than 1–2 hours clinically
• If imaging is unavailable and symptoms last >24 hours → classified as clinical stroke

---

Why TIA Is a Medical Emergency

---

Causes of TIA (Same as Ischemic Stroke)

---

Clinical Features of TIA

Carotid (Anterior Circulation) TIA

• Contralateral hemiplegia or hemiparesis (face/arm > leg)
• Contralateral hemisensory loss
• Aphasia (dominant hemisphere)
• Amaurosis fugax — transient monocular blindness ("curtain descending") from ophthalmic artery ischemia — classic TIA symptom

Vertebrobasilar (Posterior Circulation) TIA

• Vertigo, diplopia, dysphagia, dysarthria
• Ataxia, drop attacks
• Bilateral weakness or sensory loss
• Hemianopia or cortical blindness

Important: Isolated dizziness, isolated syncope, amnesia, or confusion alone are not TIA until proven otherwise.

---

ABCD2 Score — Risk Stratification

Score Interpretation

Per the meta-analysis by Wardlaw et al (2015) cited in Adult Patients With Suspected TIA in the Emergency Department (p. 33):

• ABCD2 ≥4 at 7 days: stroke risk 5.2%; at 90 days: 8.9%
• ABCD2 <4 at 7 days: stroke risk 1.4%; at 90 days: 2.4%
• Sensitivity of ABCD2 ≥4 for 7-day stroke: 86.7%

---

Investigations for TIA

Immediate (within 24 hours)

Within 48–72 Hours

---

Management of TIA

Immediate (Emergency Department)

• Aspirin 300–325 mg loading dose immediately (if no hemorrhage on CT)
• Dual antiplatelet therapy (DAPT): Aspirin + Clopidogrel (75 mg)
  • For high-risk TIA (ABCD2 ≥4) or minor ischemic stroke (NIHSS ≤3)
  • Continue for 21 days, then switch to monotherapy
  • Based on POINT and CHANCE trials — reduces 90-day stroke risk by ~25%
• Do NOT use anticoagulation as first-line for non-AF TIA

• Start anticoagulation (NOAC preferred over warfarin) once hemorrhage excluded
• Timing after TIA: can start immediately (no significant infarct burden)
• Target INR 2–3 if warfarin used

• Target <130/80 mmHg long-term (AHA 2021)
• In the acute phase: do not lower aggressively if BP <220/120 (unless hypertensive emergency)
• Start or resume antihypertensives within 24–48 hours

• High-intensity statin (atorvastatin 40–80 mg) for all non-cardioembolic TIA
• Target LDL <70 mg/dL (or <55 mg/dL in high-risk)

Hospitalization vs. Outpatient?

Carotid Revascularization

• Carotid endarterectomy (CEA) or carotid artery stenting (CAS) for ipsilateral carotid stenosis ≥50%
• Greatest benefit with stenosis 70–99%
• Should be performed within 2 weeks of TIA (ideally within 48–72 hours if stable)

Secondary Prevention (Long-term)

---

PART 2 — ACUTE MANAGEMENT OF STROKE (DETAILED)

---

The "Time = Brain" Principle

Every minute during stroke, approximately 1.9 million neurons die. Every hour without treatment = 3.6 years of accelerated brain aging.

---

Step 1 — Pre-Hospital / EMS

---

Step 2 — Emergency Department — Initial Assessment (Target: Door-to-CT <25 min)

Primary Survey — ABCs

Rapid History

• Exact time of symptom onset (or last known well)
• Recent surgery, trauma, bleeding history
• Medications (anticoagulants, antiplatelets)
• Prior stroke/TIA
• Contraindications to tPA

NIHSS (NIH Stroke Scale)

---

Step 3 — Emergency Imaging (Target: Door-to-CT-read <45 min)

Early CT Signs of Ischemia

• Hyperdense MCA sign — clot in MCA visible as bright vessel
• Loss of insular ribbon — loss of gray-white differentiation in insula
• ASPECTS score — 0–10; score <6 = large infarct, poor prognosis, consider excluding from thrombectomy

---

Step 4 — IV Thrombolysis (tPA / Alteplase)

Mechanism

Eligibility Criteria

Absolute Contraindications to tPA

Relative Contraindications (Risk-Benefit Discussion)

• Minor or rapidly improving symptoms
• Seizure at stroke onset
• Major surgery within 14 days
• GI/urinary bleeding within 21 days
• Recent MI within 3 months
• Pregnancy (relative — can be used if benefit outweighs risk)

Dosing

• 0.9 mg/kg IV (max 90 mg)
• 10% as IV bolus over 1 minute, remainder over 60 minutes
• Admit to ICU/stroke unit post-tPA; monitor BP every 15 minutes

Post-tPA Monitoring

• No antiplatelets or anticoagulants for 24 hours after tPA
• Watch for symptomatic intracranial hemorrhage (sICH) — ~6%
• BP target after tPA: <180/105 mmHg for 24 hours
• Repeat CT/MRI at 24 hours before starting antiplatelets

Tenecteplase — Newer Alternative

• Single IV bolus (0.25 mg/kg, max 25 mg)
• Easier to administer; similar efficacy to alteplase in recent trials (AHA 2022 guidelines now include as alternative)

---

Step 5 — Mechanical Thrombectomy (Endovascular Therapy)

Eligible Vessels

• Internal carotid artery (ICA)
• M1 and M2 segments of MCA
• Basilar artery
• Vertebral artery

Time Windows

Bridging Strategy

• If patient is eligible for both tPA AND thrombectomy → give tPA first without waiting to assess response
• Do NOT delay thrombectomy to assess tPA response (Endovascular Therapy of Acute Ischemic Stroke, p. 3)
• Rate of tPA-induced recanalization before thrombectomy is <10% — don't wait

Direct Thrombectomy (No tPA)

• When tPA is contraindicated (hemorrhage risk, >4.5 hours, INR elevated, recent surgery)
• Proceed directly to catheter-based clot retrieval

Technique

• Stent retriever (Solitaire, Trevo) — mesh device captures and extracts clot
• Aspiration thrombectomy — direct suction catheter
• Combined approach — both techniques
• Goal: TICI 2b/3 reperfusion (≥50% territory reperfused)

Outcomes

• mTICI 2b-3 reperfusion → 50–60% achieve functional independence at 90 days
• Number needed to treat (NNT) to prevent disability: ~2.6

---

Step 6 — General Stroke Unit Care (Neuroprotection)

Blood Pressure Management

Glucose Management

• Hyperglycemia (>180 mg/dL) worsens infarct — treat with insulin
• Hypoglycemia mimics stroke and worsens outcome — treat immediately with dextrose
• Target: 140–180 mg/dL in acute phase

Temperature

• Fever (>37.5°C) dramatically worsens outcomes — use acetaminophen aggressively
• Therapeutic hypothermia: investigational, not standard of care

Oxygen

• Supplemental O2 only if SpO2 <94%
• Routine O2 supplementation does NOT improve outcomes (IST-3)

Positioning

• Head of bed flat (0°) for ischemic stroke — improves cerebral perfusion
• HOB 30° for hemorrhagic stroke, risk of aspiration

Dysphagia Screening

• Screen before any oral intake
• Nil by mouth until formal swallow assessment
• NG tube / PEG if persistent dysphagia

Cardiac Monitoring

• Continuous telemetry for ≥24 hours (ideally 72 hours)
• Detect paroxysmal AF — found in ~15% of cryptogenic strokes
• Neurogenic cardiac injury (Takotsubo, ST changes, troponin elevation) — common post-stroke

---

Step 7 — Acute Hemorrhagic Stroke Management

Intracerebral Hemorrhage (ICH)

Subarachnoid Hemorrhage (SAH)

---

Step 8 — Secondary Prevention (Post-Stroke)

---

Step 9 — Stroke Unit Care & Rehabilitation

---

Acute Stroke Management Summary Algorithm

SYMPTOM ONSET / LAST KNOWN WELL
         ↓
   EMS: BE-FAST, glucose, IV access, alert hospital
         ↓
   ED ARRIVAL → Stroke Alert
         ↓
   ABCs + NIHSS + Blood glucose
         ↓
   STAT Non-contrast CT Brain (<25 min)
         ↓
   ┌─────────────────────────────────────┐
   │ HEMORRHAGE?                         │
   │  YES → ICH/SAH protocol             │
   │  NO → Ischemic stroke pathway       │
   └─────────────────────────────────────┘
         ↓ (Ischemic)
   CTA Head & Neck → LVO?
         ↓
   ┌─────────────────────────────────────────────────────────┐
   │ tPA ELIGIBLE? (≤4.5 hrs, no contraindications)          │
   │  YES → Give tPA immediately (Door-to-Needle <60 min)    │
   │   + If LVO → proceed to thrombectomy (don't wait)       │
   │  NO + LVO → Direct thrombectomy (≤24 hrs with mismatch) │
   └─────────────────────────────────────────────────────────┘
         ↓
   STROKE UNIT ADMISSION
   BP / Glucose / Temp / O2 / Dysphagia screen / Cardiac monitor
         ↓
   SECONDARY PREVENTION + REHABILITATION

---

• Adult Patients With Suspected TIA in the Emergency Department (p. 2, p. 33)
• Endovascular Therapy of Acute Ischemic Stroke (p. 3)
• Harrison's Principles of Internal Medicine, 21st Edition (p. 12128)
• AHA/ASA Guidelines for Early Management of Acute Ischemic Stroke (2019)
• AHA/ASA Guidelines for Management of Spontaneous ICH (2022)
• DAWN, DEFUSE-3, POINT, CHANCE, AVERT trials

---

MANAGEMENT OF STROKE — 10-Marker Answer

🧠 Master Mnemonic: "FAST BE SAFE RECOVER"

Use this to remember ALL domains of stroke management in sequence.

---

TRICK 1 — "TIME = BRAIN" 🕐

Every 1 minute of stroke = 1.9 million neurons lost Every 1 hour = 3.6 years of accelerated brain aging

---

TRICK 2 — Pre-Hospital: Mnemonic "BE-FAST"

• Check blood glucose immediately (hypoglycemia = #1 stroke mimic)
• Do NOT lower BP in field
• Pre-notify hospital → Stroke Alert

---

TRICK 3 — ED Initial Assessment: Mnemonic "ABCDE"

• 0 = Normal | 1–4 = Minor | 5–15 = Moderate | 16–20 = Mod-Severe | 21–42 = Severe

---

TRICK 4 — Emergency Imaging: Mnemonic "CT FIRST, MRI CONFIRMS"

• Hyperdense MCA sign = clot in MCA (visible as bright vessel on CT)
• Hypodense area = ischemic infarct
• Hyperdense area = hemorrhage

---

TRICK 5 — Separate Ischemic from Hemorrhagic: Mnemonic "HICH"

Hemorrhage → Image first → Contraindicated for tPA → Hypertension control

---

TRICK 6 — IV tPA (Thrombolysis): Mnemonic "4.5 HOURS, 0.9 mg/kg, 90 MAX"

• 0.9 mg/kg IV (max 90 mg)
• 10% as bolus over 1 min → rest over 60 min

Contraindications Trick: "BRAIN BLEED"

---

TRICK 7 — Mechanical Thrombectomy: Mnemonic "LVO = GO"

If Large Vessel Occlusion found → GO for thrombectomy

Give tPA first + proceed to thrombectomy WITHOUT WAITING for tPA response Direct thrombectomy if tPA contraindicated

---

TRICK 8 — General Stroke Unit Care: Mnemonic "GOFTS"

---

TRICK 9 — BP Management: Mnemonic "Three Targets"

Drug of choice for BP lowering: IV Labetalol, IV Nicardipine, or IV Clevidipine

---

TRICK 10 — Hemorrhagic Stroke — Mnemonic "REVERSE BLEED"

---

TRICK 11 — SAH Specific: Mnemonic "ANNS"

---

TRICK 12 — Secondary Prevention: Mnemonic "ABCDS"

• PFO closure — in young cryptogenic stroke with PFO
• AF management — cardioversion, rate control, anticoagulation
• Long-term cardiac monitoring — implantable loop recorder for cryptogenic stroke

---

TRICK 13 — Rehabilitation: Mnemonic "MOSS"

---

COMPLETE 10-MARK ANSWER OUTLINE

---

One-Page Visual Summary

STROKE MANAGEMENT — QUICK RECALL

PRE-HOSPITAL          ED ARRIVAL              IMAGING
BE-FAST               ABCs + NIHSS            NCCT Brain
Glucose check         IV access + ECG         → No bleed? = Ischemic
Stroke alert          BP monitoring           → Bleed? = Hemorrhagic
Time = Brain          Glucose control         CTA → LVO?

ISCHEMIC                                    HEMORRHAGIC
↓                                           ↓
tPA (≤4.5 hrs)                             Reverse anticoag (PCC/Vit K)
0.9 mg/kg, max 90 mg                       SBP <140 mmHg
BP <185/110 before                         Surgery if cerebellar >3cm
LVO → Thrombectomy                         NO tPA EVER
(0–24 hrs, don't wait)                     Nimodipine if SAH

SUPPORTIVE CARE (GOFTS)
Glucose 140–180 | O₂ if <94% | Fever treat | HOB flat | Swallow screen

SECONDARY PREVENTION (ABCDS)
Antiplatelet/AC | BP <130/80 | Carotid Rx | Diabetes/Diet/Dyslipid | Smoking

REHAB (MOSS)
MDT | OT + Mobilise | Speech | Support (psychology)

---

---

LACUNAR STROKE — Detailed Description

---

1. DEFINITION

"Lacunar infarction refers to infarction following atherothrombotic or lipohyalinotic occlusion of a small artery in the brain. The term small-vessel stroke is now the preferred term."

Key Defining Features:

---

2. ANATOMY — WHERE DO LACUNAR INFARCTS OCCUR?

Most Common Sites (Memorize):

1. Putamen (most common)
2. Thalamus
3. Pons (basis pontis)
4. Internal capsule (posterior limb and genu)
5. Caudate nucleus
6. Cerebellum (less common)

Lacunar infarcts do NOT occur in the cortex — cortical involvement always suggests embolism or large vessel disease.

---

3. PATHOPHYSIOLOGY

Two Main Mechanisms:

A. Lipohyalinosis (Primary Small Vessel Disease)

• The most common mechanism
• Chronic hypertension and diabetes cause degenerative changes in the wall of small penetrating arteries
• The normal vessel wall is replaced by lipid deposits and hyaline material → vessel wall thickens → lumen narrows → occlusion
• Affects arteries 40–200 µm in diameter
• Leads to fibrinoid necrosis in acute hypertensive crises

B. Microatheroma

• Small atherosclerotic plaque forms at the origin of the penetrating artery (where it branches off the parent vessel)
• Causes in-situ thrombotic occlusion
• More common in larger penetrating arteries (200–800 µm)
• Associated with diabetes mellitus and dyslipidemia

C. Other (Less Common) Mechanisms

Pathological Sequence:

Hypertension / Diabetes
        ↓
Lipohyalinosis / Microatheroma
        ↓
Lumen narrowing of penetrating artery
        ↓
Thrombotic occlusion
        ↓
Small deep infarct (<15 mm)
        ↓
Necrosis → macrophage infiltration
        ↓
Cavitation → small fluid-filled cavity ("lacune")

---

4. RISK FACTORS

Primary (Strongest):

Secondary:

Key distinction: Lacunar strokes are NOT primarily caused by atrial fibrillation or carotid atherosclerosis — those cause cortical/embolic infarcts. If a "lacunar" infarct is found with AF, a cardioembolic cause must be excluded.

---

5. CLASSICAL CLINICAL SYNDROMES

Syndrome 1 — Pure Motor Hemiparesis (PMH)

Most common lacunar syndrome (~50% of lacunar strokes)

Syndrome 2 — Pure Sensory Stroke (PSS)

Syndrome 3 — Ataxic Hemiparesis (AH)

Syndrome 4 — Dysarthria-Clumsy Hand Syndrome (DCHS)

Summary Table of Classic Syndromes:

Additional / Less Common Syndromes:

• Sensorimotor stroke — combined motor + sensory; thalamocapsular infarct
• Hemichorea-hemiballismus — involuntary movements; subthalamic nucleus infarct
• Thalamic dementia — bilateral thalamic infarcts; severe memory loss
• Locked-in syndrome — bilateral pontine base infarcts (rare but important)

---

6. WHAT LACUNAR STROKE DOES NOT CAUSE

Presence of ANY cortical feature in a suspected lacunar stroke → reconsider the diagnosis → look for embolic or large vessel cause.

---

7. IMAGING

CT Brain

MRI Brain

White Matter Changes (Leukoaraiosis):

• Seen on FLAIR/T2 as diffuse white matter hyperintensities
• Marker of widespread small vessel disease
• Associated with cognitive decline, gait disturbance, and recurrent lacunar strokes
• Graded by Fazekas scale (0–3)

---

8. DIAGNOSIS

Diagnostic Criteria for Lacunar Stroke:

1. Clinical syndrome consistent with one of the classic lacunar syndromes
2. No cortical signs
3. Lesion <15 mm on imaging in a deep location
4. No large vessel source (carotid stenosis, cardioembolic)
5. Risk factors present (hypertension, diabetes)

Investigations:

Differential Diagnosis:

---

9. PROGNOSIS

Lacunar State (État Lacunaire):

• Multiple recurrent lacunar infarcts over years
• Pseudobulbar palsy — bilateral UMN lesions → emotional lability, dysarthria, dysphagia
• Marche à petits pas — short-stepped, shuffling gait
• Vascular dementia — stepwise cognitive decline
• Urinary incontinence
• Mimics Parkinson's disease but lacks tremor; rigidity is symmetrical

---

10. MANAGEMENT

Acute Phase

A. Thrombolysis (tPA)

• Lacunar strokes CAN receive IV tPA if within 4.5 hours and no contraindications
• However, benefit may be less clear than for large vessel strokes (smaller penumbra)
• Still recommended by AHA guidelines if eligible

B. General Supportive Care

• BP management: permissive hypertension acutely (do not lower unless >220/120)
• Glucose: target 140–180 mg/dL
• Temperature: treat fever aggressively
• Swallowing screen before oral intake

Antiplatelet Therapy (Key Treatment)

Anticoagulation (warfarin/NOAC) is NOT superior to antiplatelet therapy for small vessel lacunar stroke (SPS3 trial) and increases bleeding risk — do NOT use unless AF is present.

Risk Factor Control (Most Important Long-term Intervention)

Intensive BP lowering is the single most important intervention to prevent recurrent lacunar strokes — target SBP <130 mmHg (SPS3 trial showed benefit).

Secondary Prevention Summary:

Rehabilitation

• Physiotherapy — strength training, gait rehabilitation
• Occupational therapy — ADL retraining
• Speech therapy — dysarthria, dysphagia
• Cognitive rehabilitation — for vascular mild cognitive impairment
• Psychological support — post-stroke depression (SSRIs effective)

---

11. QUICK EXAM SUMMARY TABLE

---

• Harrison's Principles of Internal Medicine, 21st Edition (p. 12146, 12148)
• AHA/ASA Ischemic Stroke Guidelines (2019)
• SPS3 Trial (Secondary Prevention of Small Subcortical Strokes)
• CHANCE and POINT Trials (dual antiplatelet therapy)
• PROGRESS Trial (perindopril + indapamide for BP)

---

BLOOD SUPPLY OF THE BRAIN — Complete Detail

---

OVERVIEW

---

PART 1 — ANTERIOR CIRCULATION (CAROTID SYSTEM)

---

A. Common Carotid Artery (CCA)

• Right CCA — arises from the brachiocephalic trunk (innominate artery)
• Left CCA — arises directly from the aortic arch
• Bifurcates at the level of C4 (upper border of thyroid cartilage) into:
  • External carotid artery (ECA) → face, scalp, meninges
  • Internal carotid artery (ICA) → brain

---

B. Internal Carotid Artery (ICA) — Segments

ICA Terminates by dividing into:

• Anterior Cerebral Artery (ACA)
• Middle Cerebral Artery (MCA)

---

C. Ophthalmic Artery

• First intracranial branch of ICA (C6 segment)
• Enters orbit via optic canal
• Branches: Central retinal artery (supplies retina), posterior ciliary arteries, supraorbital, supratrochlear arteries
• Central retinal artery occlusion → sudden painless monocular blindness (like "curtain" descending) — amaurosis fugax in TIA

---

D. Anterior Choroidal Artery (AChA)

• Arises from ICA (C7 segment)
• Small but critically important
• Supplies:
  • Posterior limb of internal capsule (genu and retrolenticular part)
  • Optic tract
  • Lateral geniculate body
  • Hippocampus
  • Amygdala
  • Choroid plexus of lateral ventricle
• Occlusion → Hemiplegia + hemianesthesia + hemianopia (three H's)

---

E. Anterior Cerebral Artery (ACA)

A1 Deep Branches (Medial Lenticulostriate Arteries):

• Anterior limb of internal capsule
• Anterior perforated substance
• Amygdala
• Anterior hypothalamus
• Inferior head of caudate nucleus

A2 Cortical Branches:

ACA Cortical Territory:

• Medial surface of frontal and parietal lobes
• Superior 1 cm of lateral cortex (parasagittal strip)
• Paracentral lobule (motor/sensory for leg and foot)
• Anterior corpus callosum
• Anterior cingulate gyrus

ACA Occlusion Syndrome:

---

F. Middle Cerebral Artery (MCA)

Segments:

M1 Deep Branches — Lenticulostriate Arteries (LSA):

• Arise at right angles from M1
• Penetrate anterior perforated substance
• Supply: Putamen, caudate nucleus, globus pallidus, posterior limb of internal capsule, corona radiata
• These are the vessels most commonly involved in hypertensive hemorrhage and lacunar stroke

MCA Cortical Branches (M2–M4):

MCA Cortical Territory:

• Entire lateral surface of cerebral hemisphere EXCEPT:
  • Superior 1 cm strip (ACA)
  • Occipital pole and inferior temporal (PCA)
• Primary motor cortex (face + arm > leg)
• Primary sensory cortex (face + arm > leg)
• Broca's area (dominant inferior frontal gyrus — speech production)
• Wernicke's area (dominant superior temporal gyrus — speech comprehension)
• Angular gyrus (reading, writing)
• Insula
• Basal ganglia, internal capsule (via LSA)

MCA Occlusion Syndromes:

• Broca's (expressive) aphasia — dominant
• Contralateral face + arm weakness (leg spared)
• Contralateral face + arm sensory loss

• Wernicke's (receptive) aphasia — dominant
• Contralateral homonymous superior quadrantanopia
• Hemispatial neglect — non-dominant

---

PART 2 — POSTERIOR CIRCULATION (VERTEBROBASILAR SYSTEM)

---

A. Vertebral Arteries (VA)

• Arise from subclavian arteries bilaterally
• Enter skull through foramen magnum
• Travel along anterior surface of medulla
• Unite at pontomedullary junction to form the Basilar Artery

Branches of Vertebral Artery:

PICA Occlusion — Lateral Medullary Syndrome (Wallenberg Syndrome):

Memory trick: In Wallenberg — CROSS pattern — ipsilateral face, contralateral body for pain/temp loss

---

B. Basilar Artery

Named Branches of Basilar Artery:

• Supplies: Lateral lower pons + inferior cerebellum + inner ear (labyrinthine artery often a branch)
• Occlusion → Lateral inferior pontine syndrome (similar to Wallenberg but at pontine level):
  • Ipsilateral facial weakness (CN VII nucleus)
  • Ipsilateral hearing loss, tinnitus, vertigo (CN VIII)
  • Ipsilateral facial numbness (CN V)
  • Ipsilateral Horner's syndrome
  • Ipsilateral limb ataxia
  • Contralateral body pain/temp loss

• Occlusion → Medial pontine syndromes:
  • CN VI palsy (ipsilateral) + contralateral hemiplegia = Millard-Gubler syndrome
  • Bilateral pontine base infarct → Locked-in syndrome (quadriplegia + preserved consciousness)
  • Internuclear ophthalmoplegia (INO) — MLF lesion

• Supplies: Superior cerebellum + dorsolateral upper pons
• Occlusion:
  • Ipsilateral limb ataxia, dysmetria
  • Contralateral pain/temp loss (body + face)
  • Ipsilateral Horner's syndrome
  • Ipsilateral partial CN IV palsy

---

C. Posterior Cerebral Artery (PCA)

P1 Deep Branches — Thalamoperforating Arteries:

• Supply thalamus (anterolateral, posteromedial nuclei)
• Posterior perforated substance
• Subthalamic nucleus
• Midbrain (cerebral peduncle, red nucleus, substantia nigra)

P2 Cortical Branches:

PCA Cortical Territory:

• Occipital lobe (primary + association visual cortex)
• Inferior and medial temporal lobe (fusiform, parahippocampal gyrus, hippocampus)
• Posterior thalamus
• Midbrain
• Splenium of corpus callosum

PCA Occlusion Syndromes:

---

PART 3 — CIRCLE OF WILLIS

         ACA (left) ——— ACoA ——— ACA (right)
              |                        |
         ICA (left)               ICA (right)
              |                        |
         PCoA (left)              PCoA (right)
              |                        |
         PCA (left) ——— Basilar ——— PCA (right)
                             |
                    Vertebral ×2

Components:

Function of Circle of Willis:

• Collateral circulation — if one artery is occluded, blood can reach the territory via the circle
• Provides pressure equalization across cerebral vasculature
• Only 20–25% of people have a complete, functional Circle of Willis — many have hypoplastic or absent segments

Clinical Importance:

---

PART 4 — INTERNAL CAPSULE BLOOD SUPPLY

A small infarct in the posterior limb of IC → pure motor hemiparesis (entire body — face + arm + leg) — classic lacunar syndrome

---

PART 5 — BRAINSTEM BLOOD SUPPLY SUMMARY

Key Brainstem Stroke Syndromes:

---

PART 6 — VENOUS DRAINAGE OF THE BRAIN

Superficial (Cortical) Veins:

Deep (Central) Veins:

Dural Venous Sinuses:

Cavernous Sinus — Special Importance:

• CN III, IV, V1, V2, VI in its walls/lumen
• ICA (with sympathetic plexus) traversing it
• Communicates across midline via intercavernous sinuses

Cerebral Venous Sinus Thrombosis (CVST):

• Clotting in dural venous sinuses
• Causes: hypercoagulability, OCP, pregnancy, dehydration, infection, malignancy
• SSS most commonly affected
• Presents: headache, seizures, focal deficits, papilledema, venous infarction (often hemorrhagic)
• Treatment: anticoagulation (even with hemorrhagic infarct)

---

COMPLETE SUMMARY TABLE

---

• Harrison's Principles of Internal Medicine, 21st Edition (p. 12109, 12115, 12148)
• Gray's Anatomy for Students
• Neuroanatomy: An Illustrated Colour Text
• AHA/ASA Stroke Guidelines (2019)