Overview

This lecture provides an in-depth review of stroke types, focusing on cerebrovascular anatomy, diagnosis and management of acute ischemic and hemorrhagic strokes, stroke mechanisms, and prevention strategies.

Cerebrovascular Anatomy & Vascular Territories

• The cerebral circulation is divided into anterior (carotid) and posterior (vertebral-basilar) systems.
• The Circle of Willis allows collateral blood flow; only 1/3 of people have a complete circle.
• ACA supplies medial frontal lobes (leg weakness, abulia); MCA supplies most of the hemispheres (hemiparesis, aphasia, neglect); PCA supplies thalamus and occipital lobe (vision, sensory loss).
• Brainstem and cerebellum supplied by branches of vertebrobasilar system (basilar, SCA, AICA, PICA).

Acute Ischemic Stroke: Diagnosis & Management

• Acute focal neurologic deficit differential includes stroke, seizure, hypoglycemia, tumor, demyelination, infection, migraine.
• CT head is first-line to rule out hemorrhage; early CT is often normal in ischemia.
• NIH Stroke Scale quantifies deficits; higher scores mean more severe strokes.
• Ischemic core: irreversible damage; penumbra: salvageable tissue.
• Fast treatment with IV tPA (within 4.5 hours) or endovascular thrombectomy for large vessel occlusion.
• "Time is brain"—every minute delay results in neuronal loss.

Secondary Injury Prevention & Stroke Workup

• Post-recanalization: strict BP control (140–160 systolic) to avoid hemorrhagic transformation.
• Secondary prevention: address homeostasis (glucose, fever, electrolytes), prevent cerebral edema.
• Full workup: MRI, vascular imaging (CTA/MRA), cardiac evaluation (EKG, echocardiogram, monitoring), risk factor modification.

Ischemic Stroke Mechanisms

• Five main mechanisms: large vessel disease, small vessel (lacunar), cardioembolic, rare causes (dissection, hypercoagulation, vasculitis), cryptogenic.
• Large vessel strokes cause TIAs and are due to atherosclerosis; small vessel strokes are subcortical and milder.
• Cardioembolic strokes (e.g., atrial fibrillation) are larger, more severe, and have highest recurrence risk.
• Rare causes include dissection, sickle cell, vasculitis, and genetic conditions.

Hemorrhagic Stroke: Diagnosis & Management

• Includes intraparenchymal (deep or lobar) and subarachnoid hemorrhages.
• Deep (hypertensive) hemorrhages often in basal ganglia, thalamus; lobar hemorrhages caused by AVMs, amyloid angiopathy, tumors.
• Main goals: prevent expansion (BP control, reverse coagulopathy), address mass effect, investigate cause.
• Minimally invasive surgery with TPA (MISTIE) can reduce hematoma size.

Subarachnoid Hemorrhage (SAH)

• Most non-traumatic SAH caused by ruptured saccular aneurysms at Circle of Willis branch points.
• Classic symptoms: thunderclap headache, neck stiffness, nausea, lethargy.
• Early complications: rebleeding, hydrocephalus, vasospasm.
• Secure aneurysm, aggressive BP control, monitor for complications, secondary prevention (stop smoking, consider aspirin).

Key Terms & Definitions

• Ischemic core — brain region with irreversible damage due to loss of blood flow.
• Penumbra — at-risk brain tissue that may be saved with timely reperfusion.
• NIH Stroke Scale — a standardized exam to quantify stroke severity.
• tPA (tissue plasminogen activator) — medication to dissolve clots in acute ischemic stroke.
• Thrombectomy — mechanical removal of a clot from a cerebral artery.
• Lacunar stroke — small, deep infarct due to small vessel disease.
• Cardioembolic stroke — stroke caused by emboli from the heart.
• MISTIE — minimally invasive surgery using TPA to evacuate brain hematomas.
• Subarachnoid hemorrhage — bleeding into the space between the pia and arachnoid mater.

Action Items / Next Steps

• Review cerebrovascular anatomy, vascular territories, and stroke syndromes.
• Practice reading non-contrast head CT for acute stroke.
• Know the indications, contraindications, and time limits for tPA and thrombectomy.
• Complete any homework: List non-stroke causes of thunderclap headache.
• Study risk factor modification and secondary stroke prevention strategies.

Certainly! Here is a comprehensive, detailed summary and review of the lecture on stroke, covering all key points and concepts presented:

Comprehensive Summary and Review: Stroke Neurology Lecture

Introduction

• The lecture is delivered by Dr. Igor Ribbiting, a vascular neurologist.
• Goal: To train listeners to manage acute cerebrovascular emergencies, focusing on ischemic and hemorrhagic strokes.
• Objectives:
  • Review cerebrovascular anatomy and vascular syndromes.
  • Discuss diagnosis and management of acute ischemic stroke.
  • Review ischemic stroke mechanisms and prevention.
  • Discuss diagnosis and management of acute hemorrhagic stroke.
  • Review hemorrhagic stroke mechanisms and prevention.

Cerebrovascular Anatomy and Vascular Territories

Overview of Circulation

• The cerebral circulation is divided into:
  • Anterior circulation: supplied by the internal carotid arteries (ICA).
  • Posterior circulation: supplied by vertebral arteries merging into the basilar artery.
• The Circle of Willis connects anterior and posterior circulations, allowing collateral flow.
  • Only about 1/3 of people have a complete Circle of Willis.
• Key vessels:
  • Common carotid arteries bifurcate into external carotid (supplies face/neck) and internal carotid (supplies brain).
  • Vertebral arteries arise from subclavian arteries, join to form basilar artery.
  • Basilar artery branches: anterior inferior cerebellar artery (AICA), superior cerebellar artery (SCA), posterior cerebral arteries (PCA).
  • Posterior communicating arteries connect PCAs to ICAs.

Vascular Territories and Corresponding Deficits

• Anterior cerebral artery (ACA):
  • Supplies medial frontal lobes.
  • Deficits: contralateral leg weakness, abulia (lack of motivation), amnesia.
• Middle cerebral artery (MCA):
  • Supplies most of the lateral hemispheres.
  • Deficits: contralateral hemiparesis (face and arm > leg), gaze preference toward lesion side, sensory loss, aphasia (dominant hemisphere), neglect (non-dominant hemisphere), apraxia, dysarthria.
• Posterior cerebral artery (PCA):
  • Supplies thalamus, occipital lobes, midbrain.
  • Deficits: contralateral sensory loss, homonymous hemianopia, behavioral abnormalities, transcortical aphasia (dominant thalamus), neglect (non-dominant thalamus).
• Brainstem and cerebellar arteries:
  • Basilar artery supplies pons and anterior medulla.
  • SCA supplies anterior superior cerebellum.
  • AICA supplies cerebellar peduncles and inner ear (labyrinthine artery).
  • PICA supplies lateral medulla and posterior inferior cerebellum.
  • Deficits include cranial nerve palsies, ataxia, Horner’s syndrome, dysarthria, dysphagia, sensory loss, and crossed signs.

Acute Ischemic Stroke: Diagnosis and Management

Clinical Presentation and Differential Diagnosis

• Acute focal neurologic deficits can be caused by:
  • Ischemic stroke.
  • Hemorrhagic stroke.
  • Seizures with postictal paralysis.
  • Hypoglycemia.
  • Brain tumors.
  • Demyelinating diseases (e.g., multiple sclerosis).
  • Infections (abscess, encephalitis, meningitis).
  • Complicated migraine.
• Example case: 74-year-old man with left facial droop, left hemiparesis, neglect, right gaze deviation consistent with right MCA stroke.

Imaging and Stroke Scales

• Non-contrast head CT:
  • First-line to exclude hemorrhage.
  • Early ischemic changes may not be visible for 6+ hours.
  • Hyperdense vessel sign (e.g., dense MCA sign) indicates clot.
• NIH Stroke Scale (NIHSS):
  • Quantifies stroke severity across 11 domains.
  • Higher scores indicate more severe stroke.
  • Used for rapid assessment and monitoring.

Pathophysiology: Ischemic Core and Penumbra

• Ischemic core: brain tissue with irreversible damage.
• Ischemic penumbra: at-risk but salvageable tissue supported by collateral flow.
• Goal: restore blood flow quickly to save penumbra.

Acute Treatment

• IV tPA (tissue plasminogen activator):
  • Administered within 4.5 hours of symptom onset.
  • Contraindications: active bleeding, high bleeding risk, recent surgery, uncontrolled hypertension (>185/105), coagulopathy.
• Endovascular thrombectomy:
  • Mechanical clot removal for large vessel occlusions.
  • Most effective treatment with number needed to treat (NNT) of 2-3.
  • Usually performed within 6-7 hours, sometimes up to 24 hours in select cases.
• IV tPA is given first because it is faster; thrombectomy follows if needed.
• "Time is brain": every minute delay causes loss of millions of neurons.

Secondary Injury Prevention and Stroke Workup

Post-Recanalization Management

• Blood pressure control:
  • Before reperfusion: permissive hypertension allowed.
  • After reperfusion: target systolic BP 140-160 mmHg to prevent hemorrhagic transformation.
• Monitor for neurological deterioration (increase in NIHSS by ≥4 points).
• Maintain homeostasis: control glucose, fever, oxygenation.
• Cerebral edema peaks 3-5 days post-stroke; may require intervention.

Stroke Workup: Finding the Cause ("Wolf Among Sheep")

• Purpose: identify high-risk sources of emboli or vascular disease to prevent recurrence.
• Stroke mechanisms:
  • Large vessel atherosclerosis.
  • Small vessel (lacunar) disease.
  • Cardioembolism.
  • Rare causes (dissection, hypercoagulability, vasculitis).
  • Cryptogenic (embolic stroke of undetermined source).
• Workup includes:
  • Brain MRI with diffusion-weighted imaging (DWI) for infarct detection.
  • Vascular imaging: CTA or MRA.
  • Cardiac evaluation: EKG, transthoracic echo, transesophageal echo, prolonged cardiac monitoring.
  • Labs for hypercoagulable states or vasculitis if indicated.

Ischemic Stroke Mechanisms in Detail

Large Vessel Disease

• Caused by atherosclerosis of carotid, vertebral, or major cerebral arteries.
• Causes stenosis or occlusion.
• Often causes TIAs.
• Symptoms often cortical (aphasia, neglect, visual field cuts).
• Imaging shows stenosis or occlusion.

Small Vessel Disease (Lacunar Stroke)

• Affects small perforating arteries supplying deep brain structures.
• Risk factors: hypertension, diabetes.
• Symptoms: pure motor or sensory deficits without cortical signs.
• Imaging: small, deep infarcts.
• Does not cause aphasia, neglect, or visual field cuts.

Cardioembolic Stroke

• Emboli from heart (atrial fibrillation, thrombus, valvular disease).
• Sudden onset, large infarcts, multiple vascular territories.
• Highest risk of recurrence.
• Requires anticoagulation for prevention.

Rare Causes

• Arterial dissection (young patients, trauma).
• Hypercoagulable states.
• Vasculitis.
• Paradoxical embolism via patent foramen ovale.
• Genetic disorders.

Hemorrhagic Stroke: Diagnosis and Management

Types of Hemorrhagic Stroke

• Intraparenchymal hemorrhage:
  • Deep (basal ganglia, thalamus) – often hypertensive.
  • Lobar – caused by amyloid angiopathy, AVMs, tumors.
• Subarachnoid hemorrhage (SAH):
  • Bleeding into subarachnoid space.
  • Most commonly from ruptured saccular aneurysms.

Clinical Presentation

• Sudden headache, neurological deficits, decreased consciousness.
• SAH: "worst headache of life," neck stiffness, nausea, vomiting.

Imaging

• Non-contrast CT shows hyperdense blood.
• MRI with gradient echo (GRE) or susceptibility weighted imaging (SWI) detects microbleeds.
• CTA/MRA to identify vascular malformations or aneurysms.

Management

• Prevent hematoma expansion:
  • Aggressive blood pressure control.
  • Reverse anticoagulation/coagulopathy.
• Manage mass effect and cerebral edema.
• Surgical options:
  • Open craniotomy generally not beneficial.
  • Minimally invasive surgery with TPA (MISTIE) to evacuate hematoma.
• Monitor in ICU with frequent neuro checks.

Subarachnoid Hemorrhage (SAH)

Pathophysiology

• Blood in subarachnoid space causes chemical meningitis.
• Common causes:
  • Trauma (most common overall).
  • Ruptured saccular aneurysms (most common non-traumatic).
  • Vascular malformations (AVMs).

Complications

• Rebleeding (highest risk in first 24-48 hours).
• Obstructive hydrocephalus (clot blocks CSF flow).
• Vasospasm (peaks ~7 days, lasts up to 20 days).

Diagnosis

• Non-contrast CT shows blood outlining sulci and ventricles.
• CTA to identify aneurysm.
• Lumbar puncture if CT negative but suspicion high.

Treatment

• Secure aneurysm early (clipping or coiling).
• Blood pressure control.
• Reverse coagulopathy.
• Monitor and treat hydrocephalus (external ventricular drain if needed).
• Prevent vasospasm with calcium channel blockers (nimodipine).
• Consider intra-arterial or intrathecal calcium channel blockers if vasospasm refractory.
• Secondary prevention: smoking cessation, aspirin for inflammation reduction, surveillance for other aneurysms.

Stroke Prevention and Risk Factor Modification

Major Modifiable Risk Factors

• Hypertension (most important; increases ischemic stroke risk 4-fold, hemorrhagic 9-fold).
• Dyslipidemia (statins stabilize plaques).
• Diabetes (glycemic control).
• Smoking cessation.
• Antithrombotic therapy:
  • Antiplatelets for atherosclerotic disease.
  • Anticoagulation for cardioembolic stroke (e.g., atrial fibrillation).

Summary and Take-Home Points

• Know cerebrovascular anatomy and vascular syndromes.
• Acute ischemic stroke is a neurological emergency; rapid diagnosis and treatment with IV tPA and thrombectomy are critical.
• Stroke workup is essential to identify high-risk patients and guide secondary prevention.
• Cardioembolic strokes have the highest recurrence risk.
• Hemorrhagic strokes require aggressive blood pressure control and coagulopathy reversal.
• MISTIE is a promising minimally invasive surgical technique for hematoma evacuation.
• SAH requires early aneurysm repair and vigilant monitoring for complications.
• Stroke prevention focuses on controlling hypertension, statin therapy, antithrombotics, and lifestyle modification.

If you want, I can also help you create a detailed study guide or clarify any specific section! Would you like that?