Cerebrovascular Disease

Slide 1 · Cerebrovascular Disease

Vascular mechanisms · cerebral injury · clinicopathologic patterns

A pathology lecture

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Separate ischemic injury from primary hemorrhage and explain their convergent neuronal damage.

Relate vascular occlusion, collateral flow, and ischemic duration to infarct distribution.

Recognize evolving cerebral infarction morphology and the major hemorrhagic patterns.

Explain aneurysms, vascular malformations, and cumulative vascular cognitive injury.

Slide 3 · Two major pathways to cerebrovascular injury

Altered cerebral blood supply

Hypoxia / ischemia OR vessel rupture

Neuronal and glial injury

Both mechanisms can ultimately produce tissue infarction or parenchymal destruction.

Slide 4 · Ischemic and hemorrhagic stroke

Predominantly ischemic mechanism

Reduced perfusion or oxygen delivery to neural tissue.

Localized arterial obstruction or generalized circulatory failure.

Infarction reflects sustained irreversible damage.

Predominantly hemorrhagic mechanism

Rupture of intracranial arteries or other vessels.

Extravasated blood displaces and injures parenchyma.

Secondary compression and ischemic tissue injury can coexist.

Slide 5 · What is meant by stroke?

An acute neurological syndrome attributed to a vascular mechanism.

The Robbins text describes a duration-based definition: Symptoms persisting beyond 24 hours.

The clinical deficit is determined chiefly by the injured anatomic territory.

Mechanisms include arterial occlusion and vessel rupture.

Slide 6 · Transient ischemic attack in the source

The traditional symptom-duration threshold: Resolution within 24 hours.

A transient syndrome indicates reversible clinical dysfunction, not necessarily a harmless event.

The book’s operational description is presented here as a source-specific definition, not a contemporary diagnostic guideline.

Slide 7 · The brain has extraordinary metabolic demand

Approximately 1%–2% of total body weight, but about 15% of resting cardiac output.

Approximately 20% of body oxygen consumption is attributed to the brain.

Continual aerobic ATP supply makes nervous tissue susceptible to interrupted perfusion.

Slide 8 · Why perfusion failure rapidly threatens neurons

Continuous aerobic metabolism

Interrupted oxygen / substrate delivery

Energy-dependent functions fail

Neuronal injury

Severity depends on residual perfusion, collateral vessels, and duration of the insult.

Slide 9 · Cerebral autoregulation

Vascular resistance adjusts to maintain relatively stable cerebral blood flow.

This compensation operates across a substantial range of perfusion pressures.

Severe hypotension or vascular occlusion may overwhelm compensatory capacity.

Slide 10 · Hypoxemia is not identical to ischemia

Hypoxemia

Reduced oxygen content of circulating blood.

Oxygen delivery falls even if some perfusion is maintained.

Example in the source: Carbon monoxide poisoning.

Ischemia

Insufficient blood flow to the brain or a region.

Caused by low perfusion pressure, vessel obstruction, or both.

May be global or confined to a vascular territory.

Slide 11 · Four determinants of infarct expression

Magnitude of flow reduction

Rapidity and duration of insult

Collateral supply

Site and size of injury

These variables determine both lesion morphology and clinical consequences.

Slide 12 · CNS excitotoxicity after ischemia

Reduced blood flow

Excess extracellular glutamate

NMDA receptor activation

Excess neuronal Ca²⁺ influx

Neuronal injury

CNS-specific amplification occurs alongside general mechanisms of ischemic cell damage.

Slide 13 · Infarct core versus penumbra

Irreversibly injured core

Severely compromised perfusion with established cell death.

Morphology reflects time from the ischemic insult.

Ischemic penumbra

Adjacent hypoperfused tissue remains at risk.

Viability may persist and recovery is possible with timely restoration of flow.

Apoptotic pathways may contribute to neuronal loss.

Slide 14 · Focal cerebral ischemia: Territorial injury

Partial or complete arterial occlusion

Regional perfusion decrease

Sustained ischemia

Vascular-territory infarction

Infarct geometry depends on arterial territory, collateral routes, and time.

Slide 15 · Major mechanisms of arterial occlusion

Mechanism

Typical initiating process

Relevant consequence

Embolization

Material travels from heart or proximal artery

Abrupt distal territorial occlusion

In-situ thrombosis

Occlusion develops at diseased arterial wall

Reduced luminal flow or distal embolization

Vasculitic injury

Inflammatory narrowing or thrombosis

Single or multiple cerebral infarcts

Small-vessel disease

Hypertensive penetrating-arteriole damage

Lacunar infarction or hemorrhage

Slide 16 · Cardiac sources of cerebral emboli

Mural thrombi associated with myocardial infarction may embolize to cerebral arteries.

Atrial fibrillation and valvular disease are important predisposing conditions.

Other embolic material can include tumor, fat, or air.

The occlusion site often lies at a branch point or pre-existing stenosis.

Slide 17 · Artery-to-artery thromboembolism

Carotid atheromatous plaque

Thrombus formation / fragmentation

Embolus travels intracranially

Distal cerebral infarction

The carotid arteries are major extracranial sources of atherothrombotic cerebral emboli.

Slide 18 · Why the MCA territory is often affected

The middle cerebral artery is a direct continuation of internal carotid arterial flow.

It is the cerebral arterial distribution most often involved by embolic infarcts in the source.

Deficits vary with the involved cortical and deep structures.

An embolus may obstruct a branch point or stenotic segment.

Slide 19 · Large-artery thrombosis: Characteristic sites

Thrombotic disease commonly complicates unstable atherosclerotic plaques.

Important locations include carotid bifurcation, MCA origin, and ends of the basilar artery.

Thrombus can propagate locally or fragment into downstream emboli.

Hypertension and diabetes often coexist with atherosclerotic cerebrovascular disease.

Slide 20 · Small-vessel injury in chronic hypertension

Penetrating vessel wall damage

Hyaline arteriolosclerosis

Luminal narrowing / wall weakening

Occlusion or rupture

The same vessel disease can therefore underlie lacunar infarction or deep brain hemorrhage.

Slide 21 · Deep perforators have limited collateral supply

Penetrating vessels feed basal ganglia, thalamus, deep white matter, and brainstem.

Leptomeningeal collaterals primarily connect cortical arterial territories.

Small-vessel occlusion may consequently injure a discrete deep region.

Clinical severity can be substantial despite a small lesion.

Slide 22 · Lacunar infarction: Deep location

Simplified cerebral section — location only

A lacune is a small cavitary infarct.

Typical locations include putamen, thalamus, internal capsule and pons.

Microscopy shows tissue loss bordered by gliosis.

Slide 23 · Lacunes: Pathological size and outcome

The source describes an arbitrary gross cutoff of less than 15 mm in greatest dimension.

They are often multiple in chronic hypertensive small-vessel disease.

Depending on location, they may be silent or produce severe impairment.

Enlarged perivascular spaces without infarction are termed état criblé.

Slide 24 · How collateral circulation influences injury

Arterial obstruction

Collateral supply via circle of Willis

Variable cortical leptomeningeal flow

Smaller or larger infarct

Deep perforating territories have comparatively few alternatives to their parent vessel.

Slide 25 · Additional focal ischemic etiologies

Primary CNS angiitis and systemic inflammatory vasculitides can compromise arterial lumina.

Infectious vasculitis may occur, including in immunosuppressed patients.

Hypercoagulable states and cervical arterial dissection may precipitate stroke.

The source also lists selected vasoactive substance exposures.

Slide 26 · Pale infarction and hemorrhagic transformation

Nonhemorrhagic infarct

Most occlusive infarcts begin with little extravasated blood.

Early gross appearance can be pale and swollen.

Ischemia remains the underlying lesion mechanism.

Hemorrhagic infarct

Previously ischemic vessels are damaged.

Reperfusion can cause punctate or confluent extravasation.

Blood may appear within the territory of a recent infarct.

Slide 27 · Mechanism of hemorrhagic transformation

Arterial occlusion

Ischemic microvascular injury

Recanalization / reperfusion

Blood leaks into infarct

This secondary hemorrhage is distinct from rupture of a previously intact deep parenchymal vessel.

Slide 28 · Primary hemorrhage versus hemorrhagic infarction

Feature

Primary parenchymal hemorrhage

Hemorrhagic transformation

Initiating event

Vessel rupture with a hematoma

Occlusion and ischemic infarction

Role of blood

Primary space-occupying lesion

Secondary extravasation into infarct

Pattern

Commonly central blood clot

Often punctate hemorrhage in infarct territory

Background

Hypertension, amyloid angiopathy, etc.

Reperfusion after vessel obstruction

Slide 29 · Gross evolution of nonhemorrhagic infarction

0–6 hours

Little visible gross change

Irreversible injury may already exist

~48 hours

Pale, soft and swollen

Gray–white margin obscured

2–10 days

Gelatinous and friable

Infarct margin becomes clearer

10 d–3 wk

Liquefactive breakdown

Progressive cavity formation

Slide 30 · Acute neuronal injury: The “red neuron”

Abstract cell-level schematic — not H&E microscopy

After roughly 6–12 hours, neurons develop deeply eosinophilic cytoplasm.

Nuclear pyknosis and karyorrhexis follow.

Neuronal necrosis coexists with cellular swelling and edema.

Slide 31 · Early microscopy beyond neuronal necrosis

The normal staining distinction of gray and white matter deteriorates.

Endothelial cells and astrocytes swell; Myelinated fibers begin disintegrating.

Neutrophils progressively enter for up to about 48 hours.

The neutrophilic response is less conspicuous than in myocardial infarction.

Slide 32 · Subacute infarction: Phagocytic response

Abstract cell-level schematic — not H&E microscopy

At about 48–72 hours, monocyte-derived macrophages and activated microglia appear.

Phagocytes dominate the lesion over the next 2–3 weeks.

Foamy cells ingest myelin products and sometimes blood remnants.

Slide 33 · Gliosis and vascular repair at the infarct edge

Reactive astrocytes and newly formed vessels can be seen from about 1 week.

Astrocytes enlarge, proliferate, and elaborate interlacing processes.

The injury is cleared from its periphery inward.

Different regions of one lesion may show different stages at one time.

Slide 34 · Healed cerebral infarction

Neuronal and glial tissue loss

Microglial / macrophage clearance

Liquefactive cavitation

Peripheral astroglial scar

After several months, a cystic cavity remains with a dense gliotic rim and new capillaries.

Slide 35 · Microscopic evolution of cerebral infarction

Phase

Dominant pathological findings

Acute

Red neurons, edema, glial swelling; subsequent neutrophils

Subacute

Foamy macrophages, activated microglia, reactive astrocytes and vessels

Remote

Cystic tissue loss bordered by a dense glial scar

Slide 36 · Clinical deficit follows anatomy

Neurological signs arise from the structures injured, not simply the embolic or thrombotic source.

Deficits often appear over minutes and can evolve over hours.

Edema and ischemic penumbra may contribute to temporarily impaired function.

Recovery can occur over months, but established tissue necrosis is not restored.

Slide 37 · Why the infarct boundary matters clinically

The infarct core contains nonviable parenchyma.

The penumbra and edematous adjacent brain can be functionally impaired but potentially viable.

Timely diagnosis and restoration of flow can prevent additional permanent injury.

Primary hemorrhage must be distinguished before therapies that increase bleeding risk.

Slide 38 · Global cerebral hypoxia / ischemia

Cardiac arrest / severe shock OR reduced oxygen content

Generalized oxygen delivery failure

Diffuse neuronal injury

Variable recovery or severe encephalopathy

Unlike a focal arterial occlusion, global injury can involve both hemispheres and multiple structures.

Slide 39 · Global insults: Major contexts

Generalized perfusion loss can follow cardiac arrest, shock, or profound hypotension.

Reduced blood oxygen-carrying capacity can produce global hypoxic injury.

Outcome depends on the intensity and duration of oxygen deprivation.

Milder episodes may result in transient confusion and recovery.

Slide 40 · Selective neuronal vulnerability

Neurons are generally more sensitive than glia to global hypoxia–ischemia.

Especially vulnerable: Hippocampal CA1 pyramidal neurons.

Cerebellar Purkinje cells are also selectively susceptible.

Cortical layers III and V contain particularly sensitive pyramidal neurons.

Slide 41 · Watershed infarcts occur at arterial borders

Simplified cerebral section — location only

Distal arterial boundary zones have relatively marginal flow.

The anterior–middle cerebral artery border is particularly vulnerable.

Severe systemic hypotension may produce bilateral lesions.

Slide 42 · Mechanism of watershed injury

Systemic pressure falls markedly

Border-zone perfusion becomes critical

Bilateral cortical border-zone ischemia

Wedge-shaped infarcts

Secondary hemorrhagic transformation can be present; The source emphasizes ACA–MCA border regions.

Slide 43 · Global ischemia: Gross morphology

Diffuse cerebral edema causes swollen, broad gyri and narrowed sulci.

Gray-white differentiation becomes difficult to identify on cut surfaces.

Microscopically, changes follow stages resembling those of focal infarction.

Early red neurons precede macrophage recruitment and gliosis.

Slide 44 · Global ischemia: Histopathological course

6–12 h

Acute red neurons

Early cytotoxic injury

24 h–2 wk

Tissue necrosis

Phagocytes + gliosis

After ~2 wk

Removal of necrosis

Cysts + residual gliosis

Slide 45 · Laminar cortical necrosis

Hypoxic injury may affect cortical layers unevenly.

Selective loss of neurons in some layers and preservation of others creates a laminar pattern.

The tissue response includes neuronal loss and reactive gliosis.

This represents a morphological pattern of cortical global ischemic injury.

Slide 46 · Consequences of severe global injury

Widespread neuronal death may cause sustained loss of meaningful responsiveness.

Severe diffuse injury may involve cerebral cortex and brainstem.

The chapter describes clinical brain death using irreversible neurologic injury criteria.

Brain death is a clinical determination; Histology alone does not establish it.

Slide 47 · Ischemic lesions: The essential distinctions

Territorial · lacunar · border-zone · diffuse

Territorial infarcts reflect focal arterial occlusion and variable collateral flow.

Lacunar lesions reflect deep perforating small-vessel injury.

Watershed lesions reflect vulnerable border-zone flow during severe hypotension.

Slide 48 · Where can intracranial blood accumulate?

Compartment

Typical context

Pathologic consequence

Epidural

Most often trauma

Extra-axial compression

Subdural

Most often trauma

Extra-axial blood collection

Subarachnoid

Trauma or aneurysmal / vascular lesion

Blood within CSF-containing space

Intraparenchymal

Hypertension, CAA, lesions, tumors

Tissue destruction and hematoma

Slide 49 · Primary intraparenchymal hemorrhage

Rupture of a small vessel deposits blood directly within the brain parenchyma.

The hematoma can compress adjacent tissue, producing edema and secondary ischemic damage.

Two major spontaneous patterns are deep ganglionic and superficial lobar hemorrhage.

The underlying vessel disease is a strong clue to location and morphology.

Slide 50 · Hypertensive hyaline arteriolosclerosis

Vessel lumen

Schematic wall section

Chronic hypertension causes thickening and fibrosis of small penetrating arteriolar walls.

Affected walls become rigid and structurally vulnerable.

Occlusion can cause a lacune; Rupture can produce deep hemorrhage.

The process preferentially injures basal ganglia and deep white-matter vessels.

Slide 51 · One arteriolar disease, two outcomes

Hypertensive arteriolosclerosis

Luminal obstruction OR wall failure

Lacunar infarct OR deep hematoma

Vessel-wall pathology connects the ischemic and hemorrhagic manifestations of chronic hypertension.

Slide 52 · Hypertensive hemorrhage: Deep location

Simplified cerebral section — location only

The putamen and thalamus are common sites.

Cerebellum and pons can also be affected.

A large hematoma may rupture into the ventricular system.

Slide 53 · Cerebral amyloid angiopathy: Lobar hemorrhage

Simplified cerebral section — location only

β-amyloid accumulates in meningeal and cortical arterial walls.

Rigid, amyloid-laden vessels are prone to bleeding.

A characteristic consequence is superficial or lobar hemorrhage.

Slide 54 · Cerebral amyloid angiopathy: Vessel-wall injury

Vessel lumen

Schematic wall section

Amyloid deposition involves leptomeningeal, cortical and cerebellar vessels.

Accumulation is β-amyloid rather than the collagen of ordinary hyaline sclerosis.

Vessel-wall fragility may cause lobar hemorrhage and multiple microbleeds.

CAA is distinct from hypertensive basal ganglia arteriolosclerosis.

Slide 55 · CAA: Genotype and pathological risk

The source associates APOE ε2 and ε4 alleles with increased bleeding risk.

Some hereditary CAA variants involve APP mutations.

Vessel-wall β-amyloid can be highlighted by appropriate amyloid studies.

On ordinary H&E, CAA and hyaline vascular thickening may look similar.

Slide 56 · Other inherited small-vessel diseases

CADASIL is associated with autosomal dominant pathogenic NOTCH3 variants.

It can manifest with recurrent small-vessel strokes, white-matter injury and dementia.

The source also describes COL4A1-associated small-vessel disease.

COL4A1-related injury can involve brain hemorrhage and extra-neural manifestations.

Slide 57 · CADASIL: Molecular defect to clinical injury

NOTCH3 gene alteration

Abnormal receptor extracellular domain

Small-vessel pathology

Subcortical ischemia and cognitive decline

This inherited arteriopathy is distinct from sporadic hypertensive or amyloid-related disease.

Slide 58 · COL4A1-associated cerebrovascular pathology

Type IV collagen contributes to vascular basement membranes.

Pathogenic COL4A1 variants can be associated with cerebral vessel fragility.

Reported accompanying manifestations include cataract, hematuria and epilepsy.

Inherited small-vessel pathology should be considered apart from conventional vascular risk factors.

Slide 59 · Evolution of a primary intracerebral hematoma

Primary small-vessel rupture

Clotted blood compresses brain

Secondary anoxic injury + edema

Macrophages, gliosis and cavity

The final defect may have a hemosiderin-stained rim after prior bleeding.

Slide 60 · Morphology of remote hemorrhage

The early lesion contains a central coagulum of blood surrounded by compressed tissue.

Hemosiderin-laden and lipid-laden macrophages accumulate during clearance.

Reactive astrocytes form a gliotic lesion rim.

Old destructive hemorrhages may leave a cavity with brown discoloration.

Slide 61 · Deep ganglionic versus lobar hemorrhage

Deep / ganglionic

Hypertensive arteriolosclerosis is the canonical association.

Putamen, thalamus, pons, or cerebellum may be involved.

Ventricular extension can complicate major bleeds.

Lobar / superficial

Cerebral amyloid angiopathy is a principal association.

Cortical and subcortical territories are affected.

Adjacent subarachnoid extension or microbleeds may coexist.

Slide 62 · Subarachnoid hemorrhage: Vascular mechanism

Blood enters the cerebrospinal-fluid-containing subarachnoid space.

Ruptured saccular intracranial aneurysm is a leading spontaneous cause.

Vascular malformations, hematologic disorders and trauma are alternative etiologies.

An arterial source produces abrupt pressure-related symptoms and complications.

Slide 63 · Saccular aneurysm at an arterial branch point

Focal defect in arterial wall

Progressive saccular outpouching

Wall thins near aneurysm dome

Rupture into subarachnoid space

Aneurysms may also bleed into nearby brain tissue.

Slide 64 · Aneurysm predisposition

Aneurysms often develop near major arterial branching points in the anterior circulation.

Underlying attenuation of vascular media and internal elastic lamina is important.

Familial susceptibility and selected connective-tissue disorders increase risk.

Smoking, hypertension and hemodynamic wall stress contribute.

Slide 65 · Saccular aneurysm: Gross structural features

A rounded, thin-walled, shiny outpouching arises near the circle of Willis.

Size and neck width vary; Sac walls can contain mural thrombus or calcification.

Smooth muscle and internal elastic lamina are absent from the sac itself.

Rupture typically occurs at or near its dome.

Slide 66 · Ruptured aneurysm: Early clinical sequence

Aneurysm rupture

Arterial blood enters subarachnoid space

Abrupt severe headache ± unconsciousness

Risk of rebleeding and secondary ischemia

The pathology lecture focuses on mechanism and consequences, not acute management algorithms.

Slide 67 · Secondary injury after subarachnoid blood

Blood bathing cerebral arteries can provoke arterial vasospasm.

Vasospasm may reduce blood flow and cause additional ischemic injury.

Meningeal fibrosis in the healing phase can obstruct CSF circulation or resorption.

Thus, delayed injury is not limited to the initial hemorrhage volume.

Slide 68 · Cerebral vascular malformations

Type

Basic architecture

Major teaching consequence

Arteriovenous malformation

High-flow abnormal arteries and veins

Hemorrhage, seizure, hemodynamic shunt

Cavernous malformation

Back-to-back low-flow vascular spaces

Focal bleeding or seizures

Capillary telangiectasia

Small capillary-level abnormality

Distinct structural category

Venous angioma

Abnormal venous drainage pattern

Distinct structural category

Slide 69 · Arteriovenous malformation: Direct shunting

Arterial inflow

No normal capillary resistance

High-flow venous channels

Hemorrhage or shunt-related symptoms

Large lesions can cause clinically significant altered hemodynamics.

Slide 70 · AVM morphology and clinical presentation

Grossly, AVMs form tangled, enlarged, wormlike vascular channels.

Abnormal vessels are separated by reactive gliotic tissue and may show old bleeding.

Patients may present with seizures or intracranial hemorrhage.

Prominent high-flow lesions can create substantial arteriovenous shunting.

Slide 71 · AVM versus cavernous malformation

Arteriovenous malformation

High-flow artery–vein connections with shunting.

Vascular channels may display arterial wall abnormalities.

Intervening gliotic tissue and previous hemorrhage may be present.

Cavernous malformation

Back-to-back, distended vascular channels with collagenized walls.

Usually little or no brain tissue between the abnormal channels.

Low-flow lesion without a typical AV shunt.

Slide 72 · Molecular pathology of vascular malformations

The source reports activating somatic KRAS mutations in many arteriovenous malformations.

Familial cavernous malformations can involve CCM-complex genes.

Progressive cavernous lesions may additionally acquire activating PIK3CA changes.

Somatic driver alterations support a disease mechanism involving endothelial signaling.

Slide 73 · Cumulative infarction and vascular dementia

Recurrent vascular injury

Multiple bilateral cortical / white-matter lesions

Disconnection and neuronal loss

Gait, cognition and focal deficits

Underlying mechanisms may include atherosclerosis, thromboembolism and chronic arteriolosclerosis.

Slide 74 · Subcortical vascular dementia / Binswanger pattern

Predominant subcortical white-matter vascular injury forms a recognizable distribution.

The Robbins chapter uses Binswanger disease for this subcortical arteriolosclerotic pattern.

Cognitive impairment may coexist with gait disturbance and pseudobulbar signs.

Other white-matter diseases must be differentiated radiologically and clinically.

Slide 75 · Integrating location, mechanism, and morphology

Lesion

Dominant mechanism

Morphological clue

Large territorial infarct

Arterial embolus / thrombosis

Territorial softening → cavitation

Lacune

Deep small-vessel occlusion

Small gliosis-rimmed cavity

Watershed infarct

Generalized hypoperfusion

Border-zone wedge-shaped lesion

Deep hematoma

Hypertensive arteriolosclerosis

Ganglionic clot and compression

Lobar hematoma

Cerebral amyloid angiopathy

Cortical/subcortical bleeding

Subarachnoid bleed

Often ruptured saccular aneurysm

Blood in subarachnoid space

Slide 76 · Clinicopathologic problem: Sudden focal deficit

An acute arterial deficit is not defined solely by the mechanism

Which vascular territory corresponds to the neurological findings?

Is there arterial occlusion with infarction or primary bleeding?

How might collateral perfusion alter the extent of injury?

Slide 77 · Clinicopathologic problem: Deep cerebral hematoma

A deep putaminal hemorrhage points toward small-vessel disease

Link long-standing hypertension to arteriolar wall thickening.

Explain the alternative endpoints: Luminal closure or rupture.

Predict an adjacent zone of edema and secondary parenchymal injury.

Slide 78 · Clinicopathologic problem: Explosive headache

Blood in the subarachnoid space suggests a ruptured vascular lesion

Consider a saccular aneurysm at an intracranial branch point.

Distinguish the initial bleed from vasospasm-related delayed ischemia.

Explain how later meningeal fibrosis can disturb CSF dynamics.

Slide 79 · Pathology synthesis

Vascular injury is defined by mechanism + location + time

Regional occlusion, global flow failure, and vascular rupture produce different initial lesions.

Cerebral ischemia characteristically evolves toward liquefaction and gliotic cavitation.

Vessel pathology links the ischemic and hemorrhagic presentations of cerebrovascular disease.

Slide 80 · Source and visual provenance

Primary textbook

Robbins, Cotran & Kumar: Pathologic Basis of Disease. 11th ed. (2026). Chapter 28, The Central Nervous System, pp. 1136–1143.

Teaching scope

Introductory Cerebrovascular Disease section, supplemented by contiguous focal/global ischemia, hemorrhage, vascular malformation, and vascular dementia sections from the same chapter.

Diagrams are authored editable schematics, not diagnostic specimens.