Vascular Dementia

Slide 1 · Vascular Dementia

Cerebrovascular mechanisms, brain pathology and clinical consequences

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Define vascular dementia in its neuropathologic and clinical context.

Relate vascular lesions and their distribution to cognitive and neurologic impairment.

Distinguish large-vessel infarction, lacunar injury and diffuse subcortical white-matter disease.

Integrate coexisting vascular and degenerative changes without assuming a single cause.

Slide 3 · Definition: Cumulative vascular brain injury

A syndrome arising from multifocal vascular disease.

A syndrome of dementia developing with multifocal cerebrovascular damage over months to years.

Multiple bilateral infarcts may affect both gray and white matter.

The hallmark is an anatomic burden of vascular injury, not one specific histologic lesion.

Clinical findings commonly extend beyond isolated memory impairment.

Slide 4 · Why the syndrome is clinically distinctive

Dementia coexists with gait abnormalities and pseudobulbar signs.

Superimposed focal neurologic deficits may be present.

The vascular injuries may arise through several mechanisms.

Multiple anatomic systems may be impaired by bilateral lesions.

Slide 5 · Bilateral multifocal lesions

Conceptual distribution map

Outer rim = cortex | Inner field = deep tissue

Infarcts occur in both cerebral hemispheres.

Gray and white matter can be involved together.

Distinct lesion sites provide an anatomic basis for multi-domain impairment.

Schematic — not an MRI, gross specimen, or mapped anatomy

Slide 6 · From vascular disease to cognitive impairment

Vascular disorder

Recurrent ischemic events

Cumulative brain lesions

Cognitive + neurologic syndrome

The syndrome generally develops across months and years, rather than from a single acute event.

Consequences depend on the amount and location of injured brain tissue.

Schematic causal sequence

Slide 7 · Clinical stroke versus vascular dementia

Stroke (episode)

Acute neurologic manifestations explained by a vascular event.

The focal deficit depends on the vascular territory affected.

An episode may contribute to later accumulated injury.

Vascular dementia (syndrome)

Cognitive syndrome associated with multiple or widespread vascular lesions.

Gait and pseudobulbar abnormalities may coexist.

May have superimposed focal deficits.

Related concepts, not interchangeable clinical labels

Slide 8 · A syndrome with more than one vascular cause

Cerebral atherosclerosis is a major etiologic substrate.

Thrombosis or embolization from carotid vessels or the heart may produce infarcts.

Chronic hypertension causes cerebral arteriolosclerosis and small-vessel injury.

Different mechanisms can coexist in the same brain.

Slide 9 · Three principal vascular pathways

Cumulative brain injury

Cerebral atherosclerosis

Cardiac / carotid emboli

Hypertensive arteriolosclerosis

Multifocal cerebral infarcts

Three causative vascular categories; The fourth box represents their shared tissue outcome.

Schematic relationships (not quantitative)

Slide 10 · The key determinant is lesion anatomy

Cerebral infarction produces deficits related to its anatomic distribution.

Infarct size and location reflect duration of ischemia and adequacy of collateral perfusion.

Small injuries in strategically important tracts can cause prominent functional deficits.

Do not infer syndrome severity solely from counting visible lesions.

Slide 11 · Atherosclerosis as an upstream substrate

Arterial plaque

Luminal narrowing / plaque change

Thrombus or embolus

Regional infarction

Large-artery atherosclerosis can compromise blood supply directly or supply thromboemboli.

The carotid bifurcation and origin of the middle cerebral artery are important sites.

Schematic causal sequence

Slide 12 · Atherosclerotic occlusion: Common sites

The carotid bifurcation is a common site of thrombotic occlusion.

The origin of the middle cerebral artery is another frequent location.

Either end of the basilar artery may also be involved.

Atherosclerotic cerebrovascular disease often coexists with hypertension or diabetes.

Slide 13 · Carotid-to-cerebral thromboembolism

Carotid plaque

Thrombus formation

Distal embolization

Cerebral infarction

Thrombi can fragment and move distally from their site of formation.

Occlusion of cerebral branches may generate distinct territories of ischemic necrosis.

Schematic causal sequence

Slide 14 · Cardiac sources of cerebral emboli

Cardiac mural thrombi are important embolic sources.

Myocardial infarction, valvular disease and atrial fibrillation are relevant predispositions.

Emboli can lodge at branch points or previously narrowed segments.

Recurrent embolization can create anatomically separated infarcts.

Slide 15 · Mechanism of cardioembolic cerebral injury

Cardiac thrombus

Embolus enters circulation

Brain artery occlusion

Focal ischemic necrosis

The middle cerebral artery territory is frequently affected by cerebral embolism.

Clinical outcome depends on the distribution of damaged tissue.

Schematic causal sequence

Slide 16 · Embolism versus in-situ thrombosis

Embolic occlusion

Occlusive material arrives from a distant source.

Cardiac or carotid origin is common.

Vessel branching points are frequent lodging sites.

Local thrombotic occlusion

Thrombus arises at a diseased intracranial or extracranial artery.

Acute change in a vulnerable plaque may initiate thrombosis.

Extension and distal fragmentation may also occur.

Slide 17 · Blood flow and cerebral vulnerability

The brain has substantial continuous oxygen and energy requirements.

Cerebral autoregulation helps maintain relatively constant perfusion.

Reduced oxygen delivery may follow low flow, impaired oxygenation or both.

Collateral supply, insult duration and flow reduction shape tissue survival.

Slide 18 · What determines infarct extent?

Vascular occlusion

Collateral circulation

Ischemia duration

Tissue injury extent

Magnitude and rapidity of the flow reduction also modify injury.

These determinants influence lesion shape, anatomic site and clinical manifestations.

Simplified determinant chain, not a numerical risk model

Slide 19 · Cortical versus deep arterial supply

Cortical arterial territories

Additional leptomeningeal anastomoses may contribute collateral supply.

Larger territory infarcts may follow occlusion of major branches.

Cortical involvement can accompany cognitive deficits.

Deep penetrating territories

Deep penetrating arteries have little or no collateral supply.

They supply basal ganglia, thalamus and deep white matter.

Small-vessel occlusion can create lacunar infarcts.

Slide 20 · Hypertension and the cerebral microvasculature

Chronic hypertension affects penetrating arteries and arterioles.

Wall thickening and hyaline arteriolosclerosis alter vessel function.

Affected vessels supply deep gray nuclei, white matter and brainstem.

Occlusion may produce lacunar infarcts; Rupture may cause hemorrhage.

Slide 21 · Hyaline arteriolosclerosis reduces the lumen

Cross-sectional vessel schematic

Comparator

Affected vessel

Vessel walls become thickened by hyaline change.

Lumen narrowing predisposes to distal ischemic injury.

Wall rigidity is associated with vulnerability to rupture.

This pattern is prominent in deep brain structures.

Schematic — lumen and wall not drawn to scale

Slide 22 · Small-vessel occlusive pathway

Long-standing hypertension

Arteriolar wall disease

Luminal occlusion

Lacunar infarct

The causal sequence contrasts with embolic occlusion of a larger arterial branch.

Repeated small infarcts can accumulate in subcortical structures.

Schematic causal sequence

Slide 23 · Lacunar infarcts: Deep distribution

Conceptual distribution map

Outer rim = cortex | Inner field = deep tissue

Lacunes affect deep gray nuclei, deep white matter and pons.

Illustrated locations are conceptual, not a diagnostic map.

Cumulative bilateral small lesions contribute to vascular impairment.

Schematic — not an MRI, gross specimen, or mapped anatomy

Slide 24 · Lacunes: Gross and microscopic identity

Lacunar infarcts as small occlusive infarcts below 15 mm in maximal dimension.

Grossly, healed lesions form small lake-like spaces.

Microscopically, there is tissue loss with surrounding gliosis.

This definition characterizes a lesion, not by itself the clinical diagnosis of dementia.

Slide 25 · Common lacunar locations

Anatomic site

Pathology context

Clinical teaching interpretation

Putamen / globus pallidus

Deep perforator territory

Potential motor-network disturbance

Thalamus

Deep gray-matter infarct

Disruption of distributed brain circuits

Internal capsule

Compact white-matter tracts

Focal neurologic deficits possible

Deep white matter

Subcortical ischemic injury

Disconnection of long association pathways

Caudate nucleus / pons

Additional lacunar locations

Heterogeneous focal signs

Specific clinical outcomes depend on precise lesion location; Table is explanatory, not a fixed rule.

Slide 26 · Large territorial infarcts versus lacunes

Territorial infarction

Follows occlusion of a major arterial supply.

Often has wedge- or territory-related distribution.

Can involve cortical gray matter and subjacent structures.

Lacunar infarction

Small, deep occlusive lesion.

Often reflects disease of penetrating arterioles.

Remote lesion shows cavity and surrounding gliosis.

Slide 27 · Small-vessel disease has two major outcomes

Arteriolar occlusion can produce a lacunar infarct.

An abnormal rigid vessel wall can rupture into brain parenchyma.

Both are consequences of vascular pathology in deep cerebral territories.

The occurrence of either lesion should prompt attention to the underlying vasculopathy.

Slide 28 · Hypertensive injury: Occlusion or rupture

Chronic hypertension

Arteriolar wall alteration

Occlusion OR rupture

Infarct OR hemorrhage

The tissue phenotype reflects the mode of vessel failure.

Lacunar infarcts and hypertensive intraparenchymal hemorrhages have related vascular substrates.

Schematic causal sequence

Slide 29 · Cerebral amyloid angiopathy: Distinct vessel injury

Amyloid-β peptide accumulates within meningeal and cortical vessel walls.

The altered walls become rigid and vulnerable to bleeding.

Lobar hemorrhages and small microbleeds are characteristic manifestations.

This distribution contrasts with hypertensive deep arteriolosclerosis.

Slide 30 · Amyloid deposition in cerebral vessel walls

Cross-sectional vessel schematic

Comparator

Affected vessel

The deposits are amyloid-β, not the collagen of hyaline arteriolosclerosis.

Cortical and leptomeningeal vessels are preferentially involved.

Cerebral amyloid angiopathy is an important alternative vascular substrate.

Schematic — lumen and wall not drawn to scale

Slide 31 · Two small-vessel disease patterns

Feature

Hypertensive arteriolosclerosis

Cerebral amyloid angiopathy

Typical vascular territory

Deep penetrating arterioles

Cortical / leptomeningeal vessels

Dominant wall alteration

Hyaline thickening

Amyloid-β deposition

Infarct/bleeding pattern

Lacunes and deep hemorrhage

Lobar bleeding and microbleeds

Major contextual association

Long-standing hypertension

Amyloidogenic peptide accumulation

Slide 32 · CADASIL: Hereditary small-vessel injury

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.

Caused by pathogenic NOTCH3 variants affecting its extracellular receptor domain.

Recurrent small-vessel strokes and progressive white-matter changes may be accompanied by dementia.

An inherited vascular disorder is a distinctive alternative to common hypertensive injury.

Slide 33 · CADASIL: Molecular lesion to syndrome

NOTCH3 mutation

Abnormal receptor domain

Hereditary small-vessel disease

Infarcts + leukoencephalopathy

The Robbins description links this genetic arteriopathy to recurrent small-vessel events and dementia.

The pathway is a teaching simplification, not a complete molecular model.

Schematic causal sequence

Slide 34 · Other hereditary cerebral microangiopathy

Variants affecting COL4A1, a vascular basement-membrane component, cause inherited small-vessel disease.

Brain hemorrhage may coexist with cataract, hematuria or epilepsy.

The multisystem phenotype helps distinguish this disorder from sporadic hypertensive vasculopathy.

Not every hereditary cerebral vasculopathy necessarily causes vascular dementia.

Slide 35 · Acquired and inherited small-vessel mechanisms

Common acquired pathway

Long-standing hypertension.

Hyaline arteriolar wall alteration.

Deep lacunar infarcts or hemorrhage.

Hereditary pathway

CADASIL: NOTCH3-associated vasculopathy.

COL4A1-associated basement membrane disease.

Clinical and family context may aid recognition.

Slide 36 · Gray-matter and white-matter injury

Conceptual distribution map

Outer rim = cortex | Inner field = deep tissue

Cumulative vascular damage may affect cortical and deep gray matter.

White-matter infarcts can interrupt cerebral connections.

The syndrome cannot be reduced to a single microscopic pattern.

Schematic — not an MRI, gross specimen, or mapped anatomy

Slide 37 · Cortical and subcortical injury patterns

Cortical gray matter

May sustain infarction in an arterial territory.

Focal neuronal loss and subsequent gliosis reflect chronic injury.

Can coexist with subcortical infarcts.

Subcortical structures

Deep nuclei and connecting white matter may be damaged.

Penetrating vessel disease is an important substrate.

Extensive white-matter involvement defines Binswanger pattern.

Slide 38 · Binswanger disease: Defining feature

The defining distinction is topographic: Extensive subcortical white-matter injury.

Also termed subcortical arteriosclerotic encephalopathy.

Vascular injury preferentially involves large areas of subcortical white matter.

It represents a distinct distribution within vascular cognitive disease.

Other causes of extensive hemispheric white-matter abnormalities must be excluded.

Slide 39 · Binswanger pattern: Broad subcortical injury

Conceptual distribution map

Outer rim = cortex | Inner field = deep tissue

The predominant injury involves large subcortical white-matter regions.

This differs from a few discrete cortical infarcts.

The schematic is conceptual and cannot substitute for clinical imaging.

Schematic — not an MRI, gross specimen, or mapped anatomy

Slide 40 · Why white-matter lesions matter

Vascular white-matter injury

Loss of axons / tissue

Disrupted cerebral connections

Gait and cognitive impairment

The final step is a clinicopathologic interpretation of disconnection in a multi-region syndrome.

Exact clinical deficits still depend on lesion distribution.

Schematic causal sequence

Slide 41 · Binswanger pattern: Differential principle

Extensive hemispheric white-matter damage is not specific for vascular disease.

The distribution requires correlation with the clinical course and vascular context.

Both clinical and radiologic distinction from other white-matter diseases are essential.

Do not diagnose the cause solely from a broad white-matter abnormality.

Slide 42 · From ischemia to cell death

Reduced blood flow

Energy supply failure

Glutamate excitotoxicity

Neuronal injury / necrosis

Glutamate-mediated NMDA receptor activation allows excessive intracellular calcium entry.

This mechanism contributes to vulnerability of ischemic CNS tissue.

Schematic causal sequence

Slide 43 · Early morphology of cerebral infarction

Acute ischemic neuronal injury produces eosinophilic “red neurons.”

Nuclear condensation and fragmentation accompany irreversible neuronal damage.

Glial and endothelial swelling, edema and myelin injury emerge.

A remote infarct has a very different appearance from an acute lesion.

Slide 44 · Infarct histology evolves with time

Acute

Eosinophilic neurons; Edema; Neutrophils

Subacute

Microglia / macrophages; Phagocytosis

Repair

Reactive astrocytes; Neovascular response

Remote

Cavitation; Tissue loss; Glial rim

The diagram summarizes Robbins descriptions of focal infarct evolution.

Different regions of the same lesion may exhibit different stages.

Slide 45 · Macrophage-mediated clearance of an infarct

Necrotic brain tissue

Microglial / monocyte response

Debris phagocytosis

Cavity and gliotic margin

Phagocytes remove myelin debris and products of damaged tissue.

Reactive astrocytes form a glial meshwork at the lesion edge.

Schematic causal sequence

Slide 46 · Remote infarct: The neuropathologic endpoint

Old ischemic lesions contain a cystic space left by lost parenchyma.

A glial scar with capillaries rims the defect.

Multiple remote cavities indicate an accumulated history of tissue destruction.

The size and distribution of remote lesions provide anatomic context for the syndrome.

Slide 47 · Chronic lacunes on histologic examination

A lacune is a small remote cavity in a deep cerebral structure.

Microscopy demonstrates tissue loss and reactive gliosis.

The surrounding parenchyma may reflect chronic microvascular disease.

Multiple lacunes should be considered together with coexisting white-matter injury.

Slide 48 · Pale versus hemorrhagic infarction

Initially nonhemorrhagic infarct

An occluded end artery deprives its downstream parenchyma of blood.

Grossly a lesion becomes pale and soft after evolving ischemic injury.

Cavitation appears as tissue is removed.

Hemorrhagic transformation

Reperfusion may follow dissolution or fragmentation of occluding material.

Damaged microvessels permit punctate or confluent bleeding.

Underlying ischemia remains the initiating event.

Slide 49 · Distribution is more informative than lesion label

A lesion may be large, lacunar, cortical or subcortical.

Multiple lesion types can accumulate in the same patient.

Network disturbance depends on the combined location of tissue loss.

The clinicopathologic assessment therefore integrates lesion types and distribution.

Slide 50 · Core clinical triad

Dementia developing over months or years.

Gait abnormalities suggesting broader neural-network involvement.

Pseudobulbar signs accompanying bilateral cerebral injury.

Focal neurologic deficits may be superimposed.

Slide 51 · Clinical manifestations and lesion geography

Bilateral vascular injury

Disruption of multiple systems

Cognitive + gait dysfunction

Possible focal deficits

A strictly focal stroke syndrome is not the same as the accumulated vascular dementia phenotype.

The symptom combination reflects the distributed anatomical lesions.

Schematic causal sequence

Slide 52 · Gait abnormalities: Clinicopathologic relevance

Gait change is a characteristic associated feature in the Robbins account.

Deep and subcortical tissue injury can disturb distributed motor pathways.

Its coexistence with cognitive impairment increases concern for widespread brain involvement.

A gait complaint alone does not establish vascular dementia.

Slide 53 · Pseudobulbar signs: Bilateral network injury

Pseudobulbar findings may accompany vascular dementia.

They are compatible with interruption of bilateral descending supranuclear pathways.

Their presence supports a broader lesion burden than an isolated cognitive complaint.

Pseudobulbar signs do not uniquely identify the cause of vascular injury.

Slide 54 · Focal deficits may be superimposed

A focal deficit may arise with an additional vascular event.

Different vascular territories yield different neurologic deficits.

An acute deficit should not be interpreted as merely part of chronic dementia.

Clinicopathologic interpretation requires both event timing and lesion location.

Slide 55 · Clinical phenotype: Focal and distributed effects

Focal vascular effect

Acute territorial or deep-structure insult.

Deficit linked to a particular lesion location.

Can coexist with chronic vascular cognitive impairment.

Distributed chronic effect

Numerous bilateral lesions or extensive white-matter injury.

Combined cognitive, gait and pseudobulbar findings.

May reflect heterogeneous vascular mechanisms.

Slide 56 · Clinical–radiologic correlation is indispensable

Identify whether brain lesions are cortical, deep gray-matter or subcortical white-matter predominant.

Examine whether the distribution plausibly relates to observed neurologic deficits.

Consider large-artery, embolic and small-vessel substrates.

The amount of visible vascular injury alone is not a complete attribution test.

Slide 57 · Anatomical patterns and pathologic substrates

Observed pattern

Mechanism to consider

Interpretive caution

Multiple cortical infarcts

Large-artery or embolic events

Different events may coexist

Deep lacunar cavities

Penetrating small-vessel disease

Do not equate any lacune with dementia

Confluent subcortical injury

Diffuse white-matter vascular disease

Exclude other white-matter disorders

Lobar microbleeds

Cerebral amyloid angiopathy

Pattern differs from deep hypertension

Pattern-to-mechanism links reflect supplied Robbins pathology, not formal imaging criteria.

Slide 58 · The Binswanger differential cannot be skipped

Widespread white-matter disease has multiple possible causes.

A vascular cause requires compatible history and lesion distribution.

Clinical–radiologic correlation is explicitly emphasized by Robbins.

A generic label of “white-matter change” is not a definitive etiology.

Slide 59 · Mixed vascular and neurodegenerative pathology

Cerebrovascular lesions often coexist with neurodegenerative disease.

The additional vascular burden can increase neurologic impairment.

For comparable degenerative lesion severity, vascular disease increases the risk of cognitive impairment.

Avoid forcing patients with overlapping disease into a single exclusive category.

Slide 60 · Overlapping pathologies and clinical impairment

Clinical cognitive impairment

Neurodegenerative lesions

Cerebrovascular lesions

Distribution of brain damage

Combined pathologic burden

The source emphasizes the additive contribution of cerebrovascular pathology in degenerative disorders.

Schematic relationships (not quantitative)

Slide 61 · Vascular and degenerative contributors

Vascular contribution

Infarcts, lacunes and white-matter vascular injury.

Spatial heterogeneity and focal deficits may be present.

Gait and pseudobulbar features may coexist.

Degenerative contribution

Neurodegenerative pathology may independently impair cognition.

Often coexists with vascular abnormalities.

Neurologic outcome reflects overlapping pathologic burdens.

Do not treat this table as a stand-alone diagnostic algorithm.

Slide 62 · Common attribution errors

Assuming all white-matter abnormalities signify Binswanger disease.

Calling any isolated lacunar infarct sufficient evidence of vascular dementia.

Attributing cognitive dysfunction exclusively to one pathologic process when lesions coexist.

Ignoring a new focal deficit because a chronic cognitive syndrome is already present.

Slide 63 · A structured clinicopathologic interpretation

Identify clinical syndrome

Map lesion distribution

Assess vascular substrate

Integrate co-pathology

Correlate dementia, gait, pseudobulbar and focal findings.

Keep morphologic observation separate from etiologic inference.

Schematic causal sequence

Slide 64 · Case 1: Multifocal vascular brain injury

Clinical vignette

A patient has developed progressive cognitive impairment over several years. Examination identifies an abnormal gait and bilateral supranuclear motor signs. Brain studies show multiple remote cortical and deep infarcts.

Questions for interpretation

Which pathologic syndrome is suggested?

Why is the distribution of lesions important?

Slide 65 · Case 1: Interpretation

Multifocal bilateral infarction with dementia, gait and pseudobulbar features suggests vascular dementia.

Both gray-matter and white-matter lesions may contribute.

The differential vascular substrate includes atherosclerosis, embolism and hypertensive arteriolosclerosis.

Additional clinical evidence is still required to establish the patient-level diagnosis.

Slide 66 · Case 2: Subcortical disease

Clinical vignette

A patient with a history of chronic hypertension has slowly evolving cognitive and gait difficulties. Brain imaging demonstrates extensive injury preferentially affecting the subcortical white matter.

Questions for interpretation

What named vascular pattern should be considered?

What essential Diagnostic consideration: Remains?

Slide 67 · Case 2: Interpretation

The distribution suggests Binswanger disease (subcortical arteriosclerotic encephalopathy).

Chronic hypertensive disease provides a plausible small-vessel substrate.

The same extensive white-matter appearance can be seen in other disorders.

Clinical and radiologic differentiation.

Slide 68 · Case 3: Combined pathology

Clinical vignette

An older adult with established neurodegenerative brain disease also has several remote vascular infarcts and a greater burden of cognitive impairment than expected from degenerative lesions alone.

Questions for interpretation

Does the presence of a degenerative disorder exclude vascular contribution?

How should the coexisting infarcts be interpreted?

Slide 69 · Case 3: Interpretation

Neurodegenerative and vascular lesions may coexist.

Cerebrovascular lesions can increase neurologic impairment for a given degenerative disease burden.

The appropriate conclusion is combined neuropathologic contribution, not automatic exclusive attribution.

This relationship is emphasized in the Robbins vascular dementia paragraph.

Slide 70 · Integrative model of vascular dementia

Vessel disease

Bilateral infarcts / white-matter injury

Network and tissue loss

Dementia ± gait / focal signs

Three important upstream causes: Atherosclerosis, embolic/thrombotic disease and hypertensive small-vessel disease.

Coexisting neurodegenerative pathology may amplify clinical impairment.

Schematic causal sequence

Slide 71 · High-yield distinctions

Entity

Core feature

Important caveat

Vascular dementia

Dementia with multifocal vascular brain disease

Mixed degenerative pathology is common

Lacunar infarct

Small deep infarct; remote cavity / gliosis

A lesion type, not a syndrome

Binswanger disease

Extensive subcortical white-matter vascular injury

Other white-matter disorders can resemble it

CADASIL

Hereditary NOTCH3 small-vessel disease

One specific etiology, not all vascular dementia

Slide 72 · Discussion and retrieval questions

Which three principal vascular mechanisms are named in the Robbins vascular dementia section?

What pathologic characteristic distinguishes a lacune from a large territorial infarct?

What makes the Binswanger pattern distinctive, and why is its differential necessary?

Why does coincident neurodegenerative pathology complicate disease attribution?

Slide 73 · References and source boundaries

Robbins, Cotran & Kumar: Pathologic Basis of Disease, 11th ed. (2026), ch. 28, “Vascular Dementia,” p. 1143.

Related chapter sections: “Cerebrovascular Disease,” “Focal Cerebral Ischemia,” and “Intraparenchymal Hemorrhage,” pp. 1136–1141.

All maps, vessel cross-sections and causal diagrams are original editable schematics; none depict a real specimen or scan.

Source limitations: original chapter PDF pages and licensed diagnostic images were not included; radiologic criteria were not independently updated.