Intracranial Hemorrhage

Slide 1 · Intracranial hemorrhage

Anatomical compartments, vascular mechanisms, morphology and clinical consequences

Epidural

Subdural

Subarachnoid

Intraparenchymal

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Localize intracranial bleeding to the correct anatomical compartment.

Connect hemorrhage patterns to their principal vascular lesions.

Explain acute tissue injury and the evolution of hematomas.

Differentiate common traumatic and spontaneous hemorrhages.

Slide 3 · Hemorrhage can occur in four compartments

Epidural: Between inner skull and dura.

Subdural: Within the dural border region.

Subarachnoid: Within CSF-filled meningeal space.

Intraparenchymal: Within neural tissue.

Skull

Epidural interface

Dura

Subdural border

Arachnoid

Subarachnoid space (CSF)

Pia + cerebral cortex

Slide 4 · Anatomical location determines the pathology

Extra-axial collections primarily compress underlying brain.

Parenchymal hematomas destroy, displace and infarct adjacent tissue.

Subarachnoid blood contacts cerebral vessels and CSF pathways.

Site of bleeding

Local tissue effect

Secondary damage

Slide 5 · Trauma and vascular disease produce different patterns

Pattern

Typical setting

Important mechanism

Epidural / subdural

Trauma

Meningeal artery / bridging vein

Deep parenchymal

Chronic hypertension

Fragile penetrating arterioles

Lobar parenchymal

Cerebral amyloid angiopathy

Amyloid-bearing cortical vessels

Subarachnoid

Ruptured aneurysm

Failure at arterial branch point

Slide 6 · Blood distribution is not the same as bleeding origin

A primary brain hemorrhage may enter ventricles or the subarachnoid space.

A traumatic contusion may extend into the subarachnoid space.

The secondary site of blood does not necessarily identify its source.

Primary source

Anatomic extension

Observed blood pattern

Slide 7 · The rigid cranial cavity magnifies hemorrhagic injury

Expanding blood collections compress adjacent tissue.

Compression reduces local perfusion and aggravates ischemic damage.

Large lesions can rapidly deteriorate despite an initially limited deficit.

Vessel rupture

Hematoma expansion

Compression / edema

Neurologic decline

Slide 8 · Clot expansion and edema cause secondary tissue injury

Accumulating blood increases pressure on nearby parenchyma.

Associated edema intensifies tissue compression.

Local tissue ischemia contributes to neurological dysfunction.

Clotted blood

Parenchymal compression

Secondary infarction

Edema

Slide 9 · A location-based approach starts with three questions

Is blood extra-axial, subarachnoid, or intraparenchymal?

Is the likely initiating event traumatic or spontaneous?

Does the anatomic distribution suggest a particular vessel lesion?

Where?

Compartment

Why?

Vascular or traumatic cause

What next?

Tissue effects

Slide 10 · Acute hemorrhage is not identical to hemorrhagic infarction

Feature

Primary hemorrhage

Hemorrhagic infarction

Initiating event

Vessel rupture

Occlusion / ischemia

Typical blood pattern

Hematoma / clot

Punctate, potentially confluent

Core tissue process

Compression + secondary infarct

Ischemic necrosis preceding bleed

Slide 11 · Intraparenchymal hemorrhage begins inside brain tissue

Rupture of an intraparenchymal vessel creates a primary hematoma.

Sudden neurological deficits often resemble other stroke syndromes.

Anatomical site determines the observed deficits.

Deep focus

Schematic anatomical localization — not a specimen

Slide 12 · Deep and lobar hemorrhages are distinct patterns

Deep or ganglionic hemorrhage involves basal ganglia or thalamus.

Lobar hemorrhage lies more superficially within cerebral hemispheres.

These patterns suggest different underlying vasculopathies.

Deep

Lobar

Schematic anatomical localization — not a specimen

Slide 13 · Deep hemorrhage points toward chronic hypertension

Hypertension is the dominant association for deep parenchymal hemorrhage.

Typical locations include putamen, thalamus, pons and cerebellum.

Long-standing small-artery damage makes rupture more likely.

Putamen

Thalamus

Pons

Cerebellum

Slide 14 · Hypertension remodels arteries at several calibers

Large arteries can develop accelerated atherosclerosis.

Small arteries develop hyaline arteriolosclerosis.

Severe hypertension may produce proliferative change and arteriolar necrosis.

Chronic hypertension

Small-vessel wall injury

Thickened rigid arteriole

Susceptibility to rupture

Slide 15 · Hyaline arteriolosclerosis creates a rigid vessel wall

Hyaline thickening reduces normal vessel-wall compliance.

Affected small arteries are especially prominent in basal ganglia and white matter.

The resulting wall is vulnerable to rupture under pressure.

Lumen

Thickened vessel wall

Hyaline arteriolosclerosis

Slide 16 · One small-vessel lesion causes two vascular outcomes

Luminal narrowing or occlusion can produce lacunar infarction.

Failure of the damaged vessel wall can cause parenchymal hemorrhage.

Both outcomes can arise from hypertensive arteriolosclerosis.

Hypertensive arteriolosclerosis

Luminal occlusion

Lacunar infarction

Wall rupture

Intracerebral hemorrhage

Slide 17 · The putamen is a characteristic hemorrhage site

Hypertensive hematomas frequently originate in the putamen.

Blood may involve neighboring deep structures and white matter.

Extension into the ventricular system can worsen the injury.

Deep focus

Schematic anatomical localization — not a specimen

Slide 18 · Thalamic and brainstem lesions affect compact pathways

A small deep hematoma can interrupt tightly packed circuits.

The clinical deficit follows the neuroanatomic location, not simply clot size.

Hypertensive hemorrhage may also involve the cerebellum and pons.

Deep focus

Schematic anatomical localization — not a specimen

Slide 19 · Intraventricular extension increases the affected territory

Deep hematomas may rupture into the ventricular system.

Ventricular blood signifies spread beyond the original parenchymal focus.

Large or extensive hemorrhage may cause severe neurological deterioration.

Deep parenchymal bleed

Ventricular rupture

More extensive intracranial blood

Slide 20 · Amyloid angiopathy preferentially causes lobar bleeding

Cerebral amyloid angiopathy deposits Aβ in vessel walls.

Affected vessels are predominantly cortical and leptomeningeal.

Vessel wall fragility favors superficial or lobar hemorrhage.

Superficial / lobar

Schematic anatomical localization — not a specimen

Slide 21 · CAA damages vessels by extracellular Aβ deposition

Amyloid accumulates in small and medium meningeal and cortical vessels.

The vessel wall becomes rigid and prone to rupture.

H&E may resemble hyaline change, but the deposited material is Aβ.

Lumen

Thickened vessel wall

Aβ deposition

Slide 22 · CAA and hypertension have different tissue distributions

Feature

Hypertensive arteriopathy

Cerebral amyloid angiopathy

Typical site

Deep / ganglionic

Lobar / superficial

Affected vessels

Deep small arteries

Cortical / leptomeningeal

Wall deposit

Hyaline / collagenous

Aβ amyloid

Other manifestation

Lacunar infarcts

Multiple small bleeds

Slide 23 · CAA may produce multiple small hemorrhages

Amyloid-containing vessel walls can fail repeatedly.

Small cerebral microbleeds may accompany a major lobar hematoma.

Imaging studies can reveal these small hemorrhagic foci.

Superficial / lobar

Schematic anatomical localization — not a specimen

Slide 24 · CAA-associated genetic factors modify bleeding susceptibility

APOE ε2 or ε4 alleles are associated with increased hemorrhage risk in CAA.

Some autosomal dominant CAA forms involve APP mutations.

Genetic susceptibility is not equivalent to a deterministic diagnosis.

CAA genetic associations

APOE risk alleles

Bleeding susceptibility

APP mutation

Hereditary CAA

Slide 25 · CADASIL is a contrasting hereditary small-vessel disorder

Pathogenic NOTCH3 variants lead to abnormal extracellular receptor protein.

Recurrent small-vessel infarcts are typical; Hemorrhage is less common.

White-matter changes and cognitive impairment are characteristic features.

NOTCH3 variant

Small-vessel disorder

Subcortical infarcts

White-matter injury

Slide 26 · COL4A1-associated disease can include intracranial bleeding

COL4A1 encodes a component of the vascular basement membrane.

Inherited variants may be associated with brain hemorrhage.

Other manifestations described include cataract, hematuria and epilepsy.

COL4A1 variant

Basement membrane abnormality

Vascular vulnerability

Multisystem manifestations

Slide 27 · A primary hematoma has a central blood clot

Acute bleeding creates a central mass of coagulated blood.

The hematoma displaces and compresses surrounding tissue.

The surrounding parenchyma develops ischemic injury and edema.

Deep focus

Schematic anatomical localization — not a specimen

Slide 28 · Adjacent ischemic injury is secondary to compression

Clot expansion mechanically compresses neural tissue.

Damaged surrounding cells show anoxic neuronal and glial changes.

Edema adds further tissue injury around the hematoma.

Expanding blood clot

Tissue compression

Secondary ischemia

Edema / cell injury

Slide 29 · Healing begins with hematoma clearance

Extravasated blood is gradually removed over weeks to months.

Macrophages accumulate lipid and hemosiderin from injured tissue.

Reactive astrocytes proliferate at the lesion margin.

Acute clot

Macrophage cleanup

Astrocytic reaction

Residual damage

Slide 30 · Old hemorrhages leave characteristic cavities

Severely injured parenchyma is permanently lost.

Chronic lesions may form cavities with brown hemosiderin staining at the edge.

Residual structural injury does not disappear when blood is cleared.

Cavity + rim

Schematic anatomical localization — not a specimen

Slide 31 · A large hematoma or ventricular extension predicts severe injury

Distribution

Tissue impact

Clinical course

Small focal hematoma

Limited adjacent damage

May improve during resorption

Large parenchymal hematoma

Extensive destruction / edema

Often severe neurological deficit

Ventricular extension

More extensive blood distribution

Potentially devastating

Slide 32 · Hemorrhagic transformation follows an ischemic event

An occlusive infarct initially may be nonhemorrhagic.

Recanalization or fragmentation of the obstruction restores flow.

Damaged microvessels then permit secondary hemorrhage.

Occlusive ischemia

Microvascular injury

Reperfusion

Punctate bleeding

Slide 33 · Secondary hemorrhage commonly appears punctate

Hemorrhagic transformation often produces multiple small hemorrhages.

Blood may follow the previously ischemic cortical ribbon.

More confluent secondary bleeding can also occur.

Multiple punctate foci

Schematic anatomical localization — not a specimen

Slide 34 · Contusions are traumatic intraparenchymal hemorrhages

Blunt kinetic force disrupts superficial tissue and blood vessels.

Hemorrhage develops with parenchymal damage and edema.

The crests of gyri are particularly susceptible to impact.

Cortical surface injury

Schematic anatomical localization — not a specimen

Slide 35 · Coup and contrecoup describe impact geometry

Feature

Coup

Contrecoup

Location

At point of impact

Opposite point of impact

Mechanism

Direct contact force

Brain strikes opposite skull

Morphology

Hemorrhagic contusion

Hemorrhagic contusion

Slide 36 · Frontal and temporal surfaces are prone to contusions

Orbital frontal and temporal cortex overlie irregular skull surfaces.

The superficial gyri may develop wedge-shaped hemorrhagic lesions.

Old contusions may leave yellow-brown, depressed plaques (plaque jaune).

Cortical surface injury

Schematic anatomical localization — not a specimen

Slide 37 · Additional causes complicate hemorrhage localization

Coagulopathies may aggravate bleeding in several compartments.

Neoplasms can bleed within parenchyma.

Vasculitis, aneurysms and vascular malformations can also cause hemorrhage.

Slide 38 · Some tumors are predisposed to intratumoral hemorrhage

High-grade gliomas among relevant primary tumors.

Examples of hemorrhage-prone metastases include melanoma.

Choriocarcinoma and renal cell carcinoma metastases are also cited.

Slide 39 · Subarachnoid blood occupies the CSF compartment

Blood fills spaces around the brain normally containing CSF.

Bleeding can arise from trauma or a ruptured vascular lesion.

Rupture of a saccular aneurysm is the leading spontaneous cause.

Skull

Epidural interface

Dura

Subdural border

Arachnoid

Subarachnoid space (CSF)

Pia + cerebral cortex

Slide 40 · Spontaneous subarachnoid hemorrhage has several causes

Ruptured saccular aneurysm is the principal cause.

Other causes include vascular malformations and blood disorders.

A primary cerebral hemorrhage or tumor may also contribute.

Subarachnoid blood

Saccular aneurysm

Vascular malformation

Parenchymal extension

Other disorders

Slide 41 · Saccular aneurysms arise near major branch points

Saccular outpouchings commonly occur along the circle of Willis.

Most are located in the anterior cerebral circulation.

Branch-point flow stress is implicated in their development.

Bifurcation

Saccular sac

Branch-point wall vulnerability

Slide 42 · The aneurysm sac lacks normal arterial wall support

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

The wall consists mainly of hyalinized intima and adventitia.

The weakened sac is susceptible to rupture.

Artery

Saccular dome

Sac lacks media and internal elastic lamina

Slide 43 · A saccular aneurysm has a neck, dome and apex

A narrow or broad neck connects the sac to the parent artery.

The dome forms a thin-walled rounded outpouching.

Rupture generally occurs near the apex.

Artery

Saccular dome

Apex

Neck

Slide 44 · Aneurysms evolve rather than existing fully formed at birth

Underlying structural susceptibility predisposes to sac formation.

Hemodynamic stress at an arterial branch point contributes.

The term “congenital aneurysm” is therefore potentially misleading.

Vessel-wall susceptibility

Branch-point flow stress

Progressive sac formation

Possible rupture

Slide 45 · Aneurysm predisposition includes inherited and acquired factors

First-degree family history suggests a genetic contribution.

Associated disorders include autosomal dominant polycystic kidney disease.

Smoking and chronic hypertension are recognized risk factors.

Slide 46 · Rupture introduces arterial blood into the subarachnoid space

A sac may break at its dome/apex.

High-pressure arterial blood spreads around the brain.

Some ruptures extend into the brain parenchyma as well.

Sac wall failure

Arterial extravasation

Subarachnoid blood

Acute neurological injury

Slide 47 · Aneurysmal SAH often causes abrupt severe headache

Classically described as sudden, excruciating headache.

Rapid loss of consciousness or deterioration may accompany rupture.

The presentation reflects acute bleeding into a sensitive intracranial space.

Slide 48 · Rebleeding worsens the prognosis after aneurysm rupture

Survivors of initial rupture may recover consciousness.

Additional episodes of hemorrhage can occur unpredictably.

Each further bleeding episode can worsen the outlook.

First rupture

Early survival

Risk of recurrence

Further injury

Slide 49 · Subarachnoid blood can provoke arterial vasospasm

Extravasated blood bathes basal cerebral vessels.

Arterial narrowing may cause secondary cerebral ischemia.

This risk is especially important in basal subarachnoid hemorrhage.

Blood around arteries

Vasospasm

Reduced flow

Secondary ischemia

Slide 50 · Several candidate mediators influence vasospasm

Endothelins have been implicated in vascular contraction.

Nitric oxide signaling and arachidonic acid metabolites may contribute.

These as proposed mechanisms, not a single proven pathway.

Subarachnoid blood

Endothelin pathways

Nitric oxide signaling

Arachidonic products

Vessel caliber change

Slide 51 · Healing of SAH may interfere with CSF circulation

Meningeal fibrosis and scarring develop during repair.

Scar formation can obstruct CSF flow.

Disruption of CSF resorption provides an additional mechanism of injury.

Subarachnoid blood

Meningeal scarring

Impaired CSF flow / resorption

Secondary consequence

Slide 52 · Saccular aneurysms are not the only vascular abnormalities

Other intracranial aneurysm types include fusiform and dissecting lesions.

Mycotic and traumatic aneurysms are also described.

Different vascular lesions can produce overlapping bleeding distributions.

Slide 53 · Four principal cerebral vascular malformations are recognized

Malformation class

Potential clinical importance

Arteriovenous malformation

Seizures; cerebral or subarachnoid bleed

Cavernous malformation

Bleeding and neurologic symptoms

Capillary telangiectasia

Recognized vascular malformation group

Venous angioma

Recognized vascular malformation group

Slide 54 · AVMs connect arteries to veins abnormally

Abnormal vessels form a high-flow arteriovenous shunt.

Normal intervening capillary resistance is bypassed.

Rupture can cause parenchymal or subarachnoid hemorrhage.

Feeding artery

Draining vein

Direct arteriovenous connection

Intervening capillary bed bypassed

Slide 55 · AVMs often present with seizures or bleeding

Presentations commonly occur in children and young adults.

Seizures and intracerebral or subarachnoid hemorrhage are important presentations.

High-flow neonatal shunts may cause cardiac failure.

Arteriovenous malformation

Seizures

Intracerebral bleeding

Subarachnoid bleeding

Neonatal cardiac failure

Slide 56 · Somatic signaling alterations occur in vascular malformations

Entity

Reported molecular alterations

Interpretation

AVM

Endothelial KRAS activation

RAS pathway dysregulation

Cavernous malformation

Loss of CCM-complex function

Defective vascular-growth restraint

Aggressive cavernous lesion

Additional PIK3CA activation

Growth-promoting signaling

Slide 57 · Epidural hematoma is extra-axial arterial bleeding

The middle meningeal artery is a characteristic injured vessel.

A fracture crossing its course is common in adults.

Arterial pressure strips dura from the overlying skull.

Skull

Epidural interface

Dura

Subdural border

Arachnoid

Subarachnoid space (CSF)

Pia + cerebral cortex

Slide 58 · Epidural bleeding produces rapidly expanding mass effect

Arterial blood creates a potential space against the skull.

The growing collection compresses the adjacent brain.

Without prompt treatment, dangerous herniation can develop.

Meningeal vessel tear

Epidural blood

Compression

Herniation risk

Slide 59 · A lucid interval is possible but not obligatory

An initially conscious patient may deteriorate as the hematoma grows.

The symptom-free period depends partly on the rate of bleeding.

A symptomatic epidural hematoma is a neurosurgical emergency.

Head trauma

Possible lucid interval

Progressive compression

Neurological decline

Slide 60 · Epidural hemorrhage can occur without an obvious fracture

In children, skull deformation may transiently tear a meningeal artery.

A permanent fracture need not accompany vascular injury.

The essential lesion is the arterial breach and expanding extradural blood.

Slide 61 · Subdural hematoma usually begins with venous tearing

Bridging veins cross from the cerebral convexity toward dural sinuses.

Brain displacement can tear veins near their dural entry.

Blood dissects within the dural border region.

Skull

Epidural interface

Dura

Subdural border

Arachnoid

Subarachnoid space (CSF)

Pia + cerebral cortex

Slide 62 · Subdural bleeding may evolve relatively slowly

Headache or confusion may appear after a delay.

Nonlocalizing symptoms are common, although focal signs can occur.

Deterioration may be progressive or occasionally acute.

Trauma

Bridging vein injury

Growing subdural collection

Progressive symptoms

Slide 63 · Brain atrophy increases bridging-vein vulnerability

Atrophy places bridging veins under greater stretch.

Consequently older adults may bleed after minor head trauma.

Infants are susceptible because the bridging veins are thin-walled.

Atrophy / fragile veins

Mechanical stretch

Venous tear

Subdural blood

Slide 64 · Epidural and subdural hematomas differ mechanistically

Feature

Epidural hematoma

Subdural hematoma

Source

Meningeal artery

Bridging veins

Typical setting

Skull fracture / trauma

Trauma; minor trauma possible

Bleeding compartment

Skull–dura interface

Dural border region

Course

May deteriorate rapidly

Often delayed / progressive

Slide 65 · Trauma may involve multiple compartments at once

An impact may injure skull, superficial brain and blood vessels together.

Parenchymal contusions often coexist with subarachnoid blood.

An extra-axial collection does not exclude additional brain injury.

Cortical surface injury

Schematic anatomical localization — not a specimen

Slide 66 · The complete compartment matrix localizes the source

Compartment

Typical lesion

Distinguishing context

Epidural

Meningeal arterial tear

Head trauma / fracture

Subdural

Bridging vein tear

Atrophy / minor trauma

Subarachnoid

Aneurysm or AVM rupture

Sudden severe headache

Parenchymal

Hypertensive / amyloid vessel rupture

Deep vs lobar location

Slide 67 · Case: Sudden deficit with a deep putaminal hematoma

Clinical vignette — interpret the pathology

An adult develops abrupt focal neurological deficit.

Bleeding is centered deep within the basal ganglia.

Which underlying arterial disease best explains this distribution?

Slide 68 · Deep putaminal hemorrhage suggests hypertensive arteriopathy

Hypertension injures deep penetrating small arteries.

Hyaline thickening makes the vessel wall prone to rupture.

Ventricular extension may complicate a large deep hematoma.

Deep focus

Schematic anatomical localization — not a specimen

Slide 69 · Case: Superficial lobar hemorrhage with microbleeds

Clinical vignette — interpret the pathology

An older adult has a superficial cerebral hematoma.

Several small prior hemorrhagic foci are also present.

Which vessel-wall deposit should be considered?

Slide 70 · Lobar hemorrhage with microbleeds raises CAA

Cortical and leptomeningeal vessels accumulate Aβ deposits.

A weakened vessel wall predisposes to superficial hemorrhage.

The distribution differs from classic deep hypertensive bleeding.

Superficial / lobar

Schematic anatomical localization — not a specimen

Slide 71 · Case: Sudden excruciating headache and collapse

Clinical vignette — interpret the pathology

A patient develops a sudden maximal-intensity headache.

Consciousness is briefly lost; Subarachnoid blood is identified.

Which ruptured arterial lesion is a leading possibility?

Slide 72 · Aneurysm rupture explains spontaneous basal SAH

The saccular arterial wall lacks normal media and elastic lamina.

Rupture releases arterial blood into the subarachnoid compartment.

Vasospasm and later CSF scarring are important secondary hazards.

Artery

Saccular dome

Apex

Neck

Slide 73 · Case: Deterioration after temporal head trauma

Clinical vignette — interpret the pathology

Following a head injury, an adult is initially responsive.

Neurological function deteriorates as an extra-axial collection grows.

What arterial injury should be considered urgently?

Slide 74 · Rapid extra-axial deterioration can indicate epidural blood

Meningeal arterial rupture may follow temporal skull fracture.

The expanding epidural collection compresses the brain.

The possibility of a lucid interval must not delay recognition.

Skull

Epidural interface

Dura

Subdural border

Arachnoid

Subarachnoid space (CSF)

Pia + cerebral cortex

Slide 75 · Synthesis: Infer mechanism from location and tissue response

Deep clot-centered hemorrhage: Think hypertensive small-vessel injury.

Lobar bleeding with microbleeds: Consider cerebral amyloid angiopathy.

Subarachnoid blood: Search conceptually for trauma or vascular lesion.

Extra-axial blood: Distinguish meningeal arterial from bridging-vein injury.

Slide 76 · References and source scope

Robbins, Cotran & Kumar: Pathologic Basis of Disease. 11th ed. (2026).

Primary parent heading: Intracranial Hemorrhage; expanded using adjacent CNS sections.

All illustrations in this deck are original editable schematics, not clinical images.

Clinical vignettes are constructed teaching examples.