MAGING IN CEREBRAL VASCULAR PATHOLOGIES: EVOLUTION OF INTRACRANIAL HEMATOMA

IMAGING IN CEREBRAL VASCULAR PATHOLOGIES:

EVOLUTION OF INTRACRANIAL HEMATOMA

1. Immediate
– liquid with 95% O2 saturated Hb, T2 hyper, T1 iso within seconds platelets thrombi form & cells aggregate

2. Hyper acute stage

4-6 hrs, fluid serum begins to disperse

Protein clot retracts, red cells become spherical,

Early peripheral edema begins, T2 iso, T1 iso

OxyHb is diamagnetic with no unpaired electrons,

CT – isodense for 1-3hrs, then becomes dense, 60-100HU


3. Acute stage
– 7-72 hrs, red cells begin to compact, deoxyhb

Central portion T2 hypo, T1 iso

DeoxyHb is paramagnetic with 4 unpaired electrons, T2 shortening

Sheilded from H2O by globin, prevents T1 shortening

No proton-electron relaxation enhancement can occur

Edema pronounced in periphery

Dense on CT, window width of 150-250 best

4. Subacute stage

1-4 wks, methemoglobin starts day 4

Begins at periphery & progresses towards anoxic center

Cells begin to lyse at 1 week releasing metHb, decrease in edema

Perivascular inflammatory reaction begins with macrophage at periphery

Ring Enhancement caused by this process

T1 BRIGHT due to 5 unpaired electrons exposed by globin change

Proton-electron relaxation enhancement does occur

Periphery affected 1st, middle remains iso initially

T2 HYPO early when methemoglobin still in RBC

BRIGHT once the cell breaks down & Hb diluted in water

CT attenuation decreases approx 1.5HU per day

CT is NOT an accurate indicator of age, due to variable Hb etc

5. Early Chronic stage


– >4wks, edema & inflammatory reaction subside

Vascular proliferation encroaches on haematoma decreasing its size

Dilute uniform pool of extracellular metHb with vascular walls

Macrophage contain ferritin & hemosiderin at periphery

T2 hypo due to strong magnetic susceptibility

T1 iso due to fact that hemosiderin is water insoluble

Hypodense on CT unless rebleeding has occurred

6. Late Chronic stage
cystic or collapsed with dense capsule

Vascular proliferation gradually forms fibrotic matrix with macrophage

Infants may resolve completely

Ferritin laden scar persists for years in adults

10% calc with residual hypodense focus in 40%

Gradient echo is helpful in detecting Haem in low field MRI’s

OVERVIEW OF HEMORRHAGE CAUSES

Underlying cause often hidden by the bleed. Intraventricular extension associated with 10% mortality

1. Neonatal Hemorrhage – germinal matrix hemorrhage secondary to prematurity

thin walled, proliferating vessels in subependyma of lateral caudothalamic groove

involution occurs at 34 wks when all cells have migrated

No hemorrhage in utero or beyond first 28 days post birth

Grade I – Hemorrhage confined to germinal matrix, can be bilateral

Grade II – rupture into normal size ventricles

Grade III – intraventricular hemorrhage with Hydrocephalus

Grade IV – extension to adjacent hemispheric white matter

Can be seen by US in acute & subacute, lucent if chronic

Term Infants – Hemorrhage usually secondary to trauma, subdural mostly

Asphyxia & infarction most commonly in non-traumatic cases

Posterolateral lentiform nuclei & ventral thalamus most susceptible

2. Hypertension – Most common cause of nontraumatic bleed in adult

Lenticulostriate & Pontine vasculatures mostly involved, penetrating branches of MCA

Usually spontaneous in elderly patients, basal ganglia mostly

Vessels often abnormal, ruptured microanuerysms etc

50% have hemorrhage dissection into ventricles, poor prognosis

Lobar white matter hemorrhage in 20%, cerebellum 10%, midbrain & brainstem rare

Originates along perforating branches near dentate nuclei

Active bleeding usually lasts <1hr

Edema progresses for 24-48hrs, 25% die in this period

Hypertensive Encephalopathy – occurs secondary to elevated BP

Toxemia (Most common) – autoregulation overwhelmed especially in posterior aspect

Overdistention of arteriole leads to BBB breakdown

Reversible vasogenic edema results, frank hemorrhage rare

Cortical petechia & subcortical hemorrhage possible, especially in occipital regions

Increased T2 in external capsule & basal ganglia more common

Chronic renal Diseases, TTP, & Hemolytic-Uremic syndrome other causes

3. Hemorrhagic Infarction

Arterial Infarction – hemorrhage when endothelium reperfused

Occurs in 50%, but only seen in 10%, sensitivity: MRI>CT

Cortex & basal ganglia from MCA distribution most commonly, 24-48hrs later

Pseudolaminar Cortical Necrosis – generalized hypoxia

Middle layers usually effected, gyriform hemorrhage

Nonhemorrhagic ischemic changes can occur, gyri calcification possible

Venous Infarction – usually associated with dural sinus thrombosis

Dura around sinus will enhance, clot stays hypodense (empty delta sign)

More likely to effect white matter than cortex

4. Aneurysms – 90% of nontraumatic subarachnoid hemorrhage

Headache common presenting sign for aneurysm, CT best for acute SAH

Blood usually fills ambient cisterns & sylvian first

90% of blood cleared from CSF in 1wk

MRI better for subacute or chronic SAH, dirty CSF

Superficial siderosis – hemosiderin deposit on meninges

Cerebellum brainstem & cranial nerves also coated – neurological dysfunction

Giant aneurysms >2.5cm often have intramural hemorrhage

most from carotid, cavernous portion most common, all ages

75% have calc if thrombosed, none otherwise

Charcot-Bushard Aneurysm – secondary to HTN

5. Vascular Malformations

AVM & Cavernous Angioma commonly

Most bleed into parenchyma rather than subarachnoid space

Arteriovenous Malformation – pial, dural or mixed, No cap bed

Pial AVM’s – hemorrhage @ 2% per year, often in previously normal young pts

70% bleed by 1st exam, repeated hemorrhage can simulate neoplasm

Central nidus with gliosis & encephalomalacia

Dural AVM’s – no central nidus, SAH or subdural

hemorrhage rare unless drainage through cortical veins

Cavernous Angioma – bleed @ .5% per year, freq repeated bleeds

Popcorn like with mixed signal foci & hemosiderin ring

Venous Angiomas – bleed rare, similar hematoma of other malformations

Medusa like collection of dilated medullary veins

Capillary Telangiectasias – usually small & clinically silent

may see multiple small foci of hemosiderin on T2

INTRACRANIAL ANEURYSMS & VASCULAR MALFORMATIONS

Charcot-Bushard Aneurysm – secondary to Hypertension

20% multiple, higher incidence in females.

Look for familial causes such as Polycystic Kid Disease

SACCULAR ANEURYSMS

Berrylike out pouching from arterial bifurcation

Include intima & adventitia, media ends with normal vessel

1. Etiology – hemodynamic induced injury, abnormal shear forces most commonly

Trauma, infection, tumor, drug abuse & AV malformations

Berry Aneurysms – associated with polycystic kidney Diseases & aortic coarctation

2. Incidence – 1% of angios & 5% of postmortems

Multiple in 20%, esp in females & polycystic kidney Diseases

Bilateral in 20%, esp at cavernous sinus, Pcom & MCA trifurcation

Occur age 40-60 unless traumatic or mycotic,

3. Associated Conditions – occur at anomalous vessels & AVM

Inc pressure ie HTN & aortic coarctation

Systemic Diseases – Marfan’s, fibromuscular dysplasia, polycystic kidney diaeases

4. Location – 30% at anterior communicating, 30% at posterior communicating, 20% MCA origin

10% in post circulation especially basilar artery bifurcation

traumatic or mycotic occur anywhere

5. Clinical Presentation – asymptomatic until rupture or giant >2.5cm

1-2% risk of rupture per year, 3.5% risk of surg

No different risk with HTN, age, sex or multiplicity

All should be repaired if >3yr life expectancy

Subarachnoid Hem – clinical grade by Hunt & Hess scale I-V

Vasospasm most common cause of morbidity, 30% die

highest bleed rate in 1st 24hrs, 50% rebleed in 2wk

CT – shows SAH in >80% of ruptured aneurysms

Cavernous sinus aneurysms can compress Nerves III-VI

TIA, Seizures & embolic ischaemia less common

Giant Aneurysms – most from supraclinoid carotid, all ages

Fibrous vascular walls, rarely rupture, Symptoms secondary to mass effect

Partially Thrombosed Aneurysms – 75% have curvilinear calcification

CT most specific for these with target seen

NO calc if not thrombosed

D/D – Meningioma, both erode sella & lat sphenoid

aneurysm has no associated hyperostosis or atherosclerosis

6. Appearance of Saccular Type – catheter angiography definitive

asses for relation to vessel, adjacent branches & vasospasm

essential in assessment of nontraumatic SAH

Thrombosed aneurysm will have no finding, 15%

may see mass effect if large

irregularity or local vasospasm can indicate rupture

D/D vascular loops & infundibuli (embryonic funnel <2mm)

CT may show bone erosion in long standing case

Patent aneurysms enhance intensely w contrast

Location of SAH can be prognostic indicator

Ambient cisterns anterior to brainstem probably just venous rupture

No repeat angio needed

Suprasellar cistern to lateral sylvian fissure

more aneurysmal pattern, must do F/U angio

MRI dependent on pattern of flow, turbulence & clot

may have wall enhancement with gadodiamide, laminated with thrombosis

7. Traumatic Aneurysm

nonpenetrating usually occur at skull base, or shear

hyperextention stretches ICA over lat C1

8. Mycotic Aneurysms – Secondary to infection of arterial wall, rare <10%

adventitia & muscularis disrupted, thoracic aorta commonly

Angio – occur dist to usual location, 2nd branch MCA commonly

most common cause of multiple MCA aneurysms

usually small, staph & strep most common, inc in child

bleed into parenchyma or SAH equal incidence

Medical Treatment usually sufficient to control, surgery if enlarge on angio

Mucor & Aspergilla invade direct from nasopharynx cause thrombosis & infarct more often than aneurysm

9. Oncotic Aneurysms – usually extra cranial, exsanguinate freq

tumor may implant or cause emboli, primary or metastatic

10. Flow-Related Aneurysms – seen with AVM’s in 30%

distal ones most likely to hemorrhage

11. Vasculopathies – rare but seen with SLE, infarct & TIA commonly

Takayasu’s Arteritis – 9:1 female, inflammation & stenosis most commonly

prox arch vessels, L subclavian commonly, often occludes

Fibromuscular Dysplasia – up to 50%, dissection & A-V fistula, 65% bilateral

Cocaine – 50% with CNS symptoms have SAH, may be secondary to HTN treatment

several drugs cause vasculitis .

FUSIFORM ANUERYSMS

Etiology – atherosclerosis, exaggerated arterial ectasia

media damaged, stretches & elongates, frequent mural thrombus

Vertebrobasilar Dolichoectasia – Common site, older patient

often thrombus producing brainstem infarcts

can also compress local stem causing nerve palsies

Imaging – enhances if patent, hyperintense if thrombosed

curvilinear calcification pathognomonic, may cause skull base erosion

DISSECTING ANEURYSMS

Etiology – intramural blood from tear in intima

may narrow or occlude lumen, may distend subadventitia

do not confuse with Pseudoaneurysm, a encapsulated hematoma

Presentation – usually extracranial unless severe trauma

Commonly in midcervical ICA & vertebral from C2 to skull base

Catheter angio remains procedure of choice for assesment

INTRACRANIAL VASCULAR MALFORMATIONS

1. Parenchymal AVM – congenital, dilated arteries & veins without capillary bed

98% solitary, multiple in Osler-Weber-Rendu & Wyburn-Mason

Incidence – 85% supratentorial, peak 20-40y, 25% children

Hemorrhage in 85% with 3% per year risk, seizure 25%, deficit 25%

Size not predictive, deeper & smaller ones bleed more

Parenchymal commonly, also common cause of SAH if

Vascular Steal – atrophy due to vasculopathy of feeding vessel

atrophic low density regions & hematoma with high density

Overlying meninges thick & hemosiderin stained

Angio – shows feeding arteries & tortuous veins

often wedge shaped, possible to appear Normal if thrombosed

GBM may simulate but usually has tissue between vessels

10% have aneurysms in feeding arteries, can bleed

Cryptic AVM’s – not seen by angio, 10%

CT – often absent w/o contrast, 25% have mild curvilinear calcification

mixed increased & decreased density if seen, Mild mass effect possible

Enlarged post venous sinuses but not cavernous sinus

Calcification seen in

MRI – honeycomb of flow voids, increased signal if thrombosed

hemorrhage in different stages often present

No significant intervening brain tissue, D/D : GBM

TX – resection if unruptured, must be completely removed

Aneurysms must be treated separately, increased risk for bleed

2. Dural AVM’s & Fistulae – form within a venous sinus

no discrete nidus, multiple microfistulae, occluding sinus frequent

Follow recanulation of thrombosed sinus, 10% of all AVM’s

Transverse or Sigmoid sinus commonly, Bruits & headache most common

Cavernous sinus AVM – proptosis, retro orbital pain, proptosis

SAH common if reflux flow forced into cortical veins

Carotid-Cavernous fistula related, follow trauma

Occipital & Meningeal branch of ext carotid #1 feeders

CT often N, MRI may show dilated cortical veins

3. Mixed – 15%, if parenchymal AVM recruits arteries from dural supply

4. Capillary Telangiectasias – multiple nests of dilated capillaries

Common in pons & Cerebellum, usually incidental

Gliosis of adjacent brain & hemosiderin staining from hem possibly

Cavernous Angiomas assoc or simply the extreme form

Osler-Weber-Rendu – hereditary hemorrhagic Telangiectasias

25% have brain abnormalities, most are true AVM’s

Visceral angio dysplasia with scalp & mucous membrane telangiectasia

2nd most common lesion to venous angioma at autopsy

Not visualized by angio, may present with epistaxis

CT may faintly enhance, faint on MRI

5. Cavernous Angiomas – Hemangioma or cavernoma

Circumscribed nodule of honeycomb sinusoidal vascular spaces

separated by fibrous bands but no intervening neural tissue

frequently MULTIPLE HEMATOMAS at different stages, reticulated core of vessels

Supratentorial 80% but can occur anywhere, 50% multiple

Most Common vascular lesion identified, 20-40y/o

Seizure, deficits & bleed most common presenting features

Angio does NOT visualize, possible faint blush in early venous

CT shows freq Calc, variable enhancement, can simulate neoplasm

MRI – popcorn like appearance on T2 due to multiple hem

multiple areas of signal drop-out due to hemosiderin

VENOUS MALFORMATIONS

1. Venous Angioma – dilated anomalous veins converge on central vein

Etiology – remnant embryonic venous system, usually solitary

assoc with migrational abnormalities & cavernous Angiomas in 30%

Asymptomatic, Hemorrhage very rare unless from associated cavernous angioma

CT – may show linear tuft of vessels post contrast

located in deep White Matter of cortex or Cerebellum, commonly adjacent to frontal horn

MRI – shows stellate tributary veins into prominent collector vein

gliosis or hemorrhage seen in only 15%

Angio – the only vascular malformation with a single draining vein

Medusa head appearance on venous phase of angio

2. Vein of Galen Aneurysm – enlargement of Galenic system

Secondary to arteriovenous fistulae from choroidal arteries

AVM in thalmus or midbrain can also cause this

Present at birth with high-out put cardiac failure, cranial bruit +

Macrocephaly with obstructive hydrocephalus, deficits & ocular symptoms

US shows bi-directional flow in vein of Galen

Angio demonstrates either choroidal artery or thalmoperforating feeder

dilation to venous varix with or without distal stenosis

if stenosed distally will often thrombose

CT – large enhancing midline mass posterior to 3rd ventricle

Hydrocephalus frequent but hemorrhage rare

enhancing serpentine vessels in thalamic region

3. Venous varix – assoc with several intracranial vascular abnormalities

Enlarged & thin veins resulting in SAH, hydrocephalus & increased ICP

Sinus Pericranii – venous haemangioma adherent to outer skull, deep to galea

supplied from intracranial sinus & blood returns to sinus

present with enlarging fluctuant soft tissue mass, enlarge with crying

often secondary to trauma, often resolved with prolonged compression

Frontal commonly, parietal next, most near sagittal sinus, can be very lateral

Skull Film – usually sharp margins, vascular honeycombs possible

CT – shows strong uniform enhancement

MRI – well delineated ovoid or fusiform areas w variable signal

Venous Cavernoma – subcutaneous lesions of scalp

blood supply from external carotid, drain to external jugular

4. Orbital Venous Varix – rare vascular malformation in orbit

Causes intermittent proptosis & diplopia with valsalva & bending over

Disappear completely with axial views, use tourniquet on jugular vein

NEONATAL HEMORRAGE

Caudothalamic groove – between head of caudate & thalamus

both make up lateral wall of lateral ventricle, terminates in Monroe

Foramen of Monroe – divides frontal & body portions of ventricles

thalmus entirely posterior, caudate head anterior, choroid enters it

1. Subependymal Hemorrhage – preterm infants <32wks

Correlates with size of germinal matrix at birth, largest 24-32wks

involutes & is absent by 40wks, last in inferior lateral wall of frontal

lies inferior to ependyma, superior to head of caudate & anterior to thalmus

Usually occurs in first 3 days, always by 7-8 days

Grade 0 – Normal

Grade I – Subependymal alone

Grade II – intraventricular with no ventriculomegaly

Grade III – Hydrocephalus,

Grade IV – intraparenchymal

grade does not predict ultimate outcome, may progress

Serial studies required, only applies to germinal matrix hemorrhage

2. Parenchymal Hemorrhage – extends farther lateral than germinal matrix

can be “grade IV”, but not all secondary to germinal matrix bleed

most extend from SHE(Subependymal haemorrhage) to frontal or parietal lobes

Hypoxia & Hypercapnia implicated as etiology

stress causes vessels to dilate & burst

Phase 1 – echogenic like SEH for 1-2wks

Phase 2 – central Hypoechoic, bright peripheral rim 2-4wks

Phase 3 – retracts & settles into dependent position

Phase 4 – necrosis & phagocytosis complete, encephalomalacia

Cerebellar hematoma best scaned in coronal behind ear

assoc with mortality of 50%.

3. Choroidal Hemorrhage – usually grade II or III

Second cause of intraventricular hemorrhage not caused by SEH

Difficult to discern from normal choroid on US

asym scanning can show marked asym in choroid size

isolated choroid hematoma simulates ventricular hematoma with no hydrocephalus

Myelomeningocele assoc with pedunculated choroid

CT more reliable than US for Dx

D/D – Choroid Papilloma, very rare, consider if CSF clear on tap

all assoc with hydrocephalus, enhance intensely on CT

HEMORRHAGIC NEOPLASMS & CYSTS

1. Malignancy Related Coagulopathy – esp with leukemia & chemotherapy

systemic neoplasms can be assoc with term coagulopathy

2. Intratumoral Hematomas – 10%, malignant , Astrocytoma’s are most common.

Neovascularity, central necrosis, plasminogen activators etc contribute

Heterogeneous, incomplete hemosiderin ring, edema persist

multiple lesions & min edema suggests nonneoplastic cause

Cysts & slow growing cystic neoplasm like cranio rarely bleed

Oligodendroglioma, neuroectodermal & teratoma hemorrhage frequently

Ependymoma & choroid tumors – frequent SAH & hemosiderosis

Pituitary Adenoma – may bleed more frequently than astrocytoma

Lymphoma rarely bleed unless with AIDS

Renal cell Ca, chorio Ca, melanoma, thyroid & lung mets, 15%

3. Nonneoplastic Hemorrhagic Cysts -rare, colloid cysts never bleed

Rathke cleft cysts & Arachnoid cysts more commonly bleed

Arachnoid cysts bleed secondary to trauma, bridging vessels rupture

sometimes assoc with subdural hematoma

MISCELLANEOUS CAUSES OF BENIGN INTRACRANIAL HEMORRHAGE

1. Amyloid Angiopathy – Most common cause of bleed in elderly patient with no HTN

nonbranching fibrillar protiens form beta-pleated sheets

Deposit is Cortical & leptomeningeal vessels

extend from small vessels to brain parenchyma

Contractile elements replaced by the crystals

Multiple hematomas frequent & occurs at cortico medullary junction

basal ganglia & brainstem not affected

2. Infection & vasculitis – rare, increased chance if immuncompromised

septic emboli – mycotic aneurysms & hemorrhagic infarct

10% of Infective endocarditis have SAH or parenchymal

Aspergillosis & other fungi directly invade vessel

Thrombosis, infarction & hem result

Herpes Simplex II – the only encephalitis assoc with hematoma

3. Recreational Drugs – 50% have preexisting AVM or aneurysm

Cocaine can induce an acute hypertensive episode, vasospasm

also enhances platelet aggregation, dural sinus thrombosis

amphetamine & PCP also associated with hemorrhage

endothelial damage & necrotizing vasculitis

4. Blood Dyscrasias & Coagulopathies – iatrogenic or acquired

Vit K deficiency, hepatocellular diseases, antibody against clot, DIC

Anticoagulants, thrombolytics, aspirin, Etoh abuse, chemo

15% of all intracranial hemorrhage on anticoagulants

Supratentorial, intraparenchymal bleeds most common

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