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 - <1%,>
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 <20yrs,>
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 <1/3,>
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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