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BRAIN VASCULAR ANATOMY ANATOMICAL VARIANT& VASCULAR LESIONSDR SOUMITRA HALDERDEPT. OF RADIOLOGYMEDICAL COLLEGE,KOLKATA

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BRAIN VASCULAR LESIONS..

PART-2

AneurysmVascular malformations

Aneurysm

Abnormal bulge of an arterial wall .

Develops where the blood vessel wall is weakened. Aneurysm

ACQABNORMAL VASCULAR HEMODYNAMCICS AND SHEAR FORSE.,Genetetic alterationAnomalous vsAcq.abnormal vascular hemodynamics.shearing stress.5

2. Sizes of Aneurysm.1.

By size-

. Small aneurysm diameter females> 40 years: females > males The sites different from gender: female supraclinoid segment of the internal carotid artery. male anterior communicating complex Age: rupture is most common between 40 and 60 years but can occur in any age, even in old age.Lateralized in 30 percent of patients, predominantly to the side of the aneurysm associated with a brief loss of consciousness

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IMAGING

An unenhanced CT scan is the preferred procedure for detection of SAH is positive in more than 90% of patients in the first 24 hours .

The location of the SAH may frequently suggest the site of the aneurysm

Rarely, the aneurysm itself might be visible.

CTA ..Sensitivity > 90%

DSA is gold standart.Right MCA aneurysm with subarachnoid hemorrhage.

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Giant vertebral aneurysm in the vertebral artery tip with nausea and vomiting due to brain stem compression.

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Treatment

ObservationSurgical clipping Endovascular occlusion.

Watchful waiting with serial scan for asymptomatic > SAH29

MR

T1W1 tightly packed mass or honeycomb of flow voidsT2W1 serpiginous honeycomb of flow voids adjacent high signal tissue gliosisFLAIR- flow voids +/- surrounding high signalGRE - blooming (Hagic residua)Left parital wedge shaped serpentine flow voids.30

ANGIOGRAPHY

Internal angioarchitecture best depiction

Depicts 3 components of AVM

Enlarged arteries+/- aneurysmNidusEarly draining veins

Feeding arteries Dilated and tortuous Flow related angiopathy dilatation , stenosis or thrombosisPedicle aneurysm(10-15%cases)Nidus Tightly packed tangle of abnormal arteries and veins with no intervening capillary bed/brain parenchym Intranidal aneurysm(50% cases)Draining Veins Opacify in mid-late arterial phase(Early draining vein) Enlarged , tortuous and may form varices exerting local mass effectStenosis can cause AVM Hage by intranidal pressure

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TREATMENT

Surgical excision for nidusAcute and emergent surgical intervention in life threatening ICH.

STEREOTACTIC RADIOSURGERY

Focussed irradiation to nidus Indication Unresectable because of locationSize < 3.5cms Risk of hage till it disappears completely

ENDOVASCULAR RX

Adjunct to Sx/ RadioSxUsed in small AVMs or 1-2 feeding arteriesEmbolisation Precedes surgery /radiosx reduce size of nidusComplete cure if : small AVM , few feeders , single draining vein

1Complete obliteration of nidus for cure.2 STEREOTACTIC RADIOSURGERYFocussed irradiation to nidusIndication Unresectable because of locationSize < 3.5cmsAdv : Non invasiveDisadv :Effect takes yearsRisk of hage till it disappears completely

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DURAL AV FISTULATiny crack like vessels that shunt blood b/w meningeal arteries and small venules within dural sinus wall.

ETIOLOGY : Acquired angiogenesis within dural sinus wall after thrombosis

Local hypoeperfusion in thrombosed dural venous sinus increased intrasinsu pressure

thrombosed transverse sinus with multiple tiny arteriovenous in the dural wall(thickarrow) . Lesion is mostly supplied bytransosseous feeders(curved arrow) from the external carotid artery.35

DURAL AV FISTULA

LOCATION: Trans Sinus>Sig sinus>Cav sinus(adults) Sup Saggital sinus (Children)SIZE : Tiny single vessel shunts to massive complex lesions with multiple feedersNUMBER : Multiple lesions are uncommon.

Malignant dAVF aggressive clinical course with Hage and NDMultiple dAVF poor clinical prognosis

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CLINICAL FEATURE

Mostly in adults(40-60yrs)

C/F varies with location and drainage patternTS-SigS - Bruit and tinnitusCav S Pulsatile proptosis , chemsois , retroorbital pain

Lesions with cortical venous drainage(Malignant dAVF) : seizures, dementia ,FND

40-60 yr. 20 y older than avmFND focal neurological deficitsPROGNOSIS98% w/o cortical venous drainage - benign courseTREATMENTConservative Observation +/- carotid compression techniqueIf rsk of HageEndovascular Embolisation of arterial feeders with particulate or liquid agents , coil embolization of venous sinus Surgical resection of involved dural venous sinusStereotactic RadioSx- 2-3 years for obliteration

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CT

CTA source ,right-sided tinnitus shows no obvious abnormality, although the right sigmoid sinus looks peculiar. 7-11B.Bone CT in the same patient shows multiple enlarged transosseous vascular channels

Ct.Normal to strikingEnlarged dural sinus or draining vein/transosseous venous channelsCECT Enlarged feeding arteries and draining veins Dural sinus may be thrombosed or stenotic

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MRI

Contrast-enhanced MRA dural sinus thrombosis , multiple enhancing vascular channels 7-11D. MRA innumerable tiny feeding arteries(bold arrow) supplying a dAVF at the transverse-sigmoid sinus junction. The sinushas partially recanalized , and the distal sigmoid sinus and jugular bulb are partially opacified.(curved arrow)

Dilated cortical vein without nidus adjacent to normal appearing brain MC finding thrombosed dural venous sinus with flow voids

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ANGIOGRAPHY

Best imaging toolDSA with superselective catheterization of dural and transosseous feeders requiredPresence of dural sinus thrombosis, flow reversal with drainage into cortical veins and engorged tortuous pial veins

Dural branches arise from ECA , ICA and vertebral arteries

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ECA

DSA of the external carotid artery in a patient with tinnitus, dAVF in the occluded transverse sinus(bold arrow) supplied by the middle meningeal artery (curved arrow), transosseous branches(straight) from the ECA.ANGIOGRAPHYHigh flow venopathy can cause stenosis . Occlusion or hemorrhageDysplastic venous pouches may cause HageIncreased Hage with cortical venous drainage and dysplastic venous dilatation

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TREATMENT

Conservative Observation

Endovascular Embolisation of arterial feeders with particulate or liquid agents , coil embolization of venous sinus .

Surgical resection of involved dural venous sinus

Stereotactic RadioSx- 2-3 years for obliteration

+/- carotid compression techniqueIf rsk of Hage

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CAROTID CAVERNOUS FISTULAAV shunting developing within cavernous sinus

The right cavernous sinus is enlarged by numerous dilated arterial and venouschannels.43

ETIOLOGY

Almost always acquired

DirectTraumatic: central skull base #Non-Traumatic: Preexisting cavernous ICA aneurysm

IndirectDegenerative sequelae of dural sinus thrombosis

Skull base# - stretch injury of ica /puncture from bony segmentDirectHigh FlowRupture of cavernous ICAIndirectSlow flow , low pressureFistula b/w dural br of ICA and the CS

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Dilated CS (Direct) Enlarged crack like vessels(Indirect)

GROSS PATHOLOGY

CLINICAL FEATURES

DIRECTINDIRECTEPIDEMIOLOGYLess commonMore commonDEMOGRAPHICSM=FAny ageWomen40-60yrsPRESENTATIONBruitPulsatile xophthalmosOrbital edemavisionGlaucomaPainless proptosis Vision changes

CTMild or striking proptosisProminent CSEnlarged SOV Enlarged ExOcMs

CECT The right cavernous sinus is enlarged , and the ipsilateral superior ophthalmic vein is more than 4 times the size of the left superior ophthalmic vein .

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MRI

T2WI enlarged right cavernous sinus containing numerous abnormal flow voidsT1 Bulging SOV and CS with flow voidsT2 Asymmetric flow related signal loss in the affected veins48

ANGIOGRAPHY

DIRECT CCFRapid flow with early opacification of CSFistula may be noted in ICA segment

INDIRECT CCFMultiple dural feeders from Cavernous br of ICA and deep br of ECAAnastomoses b/w ICA and ECA feeders are common

Narrowed ICA before terminating in a large venous pouch.Venous reflux into SOV and IOV is present.Direct CCF. LAT DSA in post trauma with multiple skull base fracture.Treatment..balloon embolization.50

VEIN OF GALEN ANEURYSMAL MALFORMATIONDirect AV fistula b/w deep choroidal arteries and persistent embryonic precursor of VOG

Large midline venous pouch behind the 3rd ventricle

Enlarged choroidal veins(staright arrow) draining directly to dilated MPV (median procencephalic vn)and to torcu via falcine culcus.Torcular heterophili(venous sinus confluence) enlarged.

Primary malformation in development of vein of Galen-AV shunts involving embryologic venous precursors (median vein of prosencephalon)-Choroidal arteriovenous fistula with no nidus-Absence of normal vein of Galen-Median vein of prosencephalon does not drain normal brain tissue-Manifests as high-output congestive heart failure (CHF) in infants and hydrocephalus in older children

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EtiologyIn normal fetal dvpt : arterial supply of choroid plexus drains via single transient midline vein median prosencephalic vein .

Internal cerebral vein drains fetal chorid plexus as MPV regresses

Persistent high flow fistula prevents regression

Absence of normal vein of Galen

Median vein of prosencephalon does not drain normal brain tissue

Manifests as high-output congestive heart failure (CHF) in infants and hydrocephalus in older children

Primary malformation in development of vein of Galen-AV shunts involving embryologic venous precursors (median vein of prosencephalon)-Choroidal arteriovenous fistula with no nidus-Absence of normal vein of Galen-Median vein of prosencephalon does not drain normal brain tissue-Manifests as high-output congestive heart failure (CHF) in infants and hydrocephalus in older children

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CLINICAL FEATURES

>30% of symptomatic VoGM in childrenRare in adultsNeonates high output CCF with cranial bruitOlder infants macrocrania + hydrocephalus +/- CCFOlder Children Developmental delay and seizuresYoung adults - Headache

Large VGAMS cerebral ischemia and dystrophic changesLeft untreated Die of progressive brain damage andintracatable CCF

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CTNECTEnlarged well delineated hyperdense mass at tentorial apexObstructive hydrocephalusHage and calcification may be present.

CECT Strong uniform enhancement

CECT scan massive VGAM(bold) draining into an enlarged falcine sinus (staright), causing obstructive hydrocephalus.54

MRI

Sagittal T2WI shows prominent arteries supplying an enlarged median prosencephalic vein . Note enlarged falcine sinus(curved ) .Enlarged serpentine arterial feeders adjacent to the lesion

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DSA in the same patient shows that the VGAM(bold arrow) is supplied by multiple direct arterial fistulas .2 forms based on angioarchitectureChoroidal Multiple br from pericallosal choroidal and thalamoperforate arteries drain into dilated midline venous sacMural single or few enlarged collicular or post choridal arteries drain into sinus wallVenous drainage into persistent embryonic FALCINE SINUS

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ULTRASOUNDAntenatallyHypoechoic to mild echogenic midline mass behind the third ventricle Bidirectional turbulent flow

Neonatal transcranial US shows a large VGAM posterior to the 3rd ventricle. Prominent vessels with arterial flow(staright) supply the lesion.57

CVMS WITHOUT AV SHUNTING

DEVELOPMENTAL VENOUS ANOMALYUmbrella shaped CVM with mature venous part.No arterial componentMay represent anatomic variant of otherwise normal venous drainage

enlarged medullary veins(BOLD) draining into a single transmantle collector vein .Also called VENOUS ANGIOMA/VENOUS MALFORMATION

DVA is an abnormal vein that provides functional venous drainage to normal brain .The presice etiology is unknown.Some investigator depict that it is due to arressted medullary vein devoploment between 8-11 wks.-

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CLINICAL FEATURES

DVA is a DO NOT Touch lesion

Usually asymptomaticHeadache/seizuresHage with FND ( if a/w cavernous malformation)MC vascular malformation at autopsy

Venous angiomas per se do not hemorrhage but are associated with cavernous malformation (30%) which do bleed-DVA is a DO NOT Touch lesion, if resected, the patient will suffer a debilitating venous infarct, the DVA must be preserved if an adjacent cavernous malformation is resectedLEAVE ME ALONE60

IMAGINGLocation : MC near the frontal horn of ventricle. (Deep WM)Size < 3cmUsually solitary

2ND MC4TH VENTRICLE.61

CTNECTNormal .enlarged draining vein may appear hyperdense

CECT

CECT , CTA classic DVA in left cerebellar hemisphere .

COLLECTOR VEINCECTNumerous linear or punctate enhancing foci and converge on single enlarged tubular draining vein

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MRT1 Normal if DVA is small Hage if mixed malformationsT1 C+ - stellate collection of linear enhancement structures joining subependymal collector vein.GRE if H;age in coexisting cavernous malformation - Occasionally hypo Not Hage but deoxyHb within venous bloodclassic DVA with enlarged WM veins(bold) and a collector vein draining into the anterior aspect of the superior sagittalsinus.

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MRA- MRV- DSANormal arterial and capillary phaseVenous phase Medusa head appearance

CAVERNOUS MALFORMATIONIntralesional hemorrhages into thin walled angiogenically immature blood filled locules called CAVERNS

Acquired /Inherited

Subacute(curved) , classic popcorn ball appearances of CCMs. Microhemorrhages are seen as multifocal blooming black dots .

CAVERNOUS ANGIOMA/CAVERNOMa

Dilated endothelial cell-lined spaces with no normal brain within lesion-Usually detectable because cavernous malformation contains blood degradation products of different stages

ACQUIRED BY POST RADIATION THERAPY.

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Gross patholgyDark blue well circumscribed lobulated lesion with raspberry /POPCORN like configCCMs do not contain brain parenchymaHemosiderin depositionMicro Hg

BLOOD FILLED COLLECTION67

CLINICAL FEATURES

2/3 are solitary Peak presentn : 40-60yrsMC presentn : Seizures(50%) Headache FNDHage risk More if DVACan occur anywhere in CNS.

3RD mc(AFTER DVA,CAPPILARY HEMANGIOMA)Can occur anywhere in CNS.FROM TINY TO GIANT Can occupy whole lobe.Small hemorrhages (usually not associated with large hemorrhages)

TREATMENT OPTIONS

Total surgical removal via microsurgical resexn for symptomatic lesions with recurrent HageStereotactic Radiosx = for inaccessible lesions

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CT

IMAGINGCT Norma if small.In large lesion Hyperdense lesion with scatteres intralesional calcification at post limb of int capsule

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T2WI shows classic popcorn ball appearance with locules of blood in different stages of evolution surrounded by hemosiderin rim

MRIMR DIAGNOSTICFocal central heterogeneity(varying hemorrhage within caverns)- POPCORN appearance on T2WI Circumferential hypointense ring of hemosiderin form around high intense central areas

T2 : Popcorn lesion : bright lobulated center with black (hemosiderin) rim-Subacute hemorrhage and degraded blood products within the lesion produce a halo of signal hyperintensity around the lesion on T1-weighted images, a useful finding for differentiating cavernous malformations from hemorrhagic tumors and other intracranial hemorrhages-Always obtain susceptibility sequences to detect coexistent smaller lesions

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Cavernoma in the [post central gyrus.

Axial T2 shows a large left parietal mass that resembles a popcorn ball with a hypointense hemosiderin rim (arrows) and loculated hyperintense compartments(b) Axial T1 at the same level shows multiple high signal intensity compartments in the lesion , findings suggestive of subacute hemorrhage , a faint halo of high signal intensity also is visible around the lesion (arrowheads)

T2 & T2* gradient echo show multiple cavernomas , notice the popcorn appearance with peripheral rim of hemosiderin on the T2 , the lesions are almost completely black on the gradient echo due to blooming artefacts , T2* and susceptibility weighted imaging (SWI) markedly increase the sensitivity of MRI to detect small cavernomas , the five black dots in the left cerebral hemisphere on the T2* are also cavernomas and are not visible on the T2WI

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Based on imaging72

ANGIOGRAPHY

No identifiable feeding arteries/veinsNegative unless mixed with other lesions

CAPILLARY TELANGIECTASIACAPILLARY ANGIOMACollection of enlarged thin walled vessels resembling capillaries.Vessels surrounded by normal brain parenchymaProbably congenital lesionsMC sites : Pons , cerebellum(can occur anywhere)

Graphic depicts pontine capillary telangiectasia with tiny dilated capillaries interspersed with normal brain

Cranial irradiation cause vascular damage thar induce devolpoment of talengiectasia.76

CLINICAL FEATURES

Peak Presentation : 30-40 yearsUsually silent, discovered incidentally at imaging

A few cases vertigo,headache,tinnitus77

IMAGING

CT Usually Normal

MRT1W1 usually normalT2 50% normal -50 % show stippled foci of hyperintensityT1+C BRUSH LIKE

T2* - Best sequence for demonstrating the lesion(poorly delineated greyish hypointensity)FLAIRGRE

Usually