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Page 1: Vascular malformations

Vascular Malformations

Ariunjargal.B

Page 2: Vascular malformations

Vascular Malformations(i) Malformations with AV shunts :a) AVMb) Dural AVFc) Pial AVF(ii) Malformations without AV shunts :a) Cavernous Malformationb) Venous Malformationsc) Capillary Telangiectasiad) Moyamoya Disease

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(i) Malformations with AV shunts :a) AVMb) Dural AVFc) Pial AVF

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Incidence :- Peak age is 20 to 40 years- 98% of AVM are solitary, - multiple (2%)associated with syndromes- Multiple lesions in various syndromes, Osler-Weber-Rendu and

Wyburn-Mason- Occurs intra-axially & 85 % are supratentorialClinical Picture :-One or combination of hemorrhage (usually parenchymal

hemorrhage, rarely subarachnoid, 40 %), seizures (30 %), neurological deficit or headache (20 %)

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Types :a) Parenchymal, 80% (ICA and vertebral artery

supply, congenital lesions)b) Dural, 10% (ECA supply, mostly acquired

lesions)c) Mixed, 10%

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Cerebrofacial Arterio-venous Metameric Syndrome (CAMS) :-CAMS (also known as Wyburn-Mason syndrome or Bonnet-

Dechaume-Blanc disease)

CAMS type 1 :-Involves the medial prosencephalon and will manifest with

AVMs located at the corpus callosum, hypothalamus (hypophysis) and nose

CAMS type 2 :-Involves the lateral prosencephalon with AVMs at the occipital

lobe and optic tract including the thalamus, retina and maxilla

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CAMS type 3 :-Involves the rhombencephalon and affected patients

will have AVMs at the cerebellum, pons and mandible

-The most important clue to the diagnosis of CAMS is the presence of multiple AVMs in both the brain parenchyma and the facial region

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CAMS type 2 in a 10-year-old girl who presented with a 1-year history of progressive right hemiparesis , chemosis and proptosis of the left eye were also noted (a, b) CT+C obtained at the level of the orbits (a) and brain (b) show an enhancing vascular lesion at the left basal ganglia , the lesion exerts a mass effect on the left lateral ventricle , in addition , serpiginous structures are seen surrounding the optic nerve , (c) Lateral LT ICA angiogram shows a proliferative type brain AVM nidus at the basal ganglia , another smaller AVM is noted surrounding the left optic nerve (solid arrow) , there is early venous drainage anteriorly into the basal frontal cortical veins (arrowheads) and posteriorly into the basal vein of Rosenthal (open arrow)

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CAMS type 2 in a 7-year-old girl who presented with recurrent episodes of bleeding from the gum due to eruption of a left molar , (a) Coronal CT scan (bone window) reveals an osteolytic lesion within the alveolar ridge of the left maxilla , (b, c) Left external (b) and internal (c) carotid angiograms show a facial osseous AVM supplied by branches of the internal maxillary and transverse facial arteries and draining into an intraosseous venous pouch (arrow in b) , this finding corresponds to the osteolytic lesion seen in a and proved to be the source of the patient’s bleeding , an AVM of the left optic nerve is also noted, thereby allowing the diagnosis of CAMS type 2

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Proliferative Angiopathy :-Cerebral proliferative angiopathy, previously known as diffuse

nidus type AVM, is present in an estimated 2%-4% of all brain AVMs

-There is a female predilection of 2:1 with a rather young mean patient age (20 years)

CT & MRI :-The typical MR imaging and CT findings include a proliferative

type nidus in which normal brain parenchyma is interspersed between the abnormal vessels

-Often an entire lobe or even brain hemisphere is affected

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(a) PD , (b) T1+C show multiple flow voids and contrast-enhanced tubular structures representing a large vascular lesion that involves the entire right cerebral hemisphere , the normal brain parenchyma is interspersed between the abnormal vessels

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Left occipital arteriovenous malformation (AVM) with multiple calcified phleboliths and numerous hyperattenuating vascular channels

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CT+C shows a tangle of intensely enhancing tubular structures embedded in the left parietal lobe , a finding that is compatible with a nidus , hyperattenuation representing intraventricular hemorrhage is noted in the ventricles

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MRI :-Serpiginous black flow voids-May be evidence of local atrophy and gliosis (as a

result of vascular steal and ischemia) or previous hemorrhage

-AVM replaces but does not displace brain tissue (i.e. mass effect is uncommon) unless complicated by hemorrhage and edema

-Edema occurs only if there is recent hemorrhage or venous thrombosis with infarction

-There are usually adjacent changes to the adjacent brain including gliosis (T2 prolongation), dystrophic calcification & blood products (blooming T2* gradient imaging), the gliosis / encephalomalacia or mineralization seen in the adjacent brain is due to alteration in vascular flow from the AVM

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T1 shows large occipital arteriovenous malformation (AVM) with parasagittal flow void

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T2 showing numerous flow voids

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Grading System : (Spetzler's Criteria)

0 1 2 3

Eloquence No Yes - -

Draining vein Superficial Deep - -

Size - < 3 cm

3-6 cm > 6 cm

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-Higher score is associated with higher chance of hemorrhage

-Other factors associated with poorer prognosis/higher risk of hemorrhage :

1-Intranidal aneurysm2-Aneurysm in the circle of Willis3-Aneurysm in arterial feeder4-Venous stasis

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-Eloquence of adjacent brain :a) Eloquence brain :-Sensorimotor, language, visual cortex,

hypothalamus, thalamus, brain stem, cerebellar nuclei or regions directly adjacent to these structures

b) Non-eloquence brain :-Frontal and temporal lobe, cerebellar

hemispheres

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Complications :a) Hemorrhage (parenchymal > SAH > intraventricular)b) Seizuresc) Cumulative risk of hemorrhage is approximately 3 % per

yearTreatment Options :a) Surgeryb) Endovascular embolizationc) Radiosurgery d) Conservative management

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b) Dural Arteriovenous Fistula (DAVF) :

1-Incidence :-Dural AVFs are abnormal connections between arteries that

would normally feed the meninges bone or muscles but not the brain and small venules within the dura mater

-Acquired lesions presenting in older population (50-70 years) compared to AVM (20-40 years)

2-Etiology :-Occur following damage to venous structures (post-thrombosis,

surgery & trauma)-They typically have multiple feeders and are usually acquired,

most frequently from as a result of neovascularisation induced by previously thrombosed dural venous sinus (typically transverse sinus)

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-Therefore supply is typically from the same branches that supply meningeal arterial supply :

a) Supratentorial : Middle meningeal artery (ECA)b) Anterior cranial fossa : Ethmoidal branches of

the ophthalmic artery (from ICA)c) Cavernous sinus : Dural branches from the ICA

and accessory meningeal branch of the maxillary artery (via foramen ovale), branch of ECA

d) Posterior cranial fossa :Dural branches from the vertebral arteries, branches from occipital and ascending pharyngeal arteries, branches of ECA

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Clinical Picture :-Symptoms & signs secondary to arterialization of venous

system :a) Bruitb) Venous hypertensionc) Pulsatile tinnitus (if primary involvement is sinuses)d) Hemorrhagee) Focal neurologyf) Seizuresg) Caroticocavernous fistula may give rise to proptosis &

chemosis

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Location :a) Transverse/ sigmoid sinus : Most commonb) Cavernous sinusc) Superior sagittal sinusd) Straight Sinuse) Other venous sinusesf) Anterior cranial fossa : Typically only ICA supply

due to meningeal supply of this regiong) Tentorium

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CT & MRI :-Often normal unless complications (e.g.

hemorrhage, enlargement of cavernous sinus and superior ophthalmic veins if caroticocavernous fistula)

-Dilated cortical veins (a condition referred to as a pseudophlebitic) which manifest as abnormal enhancing tubular structures or flow voids within the cortical sulci with no true nidus within the brain parenchyma

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Borden type 2 dural AVF in a 45-year-old woman who presented with sudden loss of consciousness , (a) CT without contrast shows a left temporo-occipital hematoma with intraventricular hemorrhage , (b) T2 shows multiple flow void vascular structures along the cortical sulci of both occipital regions , there is white matter edema with T2 hyperintensity in the left occipital lobe with evidence of a resolving hematoma , no nidus can be identified , (c) Left internal maxillary angiogram reveals a dural AVF in the left transverse sinus supplied by branches of the left middle meningeal artery , note the associated thrombosis of the proximal and distal parts of the transverse sinus creating an “isolated pouch” and thereby causing reflux from the shunt into the cortical veins

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-Hypoattenuation of the white matter at CT or hyperintense T2 signal at MR imaging indicates venous congestion or infarction which may eventually lead to venous hemorrhage

-Focal enhancement of these areas may also be observed as a sign of chronic venous ischemia

-Curvilinear subcortical calcifications can be seen at CT in patients with long-standing cortical venous reflux, possibly due to chronic venous congestion

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Classification :a) Cognard classificationb) Borden classification

a) Cognard classification :-Correlates venous drainage patterns with increasingly

aggressive neurological clinical courseType I : Confined to sinus wall, typically after thrombosisType II :IIa : Confined to sinus with reflux (retrograde) into sinus

but not cortical veinsIIb : Drains into sinus with reflux (retrograde) into cortical

veins (10-20% hemorrhage)

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Type III : Drains direct into cortical veins (not into sinus), 40% hemorrhageType IV : Drains direct into cortical veins (not into sinus) with venous

ectasia, 65% hemorrhageType V : Spinal perimedullary venous drainage, associated with

progressive myelopathy

b) Borden classification :1-Type 1 : -DAVF drainage into a dural venous sinus or meningeal vein with normal

anterograde flow- Usually benign clinical behavior-Equivalent to Cognard type I and II

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2-Type 2 :-Anterograde drainage into dural venous sinus and

onwards but retrograde flow occurs into cortical veins-May present with hemorrhage-Equivalent to Cognard type IIb and IIa+b

3-Type 3 :-Direct retrograde flow of blood from the fistula into

cortical veins causing venous hypertension with a risk of hemorrhage

-Equivalent to Cognard type III, IV and V

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7-Caroticocavernous Fistula :-Represent abnormal communication between the

carotid circulation and the cavernous sinus-Direct CCFs are often secondary to trauma, most

commonly seen in the young male patients, presentation is acute and symptoms develop rapidly

-In contrast, indirect CCFs have a predilection for the postmenopausal female patient and the onset of symptoms is often insidious

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Clinical Picture :1-Pulsatile exophthalmos / proptosis : 75 % 2-Chemosis and subconjunctival hemorrhage3-Progressive visual loss : 25-32 % 4-Pulsatile tinnitus (usually objective)5-Raised intracranial pressure6-subarachnoid hemorrhage, intracerebral

hemorrhage, otorrhagia, epistaxis : 2.5-8.5 %

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Classification :Direct : Direct communication between intra-cavernous ICA and

cavernous sinus Indirect : Communication exists via branches of the carotid circulation

(ICA or ECA)-Another method is to classify according to four main types Type A : Direct connection between the intracavernous ICA and CSType B : Dural shunt between intracavernous branches of the ICA and

CS-Type C : Dural shunt between meningeal branches of the ECA and CS-Type D : B + C

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*Direct : type A-A direct fistula is due to a direct communication

between the intracavernous ICA and the cavernous sinus

-There are a number of causes, however aneurysm rupture and trauma are by far the most common

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*Indirect : types B, C & D-Indirect fistulas are due to communication by

multiple branches between the ICA / ECA and CS-The are most frequent are type C, with meningeal

branches of the ECA forming the fistula-They are postulated to occur secondary to

cavernous sinus thrombosis with revascularization

-Other predisposing factors appear to be pregnancy, surgical procedures in the region & sinusitis

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MRI :-Findings of CCFs include a dilated CS with multiple signal

intensity void structures that are associated with proptosis and an enlarged superior ophthalmic vein

-On gradient-echo images, these flow voids shows high signal intensity

-The presence of flow-related enhancement in the CS on MRA suggests the diagnosis in the right clinical setting

-Other supporting findings are a dirty appearance of the retro-orbital fat and enlargement of the extraocular muscles, due to the presence of intracavernous communications, very high-flow fistulas may result in enlargement of both CSs

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ICA to a CS fistula , axial source image from an MRA shows flow-related enhancement in the medial (arrow) left CS from a direct-type fistula

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MRA shows an enlarged superior ophthalmic vein (arrow)

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MRA shows a right carotid cavernous fistula (arrow)

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c) Pial AVF :-Consist of a direct fistulous communication between a

pial artery and a vein without any intervening nidus-They differ from dural AVFs in that they derive their

arterial supply from pial or cortical arteries and are not located within the dura mater

Incidence :-Pial AVFs are more commonly encountered in children

and are frequently associated with hereditary hemorrhagic telangiectasia

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Location :-Pial AVFs are located on the surface of the brain, are

often high flow lesions and in most instances are associated with dilated venous pouches

Radiographic Findings :-Clues to the diagnosis of pial AVFs at cross sectional

imaging include the presence of :a) Dilated vessels, mainly at the brain surfaceb) Asymmetric dilatation of the pial feeding artery,

either the MCA, ACA or PCA, which is best seen at the level of the circle of Willis

-These findings can be used to differentiate pial AVFs from dural AVFs and may be accompanied by dilated venous pouches outside the brain parenchyma

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Pial AVF in a 1-week-old neonate who presented with congestive heart failure , the patient had a family history of hereditary hemorrhagic telangiectasia , (a, b) Axial T2 reveal enlargement of the right MCA at the level of the circle of Willis (arrow in a) and a large dilated vascular structure in the right perisylvian region (arrowhead in b) , findings that are suggestive of a venous pouch , the upper portion of another large flow void structure is also seen in the posterior fossa , no nidus can be identified , (c) Lateral RT ICA angiogram reveals a high-flow fistula between an MCA branch and a large venous pouch (arrowhead) , retrograde flow of contrast material into the basilar artery confirms the presence of another high-flow fistula (arrows) from the posterior inferior cerebellar artery , the high-flow fistulas and venous pouches are typical findings in a patient with hereditary hemorrhagic telangiectasia

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Pial AVF with venous pouches and venous congestion in a 7-year-old boy who presented with headaches , the patient had a family history of nosebleeds and mucosal telangiectasias suggestive of hereditary hemorrhagic telangiectasia , (a,b) T2 reveal large dilated vascular structures in the right perisylvian region suggestive of venous pouches with enlargement of the right MCA relative to the left side (arrow in b) and no identifiable nidus , findings that are compatible with a pial AVF , the hyperintense T2 signal of the white matter at the right frontal lobe (arrow in a) is suggestive of venous congestion , (c) Lateral RT ICA angiogram reveals a high-flow fistula between an MCA branch and large venous pouches

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(ii) Malformations without AV shunts :a) Cavernous Malformationb) Venous Malformationsc) Capillary Telangiectasiad) Moyamoya Disease

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a) Cavernous Malformation :-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

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Incidence :-All age group-60-80 % multiple (may be familial)-Often associated with an adjacent developmental

venous anomaly (DVA), there is increased risk of bleeding if a DVA is present, however, the DVA itself doesn’t have any bleeding risk

-When multiple, cavernous malformations represent an inherited disorder called familial cavernomatosis

Location :-80% supratentorial-Occur anywhere in CNS, common in Pons

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Clinical Picture :-Small hemorrhages -Seizures-Headache secondary to occult hemorrhage

MRI :-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 postcentral gyrus on T1 , T2 and SWI , notice popcorn appearance and blooming artifact

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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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(a) 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)

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Cavernous malformation & associated DVA , T1+C show a hypointense , centrally hyperintense nonenhancing cavernous malformation (yellow arrow) in the left cerebellar hemisphere , directly superior to the cavernoma (b) is an enhancing vascular structure with caput medusa morphology (red arrow) representing a DVA

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Giant cavernous malformation (a) CT without contrast shows a hyperattenuating complex mass (arrows) in the RT fronto-temporal lobe , (b) T1 shows the mass is predominantly cystic & hyperintense (representing blood products) , (C) FLAIR shows that the intracystic contents are primarily hyperintense , there is a complete low signal hemosiderin ring surrounding the lesion (red arrows) , there is mild surrounding edema , (d) T1+C shows no appreciable enhancement

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b) Venous Malformations :1-Developmental Venous Anomaly2-Vein of Galen Malformation3-Venous Varix

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1-Developmental Venous Anomaly (Venous Angioma) :

-DVA is an abnormal vein that provides functional venous drainage to normal brain

-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 resected

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CT :-Only enhanced scans may show linear vein draining to

ependymal lining of ventricle or cortex with inverse umbrella-shaped (caput medusa) leash of vessels draining towards anomalous veins

MRI :-Medusa head or large transcortical vein best seen on spin-echo

images or after administration of gadolinium-Location in deep cerebellar white matter or deep cerebral white

matter-Adjacent to the frontal horn (most common site)

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T1+C

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DVA & a tiny cavernous malformation , (a) T1+C shows a subtle curvilinear enhancing structure (yellow arrow) in the RT frontal white matter representing a DVA , (b) Susceptibility weighted shows a focus of susceptibility artifact (red arrow) , suggestive of an adjacent cavernous malformation

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2-Vein of Galen Malformation :-Complex group of vascular anomalies that consist of a

central AVM and resultant varix of the vein of Galen (incorrectly referred to as vein of Galen aneurysm)

Types :-Two main types exist with the common feature of a dilated

midline venous structure :1-Vein of Galen AVM2-Vein of Galen varix

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1-Vein of Galen AVM :-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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2-Vein of Galen Varix :-Primary parenchymal AVM drains into vein of

Galen which secondarily enlarges-Thalamic AVM with nidus is usually the primary

AVM-Uncommon to present in neonates-Higher risk of hemorrhage than the vein of

Galen AVM

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(a) Sagittal T1 shows the markedly enlarged median prosencephalic vein of Markowski, characteristic of VGAM (arrow), arterial feeders can be seen along the anterior wall of the vein, (b) the complex arterial maze (arrows) is well seen on this conventional angiogram obtained with injection of the left vertebral artery, coils can be seen along the right side of the varix, occluding several arterial feeders

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CT angiography axial image showing enlarged median prosencephalic vein (large arrow) with multiple arterial feeders ( small arrows)

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CT angiography sagittal image showing enlarged median prosencephalic vein (black arrow) continuing in the falcine sinus (red arrow) with enlarged confluence of sinuses

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(a & b) Sagittal reconstructions of CT angiograms showing choroidal type , vein of Galen malformation in a neonate , the falcine draining sinuses are massively enlarged because of narrowing of both sigmoid sinuses

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CT+C

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In utero diagnosis of vein of Galen malformation , MRI performed in the third trimester showing a dilated midline vascular structure in sagittal (a) , axial (b) and coronal (c) planes

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T1 T2

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T1 T2

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T2, the dilated galenic vein, namely the median vein of prosencephalon (thick arrow), located midline in the cistern of velum interpositum, drains into the parietal superior sagittal sinus (thin arrow) via the persistent primitive falcine sinus (arrowhead)

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c) Capillary Telangiectasia :Definition :-Nests of dilated capillaries with normal brain interspersed

between dilated capillaries-Commonly coexist with cavernous malformation-A Do NOT Touch lesionLocation :-pons > cerebral cortex, spinal cord > other locationsMRI :-Foci of increased signal intensity on contrast-enhanced studies-T2 : hypointense foci if hemorrhage has occurred

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(a) T1+C Patient with midbrain capillary telangiectasia showing brush-like enhancement in the right midbrain , (b) Gradient shows subtle increased susceptibility in the right midbrain

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GRE T1 T1+C

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d) Moyamoya Disease :Definition :-Uncommon occlusive disease of unknown origin that

classically involves the supraclinoid internal carotid arteries with relative sparing of the posterior fossa in the early stages

-The term moyamoya syndrome is used in cases in which no underlying cause (atherosclerosis, Down syndrome, neurofibromatosis, sickle cell disease or some other condition) can be identified

-There is usually development of extensive tiny basal perforator collateral vessels ( the moyamoya vessels ) which have been described as having a puff of smoke appearance at cerebral angiography and of transdural collateral vessels

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2-Clinical Picture :-Differs between pediatric and adult

populations: a) Most children present with transient ischemic

attack or cerebral infarctions b) Approximately one-half of adults present with

intracranial hemorrhage from rupture of the moyamoya collateral vessels

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CT & MRI :-Imaging include the presence of tiny flow voids,

commonly seen arising from the basal cisterns and extending into the basal ganglia or the thalamus

-There is no true nidus embedded within the brain parenchyma and no dilated vessels

-The diagnosis can be suggested by the presence of bilateral supraclinoid internal carotid artery stenosis at MRA and CTA

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MRA

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