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Vascular brain lesions for radiology by Dr Soumitra Halder
- 1. DR SOUMITRA HALDER DEPT. OF RADIOLOGY MEDICAL COLLEGE,KOLKATA
- 3. Aneurysm Vascular malformations
- 4. Aneurysm
- 5. Abnormal bulge of an arterial wall . Develops where the blood vessel wall is weakened. Aneurysm
- 6. 2. Sizes of Aneurysm. 1.
- 8. Clinical presentation Asymptomatic unless they rupture Usually found either incidentally or when a patient presents with SAH. Ruptured SA is the MC nontraumatic cause of SAH
- 9. Rupture of aneurysm: Headache (97 percent of cases) sudden onset, severe worst headache of life. Associated with a brief loss of consciousness Seizure, nausea, vomiting, or meningismus
- 10. 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%
- 15. Treatment… Observation Surgical clipping Endovascular occlusion.
- 16. Pseudoaneurysm Arterial dilatation with complete disruption of arterial wall. Trauma,infection,drug,post surgery Fragile cavitated blood and fibrous tissue Cavernous /paraclinoid ICA (Trauma) Distal cortical branches(infection,Drug)
- 17. Imaging Focus of contrast enhancement(Spot sign) Fusiform irregularly shaped vessel outpouching Neck is absent Delayed filling and delayed emptying on angio Positional contrast stagnation .
- 19. Treatment.. Endovascular occlusion….Coiling,liquid embolics
- 20. Malformations
- 21. Malformations Heterogenous group of disorders Morphogenetic errors affecting arteries , veins or various combinations of vessels
- 22. CLASSIFICATION HISTOPATHOLOGY AVM Venous angioma Capillary telangiectasia Cavernous malformation
- 23. CLASSIFICATION FUNCTIONAL AV SHUNTING AVM Dural Av fistula VOG malformation WITHOUT AV SHUNTING Venous angioma Capillary telangiectasia Cavernous malformation Sinus pericranii Moya Moya
- 24. AV MALFORMATION Usually congenital Tightly packed thin walled vessels (NIDUS) Direct artery to vein shunting No intervening capillary bed Most AVMs are parenchymal lesions – PIAL AVMs
- 25. AV MALFORMATION LOCATION: Supratentorial(85%) SIZE : 2-6cms NUMBER : Solitary Multiple (2%)
- 26. GROSS PATHOLOGY Wedge shaped tangled irregulary dilated vessels . Nidus.. no N brain tissue Surrounding brain parenchyma : H’age residue Gliosis ischemic changes
- 27. AV MALFORMATION CLINICAL FEATURES Presentation: 2-4th decade Headache with H’age – MC Focal neurological deficits(20-25%) Lifelong risk of H’age - 2-4% every year ,cumulative
- 28. AVM Grading..
- 29. CT NECT Normal : Very small AVM serpentine hyperdensities. (BAG OF WORMS) Calcification(25-30%) CECT Uniform Enhanced arterial feeders , nidus and draining veins
- 30. MR
- 32. ANGIOGRAPHY Internal angioarchitecture best depiction Depicts 3 components of AVM Enlarged arteries+/- aneurysm Nidus Early draining veins
- 34. TREATMENT Surgical excision for nidus …Acute and emergent surgical intervention – in life threatening ICH. STEREOTACTIC RADIOSURGERY Focussed irradiation to nidus Indication Unresectable because of location Size < 3.5cms Risk of h’age till it disappears completely ENDOVASCULAR RX Adjunct to Sx/ RadioSx Used in small AVMs or 1-2 feeding arteries Embolisation – Precedes surgery /radiosx reduce size of nidus Complete cure if : small AVM , few feeders , single draining vein
- 35. DURAL AV FISTULA Tiny 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
- 36. 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 feeders NUMBER : Multiple lesions are uncommon.
- 37. CLINICAL FEATURE Mostly in adults(40-60yrs) C/F varies with location and drainage pattern TS-SigS - Bruit and tinnitus Cav S – Pulsatile proptosis , chemsois , retroorbital pain Lesions with cortical venous drainage(Malignant dAVF) : seizures, dementia ,FND
- 38. CT
- 39. MRI
- 40. ANGIOGRAPHY Best imaging tool DSA with superselective catheterization of dural and transosseous feeders required Presence of dural sinus thrombosis, flow reversal with drainage into cortical veins and engorged tortuous pial veins
- 41. ECA
- 42. 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
- 43. CAROTID CAVERNOUS FISTULA AV shunting developing within cavernous sinus
- 44. ETIOLOGY Almost always acquired Direct Traumatic: central skull base # Non-Traumatic: Preexisting cavernous ICA aneurysm Indirect Degenerative – sequelae of dural sinus thrombosis
- 45. Dilated CS (Direct) Enlarged crack like vessels(Indirect) GROSS PATHOLOGY
- 46. CLINICAL FEATURES DIRECT INDIRECT EPIDEMIOLOGY Less common More common DEMOGRAPHICS M=F Any age Women 40-60yrs PRESENTATION Bruit Pulsatile xophthalmos Orbital edema ↓vision Glaucoma Painless proptosis Vision changes
- 47. CT Mild or striking proptosis Prominent CS Enlarged SOV Enlarged ExOcMs
- 48. MRI
- 49. ANGIOGRAPHY DIRECT CCF Rapid flow with early opacification of CS Fistula may be noted in ICA segment INDIRECT CCF Multiple dural feeders from Cavernous br of ICA and deep br of ECA Anastomoses b/w ICA and ECA feeders are common
- 51. VEIN OF GALEN ANEURYSMAL MALFORMATION Direct AV fistula b/w deep choroidal arteries and persistent embryonic precursor of VOG Large midline venous pouch behind the 3rd ventricle
- 52. Etiology In 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
- 53. CLINICAL FEATURES >30% of symptomatic VoGM in children Rare in adults Neonates – high output CCF with cranial bruit Older infants – macrocrania + hydrocephalus +/- CCF Older Children – Developmental delay and seizures Young adults - Headache
- 54. CT NECT Enlarged well delineated hyperdense mass at tentorial apex Obstructive hydrocephalus H’age and calcification may be present. CECT – Strong uniform enhancement
- 55. MRI
- 57. ULTRASOUND Antenatally Hypoechoic to mild echogenic midline mass behind the third ventricle Bidirectional turbulent flow
- 58. CVMS WITHOUT AV SHUNTING
- 59. DEVELOPMENTAL VENOUS ANOMALY Umbrella shaped CVM with mature venous part. No arterial component May represent anatomic variant of otherwise normal venous drainage
- 60. CLINICAL FEATURES DVA is a DO NOT Touch lesion Usually asymptomatic Headache/seizures H’age with FND ( if a/w cavernous malformation) MC vascular malformation at autopsy
- 61. IMAGING Location : MC near the frontal horn of ventricle. (Deep WM) Size < 3cm Usually solitary
- 62. CT NECT Normal . enlarged draining vein may appear hyperdense
- 63. CECT
- 65. MRA- MRV- DSA Normal arterial and capillary phase Venous phase – Medusa head appearance
- 66. CAVERNOUS MALFORMATION Intralesional hemorrhages into thin walled angiogenically immature blood filled locules called CAVERNS Acquired /Inherited
- 67. Gross patholgy Dark blue well circumscribed lobulated lesion with raspberry /POPCORN like config CCMs do not contain brain parenchyma Hemosiderin deposition Micro Hg
- 68. CLINICAL FEATURES 2/3 are solitary Peak presentn : 40-60yrs MC presentn : Seizures(50%) Headache FND H’age risk – More if DVA Can occur anywhere in CNS.
- 69. CT
- 75. ANGIOGRAPHY No identifiable feeding arteries/veins Negative unless mixed with other lesions
- 76. CAPILLARY TELANGIECTASIA CAPILLARY ANGIOMA Collection of enlarged thin walled vessels resembling capillaries. Vessels surrounded by normal brain parenchyma Probably congenital lesions MC sites : Pons , cerebellum(can occur anywhere)
- 77. CLINICAL FEATURES Peak Presentation : 30-40 years Usually silent, discovered incidentally at imaging
- 78. IMAGING CT – Usually NormalMR T1W1 –usually normal T2 – 50% normal -50 % show stippled foci of hyperintensity T1+C – BRUSH LIKE T2* - Best sequence for demonstrating the lesion(poorly delineated greyish hypointensity) FLAIR GRE
- 80. SINUS PERICRANII Large transcalvarial communication between intra and extra-cranial venous drainage system. Mostly congenital. May be a/w other dva.
- 81. SINUS PERICRANII CLINICAL FEATURES Rare Children and young adults NON TENDER NON PULSATILE BLUISH COMORESSIBLE SCALP MASS Increase in size with Valsalva
- 82. CT NECT Iso to hyperdense Typically well demarcated calvarial defect CECT Strong uniform enhancement
- 84. ANGIOGRAM Arterial and capillary phase normal Venous phase – Visualised on late venous phase mostly Contrast accumulating within the lesion and adjacent to the skull defect with pericranial scalp vein
- 85. Progressive stenosis of supraclinoid ICA Formation of collateral vessels at base of brain that give a "puff of smoke" appearance on angiography. Japanese and other Asian populations. Moyamoya
- 86. Clinical features. 2 peak age of presentation. Ischemic events more frequent in children. Hemorrhagic stroke Epilepsy.
- 87. Swimming worm in a bare cistern
- 89. SUMMURY
- 92. THANK YOU
Notas del editor
- ACQ…ABNORMAL VASCULAR HEMODYNAMCICS AND SHEAR FORSE., Genetetic alteration Anomalous vs Acq….abnormal vascular hemodynamics.shearing stress.
- By size- . Small aneurysm diameter <1.5 cm. . Large aneurysm(1.5to 2.5 cm). . Giant (2.5to 5 cm). . Super giant (over 5 cm). By Shape- . Saccular, most common: berry aneurysms, necks or stems resembling a berry. . Fusiform- without stem. . Dissecting- blood follows a false lumen.
- 40-60 Y Most intracranial aneurysms are Asymptomatic unless they rupture
- Incidence: Female: Male = 3:2 But the ratio varies with age: < 40 years: males > 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
- DSA is gold standart.Right MCA aneurysm with subarachnoid hemorrhage.
- Giant vertebral aneurysm in the vertebral artery tip with nausea and vomiting due to brain stem compression.
- Watchful waiting with serial scan for asymptomatic <7mm aneysysm
- FALSE ANEY The weekend arterial wall is expandas and finally ruptured,forming a paravascular hematoma, If the hematoma cavitates and commmunicate with the residual vs wall,psudoaneyrysm is created.
- NECT nonspecific,we may get only parenchymal hg. Cta…spot sigh.
- Right VA
- An AVM is a congenital high-flow vascular malformation consisting of directly connecting arteries & veins without an intervening capillary bed -The transition between artery and vein can take place via a so-called nidus (i.e. a tangle of abnormal vessels located in the brain parenchyma) Nidus – high flow low resistance vascular bed rerplacing normal arterioles
- (<2%multiple) when a/w syndromes HHT , Wyburn-Mason syndrome
- Thin wall cause hemorrhage Apex – ventricle , base near cortex Nidus contain no N brain tissue.sometimes intranidal aneurysm is seen. HPE: well defined elastic lamina(usually absent in venous channels ) with focal areas of wall thinning
- Seizures > hemorrhage(adults ) Seizures < hemorrhage(children ) Nidus – MC site for hemorrhage Location – peri/interventricular /basal ganglia PROGNOSIS All are potentially hazardous Lifelong risk of H’age- 2-4% every year cumulative Spontaneous regression – rare and unpredictable
- Eloquent area – area with identifiable neuro funxn Grade 4 n above – unresectable and untreatbale
- Left) NECT shows serpentine hyperdensities . (Right) CECT shows strong uniform enhancement . Wedge-shaped configuration is typical for AVM. Roughly 85% of AVMs are supratentorial. AVM Bleed – parenchymal , IVH >> SAH
- T1W1 – tightly packed mass or honeycomb of flow voids T2W1 – serpiginous honeycomb of flow voids adjacent high signal tissue – gliosis FLAIR- flow voids +/- surrounding high signal GRE - blooming (H’agic residua) Left parital wedge shaped serpentine flow voids.
- Feeding arteries Dilated and tortuous Flow related angiopathy – dilatation , stenosis or thrombosis Pedicle 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 effect Stenosis can cause AVM H’age by ↑ intranidal pressure
- 1Complete obliteration of nidus for cure. 2 STEREOTACTIC RADIOSURGERY Focussed irradiation to nidus Indication Unresectable because of location Size < 3.5cms Adv : Non invasive Disadv :Effect takes years Risk of h’age till it disappears completely
- 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 by transosseous feeders(curved arrow) from the external carotid artery.
- Malignant dAVF – aggressive clinical course with H’age and ND Multiple dAVF – poor clinical prognosis
- 40-60 yr. 20 y older than avm FND – focal neurological deficits PROGNOSIS 98% w/o cortical venous drainage - benign course TREATMENT Conservative – Observation +/- carotid compression technique If rsk of H’age 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
- 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 striking Enlarged dural sinus or draining vein/transosseous venous channels CECT – Enlarged feeding arteries and draining veins Dural sinus may be thrombosed or stenotic
- 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 sinus has 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
- Dural branches – arise from ECA , ICA and vertebral arteries
- 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. ANGIOGRAPHY High flow venopathy can cause stenosis . Occlusion or hemorrhage Dysplastic venous pouches may cause H’age Increased H’age with cortical venous drainage and dysplastic venous dilatation
- +/- carotid compression technique If rsk of H’age
- The right cavernous sinus is enlarged by numerous dilated arterial and venous channels.
- Skull base# - stretch injury of ica /puncture from bony segment Direct High Flow Rupture of cavernous ICA Indirect Slow flow , low pressure Fistula b/w dural br of ICA and the CS
- 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 .
- T2WI enlarged right cavernous sinus containing numerous abnormal “flow voids” T1 – Bulging SOV and CS with flow voids T2 – Asymmetric flow related signal loss in the affected veins
- 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.
- 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
- 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
- Large VGAMS – cerebral ischemia and dystrophic changes Left untreated – Die of progressive brain damage and intracatable CCF
- CECT scan massive VGAM(bold) draining into an enlarged falcine sinus (staright), causing obstructive hydrocephalus.
- Sagittal T2WI shows prominent arteries supplying an enlarged median prosencephalic vein . Note enlarged falcine sinus(curved ) . Enlarged serpentine arterial feeders adjacent to the lesion
- DSA in the same patient shows that the VGAM(bold arrow) is supplied by multiple direct arterial fistulas . 2 forms based on angioarchitecture Choroidal – Multiple br from pericallosal choroidal and thalamoperforate arteries drain into dilated midline venous sac Mural – single or few enlarged collicular or post choridal arteries drain into sinus wall Venous drainage into persistent embryonic FALCINE SINUS
- Neonatal transcranial US shows a large VGAM posterior to the 3rd ventricle. Prominent vessels with arterial flow(staright) supply the lesion.
- 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. -
- 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 LEAVE ME ALONE
- 2ND MC…4TH VENTRICLE.
- CECT , CTA classic DVA in left cerebellar hemisphere . COLLECTOR VEIN CECT Numerous linear or punctate enhancing foci and converge on single enlarged tubular draining vein
- MR T1 – Normal if DVA is small H’age if mixed malformations T1 C+ - stellate collection of linear enhancement structures joining subependymal collector vein. GRE – if H;age in coexisting cavernous malformation - Occasionally hypo – Not H’age but deoxyHb within venous blood classic DVA with enlarged WM veins(bold) and a collector vein draining into the anterior aspect of the superior sagittal sinus.
- 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.
- BLOOD FILLED COLLECTION
- 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 H’age Stereotactic Radiosx = for inaccessible lesions
- IMAGING CT – Norma if small. In large lesion Hyperdense lesion with scatteres intralesional calcification at post limb of int capsule
- T2WI shows classic “popcorn ball” appearance with locules of blood in different stages of evolution surrounded by hemosiderin rim MRI MR – DIAGNOSTIC Focal 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
- 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
- Based on imaging
- Graphic depicts pontine capillary telangiectasia with tiny dilated capillaries interspersed with normal brain Cranial irradiation cause vascular damage thar induce devolpoment of talengiectasia.
- A few cases vertigo,headache,tinnitus
- Usually <1cm C…flair faint patchy hyperintesity in pons D…GRE shows ausceptability effect with greyish hypointensiyy.
- T1 C+ scan shows the brush-like faint enhancement No treatment is reqd.
- Coronal graphic depicts a classic sinus pericranii (SP BOLD ARROW) with an expanded venous pouch under the scalp connecting to the intracranial venous system through a transcalvarial channel. a/w wd DVA Some investigator suggest that sp is cutaneous manifestation of intracranial dva as the two lesions are invarieably associated.
- TREATMENT Surgical removal of extracranial component- cosmetic purpose Reduce on upright position
- CT venogram – SP communicating with sup sagittal sinus
- Sinus pericranmii that connects to th SSS via transcalvarial venous channels
- Late venous phase DSA shows angiographic findings of sinus pericranii with enlarged venous pouches connecting directly to the superior sagittal sinus through a transcalvarial channel
- Idiopathic progressive arteriopathy. Familial. Secondary moyamoya syndrome is seen in association with neurofibromatosis, Down syndrome, Williams syndrome, sickle cell disease, and as a sequale of cranial irradiation. Intracranial hemorrhage is common in young adults. Dissection — Arterial dissection is the most common vascular abnormality in some young adult series
- 2 peak age of presentation less than 10(70%). 5th decade
- Multiple enhancing pi=unctate dots or fkloew voids in basal ganglia Swimming worm in a bare cistern(multiple tiny collateral vs in enlarged csf space) Multiple microbleed can detected in gre.
- Dsa/cta/mra shows bottle neck sign.