Brain angiography

BRAIN AGIOGRAPHYImage misinterpretation

SAMIR EL ANSARYICU PROFESSOR

AIN SHAMSCAIRO

Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/145

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Diffuse proliferative cerebral arterial disorders:

Similar appearances, different diagnosis.

Diffuse Proliferative cerebral arterial disorders.

Types.

1. Cerebral Proliferative Angiopathy

2. Moyamoya

3. Hemorrhagic Angiopathy

Clinical Features

Cerebral Proliferative

Angiopathy

Moyamoya

Seizure: 45%

Headache: 41%

Focal deficits: 16%

Hemorrhages (12%):

33% single -- 67% recurrent

Prognosis: poor

Infarction: 50-75%

TIA: 50-75%

Seizures, headaches

Hemorrhages

Rare: choreiform, cognitive or

psychiatric changes

Prognosis: variable

If a patient with suspect CPA presents with HEMORRHAGE

consider HEMORRHAGIC ANGIOPATHY

More facts about Moyamoya

• 10-20% associated with sickle cell disease, NF-1, Down Syndrome, previous cranial irradiation

• <10% associated with congenital cardiac anomalies, renal-artery stenosis, giant cervicofacial hemangiomas,

hyperthyroidism

• Genetic component: – 10% of Japanese & 6% of US pts have a 1st degree relative– Associated w/abnormalities in chromosomes 3,6,8, & 17

• None of these associations are seen with CPA

Pathology Features

Cerebral Proliferative

Angiopathy

Moyamoya

Altered internal elastic

lamina & smooth

muscle cells

Collagenous thickening

of veins

Intermingled normal

neural tissue

Smooth muscle

hyperplasia

Irregular elastic lamina

No inflamacion

CT Features

Cerebral Proliferative

Angiopathy

Moyamoya

Areas of dense contrast

enhancement which may

be focal, lobar or

hemispheric

Collateral deep perforators

& pial vessels (Ivy sign)

Cortical Infarcts

Calcium in old infarcts

Hemorrhage

Cerebellum always nl

Hemorrhage:

Consider Hemorrhagic Angiopathy

Hemorrhagic Angiopathy: CT

3 pts with Hemorrhagic Angiopathy show intraparenchymal bleeds. Hemorrhages are much less common in CPA.

Angiography Features (1)

Cerebral Proliferative

Angiopathy

Moyamoya

Intermingled nl brain

parenchyma

No dominant feeders

Fast capillary transit

Transdural blood supply

Late stenosis (ICA, M1-2, A1-2):

39%

Aneurysms (12%)

Mildly enlarged draining veins

Dilated perforating

arteries

Generally bilateral

Spares posterior

circulation arteries

Early stenosis of ICA,

M1 & A1

Aneurysms

Angiography Features (2)

Cerebral Proliferative

Angiopathy

Hemorrhagic

Angiopathy

Intermingled nl brain

parenchyma

No dominant feeders

Fast capillary transit

Transdural blood supply

Late stenosis

Aneurysms (12%)

Blush may be focal, lobar or

hemispheric

Low incidence of bleeds

Intermingled nl brain

parenchyma

No dominant feeders

Fast capillary transit

No transdural blood supply

No stenoses

No aneurysms

Small pseudo-tumoral blush;

usually subcortical

High incidence of bleeds

Cerebral Proliferative Angiopathy: Angiography

Arterial stenoses Lack of dominant feeders Fast capillary transit

Intermingled normal brain parenchyma Transdural blood

supply

Cerebral Proliferative Angiopathy: Angiography

3 frontal angiographic views show arterial proliferation without A-V shunting & filling of multiple moderate dilated veins.

Initial lateral angiogram (left) shows CPA, center shows revascularization obtained via dural branches of the middle meningeal artery after burr holes,

follow-up angiogram (right) shows diminished CPA.

Cerebral Proliferative Angiopathy: Angiography

Initial lateral angiogram (left) shows CPA, center shows revascularization obtained via dural branches of the middle meningeal artery after burr holes,

follow-up angiogram (right) shows diminished CPA.

Cerebral Proliferative Angiopathy: Angiography

Hemorrhagic Angiopathy: Angiography

Angiography demonstrates nl sized arterial feeders with a pseudo tumoral blush & no venous shunting.

Early arterial phase (left) & late arterial phase (right) demonstrates nl size arterial feeders & slightly early draining veins.

Hemorrhagic Angiopathy: Angiography

Moyamoya: angiography,

different stages

Narrowing of ICA, M1, A1 Narrowing of ICA with“Puff-of-Smoke”,

diminished cortical flow.

Obliteration of ICA,disappearance of Puff-of-Smoke,further reduction of cortical flow.

MR T2WIs & lateral angiogram show focal CPA in the right frontal lobe.

Cerebral Proliferative Angiopathy :

MR & Angiography

Cerebral Proliferative Angiopathy: MR

Source MRA (left) shows multiple hypertrophied arteries, MRA frontal view (center) shows stenosis of left MCA & CPA, T2WI (right) shows abnormal blood

vessels & gliosis in left hemisphere.

Cerebral Proliferative Angiopathy: MR

MRI studies (different pts) show multiple flow voids on T1WI (left), FLAIR (center) & after Gdt administration (right). Note intermingled normal brain in all pts.

Cerebral Proliferative Angiopathy: MR

MR T1WIs (left, center) &T2WI show CPA in left hemisphere including basal ganglia.

Cerebral Proliferative Angiopathy: MR Perfusion

MTT, rCBF & rCBV are increased due to capillary & venous ectasia. In classic brain AVMs MTT is decreased due to rapid shunting.

CBV CBF MTT

Cerebral Proliferative Angiopathy: MR Perfusion

T2 image shows diffuse CPA & gliosis, source MRA image confirms presence of vessels & Gd perfusion rCBF map shows high perfusion.

Cerebral Proliferative Angiopathy: MR Perfusion

Lasjaunias P. et al. Cerebral proliferative angiopathy, clinical and angiographic description of an entity different from cerebral AVMs. Stroke. 2008 Mar: 1-8.

T1WI post Gd, TTP, rCBV & rCBF maps in an 11-year-old girl with headaches shows left frontoparietal CPA. MRI demonstrate increase CBV & CVF indicating hypervascularization in lesion & decreased TTP in nidus and surrounding areas

suggesting the ischemic nature of the disease.

Hemorrhagic Angiopathy: MR

2 pts presenting with intraparenchymal hemorrhages. (Left) T1WI non-contrast, (Middle) FLAIR, (Right) T2WI.

Moyamoya: MR

Flow Voids in basal ganglia

Leptomeningeal enhancement (leptomeningeal blood vessel

engorgement: Ivy sign).

Moyamoya: MR

Different patients: FLAIR shows watershed chronic infarcts (far left) & acute parietal infarct (ctr left). T2WI shows left intraventricular acute hemorrhage (ctr right). T2*

shows right temporal acute bleed (far right).

Moyamoya: Vascular MR

Different patients: MRA shows stenosis of both MCAs & large perforators (left). Center shows stenosis of left MCA. MR perfusion (right) shows low rCBF in deep regions of

both hemispheres.

Treatment

Cerebral Proliferative

Angiopathy

Moyamoya

Targeted embolization

Increase cortical blood

supply: Synangiogenesis or calvarial

burr holes increase cortical

blood supply by recruiting

additional dural arteries

Antiplatelet Tx

Calcium channel

blockers

Surgery: Synangiogenesis or

calvarial burr holes

Bypass ECA to ischemic

zone is feasible

Hemorrhagic Angiopathy: Response to Radiation therapy

Pre & Post radiation Tx angiography performed on hemorrhagic angiopathy pts. Pre images demonstrate pseudo tumoral blush at time of ICH with rapid capillary transity.

Post Tx images show excellent response to irradiation.

Pre Treatment Post Treatment Pre Treatment Post Treatment

Conclusions

Both cerebral proliferative angiopathy & Moyamoya are arterial proliferative conditions leading to stenoses in proximal vessels.

Both are ischemic arterial conditions.

Proliferative angiopathy and hemorrhagic angiopathy have to be considered as a group of disorders different from classical brain AVMs.

Conclusions

Treatment of Moyamoya aims to an improvement in arterial supply by direct (bypass) or indirect (synangiogenesis or calvarial burr holes)revascularization techniques.

Proliferative angiopathy pts. can be candidates for arterial revascularisation treatments. In some instances they can benefit from targeted embolizations.

Hemorrhagic angiopathy has a rapid response to the radiotherapy.

References

Scott R. et al. Moyamoya Disease and Moyamoya Syndrome. NEJM 2009;360:1226-37.

Bacigaluppi S, Dehdashti AR, Agid R, Krings T, Tymianski M, Mikulis DJ.Neurosurg The contribution of imaging in diagnosis, preoperative assessment, and follow-up of moyamoya disease: a review. Neurosurg Focus. 2009; 26:E3a

Lasjaunias P. et al. Cerebral Proliferative Angiopathy, Clinical and Angiographic Description of an Entity Different From Cerebral AVMs. Stroke. 2008 Mar: 1-8.

Paolo Tortori-Donati, Andrea Rossi, C. Raybaud. Pediatric Neuroradiology: Brain, Head , Neck, and Spine. Springer Berlin Heidelberg New York. 2005. 291-297.

Lasjaunias P, Ter Brugge K.G., Berenstein A. Surgical Neuroangiography. Volume 3: Clinical and Interventioal Aspects in Children. Springer. 2006: 35-39.

Representative Cases

Case # 1

Patient presents withstroke symptom ofless than 2 hours.Non contrast head CTwas performed andshows a left denseMCA (arrow).

Following the CT of the head, this CTA was performed :

Do you consider the left MCA to be occluded? This MIP was interpreted as the MCA being patent.

Case # 1

Case # 1

Follow-u[ MRA shows that left ICA is occluded.

Case # 1

Catheter angiogramshows dissected leftICA. There is crossfilling from rightinjection to level ofocclusion (arrow).Pial collaterals supplyterritory of left MCAthus filling it withcontrast.

Case # 1- Teaching Point

On the CTA the dense clot-filled M1 segment ofthe left MCA appears isodense to contrast filledarteries.

Collateral filling of the ipsilateral MCA branches tothe distal end of the clot resulted in a CTA thatgave the false appearance being normal.

Catheter angiography confirms these findings. IfCTA findings do not correspond with patient’ssymptoms, additional studies using differenttechniques may be needed.

Case # 2

Patient complained of left sided hemiplegiaand left facial numbness lasting approximately1 hour.

CTA was performed, two MIP coronal views areshown (next slide), no early ischemic findingswere observed.

Vasculature and brain parenchyma weresymmetrical. Both ICAs had calcifications.

Coronal MIPs show symmetrical filling of MCAs.

Case # 2

Case # 2

Immediately after the CT the patient underwent MRA which shows occluded left ICA but cross filling of left

sided intracranial arteries via the circle of Willis.

Re-windowing the coronal and axial MIPs show calcification in the left ICA (arrow) which confirms occluded artery as seen on

MRA. Note that with narrow window settings (left) the calcification is not appreciated.

Case # 2

Case # 2 – Teaching Point

Primary collateral blood flow created asymmetrical vascular picture of the distalbrain vessels and the dense intra-arterialcalcification in the left ICA masked the totalvessel occlusion when the CTA was viewedwith narrow window settings.

We have seen similar findings in three otherpatients. Wide windows should be used toavoid this problem.

Case # 3

Patient presented with acute leftMCA stroke symptoms.

CTA showed no occlusions; VR imagesare shown (next slide).

Case # 3

Both MCAs are patent and left A1 segment of the ACA is not visualized, bone obscures visualization of the petrous portions

of the ICAs. The posterior circulation is not seen entirely.

Case # 3

Widening the window (right side image) allows one to see that the petrous portion of the left ICA (arrow) is narrowed when compared to the opposite side. This finding is difficult to see

with regular window (left image) settings due to similar densities at vessel/bone interface.

Case # 3

Axial MIPs with wide window settings show narrowed petrous (arrows) left ICA when compared to right ICA

(arrowhead).

Case # 3- Teaching Point

With normal window settings, distinguishing between adjacent bone and opacified vessel may be difficult.

Separation of blood vessel/bone interface necessitates wide window settings.

Case # 4

Patient had an acute right posteriorcirculation infarct confirmed by non-contrasthead CT.

CTA demonstrated diffuse vascular irregularitiesand narrow intracranial vessels.

The basilar artery and both P1 segments werepoorly visualized, VR images are shown (nextslide).

VRs of the circle of Willis show a narrowed basilar artery, non visualization of the PCAs and adequate proximal anterior

circulation.

Case # 4

Case # 4

Axial MIPs show apparently complete circle of Willis, noticed that, however vessel opacification is poor suggesting stenosis

(not seen) leading to poor blood flow to these arteries.

Case # 4

MIP axial image shows occlusion of the right ICA.

Case # 4- Continuation

Angiography confirmed the severe basilarstenosis and right ICA occlusion.

Most of the arterial supply to the right cerebralhemisphere was via right ophthalmic arteryand right PCA and not via the anteriorcommunicating artery as suspected from theCTA.

Case # 4

Right external carotid artery injection shows opacification of right MCA territory.

Lateral view of ECA injection shows opacification of right

MCA territory.

Left ICA injection shows poor opacification of the right MCA territory implying inadequate cross filling through ACommA.

Left vertebral artery injectionshows opacification of right MCA

territory.

Case # 4

Left vertebral artery injectionshows opacification of right MCA

territory.

Case # 4

Case # 4- Teaching Point

The status of the circle of Willis suggested bythe CTA was misinterpreted because ofpatient’s low arterial input of contrast andnon-visualization of the collateral supply bythe right ophthalmic and right posteriorcommunicator artery.

The degree of narrowing of the basilar arterywas overestimated on CT.

Hemodynamic alterations were thought to beresponsible for the patient’s symptoms.

Case # 5

Patient presented with acute stroke symptomssuggesting involvement of left posteriorcirculation. CTA showed left occipitalhypodensity.

Axial MIPs are shown (next slide).

Case # 5

The transition between left P1 and P2 segments is not well visualized, but small distal PCA branches show opacification implying that these arteries are patent

(click for sequential MIPs from CTA).

VR images show normal basilar artery. The right vertebral artery is dominant while there is a vessel in the region of the left sided one. A discrepant finding with

respect to the MIPS is that both PCAs are not seen past their proximal segments on these images probably due to the fact that they were excluded from the

reformations.

Case # 5

Case # 5

Injection into the right subclavian artery shows occlusion of proximal vertebral artery with recanalization cephalad by

collaterals.

Case # 5

The right vertebral artery filled via muscular collaterals and there was slow flow to the basilar artery. The left PCA is occluded (arrow) past its P2 segment while the right sided one is patent.

Case # 5

Injection into left vertebral artery shows that it ends in PICA thus the vessel seen on the CTA cannot be the vertebral artery

but is probably a vein draining into the marginal sinus.

Case # 5- Teaching Point

Initially, there were discrepant findings between theMIPs and VR images, the latter showing occlusion ofboth PCAs. Catheter angiogram showed occludedleft PCA. Despite visualization of the presumed leftvertebral artery on CTA, angiogram showed it beoccluded. Moreover, the right vertebral wasproximally occluded and recanalized distally. Thestatic nature of CTA does not allow one to visualizedelay circulation times which may have been relatedto patient’s symptoms.

Case # 6

Patient presented to the hospital after aperipheral interventional procedure with signsof a right MCA infarct. Embolic infarct wassuspected. CTA is shown in next slide.

Case 6

Sequential axial MIPs (on click) showing normal appearing vessels.

Case # 6

Coronal MIPs show left MCA fenestration (circle) and incompletely seen right M1 segment but with good opacification

of the ipsilateral sylvian branches.

Case # 6

VR images confirm left MCAfenestration (circle) andadequate filling of rightMCA despite symptomscorresponding to that side.

Case # 6

Angiogram confirms left fenestration (circle). On the right, there is a similar fenestration but its superior limb is occluded (arrow) explaining the patients

symptoms.

Case # 6- Teaching Point

CTA showed patent right MCA. This arterywas however fenestrated and the superiorlimb of the fenestration was occludedresulting in a basal ganglia/capsular infarction.The fact that the inferior limb of thefenestration was patent gave the falseimpression that the entire left MCA waspatent. This was suspected and lead tocatheter angiogram and attemptedthrombolysis.

Case # 7

Patient presented with posterior circulationinfarct symptoms and CTA showed an unusualconfiguration of the top of the basilar artery.

Case # 6

Sagittal MIP (left) shows irregular basilar artery termination (arrow). This finding cannot be confirmed on the VR image (right) as the basilar artery apex

is inseparable from adjacent bone.

Case # 6

Catheter angiogram shows clot occluding distal basilar artery. The definitive diagnosis could be made on CTA and required this

study.

Case # 6- Teaching Point

Contrast and/or clot may be of similar densityto bone and inseparable from it on VR images.This is dependent on window settings andtime of study acquisition. Some times,changing window setting may solve thisproblem but others times the problem maypersist. Suspected defects seen on MIPs maynecessitate confirmation by catheterangiography.

Discussion

• Stroke is the end product of a dynamic cascade ofevents that culminates with tissue death.

• CTA information is only a snapshot of entire process.

• CTA may reveal distinct phases of disease process orpatient characteristics that serve as confounding factorsin imaging, such as

– recanalization of prior occlusion

– intra-arterial clot that is as dense as IV contrast

– collateral flow that may be primary or secondary

– symmetrical collateral flow that may be insufficient underhypoperfusion situations.

Discussion

• Technical factors such as slice thickness , type ofreconstructions, suitable window settings andMIP/VR interactive assessment at the work stationmay improve assessment of distal branch occlusionand intra-vascular densities.

• Keep in mind, when assessing a patient with acutestroke symptoms, that there is a high likelihood thatchronic findings and/or unusual flow patterns maybe related to the patient’s symptoms.

Suggested Image Assessment

• Assess all acquired imaging settings

• Alter window level and center when assessing MIPs and VRs to find calcifications, clots, dissections and stenoses that may be either concealed or overestimated

• Assess 3D images dynamically, changing vessel bifurcations angles

• Keep in mind that you are dealing with a dynamic disease with possible associated chronic findings;

• Keep in mind that venous and arterial systems may be contrasted and overlapping

• Look for possible collateral flow

Anterior circulation

Posterior Circulation

Aortic Arch Angiogram

Carotid Angiogram

Internal Carotid Angiograms

Internal Carotid Angiogram

Vertebral Arteries Angiogram

Vertebral Artery Angiogram

GOOD LUCK

SAMIR EL ANSARY

ICU PROFESSOR

AIN SHAMS

CAIRO

elansarysamir@yahoo.com

Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/145

1610115129555/ Wellcome in our new group ..... Dr.SAMIR EL ANSARY