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Brain angiography


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Brain angiography

  2. 2. Global Critical Care!/groups/145 1610115129555/ Wellcome in our new group ..... Dr.SAMIR EL ANSARY
  3. 3. Diffuse proliferative cerebral arterial disorders: Similar appearances, different diagnosis.
  4. 4. Diffuse Proliferative cerebral arterial disorders. Types. 1. Cerebral Proliferative Angiopathy 2. Moyamoya 3. Hemorrhagic Angiopathy
  5. 5. 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
  6. 6. 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
  7. 7. 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
  8. 8. 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
  9. 9. Hemorrhagic Angiopathy: CT 3 pts with Hemorrhagic Angiopathy show intraparenchymal bleeds. Hemorrhages are much less common in CPA.
  10. 10. 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
  11. 11. 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
  12. 12. Cerebral Proliferative Angiopathy: Angiography Arterial stenoses Lack of dominant feeders Fast capillary transit
  13. 13. Intermingled normal brain parenchyma Transdural blood supply
  14. 14. Cerebral Proliferative Angiopathy: Angiography 3 frontal angiographic views show arterial proliferation without A-V shunting & filling of multiple moderate dilated veins.
  15. 15. 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
  16. 16. 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
  17. 17. Hemorrhagic Angiopathy: Angiography Angiography demonstrates nl sized arterial feeders with a pseudo tumoral blush & no venous shunting.
  18. 18. Early arterial phase (left) & late arterial phase (right) demonstrates nl size arterial feeders & slightly early draining veins. Hemorrhagic Angiopathy: Angiography
  19. 19. 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.
  20. 20. MR T2WIs & lateral angiogram show focal CPA in the right frontal lobe. Cerebral Proliferative Angiopathy : MR & Angiography
  21. 21. 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.
  22. 22. 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.
  23. 23. Cerebral Proliferative Angiopathy: MR MR T1WIs (left, center) &T2WI show CPA in left hemisphere including basal ganglia.
  24. 24. 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
  25. 25. 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.
  26. 26. 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.
  27. 27. Hemorrhagic Angiopathy: MR 2 pts presenting with intraparenchymal hemorrhages. (Left) T1WI non-contrast, (Middle) FLAIR, (Right) T2WI.
  28. 28. Moyamoya: MR Flow Voids in basal ganglia Leptomeningeal enhancement (leptomeningeal blood vessel engorgement: Ivy sign).
  29. 29. 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).
  30. 30. 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.
  31. 31. 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
  32. 32. 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
  33. 33. 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.
  34. 34. 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.
  35. 35. 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.
  36. 36. Representative Cases
  37. 37. Case # 1 Patient presents with stroke symptom of less than 2 hours. Non contrast head CT was performed and shows a left dense MCA (arrow).
  38. 38. 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
  39. 39. Case # 1 Follow-u[ MRA shows that left ICA is occluded.
  40. 40. Case # 1 Catheter angiogram shows dissected left ICA. There is cross filling from right injection to level of occlusion (arrow). Pial collaterals supply territory of left MCA thus filling it with contrast.
  41. 41. Case # 1- Teaching Point On the CTA the dense clot-filled M1 segment of the left MCA appears isodense to contrast filled arteries. Collateral filling of the ipsilateral MCA branches to the distal end of the clot resulted in a CTA that gave the false appearance being normal. Catheter angiography confirms these findings. If CTA findings do not correspond with patient’s symptoms, additional studies using different techniques may be needed.
  42. 42. Case # 2 Patient complained of left sided hemiplegia and left facial numbness lasting approximately 1 hour. CTA was performed, two MIP coronal views are shown (next slide), no early ischemic findings were observed. Vasculature and brain parenchyma were symmetrical. Both ICAs had calcifications.
  43. 43. Coronal MIPs show symmetrical filling of MCAs. Case # 2
  44. 44. 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.
  45. 45. 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
  46. 46. Case # 2 – Teaching Point Primary collateral blood flow created a symmetrical vascular picture of the distal brain vessels and the dense intra-arterial calcification in the left ICA masked the total vessel occlusion when the CTA was viewed with narrow window settings. We have seen similar findings in three other patients. Wide windows should be used to avoid this problem.
  47. 47. Case # 3 Patient presented with acute left MCA stroke symptoms. CTA showed no occlusions; VR images are shown (next slide).
  48. 48. 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.
  49. 49. 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.
  50. 50. Case # 3 Axial MIPs with wide window settings show narrowed petrous (arrows) left ICA when compared to right ICA (arrowhead).
  51. 51. 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.
  52. 52. Case # 4 Patient had an acute right posterior circulation infarct confirmed by non-contrast head CT. CTA demonstrated diffuse vascular irregularities and narrow intracranial vessels. The basilar artery and both P1 segments were poorly visualized, VR images are shown (next slide).
  53. 53. VRs of the circle of Willis show a narrowed basilar artery, non visualization of the PCAs and adequate proximal anterior circulation. Case # 4
  54. 54. 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.
  55. 55. Case # 4 MIP axial image shows occlusion of the right ICA.
  56. 56. Case # 4- Continuation Angiography confirmed the severe basilar stenosis and right ICA occlusion. Most of the arterial supply to the right cerebral hemisphere was via right ophthalmic artery and right PCA and not via the anterior communicating artery as suspected from the CTA.
  57. 57. Case # 4 Right external carotid artery injection shows opacification of right MCA territory. Lateral view of ECA injection shows opacification of right MCA territory.
  58. 58. Left ICA injection shows poor opacification of the right MCA territory implying inadequate cross filling through ACommA. Left vertebral artery injection shows opacification of right MCA territory. Case # 4
  59. 59. Left vertebral artery injection shows opacification of right MCA territory. Case # 4
  60. 60. Case # 4- Teaching Point The status of the circle of Willis suggested by the CTA was misinterpreted because of patient’s low arterial input of contrast and non-visualization of the collateral supply by the right ophthalmic and right posterior communicator artery. The degree of narrowing of the basilar artery was overestimated on CT. Hemodynamic alterations were thought to be responsible for the patient’s symptoms.
  61. 61. Case # 5 Patient presented with acute stroke symptoms suggesting involvement of left posterior circulation. CTA showed left occipital hypodensity. Axial MIPs are shown (next slide).
  62. 62. 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).
  63. 63. 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
  64. 64. Case # 5 Injection into the right subclavian artery shows occlusion of proximal vertebral artery with recanalization cephalad by collaterals.
  65. 65. 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.
  66. 66. 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.
  67. 67. Case # 5- Teaching Point Initially, there were discrepant findings between the MIPs and VR images, the latter showing occlusion of both PCAs. Catheter angiogram showed occluded left PCA. Despite visualization of the presumed left vertebral artery on CTA, angiogram showed it be occluded. Moreover, the right vertebral was proximally occluded and recanalized distally. The static nature of CTA does not allow one to visualize delay circulation times which may have been related to patient’s symptoms.
  68. 68. Case # 6 Patient presented to the hospital after a peripheral interventional procedure with signs of a right MCA infarct. Embolic infarct was suspected. CTA is shown in next slide.
  69. 69. Case 6 Sequential axial MIPs (on click) showing normal appearing vessels.
  70. 70. Case # 6 Coronal MIPs show left MCA fenestration (circle) and incompletely seen right M1 segment but with good opacification of the ipsilateral sylvian branches.
  71. 71. Case # 6 VR images confirm left MCA fenestration (circle) and adequate filling of right MCA despite symptoms corresponding to that side.
  72. 72. 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.
  73. 73. Case # 6- Teaching Point CTA showed patent right MCA. This artery was however fenestrated and the superior limb of the fenestration was occluded resulting in a basal ganglia/capsular infarction. The fact that the inferior limb of the fenestration was patent gave the false impression that the entire left MCA was patent. This was suspected and lead to catheter angiogram and attempted thrombolysis.
  74. 74. Case # 7 Patient presented with posterior circulation infarct symptoms and CTA showed an unusual configuration of the top of the basilar artery.
  75. 75. 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.
  76. 76. Case # 6 Catheter angiogram shows clot occluding distal basilar artery. The definitive diagnosis could be made on CTA and required this study.
  77. 77. Case # 6- Teaching Point Contrast and/or clot may be of similar density to bone and inseparable from it on VR images. This is dependent on window settings and time of study acquisition. Some times, changing window setting may solve this problem but others times the problem may persist. Suspected defects seen on MIPs may necessitate confirmation by catheter angiography.
  78. 78. Discussion • Stroke is the end product of a dynamic cascade of events that culminates with tissue death. • CTA information is only a snapshot of entire process. • CTA may reveal distinct phases of disease process or patient characteristics that serve as confounding factors in 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 under hypoperfusion situations.
  79. 79. Discussion • Technical factors such as slice thickness , type of reconstructions, suitable window settings and MIP/VR interactive assessment at the work station may improve assessment of distal branch occlusion and intra-vascular densities. • Keep in mind, when assessing a patient with acute stroke symptoms, that there is a high likelihood that chronic findings and/or unusual flow patterns may be related to the patient’s symptoms.
  80. 80. 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
  81. 81. Anterior circulation
  82. 82. Posterior Circulation
  83. 83. Aortic Arch Angiogram
  84. 84. Carotid Angiogram
  85. 85. Internal Carotid Angiograms
  86. 86. Internal Carotid Angiogram
  87. 87. Vertebral Arteries Angiogram
  88. 88. Vertebral Artery Angiogram
  89. 89. GOOD LUCK SAMIR EL ANSARY ICU PROFESSOR AIN SHAMS CAIRO Global Critical Care!/groups/145 1610115129555/ Wellcome in our new group ..... Dr.SAMIR EL ANSARY