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- 1. A Consensus Meeting <br />for The Definitions of Subcortical lesions, Lacunes, Microbleeds, and Subcortical White Matter Change<br />Jei Kim, MD<br />
- 2. M/71, 2011. 1. 28<br />
- 3. M/71, 2011. 1. 28<br />
- 4. M/71, 2011. 1. 28<br />
- 5. Subcortical lesions<br />1. Perivascular spaces (etatcrible)<br />2. Lacunes<br />3. Subcortical white matter changes<br />4. Microbleeds<br />
- 6. Perivascular spaces (etatcrible)<br />
- 7. 1. Perivascular spaces (etatcrible)<br />1) Histopathologic definition (ref. 1)<br />: the dilatation of perivascular spaces around <br /> cerebral arterioles in the brain of elderly patients <br />(Virchow-Robin space)<br />2) MRI definition (ref. 1)<br />: the punctiform dilatations of the perivascular<br /> spaces often seen by brain MRI in the white <br /> matter and in the basal ganglia<br />
- 8. 1. Perivascular spaces (etatcrible)<br />2) MRI definition<br />: the punctiform dilatations of the perivascular spaces <br /> often seen by brain MRI in the white matter and <br /> in the basal ganglia<br />: On T2WI – high intensity, <br />same as the intensity of CSF <br />: On FLAIR – dark (low), same as the intensity of CSF<br />: On T1WI – dark (low), same as the intensity of CSF<br />http://www.radiologyassistant.nl/en/4556dea65db62<br />
- 9. M/80, 2011. 10. 13<br />
- 10. Lacunes<br />
- 11. 2. Lacunes<br />1) Histopathologic definition<br />: a small, cystic cavity of the brain substance that <br /> usually results from an ischemic infarction in the <br /> territory of a penetrating arteriole (ref. 1)<br />
- 12. 2. Lacunes<br />2) Vascular pathology of lacunes<br />(ref. 13)<br />
- 13. 2. Lacunes<br />3) Perforating arteries <br />(1) Anterior perforating arteries<br />(2) Posterior perforating arteries<br />(3) Arterial supply of the brainstem<br />
- 14. (1) Anterior perforating arteries<br />
- 15. (1) Anterior perforating arteries<br />A. Perforating branches arising from ACA <br /> and the recurrent artery of Heubner<br />
- 16. (1) Anterior perforating arteries<br />B. Perforating branches arising from MCA<br />a. Perforating branches arising from MCA<br />
- 17. (1) Anterior perforating arteries<br />B. Perforating branches arising from MCA<br />b. Percentage of perforating arteries arising from MCA trunk and its branches<br />
- 18. (1) Anterior perforating arteries<br />B. Perforating branches arising from MCA<br />c. Origin of perforating arteries arising <br /> from MCA trunk and its branches<br />
- 19. (1) Anterior perforating arteries<br />B. Perforating branches arising from MCA<br />d. Number of perforating arteries arising <br /> from different distances from the origin of MCA<br />
- 20. (1) Anterior perforating arteries<br />B. Perforating branches arising from MCA<br />e. Branching characteristics of 508 perforating arteries <br /> arising from common stems of MCA<br />
- 21. (2) Posterior perforating arteries<br />
- 22. (3) Arterial supply of the brainstem<br />A. Perforating arteries of the midbrain<br />
- 23. (3) Arterial supply of the brainstem<br />B. Perforating arteries of the pons<br />
- 24. (3) Arterial supply of the brainstem<br />C. Perforating arteries of the midbrain<br />
- 25. Schematic diagram of origin of deep perforating branches from a parent artery<br />
- 26. 2. Lacunes<br />4) Pathogenic implications of microcirculation<br />(1) Perforating arteries<br />1) Stenosis or complete occlusion by atherosclerosis<br />2) Stenosis or occlusion of ostium of a branch point<br />3) Atherosclerotic narrowing of a parent artery<br />4) Proximal thrombus or embolus in atherosclerotic artery<br />(2) Cortical branches<br />
- 27. 4) Pathogenic implications of microcirculation<br />(1) Perforating arteries<br />A. Stenosis or complete occlusion by atherosclerosis<br />
- 28. 4) Pathogenic implications of microcirculation<br />(1) Perforating arteries<br />B. Stenosis or occlusion of ostium of a branch point<br />
- 29. 4) Pathogenic implications of microcirculation<br />(1) Perforating arteries<br />C. Atherosclerotic narrowing of a parent artery<br />
- 30. 4) Pathogenic implications of microcirculation<br />(1) Perforating arteries<br />D. Proximal thrombus or embolus in atherosclerotic artery<br />
- 31. 4) Pathogenic implications of microcirculation<br />(2) Cortical branches<br />
- 32. 2. Lacunes<br />5) MRI definition<br />(ref. 2)<br />: small hyperintense lesions on T2WI (ref. 2)<br />: corresponding distinctive low intensity area on T1WI<br />: Maximum size of lacune (ref. 4)<br /> - with a diameter of 5-10 mm<br />: On CT (ref. 4)<br /> - areas of more or less complete focal tissue destruction<br /> - clearly defined borders with marked central <br />hypodensity on CT<br />: On MRI (ref. 4)<br /> - low intensity on T1WI, proton-density and FLAIR scans<br /> - high intensity on T2WI<br /> -> isointense to CSF<br />
- 33. 2. Lacunes<br />5) MRI definition<br />(ref. 17)<br />
- 34. 2. Lacunes<br />1) Histopathologic definition<br />: a small, cystic cavity of the brain substance that <br /> usually results from an ischemic infarction in the <br /> territory of a penetrating arteriole (ref. 1)<br />: defined as cavitatedmicroinfarcts or encephalomalacic<br /> lesions, 2 mm or smaller in greatest dimension, not <br /> identifiable with certainty on gross inspection of the <br /> brain or non-cavitatedmicroinfarcts, focal gliotic areas <br /> without a cystic cavity (ref. 3)<br />
- 35. M/80, 2011. 10. 13<br />
- 36. 2. Lacunes<br />6) Grading of lacunes<br />(ref. 2)<br />Absent<br />(2) Mild – 1-3<br />(3) Moderate – 4-10<br />(4) Severe - >10<br />7) Locations of lacunes<br />(ref. 2)<br />Cortico-subcortical<br />(2) Basal ganglia<br />(3) Thalamus<br />(4) Brain stem<br />(5) Cerebellum<br />
- 37. Subcortical white matter change<br />
- 38. 3. Subcortical white matter change<br />1) Definition of Binswanger’s disease (1894)<br />: pronounced atrophy of the white matter, either confined <br /> to one or more gyri of the brain or in several sections <br /> of the hemisphere <br />: in the most severe cases the entire white matter <br /> of a cerebral lobe appears to have completely wasted away<br />: a severe atheromatosis of the arteries of the brain is always <br /> present in these cases<br />: extensive atrophic degeneration or fatty degeneration <br /> of the small arterial and venous vessels<br />: partial thickening of the inner and middle vascular <br /> membranes<br />: the lumen is correspondingly narrowed<br />
- 39. 3. Subcortical white matter change<br />2) Definition of leukoaraiosis<br />(Hachinski et al., 1987)<br />: loss of density of the periventricular white matter <br /> observed by CT of the brain<br />: the white matter changes commonly observed in the <br /> elderly by MRI of the brain<br />
- 40. 3. Subcortical white matter change<br />3) Mechanisms hypothesized to be involved <br /> in the pathogenesis of white matter change (ref. 14)<br />
- 41. 3. Subcortical white matter change<br />4) Small vessel changes related to white matter changes <br /> (ref. 14)<br />
- 42. 3. Subcortical white matter change<br />5) Evolution of white matter lesions (ref. 16)<br />
- 43. 3. Subcortical white matter change<br />6) Definition of ‘Periventricular’ and ‘Deep white matter’ <br /> change (ref.5)<br />(1) Periventricular<br />- Start directly at the ventricular border <br />
- 44. 3. Subcortical white matter change<br />6) Definition of ‘Periventricular’ and ‘Deep white matter’ <br /> change (ref.5)<br />(2) Both periventricular and deep white matter<br /><ul><li> If the periventricular abnormalities extend > 1 cm </li></ul> into the adjacent white matter <br />
- 45. 3. Subcortical white matter change<br />6) Definition of ‘Periventricular’ and ‘Deep white matter’ <br /> change (ref.5)<br />(3) Selective deep white matter lesion<br />- usually characterized by a rim of normal-appearing tissue which separates them from the periventricular region<br />
- 46. 3. Subcortical white matter change<br />6) Definition of ‘Periventricular’ and ‘Deep white matter’ <br /> change (ref.5)<br />(4) Basal ganglia hypodensities on CT or hyperintensity on MRI<br />(M/82)<br />
- 47. 3. Subcortical white matter change<br />6) Definition of ‘Periventricular’ and ‘Deep white matter’ <br /> change (ref.24)<br />
- 48. 3. Subcortical white matter change<br />6) Definition of ‘Periventricular’ and ‘Deep white matter’ <br /> change – (1) (ref.5)<br />Periventricularhyperintensity<br /> 0 = absence<br /> 1 = “caps” or pencil-thin lining<br /> 2 = smooth “halo”<br /> 3 = irregular PVH extending into the deep white matter<br />(2) Deep white matter hyperintense signal<br /> 0 = absence<br /> 1 = punctuate foci<br /> 2 = beginning confluence of foci<br /> 3 = large confluent areas<br />
- 49. 3. Subcortical white matter change<br />7) Definition of ‘Periventricular’ and ‘Deep white matter’ –(3) <br /> (ref. 6)<br />(1) White matter lesions<br /> 0 = no lesions <br />(including symmetrical, well-defined caps or bands)<br /> 1 = Focal lesions<br /> 2 = Beginning confluence of lesions<br /> 3 = Diffuse involvement of the entire region, <br />with or without involvement of U fibers <br />(2) Basal ganglia lesions<br /> 0 = No lesions<br /> 1 = 1 focal lesion (≥ 5 mm)<br /> 2 = > 1 focal lesion<br /> 3 = Confluent lesions<br />
- 50. 3. Subcortical white matter change<br />7) Definition of ‘Periventricular’ and ‘Deep white matter’ –(3) <br /> (ref. 6)<br />1. Score of 1<br />
- 51. 3. Subcortical white matter change<br />7) Definition of ‘Periventricular’ and ‘Deep white matter’ –(3) <br /> (ref. 6)<br />2. Score of 2<br />
- 52. 3. Subcortical white matter change<br />7) Definition of ‘Periventricular’ and ‘Deep white matter’ –(3) <br /> (ref. 6)<br />3. Score of 3<br />
- 53. 3. Subcortical white matter change<br />(1) White matter lesions<br />1 = Focal lesions<br />
- 54. 3. Subcortical white matter change<br />(1) White matter lesions<br /> 2 = Beginning confluence of lesions<br />
- 55. 3. Subcortical white matter change<br />(1) White matter lesions<br /> 3 = Diffuse involvement of the entire region, <br />with or without involvement of U fibers <br />(M/75)<br />
- 56. 3. Subcortical white matter change<br />(1) White matter lesions<br /> 3 = Diffuse involvement of the entire region, <br />with or without involvement of U fibers <br />(M/60)<br />
- 57. 3. Subcortical white matter change<br />(2) Basal ganglia lesions<br /> 1 = 1 focal lesion (≥ 5 mm)<br />
- 58. 3. Subcortical white matter change<br />(2) Basal ganglia lesions<br /> 2 = > 1 focal lesion<br />
- 59. 3. Subcortical white matter change<br />(2) Basal ganglia lesions<br />3 = Confluent lesions<br />
- 60. Microbleeds<br />
- 61. 4. Microbleeds<br />1) Histopathologic and MRI definition<br />: paramagnetic material which produces local susceptibility <br /> gradients and thereby causes a faster decay of transverse <br /> magnetization on gradient-echo acquisition (ref. 18)<br />: remnants of even minor blood leakage through <br /> damaged vessel walls<br />
- 62. 4. Microbleeds<br />1) Histopathologic definition<br />: Postmortem gradient-echo-T2*-weighted MRI and <br />histopathologic finding (ref. 19)<br />
- 63. 4. Microbleeds<br />2) Severity of amyloidangiopathy (ref. 27)<br />Figure 1. Grading of CAA severity in single brain samples (ref. 27) <br />0: No cerebral vessels showed immunopositivity<br />for beta amyloid<br />1+: Amyloid is restricted to a rim around smooth <br />muscle fibers in the media of occasional <br />normal vessels<br />2+: The media is thicker than normal and <br />circumferentially replaced by amyloid<br />in a few vessels <br />3+: Widespread medial thickening and <br />circumferential amyloid deposition <br />with a small halo of immunoreactivity<br />in the surrounding parenchyma <br />: A focus of wall leakage as evidenced <br />by fresh hemorrhage or hemosiderin-laden <br />macrophages, or occlusion, or recanalization<br />
- 64. 4. Microbleeds<br />3) MRI definition of microbleed (ref. 2, 19, 20, 21)<br />(1) Homogeneous round signal loss lesion with a diameter of up to 5 mm (or <10 mm) <br /> on gradient echo image<br />Distinct from <br /> a. Vascular flow voids on subarachnoid space<br /> b. Leptomeningealhemasiderosis<br /> c. Non-hemorrhagic subcortical mineralization<br />
- 65. <ul><li> Non-hemorrhagic subcortical mineralization</li></ul>(ref. 26)<br />
- 66. <ul><li> Non-hemorrhagic subcortical mineralization</li></ul>(M/80)<br />
- 67. <ul><li>Leptomeningealhemasiderosis</li></ul>1. Superficial cortical hemosidersosis (ref. 25)<br />
- 68. <ul><li>Leptomeningealhemasiderosis</li></ul>2. Subarachnoid hemosidersosis (ref. 25)<br />
- 69. <ul><li>Leptomeningealhemasiderosis</li></ul>3. Schematic drawing illustrating subarachnoid hemosiderosis<br /> and superficial coricalhemosidersosi (ref. 25)<br />
- 70. 4. Microbleeds<br />3) MRI definition of microbleed (ref. 20)<br /><ul><li> In CAA Pt.
- 71. In CADASIL Pt.
- 72. In H/T Pt.</li></li></ul><li>4. Microbleeds<br />3) MRI definition of microbleed (ref. 21)<br />
- 73. 4. Microbleeds<br />4) Degree of severity of microbleeds (ref. 2)<br />(1) Absent<br />(2) Mild – total number of MBs, 1-5<br />(3) Moderate – total number of MBs, 6-15<br />(4) Severe – total number of MBs, >15<br />
- 74. 4. Microbleeds<br />5) The locations of the microbleeds and lacunes (ref. 2)<br />(1) Cortico-subcortical<br />(2) Basal ganglia<br />(3) Thalamus<br />(4) Brain stem<br />(5) Cerebellum<br />
- 75. Evaluation of the vessel stenosis<br />
- 76. Definition of coronary artery stenosis (ref. 8)<br />1) Significant stenosis - >50%<br />2) No significant stenosis - <50%<br />
- 77. The degrees of stenoocclusive disease (ref. 7)<br />1) Normal – 0% - 29% diameter stenosis<br />2) Mildly stenotic – 30% - 49%<br />3) Moderately stenotic – 50% - 79%<br />4) Severely stenotic – 80%- 99%<br />5) Occluded<br />
- 78. Regional location of stenosis (ref. 9)<br />: Schematic representation of 11 arterial segments studied <br /> by transcranial Doppler and duplex ultrasound<br />MCA – 1 and 2<br />ACA – 3 and 4<br />PCA – 5 and 6<br />Siphon ICA – 7 and 8<br />Extracranial ICA - 9 and 10<br />Vertebrobasilar artery – 11<br />
- 79. Measuement of vessel stenosis (ref. 10)<br />1. Equation for measuring intracranial arterial stenosis<br />: Percent stenosis = [(1-(Dstenosis/Dnormal))] x 100<br /><ul><li> Dstenosis: the diameter of the artery at the site of the </li></ul> most severe degree of stenosis<br /><ul><li> Dnormal: the diameter of the proximal normal artery</li></li></ul><li>Measuement of vessel stenosis (ref. 10)<br />2. Criteria for normal proximal artery<br />1) For the MCA, intracranial VA, and BA<br />(1) First choice<br /><ul><li> the diameter of the proximal part of the artery </li></ul> at its widest , non-tortuous, normal segment was <br /> chosen<br />(2) Second choice<br />- if the proximal artery was diseased <br />-> the diameter of the distal portion of the artery <br /> at its widest, parallel<br />
- 80. Measuement of vessel stenosis (ref. 10)<br />2. Criteria for normal proximal artery<br />(3) Third choice<br />A. If the entire intracranial artery was diseased<br />-> the most distal, parallel, non-tortous normal <br /> segment of the feeding artery <br />B. If the entire middle cerebral artery was diseased<br />-> measured at the most distal, parallel segement <br /> of the supraaclinoid carotid artery<br />C. If the entire intracranial vertebral artery was diseased <br />-> measured at the most distal, parallel, <br /> non-tortous normal segment of the extracranial <br /> vertebral artery<br />
- 81. Measuement of vessel stenosis (ref. 10)<br />2. Criteria for normal proximal artery<br />2) For the ICA<br />(1) First choice<br />: The precavernous, cavernous, and postcavernous <br /> stenoses of ICA<br />-> measured at the widest, non-tortous, normal <br /> portion of the petrous carotid artery that had <br /> parallel margins<br />
- 82. Measuement of vessel stenosis (ref. 10)<br />2. Criteria for normal proximal artery<br />2) For the ICA<br />(2) Second choice<br />- If the entire petrous carotid was diseased<br />-> the most distal, parallel part of the extracranial <br /> internal carotid artery was substituted<br />- If tandem intracranial lesions were present<br />-> percent stenosis of both sites was measured <br /> and the more severe stenosis was selected <br />- When a “gap sign” was present<br />-- the lumen of the vessel could not be visualized <br /> at the site of severe stenosis<br />-- could not be measured<br />-- defined as 99% luminal stenosis<br />
- 83. Measuement of vessel stenosis (ref. 10)<br />1. Equation for measuring intracranial arterial stenosis<br />
- 84. Measuement of vessel stenosis<br />2. Equation for measuring extracranial arterial stenosis<br />1) Severity of intracranial stenosis (ref. 11, 12)<br />(1) Mild - <30%<br />(2) Moderate – 30% - 69%<br />(3) Severe – 70% - 99%<br /> - in case of segmental signal void<br /> -> the stenosis was graded as severe (>70%)<br />(4) Occluded<br />
- 85. Measuement of vessel stenosis<br />2. Equation for measuring extracranial arterial stenosis<br />2) Measurement of the carotid artery stenosis (ref. 12)<br />(1) NASCET<br /> : (1-md/C)x100%<br />(2) ECST <br /> : (1-md/B)x100%<br />(3) CC<br /> : (1-md/A)x100%<br />

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