Subcortical lesion-classification-presentation-2011-10-10

A Consensus Meeting for The Definitions of Subcortical lesions,

Lacunes, Microbleeds, and Subcortical White Matter Change

Jei Kim, MD

M/71, 2011. 1. 28

M/71, 2011. 1. 28

M/71, 2011. 1. 28

Subcortical le-sions

4. Microb-leeds

3. Subcortical white matter changes

1. Perivascular spaces (etat crible)2. Lacunes

Perivascular spaces (etat crible)

1) Histopathologic definition (ref. 1)

1. Perivascular spaces (etat crible)

: the dilatation of perivascular spaces around cerebral arterioles in the brain of elderly patients (Virchow-Robin space)

2) MRI definition (ref. 1)

: the punctiform dilatations of the perivascular spaces often seen by brain MRI in the white matter and in the basal ganglia

1. Perivascular spaces (etat crible)2) MRI definition

: the punctiform dilatations of the perivascular spa-ces often seen by brain MRI in the white matter and in the basal ganglia: On T2WI – high intensity, same as the intensity of CSF : On FLAIR – dark (low), same as the intensity of CSF: On T1WI – dark (low), same as the intensity of CSF

http://www.radiologyassistant.nl/en/4556dea65db62



M/80, 2011. 10. 13

La-cunes

2. La-cunes

1) Histopathologic definition: a small, cystic cavity of the brain sub-stance that usually results from an ischemic infarction in the territory of a penetrating arteriole (ref. 1)

2. La-cunes

2) Vascular pathology of lacunes(ref. 13)

3) Perforating ar-teries

(1) Anterior perforating arter-ies

(2) Posterior perforating ar-teries

(3) Arterial supply of the brain-stem

2. La-cunes


A. Perforating branches arising from ACA

and the recurrent artery of Heubner


B. Perforating branches arising from MCAa. Perforating branches arising from

MCA


b. Percentage of perforating arteries arising from MCA trunk and its branches

(1) Anterior perforating arter-iesB. Perforating branches arising from MCA

c. Origin of perforating arteries aris-ing

from MCA trunk and its branches


d. Number of perforating arteries arising from different distances from the origin of MCA


e. Branching characteristics of 508 perforating arteries

arising from common stems of MCA


(2) Posterior perforating ar-teries

(3) Arterial supply of the brain-stemA. Perforating arteries of the mid-

brain

B. Perforating arteries of the pons


C. Perforating arteries of the mid-brain


Schematic diagram of origin of deep perforating branches from a parent artery

4) Pathogenic implications of microcircula-tion

1) Stenosis or complete occlusion by athero-sclerosis

2) Stenosis or occlusion of ostium of a branch point

3) Atherosclerotic narrowing of a parent artery

4) Proximal thrombus or embolus in atheroscle-rotic artery

(1) Perforating ar-teries

(2) Cortical branches

2. La-cunes


A. Stenosis or complete occlusion by athero-sclerosis

(1) Perforating ar-teries

B. Stenosis or occlusion of ostium of a branch point

4) Pathogenic implications of microcircula-tion(1) Perforating ar-teries

C. Atherosclerotic narrowing of a parent artery


D. Proximal thrombus or embolus in atheroscle-rotic artery


(2) Cortical branches


5) MRI defini-tion

2. La-cunes(ref. 2)

: small hyperintense lesions on T2WI (ref. 2): corresponding distinctive low intensity area on T1WI: Maximum size of lacune (ref. 4) - with a diameter of 5-10 mm

: On CT (ref. 4) - areas of more or less complete focal tissue de-struction - clearly defined borders with marked central hypodensity on CT: On MRI (ref. 4) - low intensity on T1WI, proton-density and FLAIR scans - high intensity on T2WI -> isointense to CSF

5) MRI defini-tion

2. La-cunes(ref. 17)

2. La-cunes

1) Histopathologic definition: a small, cystic cavity of the brain sub-stance that usually results from an ischemic infarction in the territory of a penetrating arteriole (ref. 1): defined as cavitated microinfarcts or en-cephalomalacic lesions, 2 mm or smaller in greatest dimension, not identifiable with certainty on gross inspection of the brain or non-cavitated microinfarcts, focal gliotic ar-eas without a cystic cavity (ref. 3)

M/80, 2011. 10. 13

6) Grading of la-cunes

2. La-cunes

(ref. 2)

(1)Absent(2) Mild – 1-3(3) Moderate – 4-10(4) Severe - >10

7) Locations of la-cunes

(ref. 2)

(1)Cortico-subcorti-cal

(2) Basal ganglia(3) Thalamus(4) Brain stem(5) Cerebellum

Subcortical white matter change

3. Subcortical white matter change

1) Definition of Binswanger’s disease (1894): pronounced atrophy of the white matter, either confined to one or more gyri of the brain or in several sections of the hemisphere : in the most severe cases the entire white matter of a cerebral lobe appears to have completely wasted away: a severe atheromatosis of the arteries of the brain is always present in these cases: extensive atrophic degeneration or fatty degen-eration of the small arterial and venous vessels : partial thickening of the inner and middle vascu-lar membranes: the lumen is correspondingly narrowed


: loss of density of the periventricular white matter observed by CT of the brain: the white matter changes commonly observed in the elderly by MRI of the brain

2) Definition of leukoaraiosis (Hachinski et al., 1987)

3. Subcortical white matter change3) Mechanisms hypothesized to be involved

in the pathogenesis of white matter change (ref. 14)

4) Small vessel changes related to white matter changes (ref. 14)


3. Subcortical white matter change5) Evolution of white matter lesions (ref. 16)

3. Subcortical white matter change6) Definition of ‘Periventricular’ and ‘Deep white

matter’ change (ref.5)(1) Periventricu-

lar- Start directly at the ventricular border


matter’ change (ref.5)

(2) Both periventricular and deep white mat-ter- If the periventricular abnormalities extend > 1 cm into the adjacent white matter

6) Definition of ‘Periventricular’ and ‘Deep white matter’ change (ref.5)


(3) Selective deep white matter lesion

- usually characterized by a rim of normal-appear-ing tissue which separates them from the periven-tricular region


matter’ change (ref.5)(4) Basal ganglia hypodensities on CT or hyperintensity

on MRI(M/82)

6) Definition of ‘Periventricular’ and ‘Deep white matter’ change (ref.24)



6) Definition of ‘Periventricular’ and ‘Deep white matter’ change – (1) (ref.5)(1) Periventricular hyperintensity

0 = absence 1 = “caps” or pencil-thin lining 2 = smooth “halo” 3 = irregular PVH extending into the deep white matter(2) Deep white matter hyperintense signal 0 = absence 1 = punctuate foci 2 = beginning confluence of foci 3 = large confluent areas

3. Subcortical white matter change7) Definition of ‘Periventricular’ and ‘Deep white mat-

ter’ –(3) (ref. 6)(1) White matter lesions 0 = no lesions (including symmetrical, well-defined caps or

bands) 1 = Focal lesions 2 = Beginning confluence of lesions 3 = Diffuse involvement of the entire region, with or without involvement of U fibers

(2) Basal ganglia lesions 0 = No lesions 1 = 1 focal lesion (≥ 5

mm) 2 = > 1 focal lesion 3 = Confluent lesions


ter’ –(3) (ref. 6)

1. Score of 1


ter’ –(3) (ref. 6)

2. Score of 2


ter’ –(3) (ref. 6)

3. Score of 3

1 = Focal lesions

(1) White matter le-sions


(1) White matter lesions 2 = Beginning confluence of

lesions


(1) White matter lesions 3 = Diffuse involvement of the entire

region, with or without involvement of U fibers

(M/75)


(1) White matter lesions 3 = Diffuse involvement of the entire region, with or without involvement of U

fibers

(M/60)


(2) Basal ganglia lesions 1 = 1 focal lesion (≥ 5

mm)


(2) Basal ganglia lesions 2 = > 1 focal lesion


(2) Basal ganglia lesions3 = Confluent lesions


Microb-leeds

4. Microb-leeds

1) Histopathologic and MRI definition

: paramagnetic material which produces local sus-ceptibility gradients and thereby causes a faster decay of transverse magnetization on gradient-echo acquisition (ref. 18): remnants of even minor blood leakage through damaged vessel walls

4. Microb-leeds

1) Histopathologic definition

: Postmortem gradient-echo-T2*-weighted MRI and histopathologic finding (ref. 19)

4. Microb-leeds

Figure 1. Grading of CAA severity in single brain samples (ref. 27) 0: No cerebral vessels showed immunoposi-tivity for beta amyloid1+: Amyloid is restricted to a rim around smooth muscle fibers in the media of occasional normal vessels2+: The media is thicker than normal and circumferentially replaced by amyloid in a few vessels 3+: Widespread medial thickening and circumferential amyloid deposition with a small halo of immunoreactivity in the surrounding parenchyma

: A focus of wall leakage as evidenced by fresh hemorrhage or hemosiderin-

laden macrophages, or occlusion, or

recanalization

2) Severity of amyloid angiopathy (ref. 27)

4. Microb-leeds3) MRI definition of microbleed (ref. 2, 19, 20,

21)(1) Homogeneous round signal loss lesion

with a diameter of up to 5 mm (or <10 mm)

on gradient echo image

(2)Distinct from a. Vascular flow voids on subarachnoid space b. Leptomeningeal hemasiderosis c. Non-hemorrhagic subcortical mineraliza-tion

• Non-hemorrhagic subcortical mineral-ization

(ref. 26)

• Non-hemorrhagic subcortical mineral-ization

(M/80)

• Leptomeningeal hemasiderosis

1. Superficial cortical hemosidersosis (ref. 25)


2. Subarachnoid hemosidersosis (ref. 25)


3. Schematic drawing illustrating subarachnoid hemosiderosis and superficial corical hemosidersosi (ref. 25)

4. Microb-leeds3) MRI definition of microbleed (ref. 20)

• In CAA Pt. • In CADASIL Pt.

• In H/T Pt.

4. Microb-leeds3) MRI definition of microbleed (ref. 21)

4. Microb-leeds

4) Degree of severity of microbleeds (ref. 2)

(1) Absent(2) Mild – total number of MBs, 1-5(3) Moderate – total number of MBs, 6-15(4) Severe – total number of MBs, >15

4. Microb-leeds

5) The locations of the microbleeds and lacunes (ref. 2)

(1) Cortico-subcortical(2) Basal ganglia(3) Thalamus(4) Brain stem(5) Cerebellum

Evaluation of the vessel stenosis

1) Significant stenosis - >50%2) No significant stenosis - <50%

Definition of coronary artery stenosis (ref. 8)

The degrees of stenoocclusive disease (ref. 7)

1) Normal – 0% - 29% diameter stenosis2) Mildly stenotic – 30% - 49%3) Moderately stenotic – 50% - 79%4) Severely stenotic – 80%- 99%5) Occluded

Regional location of stenosis (ref. 9)

: Schematic representation of 11 arterial segments studied by transcranial Doppler and duplex ultrasound

MCA – 1 and 2ACA – 3 and 4PCA – 5 and 6Siphon ICA – 7 and 8Extracranial ICA - 9 and 10Vertebrobasilar artery – 11

Measuement of vessel stenosis (ref. 10)

1. Equation for measuring intracranial arterial stenosis

: Percent stenosis = [(1-(Dstenosis/Dnormal))] x 100• Dstenosis: the diameter of the artery at the site of the most severe degree of stenosis• Dnormal: the diameter of the proximal normal artery


2. Criteria for normal proximal artery1) For the MCA, intracranial VA, and BA

(1) First choice- the diameter of the proximal part of the artery at its widest , non-tortuous, normal segment was chosen

(2) Second choice

- if the proximal artery was diseased -> the diameter of the distal portion of the artery at its widest, parallel


2. Criteria for normal proximal artery(3) Third choice

A. If the entire intracranial artery was dis-eased-> the most distal, parallel, non-tortous

normal segment of the feeding artery B. If the entire middle cerebral artery was dis-

eased-> measured at the most distal, parallel sege-ment of the supraaclinoid carotid arteryC. If the entire intracranial vertebral artery was dis-

eased -> measured at the most distal, parallel, non-tortous normal segment of the ex-tracranial vertebral artery


2. Criteria for normal proximal artery2) For the ICA

(1) First choice

: The precavernous, cavernous, and postcav-ernous stenoses of ICA-> measured at the widest, non-tortous, nor-

mal portion of the petrous carotid artery that had parallel margins


2. Criteria for normal proximal artery2) For the ICA

(2) Second choice

- If the entire petrous carotid was dis-eased-> the most distal, parallel part of the ex-

tracranial internal carotid artery was substituted- If tandem intracranial lesions were

present-> percent stenosis of both sites was mea-sured and the more severe stenosis was se-lected

- When a “gap sign” was present-- the lumen of the vessel could not be visu-alized at the site of severe stenosis-- could not be measured

-- defined as 99% luminal stenosis

1. Equation for measuring intracranial arterial stenosis


2. Equation for measuring extracranial arterial stenosis

Measuement of vessel stenosis

1) Severity of intracranial stenosis (ref. 11, 12)

(1) Mild - <30%(2) Moderate – 30% - 69%(3) Severe – 70% - 99% - in case of segmental signal void -> the stenosis was graded as severe (>70%)(4) Occluded

2. Equation for measuring extracranial arterial stenosis

Measuement of vessel stenosis

2) Measurement of the carotid artery stenosis (ref. 12)

(1) NASCET : (1-md/C)x100%(2) ECST : (1-md/B)x100%(3) CC : (1-md/A)x100%

Education

Subcortical lesion-classification-presentation-2011-10-10