CEREBRAL INFARCTS Pathophysiology Significantly diminished blood supply to all parts(global ischemia) or selected areas(regional or focal ischemia) of the brain Focal ischemia- cerebral infarction Global ischemia-hypoxic ischemic encephalopathy(HIE), hypotensive cerebral infarction Infarct vs pneumbra In the central core of the infarct, the severity of hypoperfusion results in irreversible cellular damage Around this core, there is a region of decreased flow in which either: The critical flow threshold for cell death has not reached Or the duration of ischemia has been insufficient to cause irreversible damage. Current therapies attempt to rescue these ‘at risk’ cells Goal of imaging Exclude hemorrhage Identify the presence of an underlying structural lesion such as tumour , vascular malformation, subdural hematoma that can mimic stroke Identify stenosis or occlusion of major extra- and intracranial arteries Differentiate between irreversibly affected brain tissue and reversibly impaired tissue (dead tissue versus tissue at risk) Imaging modalities CT MRI Diffusion weighted imaging MRA MRS CT angiography CT perfusion imaging Perfusion-weighted MR Imaging Trans cranial doppler Cerebral angiography Classification Hyper acute infarct (<12 hours) Acute infarct (12 to 48 hours) Subacute infarct (2 to 14 days) Chronic infarct (>2 weeks) Old infarct (> 8 to 10 weeks) CT-Hyperacute infarct Normal in 50 – 60% Hyperdense MCA sign-acute intraluminal thrombus Obscuration of lentiform nulei Dot sign-occluded MCA branch in sylvian fissure Insular ribbon sign –grey white interface loss along the lateral insula Hyperdense MCA sign Obscuration of lentiform nuclei Insular ribbon sign Insular ribbon sign MRI –Hyperacute infarct Absence of normal flow void with intra vascular arterial enhancement Anatomic changes in T1WI Sulcal effacement, Gyral edema, Loss of grey white interface Sulcal effacement CT- Acute infarct Low density basal ganglia Sulcal effacement Wedge shaphed parenchymal hypo density area that involves both grey and white matter Increasing mass effect Hemorrhagic transformation may occur -15 to 45% ( basal ganglia and cortex common site) in 24 to 48 hours Sulcal effacement MRI –Acute infarct T2WI-hyperintensity in affected area Meningeal enhancement adjacent to infarct(12 to 24 hours) Early parenchymal enhancement Hemorrhagic transformation becomes evident MRI –Acute infarct MRI –Acute infarct CT – sub acute infarct NECT Wedge-shaped area of decreased attenuation involving gray/white matter in typical vascular distribution Mass effect initially increases, then begins to diminish by 7-10 days HT of initially ischemic infarction occurs in 15-20% of MCA occlusions, usually by 48-72 hrs CECT Enhancement patterns typically patchy or gyral May appear as early as 2-3 days after ictus, persisting up to 8-10 weeks

1. CEREBRAL INFARCTS

2. Pathophysiology
 Significantly diminished blood supply
to all parts(global ischemia) or
selected areas(regional or focal
ischemia) of the brain
 Focal ischemia- cerebral infarction
 Global ischemia-hypoxic ischemic
encephalopathy(HIE), hypotensive
cerebral infarction

3. Infarct vs pneumbra
 In the central core of the infarct, the severity
of hypoperfusion results in irreversible
cellular damage
 Around this core, there is a region of
decreased flow in which either:
◦ The critical flow threshold for cell death
has not reached
◦ Or the duration of ischemia has been
insufficient to cause irreversible damage.
 Current therapies attempt to rescue these
‘at risk’ cells

5. Goal of imaging
 Exclude hemorrhage
 Identify the presence of an underlying
structural lesion such as tumour , vascular
malformation, subdural hematoma that can
mimic stroke
 Identify stenosis or occlusion of major extra-
and intracranial arteries
 Differentiate between irreversibly affected
brain tissue and reversibly impaired tissue

6. Imaging modalities
 CT
 MRI
 Diffusion weighted imaging
 MRA
 MRS
 CT angiography
 CT perfusion imaging
 Perfusion-weighted MR Imaging
 Trans cranial doppler
 Cerebral angiography

7. Classification
 Hyper acute infarct (<12 hours)
 Acute infarct (12 to 48 hours)
 Subacute infarct (2 to 14 days)
 Chronic infarct (>2 weeks)
 Old infarct (> 8 to 10 weeks)

8. CT-Hyperacute infarct
 Normal in 50 – 60%
 Hyperdense MCA sign-acute
intraluminal thrombus
 Obscuration of lentiform nulei
 Dot sign-occluded MCA branch in
sylvian fissure
 Insular ribbon sign –grey white
interface loss along the lateral insula

9. Hyperdense MCA sign
Axial unenhanced CT
images in a proximal
segment of the left MCA in
a 53-year-old man
obtained 2 hours after the
onset of right hemiparesis
and aphasia, show areas
of hyperattenuation (arrow)
suggestive of intravascular
thrombi.

10. Obscuration of lentiform
nuclei
Axial unenhanced CT
image obtained in a 53-
year-old man shows
hypoattenuation and
obscuration of the left
lentiform nucleus
(arrows), which,
because of acute
ischemia in the
lenticulostriate
distribution, appears
abnormal in comparison
with the right lentiform
nucleus.

11. Insular ribbon sign
Axial unenhanced CT
image, obtained in a 73-
year-old woman 21/2
hours after the onset of
left hemiparesis, shows
hypoattenuation and
obscuration of the
posterior part of the right
lentiform nucleus (white
arrow) and a loss of gray
matter–white matter
definition in the lateral
margins of the right
insula (black arrows).
The latter feature is
known as the insular
ribbon sign.

12. Insular ribbon sign

13. MRI –Hyperacute infarct
 Absence of normal flow void with intra
vascular arterial enhancement
 Anatomic changes in T1WI
◦ Sulcal effacement,
◦ Gyral edema,
◦ Loss of grey white interface

14. Sulcal effacement

15. CT- Acute infarct
 Low density basal ganglia
 Sulcal effacement
 Wedge shaphed parenchymal hypo
density area that involves both grey
and white matter
 Increasing mass effect
 Hemorrhagic transformation may
occur -15 to 45% ( basal ganglia and
cortex common site) in 24 to 48 hours

16. Sulcal effacement
CT scans show subtle
hypoattenuation and sulcal
effacement in the right
MCA territory (arrows)

17. MRI –Acute infarct
 T2WI-hyperintensity in affected area
 Meningeal enhancement adjacent to
infarct(12 to 24 hours)
 Early parenchymal enhancement
 Hemorrhagic transformation becomes
evident

18. MRI –Acute infarct
Axial T2-weighted images
show areas with increased
signal intensity.

19. MRI –Acute infarct
Acute stroke of the
posterior circulation in a
77-year-old man.
Diffusion-weighted MR
image) shows bilateral
areas of increased
signal intensity (arrows)
in the thalami and
occipital lobes.

20. CT – sub acute infarct
 NECT
 Wedge-shaped area of decreased attenuation involving gray/white
matter in typical vascular distribution
 Mass effect initially increases, then begins to
diminish by 7-10 days
 HT of initially ischemic infarction occurs in 15-20% of MCA
occlusions, usually by 48-72 hrs
 CECT
 Enhancement patterns typically patchy or gyral
 May appear as early as 2-3 days after ictus, persisting up to 8-10
weeks
 "2-2-2" rule = enhancement begins at 2 days, peaks at 2 weeks,
disappears by 2 months

21. CT – sub acute infarct
Subacute infarct
involving the right
Parieto-occipital region

22. MRI –Sub acute infarct
 Intravascular and meningeal enhancement begin to diminish
TIWI- edema becomes prominent and appear hypointense with decreasing mass
effect
T1WI Contrast
 Intra vascular , meningeal enhancement disappear
 Striking parenchymal enhancement (patterns typically patchy or gyral)
 May appear as early as 2-3 days after ictus
 Can persist up to 8-10 weeks
 HT: Signal changes of evolving hemorrhage
T2WI
 Hyperintense edema with decreasing mass effect
 Fogging effect- in 2nd week sometime decrease in T2 hyper intensity due to
reduction in edema and leakage of protein from cell lysis
 Early Wallerian degeneration -well-defined hypointense band in corticospinal tract
 If HT occurs, signal changes of evolving hemorrhage are observed

23. MRI –Sub acute infarct
The MRI showing an area of
high signal within the left corona
radiata and body of the caudate
nucleus (arrow).

24. CT & MRI –Sub acute infarct
Subacute infarct appears as a hypodensity on a CT scan (Image A)
obtained within 5-6 hours of onset and as a region of hyperintensity on a
T2-weighted MRI (Image B), on a fluid-attenuated inversion recovery
(FLAIR) MRI (Image C), and on a diffusion-weighted MRI (Image D).

25. CT-chronic infarct
NECT
 Focal, well-delineated low-attenuation
areas in affected vascular distribution
 Adjacent sulci become prominent;
ipsilateral ventricle enlarges
 Dystrophic Ca++ may occur in
infarcted brain but is very rare
CECT
 No enhancement

26. CT-chronic infarct
Left PCA
territory
(medial
temporal,
occipital) and
MCA territory
(lateral
temporal)
infarcts caused
by two
separate
ischaemic
episodes both
well in the
past.

27. MRI- chronic infarct
TlWI
 Isointense to CSF in affected areas
 Adjacent sulci become prominent
 Ipsilateral ventricle enlarges
T2WI
 Isointense to CSF in affected areas
 Borders of infarction may show increased
signal secondary to gliosis
FLAIR
 Hyperintense gliotic white matter at margins
 Low signal in encephalomalacic area

28. MRI- chronic infarct
Chronic infarcts in a 71-year-
old man with a remote history
of multiple strokes. Diffusion-
weighted MR image shows
areas of decreased signal
intensity in the left frontal
lobe.

29. MRI- chronic infarct
ADC map shows
increased ADC values in
the white matter of the
right frontal lobe
suggestive of chronic
infarction.

30. CT and MR Angiogram
 Identifies occlusions, stenosis, status of
Collaterals

31. Cerebral Angiography
 Angiographic signs of acute infarction:
1. Vessel occlusion 45-50%.
2. Slow antegrade flow with delayed arterial
emptying 15%.
3. Collateral retrograde filling 15-25%.
4. Bare non-perfused areas 5-10%.
5. Vascular blush15-25 %.
6. AV shunting with early appearing draining vain10-
15 %.
7. Mass effect 25-50%

32. Lacunar infarction
 Small, deep cerebral infarcts typically
located in basalganglia (BG),
thalamus
 Multiple & due to embolic, thrombotic
or atheromatous lesions in long single
penetrating end arterioles
 Most not seen in CT
 Tl WI : Rounded or slit like lesions that
are hypointense to brain
 T2WI : Well delineated hyperintense
areas

33. Cerebral Arterial Territory
 MCA-most of lateral hemisphere,
anterior and lateral temporal lobe,Basal
ganglia, insula,
 ACA-Inferomedial basal
ganglia,ventromedial frontal lobes,
anterior 2/3rd medial cerebral
hemispheres, 1 cm supero medial brain
convexity
 PCA-Thalami, midbrain, posterior 1/3of
medial hemisphere, occipital lobe,
postero medial temporal lobe

35.  Anterior Choroidal artery
branch of ICA supply part of the
hippocampus, the posterior limb of the
internal capsule
 Medial lenticulostriate arteries
They supply the anterior inferior parts of the
basal nuclei and the anterior limb of the
internal capsule.
 Lateral lenticulostriate arteries
They supply the superior part of the head and
the body of the caudate nucleus, most of the
globus pallidus and putamen and the
posterior limb of the internal capsule

37.  AICA- lateroinferior part of pons, middle
cerebellar peduncle, floccular region, anterior
petrosal surface of cerebellar hemisphere
 PICA-inferoposterior surface of cerebellar
hemisphere adjacent to occipital bone,
ipsilateral part of inferior vermis, inferior
portion of deep white matter only
 Superior cerebellar artery-superior aspect
of cerebellar hemisphere (tentorial surface),
ipsilateral superior vermis, largest part of
deep white matter including dentate nucleus,
pons

39. Water shed infarct

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