Cerebral Infarcts . pptx

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 (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

4. 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)

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

6. 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)

7. 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

8. 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 .

9. 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 .

10. Insular ribbon sign Axial unenhanced CT image, obtained in a 73-year-old woman 2 1 / 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 .

11. Insular ribbon sign

12. 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

13. Sulcal effacement

14. 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

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

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

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

18. 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 lobe s.

19. 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

20. CT – sub acute infarct Subacute infarct involving the right Parieto -occipital regio n

21. 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 2 nd 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

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

23. 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).

24. 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

25. 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.

26. 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

27. MRI- chronic infarct Chronic infarct s 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.

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

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

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

31. 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

32. 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

33. 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

34. 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

35. Water shed infarct

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