MRI findings in CVA

1. CVA-MRI
OSR
Dr. Yash Kumar Achantani

2. Cerebrovascular accident aka "Stroke" is a generic term that
describes a clinical event characterized by sudden onset of a
neurologic deficit.
Arterial ischemia/infarction is by far the most common cause of
stroke, accounting for 80% of all cases.
The remaining 20% of strokes are mostly hemorrhagic, divided
between primary "spontaneous" intracranial hemorrhage (sICH),
nontraumatic subarachnoid hemorrhage (SAH), and venous
occlusions.

3. Arterial Infarcts

4. Acute Cerebral Ischemia-Infarction

5. Hyperacute stroke designates events within the first 6 hours.
Acute strokes are those 6-48 hours from onset.
Ischemic stroke is a heterogeneous disease with different etiologies and
several subtypes.
Stroke Subtypes : ASCO phenotypic system, which divides strokes
into four subtypes:
Atherosclerotic, (Most large artery territorial infarcts are embolic)
Small vessel disease, (lacunar infarcts, less than 15 mm in diameter,
embolic, atheromatous, or thrombotic)
Cardioembolic, (myocardial infarction, arrhythmia , and valvular heart
disease)
Other- Undetermined etiology ("cryptogenic stroke").

6. Imaging
The primary goals of emergent stroke imaging is to answer the
following questions.
1. +/- intracranial haemorrhage or stroke "mimic" (such as subdural
hematoma or neoplasm - NECT
2. Whether a major cerebral vessel is occluded- CTA/MRA
3. What part of the brain is irreversibly damaged- CT/MR Perfusion
4. Determine whether there is a clinically relevant ischemic penumbra
(potentially salvageable brain).

7. MR Findings.
T1WI- Normal within the first 3-6 hours.
Subtle gyral swelling and hypointensity seen as blurring of the GM-
WM interfaces within 12- 24 hours.
Loss of the expected "flow void“in the affected artery.
T2/FLAIR- 30-50% Show cortical swelling and hyperintensity on
FLAIR scans within the first 4 hours.
Nearly all strokes are FLAIR positive by 7 hours.
FLAIR-DWI "mismatch" (negative FLAIR, positive DWI) has been
suggested as a quick indicator of viable ischemic penumbra and
eligibility for thrombolysis.

8. T2* GRE- Intraarterial thrombus can sometimes be detected as "blooming"
hypointensity on T2* (GRE, SWI).
DWI and DTI- > 95% restriction within minutes
Hyperintense on DWI
Hypointense on ADC map.
DTI is even more sensitive than DWI, especially for pontine and medullary
lesions.
"Diffusion-negative" acute strokes
○ Small (lacunar) infarcts
○ Brainstem lesions
○ Rapid clot lysis/recanalization
○ Transient/fluctuating hypoperfusion

9. pMR- Restriction on DWI generally reflects the densely ischemic core of
the infarct, whereas pMR depicts the surrounding "at-risk" penumbra.
A DWI-PWI mismatch is one of the criteria used in determining
suitability for intraarterial thrombolysis.

10. Fast FLAIR shows left MCA cortical hyperintensity with intravascular
signal in the M3, M4 branches
DWI shows that restricted diffusion extends into the insular cortex and
external capsule with minimal involvement of the lateral putamen .

11. T2* GRE in the same case shows "blooming" thrombus in the left M1
segment and bifurcation.
pMR shows markedly reduced cerebral blood flow in the densely ischemic
core infarct, which appears smaller than the corresponding DWI and
FLAIR abnormality.

12. CBV is markedly reduced in the densely ischemic core infarct, but this
image shows a penumbra of well maintained CBV in the adjacent brain.
MTT shows the prolonged transit time in the large ischemic penumbra as
well as some islands of slowed but still-perfused brain within the core
infarct.

13. Acute stroke in a 47y man shows patchy hyperintensity in left caudate nucleus,
lateral putamen, and parietal cortex. Note multiple linear foci of intravascular
hyperintensity, consistent with slow flow in the MCA distribution.
T2* GRE shows several linear hypointensities in the affected MCA branches,
consistent with haemoglobin deoxygenation caused by slow, stagnating arterial
blood flow.

14. DWI in the same patient shows multiple patchy foci of diffusion restriction
ſt, consistent with acute cerebral infarct.
Axial source image from 2D TOF MRA shows normal signal intensity in the
right MCA and both ACA branches but no flow in the left MCA vessels.

15. Axial and Coronal T1 C+ FS scan shows intravascular enhancement in the
left MCA branches, consistent with slow flow in patent (nonthrombosed)
vessels.

16. Subacute Cerebral Infarcts

17. Refers to strokes that are between 48 hours and 2 weeks following the
initial ischemic event.
Haemorrhagic transformation (HT) of a previously ischemic infarct
occurs in 20-25% of cases between 2 days and a week after ictus.
HT is actually related to favourable outcome, probably reflecting early
vessel recanalization and better tissue reperfusion.
Early subacute strokes have significant mass effect and often exhibit
HT, whereas edema and mass effect have mostly subsided by the late
subacute period.

18. MR Findings
Signal intensity in subacute stroke varies depending on
(1)Time since ictus and
(2) The presence or absence of hemorrhagic transformation.
T1WI- Nonhemorrhagic subacute infarcts are hypointense on T1WI
and demonstrate moderate mass effect with sulcal effacement.
Strokes with HT are initially isointense with cortex and then become
hyperintense.

19. T2WI- Initially hyperintense
Isointense at 1-2 weeks (the T2 "fogging effect") .
FLAIR- Hyperintense on FLAIR .
By 1 week after ictus, "final" infarct volume corresponds to the FLAIR-
defined abnormality.
T2*
"Blooming" HT
Prominent medullary veins
DWI - Restricted diffusion with hyperintensity on DWI and hypointensity
on ADC persists for the first several days following stroke onset, then
gradually reverses to become hypointense on DWI and hyperintense with
T2 "shine-through" on ADC.

20. FLAIR and GRE in the same case
show hemorrhagic transformation in
this example of subacute stroke.
MR 2 weeks after right MCA stroke
shows HT and the intense
enhancement characteristic of
subacute infarction.

21. T2 "fogging effect" 2 weeks
after stroke.
T2WI appears normal.
T1 C+ FS shows patchy
enhancement ſt in PCA infarct.
Subacute infarct with ring
enhancement mimics
neoplasm.
pMR shows "cold" lesion with
profoundly decreased rCBV.

22. Chronic Cerebral Infarcts

23. End result of ischemic territorial strokes and are also called postinfarction
encephalomalacia.
The pathologic hallmark of chronic cerebral infarcts is volume loss with
gliosis in an anatomic vascular distribution.
MR scans show cystic encephalomalacia with CSF-equivalent signal
intensity on all sequences.
Marginal gliosis or spongiosis around the old cavitated stroke is
hyperintense on FLAIR.
DWI shows increased diffusivity (hyperintense on ADC).

24. FLAIR shows hyperintensity ſt around the cavitated,
encephalomalacic area, whereas T2* GRE shows some
HT.

25. Multiple Embolic Infarcts
Cardiac and Atheromatous Emboli
• Small, simultaneous, multiple lesions
• Bilateral, multiple vascular distributions
• Typically involve cortex, GM-WM interfaces
• May be Ca++
• ± Punctate/ring enhancement
• Usually not haemorrhagic unless septic

26. A 70y man with decreasing cognitive function for one month
became acutely worse.
Emergent MR with axial FLAIR shows multifocal bilateral
cortical and basal ganglionic hyperintensities.

27. T2* GRE shows some of the cortical lesions exhibit blooming,
consistent with petechial hemorrhages.
DWI shows restricted diffusion in the lesions. Multiple septic and
hemorrhagic embolic infarcts are seen.

28. Fat Emboli
• 12-72 h after long bone trauma, surgery
• Less commonly from bone marrow necrosis (e.g., sickle cell crisis)
• Arteriolar/capillary fat emboli
• Cause multiple tiny microbleeds
• Multiple foci of restricted diffusion in "star field" pattern (bright
spots on dark background)
• Microbleeds best seen on T2* SWI > > GRE
• Deep WM > cortex

29. Axial FLAIR scan in a
62y woman with altered
mental status following
hip surgery shows
multiple confluent
hyperintense foci in
the deep white matter of
both hemispheres.

30. DWI in the same case shows innumerable tiny foci of diffusion restriction
in the deep cerebral white matter, the so-called "star field“ pattern
characteristic of cerebral fat embolism syndrome.
T2* SWI in the same case shows literally thousands of tiny blooming
hypointense foci throughout the hemispheric WM characteristic of
microbleeds secondary to cerebral fat embolism syndrome.

31. Cerebral Gas Embolism
• Usually iatrogenic (procedural) or traumatic
• Can occur with hydrogen peroxide ingestion
• NECT may show transient round or curvilinear air densities in sulcal
vessels
• Quickly absorbed, disappear
• If massive, lethal brain swelling ensues rapidly.

32. 55y woman experienced left hemiparesis after esophageal dilatation.
Axial NECT of cerebral gas embolism shows multiple "dots" of air in the brain.
FLAIR shows a much more extensive area of diffuse cortical/subcortical WM
hyperintensity.
DWI shows restricted diffusion ſt in the cortex.
T1 C+ shows extensive patchy, linear enhancement in the cortex and subcortical
WM.

33. Lacunar Infarcts
Lacunae are 3- to 15-mm CSF-filled cavities or "holes" that most often
occur in the basal ganglia or cerebral white matter.
They are subclinical strokes. Lacunae are sometimes called "silent"
strokes, a misnomer as subtle neuropsychologic impairment is common
in these patients.
There are two major vascular pathologies involving small penetrating
arteries and arterioles:
(1)Thickening of the arterial media by lipohyalinosis, fibrinoid
necrosis, and atherosclerosis causing luminal narrowing and
(2) Obstruction of penetrating arteries at their origin by large intimal
plaques in the parent arteries.

34. Most common in the basal ganglia (putamen, globus pallidus, caudate
nucleus), thalami, internal capsule, deep cerebral white matter, and pons.
A single subclinical stroke—often a lacuna—is associated with increased
likelihood of having additional "little strokes" as well as developing overt
clinical stroke and/or
dementia.
Acute Lacunar Infarcts- Mostly invisible on NECT
Hyperintense on T2/FLAIR and may be difficult to distinguish from foci of
coexisting chronic microvascular disease.
Acute and early subacute lacunae restrict on DWI and also usually enhance
on T1 C+.
DWI overestimates the eventual size of lacunar infarcts.
Cavitation and lesion shrinkage are seen in more than 95% of deep
symptomatic lacunar infarcts on follow-up imaging.

35. Chronic Lacunar Infarcts-
Hypointense on T1WI and hyperintense on T2WI.
The fluid in the cavity suppresses on FLAIR, whereas the gliotic periphery
remains hyperintense.
Most lacunae are nonhemorrhagic and do not "bloom" on T2* sequences.
However, parenchymal microbleeds—multifocal "blooming black dots" on
T2* (GRE, SWI)—are common comorbidities.

36. Axial T2WI shows multiple bilateral rounded and irregular hyperintensities in the
basal ganglia and deep cerebral white matter.
FLAIR MR (same case) shows multiple hyperintensities in both hemispheres. Some
small subcortical lesions are also present.
Some lesions demonstrate acute restriction. DWI is helpful in distinguishing acute
from chronic lacunar infarcts.

37. Watershed ("Border Zone") Infarcts
Watershed (WS) infarcts, also known as "border zone" infarcts, are
ischemic
lesions that occur in the junction between two nonanastomosing distal
arterial distributions.
Two distinct types of vascular border zones are recognized:
External (cortical) WS zone-The two major external WS zones lie in
the frontal cortex (between the ACA and MCA) and parietooccipital
cortex (between the MCA and PCA).
Internal (deep) WS zone- Represent the junctions between penetrating
branches (e.g., lenticulostriate arteries, medullary white matter
perforating arteries, and anterior choroidal branches) and the major
cerebral vessels (MCA , ACA, and PCA).

38. Etiology
○ Emboli (cortical more common)
○ Regional hypoperfusion (deep WM common)
○ Global hypoperfusion (all 3 cortical WS zones)
Imaging
• External: wedge or gyriform
• Internal: rosary-like line of WMHs

39. T1-weighted images
show two vascular watershed
(WS) zones.
Wedge-shaped areas between
the ACAs, MCAs, and PCAs
represent "border zones"
between the three major
terminal vascular distributions.
Curved blue lines (lower right)
represent subcortical WS.
The triple "border zones"
represent confluence of all
three major vessels.
Yellow lines indicate
the internal (deep WM) WS
zone between perforating
arteries and major territorial
vessels.

40. Axial FLAIR in a 69y woman with TIAs shows hyperintensities in the deep
WM adjacent to the right lateral ventricle.
More cephalad FLAIR in the same case shows bilateral WM hyperintensities
lined up from front to back just above the level of the lateral ventricles.

41. Axial FLAIR scan demonstrates
typical findings of bilateral external
(cortical) watershed
infarcts ſt.
DWI shows multiple cortical
punctate, gyriform foci of
restricted diffusion, hypotension
with transient global
hypoperfusion.

42. Thank You