A stroke occurs when blood supply to the brain is disrupted, either from a blockage (ischemic stroke) or bleeding (hemorrhagic stroke). Imaging plays an important role in the evaluation and management of acute stroke. Non-contrast CT is used initially to rule out hemorrhage. CT angiography can identify potentially treatable vessel occlusions. CT and MRI perfusion can identify irreversibly damaged tissue and the ischemic penumbra that may be salvaged with reperfusion. The ASPECTS score on CT assesses early ischemic changes and prognosis.

1. STROKE
By Dr.Nandini Dadhich
Guide-Dr.Anu mam

2. STROKE
• DEFINATION-A stroke, sometimes called as brain
attack, occurs when something blocks blood supply
to part of the brain or when a blood vessel in the
brain bursts.
• It is a neurological deficit of;
✓Sudden onset
✓With focal rather than global dysfunction
✓In which,after adequate investigations, symptoms
are presumed to be of non-traumatic vascular origin
✓And lasts for more than 24 hours

3. Two main
causes of
stroke-which
has to be rule
out through
imaging

4. Pathophysiology
• In cerebral ischemia, the affected tissue remains viable, although blood flow
is inadequate to sustain normal cellular function. In cerebral infarction, frank
cell death occurs with loss of neurons, glia, or both.
• The center of the affected brain parenchyma—the densely ischemic core—
typically has a CBF < 6-8 cm3 /100 g/min.
• A relatively less ischemic penumbra surrounding the central core is present
in ∼ 1/2 of all patients. CBF in the penumbra is significantly reduced, falling
from a normal of 60 cm3 /100 g/min to 10-20 cm3 /100 g/min.
• This ischemic but not-yet-doomed-to-infarct tissue represents physiologically
“at risk” but potentially salvageabletissue.

5. pathophysiology

6. In patients with acute ischemic stroke caused
by a proximal occlusion of an intracranial
artery, collateral blood flow is essential to
sustainthe viability of hypo perfused but
potentially salvageable tissue distal to the
occluded artery. The ischemic penumbra refers
to tissue at risk of infarction if reperfusion does
not occur in a timely manner. This
dysfunctional but salvageable tissue has been
the target of all reperfusion and
neuroprotection therapies. The cerebral
collateral circulation exists to protect the brain
againstischemia and sustainthe penumbra

7. Anatomy
of brain
blood
supply
• The circle of Willis (COW) has 10
components: Two internal carotid
arteries (ICAs), two proximal or
horizontal (A1) anterior cerebral
artery (ACA) segments, the anterior
communicating artery (ACoA), two
posterior communicating arteries
(PCoAs), the basilar artery (BA), and
two proximal or horizontal (P1)
segments of the posterior cerebral
arteries . The middle cerebral artery
(MCA) is not part of the circle of willis.

10. • Anterior circulation
• anterior choroidal artery
• anterior cerebral artery (ACA)
• medial lenticulostriatearteries
• middle cerebral artery (MCA)
• lateral lenticulostriatearteries
• posterior circulation
• posterior cerebral artery (PCA)
• posterior choroidal arteries
• basilar artery
• superior cerebellar artery (SCA)
• anterior inferior cerebellar artery (AICA)
• posterior inferior cerebellar artery (PICA)
• SEGMENTS OF ANTERIOR CEREBRAL ARTERY-

11. •originating fromthe terminal bifurcation of the ICA, extending ~14 mm in length
•terminates at the anterior communicating artery (ACom)
A1: horizontalor pre-
communicatingsegment
•originating at the ACom, extending anterior to the lamina terminalis and along the rostrumof
the corpus callosum
•terminates either at the genu of the corpus callosumor at the origin of the callosomarginal
artery
A2: vertical,post-
communicatingor
infracallosalsegment
•extends around the genu of the corpus callosumor distal to the origin of the callosomarginal
artery
•terminates where the artery turns directly posterior abovethe corpus callosum
A3: precallosalsegment
•abovethe body of the corpus callosumanterior to the plane of the coronalsuture
A4: supracallosalsegment
•abovethe body of the corpus callosumposterior to the plane of the coronalsuture
A5: postcallosalsegment

13. Branches-
• A1
• medial lenticulostriate arteries
• anterior communicating artery
• A2
• recurrent artery of Heubner (mayarise from distal A1 segment or
proximal A2 )
• orbitofrontal artery
• frontopolar artery
• A3
• pericallosal artery
• callosomarginal artery (runs in the cingulate sulcus)

14. MCA segments;
M1: sphenoidal or
horizontal segment
• originates at the terminal
bifurcation of the
internal carotid artery
• courses laterally parallel
to the sphenoid ridge
• terminates at one of two
points :
• at the genu adjacent to
the limen insulae
• at the main bifurcation
M2: insular segment
• originates at the
genu/limen insulae or
the main bifurcation
• courses
posterosuperiorly in
the insular cleft
• terminates at the circular
sulcus of insula, where it
makes a right angle to
hairpin turn
M3: opercular segment
• originates at the circular
sulcus of the insula
• courses laterally along
the
frontoparietal operculum
• terminates at the
external/superior surface
of the Sylvian fissure
M4: cortical segment
• originates at the
external/top surface of
the Sylvian fissure
• courses superiorly on the
lateral convexity
• terminates at their final
cortical territory

16. Posterior cerebral artery
• The two PCAs are the major terminal branches of the distal BA.
• The P1 segmentextends laterally from the BA bifurcation to the junction
with the PCoA. The P1 segment has perforating branches that course
posterosuperiorly in the interpeduncular fossa to enter the undersurface
of the midbrain.
• The P2 segmentextends from the P1-PCoA junction, running in the
ambient (perimesencephalic) cistern as it sweeps posterolaterally around
the midbrain.
• P3 (quadrigeminal)- is a short segmentthat lies entirely within the
quadrigeminal cistern. It begins behind the midbrain and ends where the
PCA enters the calcarine fissure of the occipital lobe.
• The P4 segment- terminates within the calcarine fissure, where it divides
into the terminal PCA trunks, including the calcarine artery.

17. • Imageshows circle of willis, basal
brain vessels in relationship to
cranial nerves. P1 , P2 , P3 PCA
segments are shown, as is the M1
(horizontal) MCA segment.

18. ACA territories
• Cortical ACA branches supply the anterior 2/3 of the medial
hemispheres and corpus callosum, the inferomedial surface
of the frontal lobe, and the anterior 2/3 of the cerebral
convexity adjacent to the interhemispheric fissure .
• Penetrating ACA branches (mainly the medial lenticulostriate
arteries) supply the medial basal ganglia, corpus callosum
genu, and anterior limb of the internal capsule.

19. • Cortical ACA territory (green)
includes the anterior 2/3 of the
medial surface of the hemisphere ,
• a thin strip of cortex over the top of
the hemisphere vertex , and a small
wedge along the inferomedial
frontal lobe .

20. MCA Territories
• The MCA has the largest vascular territory of any of the major cerebral
arteries.
• The MCA supplies most of the lateral surface of the cerebral hemisphere
with the exception of a thin strip at the vertex (supplied by the ACA) and
the occipital and posteroinferior parietal lobes (supplied by the PCA) .
• Its penetrating branches supply most of the lateral basal brain structures -
They supply the superior part of the head and the body of the caudate
nucleus, most of the globus pallidus and putamen.
They also supply the anterior limb of the internal capsule and parts of the
posterior limb of the internal capsule, which is largely supplied by
the anterior choroidal artery.

21. • Cortical MCA territory (red)
supplies mostof the lateral surface
of the hemisphere , the anterior tip
of the temporal lobe , and the
inferolateral frontal lobe .

22. PCA territories
• The PCA supplies most of the inferior surface of the cerebral
hemisphere with the exception of the temporal tip(by MCA)
and frontal lobe. It also supplies the occipital lobe, posterior
1/3 of the medial hemisphere and corpus callosum, and most
of the choroid plexus . Penetrating PCA branches are the major
vascular supply to the midbrain and posterior thalami.

23. • Cortical PCA territory (purple)
includes the occipital lobe and
posterior 1/3 of the medial and
the posterolateral surfaces of
the hemisphere , as well as
almost the entire inferior surface
of the temporal lobe .

24. STROKE
PHASES
1. Hyperacute –less than 24 hr
2. Acute- 24hr to 1 week
3. Subacute-1 week to 3 week
4. Chronic-more than 3 week

26. Goal of imaging
• The primary goals of emergent stroke imaging are
(1) to distinguish“bland” or ischemic stroke from intracranialhemorrhage.
(2) to select/triage patientsfor possible reperfusion therapies.
• The 3- to 4.5-hour time window for IV thrombolysis following onset of stroke
symptoms is derived from population studies.
• Collateralflow is the interveningfactor that determines how long the patient can
be asymptomaticbefore stroke evolves after occlusion.
• the collateralstatusbefore endovasculartreatment (EVT) is an important
determinantof functionaloutcome, and patientswith good collateralson
baseline neuroimagingmay also derive greater benefitfrom this treatment.

27. Role of imaging in acute stroke;
Exclude intracranial
hemorrhage and other
stroke mimics
1
Identify whether a major
cerebral vessel is occluded,
intracranial thrombusthat
can be treated with
thrombolysis or
thrombectomy
2
Identifythe presence and
size of irreversiblyinfarcted
tissue core.
3
Identify hypoperfusedtissue
at risk for infarction
if adequate perfusion is not
resorted
4

28. • For exclusion of intracranial hemorrhage NCCT is performed. If a
typical hypertensive hemorrhage is identified on the screening
NCCT and the patient has a history of systemic hypertension, no
further imaging is generally required.
• CTA can be obtained immediately following the NECT scan and is
the noninvasive procedure of choice for depicting potentially
treatable major vessel occlusions.
• The third and fourth points can be answered with either CT or
MR perfusion (pCT, pMR) studies. Both can depict what part of
the brain is irreversibly damaged (i.e., the unsalvageable core
infarct) and determine whether there is a clinically relevant
ischemic penumbra (potentially salvageable brain).

29. Ischemic
stroke
mimics
• Hemorrhage
✓Intraparenchymal
✓Subarachnoid
✓Subdural and extradural
• Tumour
• Demylination
• migrain

30. Modalities that are used for stroke imaging
• CT modalities;
✓NCCT
✓CT Angiography
✓CT perfusion imaging
• MR modalities;
✓DWI/ADC
✓T2/FLAIR
✓MR Angiography
✓MR perfusion imaging
✓T2 GRE
✓SWI

31. NCCT scan
• Computed tomography-Noncontract CT is the most widely
used first line imaging tool in patients with acute stroke and is
recommendedinitially to rule out hemorrhage.
• Initial NECT scans—even those obtained in the first 6 hours—
are abnormal in 50-60% of acute ischemic strokes if viewed
with narrow window width.

32. NCCT findings in early
ischemic stroke
• The most specific but least sensitive sign is a hyperdense vessel filled with
acute thrombus.
• Hyperdense Middle Cerebral Artery Sign;
➢Intravascular blood clot in M1 segment of MCA
➢Often associated with large infarct ,sever clinical course ,and poor response
to IV t-PA.
➢Clot length more than 8mm has little recanalization potential with IV tPA.

33. • NECT shows “hyperdense MCA”
sign (thrombus in the right MCA)
compared to the normal, mild
hyperdensity of the left MCA .

34. MCA dot sign
• Hyperdensity of small arteries in sylvian fissure,seen in cross
section
• Clot in M2 and M3 branch
• Stroke is less severe than Hyperdense Middle Cerebral
Artery Sign

35. NECT in acute
onset of right
hemiparesis
shows
hyperdense
thrombus in
the left M2
(“dot” sign)
and M3 MCA
branches.

36. INDISTINCT GM-WM
• Blurring and indistinct GM-WM interfaces can be seen in 50-
70% of cases within the first three hours following occlusion.
Loss of the insular cortex (“insular ribbon” sign)
• Decreased density of the basal ganglia (“disappearing basal
ganglia” sign) are the most common findings

37. INSULAR RIBBON SIGN-This refers to hypodensity and swelling of the insular cortex.
It is a very indicative and subtle early CT-sign of infarction in the territory of the middle cerebral artery.
This region is very sensitive to ischemia because it is the furthest from collateral flow.
It has to be differentiated from herpes encephalitis.

38. • Obscuration of the lentiform
nucleus, also called blurred basal
ganglia, is an important sign of
infarction.

39. HYPODENSITY
• Hypodensity correspondsto the territory of affected vessels
• Increased water in case of cytotoxic edema appears hypodense.
• Wedge-shaped parenchymal hypodensity with indistinct GM-WM
borders and cortical sulcal effacement develops in large territorial
occlusions.
• If > 1/3 of the MCA territory is initially involved, the likelihood of a
“malignant” MCA infarct with severe brain swelling rises, as does
the risk of hemorrhagic transformation with attempted
revascularization.

40. At 24 h, the wedge-shaped
infarction is sharply
delineated. ASPECTSscore of
3, has a poor prognosis.

41. • The Alberta Stroke Program Early Computed Tomographic Score
(ASPECTS) is a straightforward, quick, and reproducible measure of early
ischemic change.
• ASPECTS score is calculated by subtracting one point for each of 10
regions affected. ASPECT score ≤ 7 equates to > 1/3 of the MCA territory
and is associated with increased risk of hemorrhage and poor outcome.
• Any ischemic lesion on axial CT cuts at the level of the caudate head or
below that is at ganglionic ASPECTS region (M1M2M3, insula, caudate
nucleus, lentiform nucleus, internal capsule); ischemic lesions above the
level of the caudate head that is at suprganglionic ASPECTS region
(M4M5M6). The caudate nucleus is assessed in both the ganglionic level
(head of caudate) and supraganglionic level (body and tail of caudate).

42. A-Anatomic regions for calculating ASPECTS score are illustrated. M1-3 represent the MCA cortex with each area
allotted 1 point. The insular cortex (I), lentiform nuclei (L), caudate head (C), and internal capsule are scored with
1 point each.B-More cephalad graphic shows the superior 3 MCA territories. ASPECTS score is calculated by
subtracting 1 point for each affected area from 10 (normal total score).

43. NCCT
• Advantage-
➢Very useful in excluding hemorrhage.
➢Widely accessible
➢Convenient
➢Short imaging time
• Disadvantage-
➢Findings are subtle
➢Not useful for posterior circulation
➢Not useful for ischemic penumbra

44. CT angiography;
• Recommended in acute stroke patient when IA fibrinolysis or mechanical
thrombectomyis being considered. But it should not delay IV tPA.
• Informations that CTA Provide in Patients Presenting With Acute Ischemic
Stroke are-
➢Presence of Occlusion-Numerous angiographic studies have shown that a
proportion of patients with acute ischemic stroke have no identifiable
occlusion.
• imaging tool for detecting intracranial occlusions in patients presenting with
acute ischemic stroke, thereby guiding in therapy

45. ➢Extent of Thrombus;
• In addition to providing information on the presence of an occlusion, CTA also
helps in estimating the extent of occlusion in the arterial tree (the thrombus
burden).
• Recanalizationrates in patients with proximal occlusions are significantly lower
with IV tPA when compared to endovascular therapy.
• CTA can be used to assess the extent of thrombus in the arterial tree using a clot
burden score(CBS).
• Thrombus extent can also be quantitated by measuring the length of a thrombus
in the arterial tree.
• Residual flow through a thrombus is associated with less tissue damage in
coronary angiography and higher rates of arterial recanalization in strokes treated
with IV tPA.

46. A-here is example of the
dense middle cerebral artery
(MCA) sign (left image, arrow).
This sign suggests MCA
thrombosis, but is not specific
B-the CT angio image on the
right confirms that there is
complete occlusion of the left
MCA (arrow).

47. • leptomeningeal collaterals (LMCs) are responsible for preserving
blood flow distal to the site of occlusion in patients with acute
ischemic strokes.
• Computed tomography angiography provides a quick and reliable
method of assessment of LMCs.
• Hypoattenuation on CTA source image is an indicator of reduced
cerebral blood volume in the area of ischemia .
• Areas of hypoattenuation on CTA source image correlate well with
lesions on diffusion-weighted image (DWI) and aretherefore a
marker of core or irreversibly infarcted brain tissue at presentation.

48. CTA
Advantage
• Widely available
• 98% sensitive in detecting acute
proximal intracranial occlusion.
• 97% sensitive in detecting
extracranial communication
• Detects extracranial stenosis
also.
Disadvantage
• Iodinated contrast
• Radiation
• STREAK ARTIFECT-
• Atherosclerotic calcification
produce streak artifact and can
result in overestimation of
stenosis.
• Flow artifact

49. PERFUSION IMAGING;
• It can be performed immediately following NCCT and has advantages of
accessibility and speed.
• Differentiation of salvageable ischemic penumbra from unsalvageable core
infarct mayhelp identify patients most likely to benefit from thrombectomyor
thrombolysis
• All three pCT parameters can also be depicted either visually on a color scale.
The standard color scale is graduated from shades of red and yellow to blue
and violet. With CBV and CBF, perfusion is portrayed in red/yellow/green
(highest) to blue/purple/black (lowest). Well-perfused gray matter.
• Perfusion Patterns:
❑NORMAL PERFUSION-CTP measures brain tissue blood perfusion.
• CTP parameters that are commonly calculated by commercially available
postprocessing software platforms include CBF, CBV, and MTT.
• CBF, CBV, and MTT are related by the central volume principle:
CBF = CBV / MTT.

50. • CBV is measured in units of milliliters of blood per 100 g of brain and is
defined as the volume of flowing blood for a given volume of brain.
• MTT is measured in seconds and defined as the average amount of time it
takes blood to transit through the given volume of brain.
• CBF is measured in units of milliliters of blood per 100 g of brain tissue per
minute and is defined as the volume of flowing blood moving through a
given volume of brain in a specific amount of time.
• In normal perfusion, there is symmetric perfusion with higher CBF and CBV
in gray matter compared with white matter, reflecting the physiologic
hemodynamic differences between these tissues

51. ❑Core Infarct versus Penumbra perfusion-In the setting of acute infarction,
areas of irreversibly infarcted tissue show matched areas of decreased CBF
and CBV with increased MTT in perfusion maps.
• On the other hand, in the setting of penumbra, it is possible to have
regions of tissue that show decreased CBF with maintained CBV indicating
potentially salvageable tissue or penumbra.
• Such areas can also be characterized by prolonged MTT extending beyond
areas of core infarct in perfusion maps and have been called CBV/MTT
mismatch.
• as MTT has both infarcted core and penumbra as it is increased in both
but CBV gets decreased only in core as final amount of CBV is almost
normal in case of penumbra due to collaterals.

52. • CT perfusion images obtainedin a patient with acute ischemic
stroke demonstrate a large perfusion defect in the left MCA
distribution,with minimalCBV/MTT or CBF mismatch. A- CBF. B-
CBV, C- MTT. signifying there is infarctedcore as compared
too penumbra- as all the three affected area is overlapping.

53. .A 64-year-old man presenting with
headache and acute aphasia. A-On
admission, NCCT and CTP were
performed. NCCT shows no
evidence of acute infarction.
B-CT perfusion CBF map shows a
region of decreased perfusion
within the posterior segment of
the left MCA territory (arrows).
C- CBV map demonstrates no
abnormality. D-MTT map shows a
corresponding prolongation within
this same region (arrows).y,
therefore, representing a CBV/MTT
mismatch or ischemic penumbra.

54. CT PERFUSION
• AutomatedpCT calculation shows
volume with CBF < 30% (pink,
representing severely ischemic core
infarct) is 68 mL.
• Volume with Tmax > 6.0 seconds
(green) is 108 mL. The mismatch
volume is 40 mL and the mismatch
ratio is 1.6.

55. In early cerebral ischemia there is
1-autoregulation
2-vasodilatation
3-CBF-dec. MTT-inc. and CBV-Normal
•Later CBF and CBV both decrease and creates ischemic core.
•Between 15-20% of large MCA infarcts cause hypoperfusion with
reduced CBF in the contralateral cerebellum, a phenomenon
called crossed cerebellar diaschisis.

56. MRI
• Although CT/CTA/pCT is often preferred because of accessibility
and speed, “expedited” rapid stroke protocols with only fast FLAIR,
T2 GRE, DWI, and pMR can be used. MR is superior to CT in
detecting small ischemic and lacunar strokes.
• T1WI-T1WI is usually normal within the first 3-6 hours. Subtle gyral
swelling and hypointensity begin to develop within 12-24 hours
and are seen as blurring of the GM-WM interfaces.
• With large vessel occlusions, loss of the expected “flow void” in
the affected artery can sometimesbe identified.

57. DWI
• DWI and DTI- Around 95% of hyperacute infarcts show
diffusion restriction on DWI with hyperintensity on DWI and
corresponding hypointensity on ADC. DTI is even more
sensitive than DWI, especially for small pontine and
medullary lesions
• Time course of restricted diffusion
➢Appears within minutes after arterial occlusion
➢Peak at 1-4 days
➢Persist up to 2 weeks.

58. T2/FLAIR;
• Only 30-50%of acute strokes show cortical swelling and hyperintensity on
FLAIR scans within the first 4 hours.
• Nearly all strokes are FLAIR positive by 7 hours following symptom onset.
Intraarterial hyperintensity on FLAIR is an early sign of stroke and
indicates slow flow, either from delayed antegrade flow or—more
commonly—retrograde collateral filling across the cortical watershed.
• the presence of restricted diffusion on DWI-ADCwith negative findings at
FLAIR indicates stroke within first 6 hours and is been enough to initiate
treatment, it is known as DWI-FLAIR mismatch.
• High signal intensity is not usually seen at T2- weighted imaging until at
least 8 hours after the initial ischemic insult.

59. A-T1-showing subtle hypointensity in right MCA territory,B-T2showing hyperintensity-
FLAIR showing hyperintensity,D-DWI showing hyperintensity conforming the cytotoxic
edema in hyperacute infarct.

60. A-NCCT, The findings in this case are
very subtle in early stroke.
There is some hypodensityand
swelling in the left frontal region with
effacement of sulci compared with
the contralateralside.
• B- but DWI clearly showing
hyperintensity .
• This is why DWI is called 'the stroke
sequence'.

61. MRA
ADVANTAGE
No need for contrast
with 2D and 3D TOF
technique.
Comparable to CTA for
detection
of extracranial disease
DISADVANTAGE
• Less practical in emergency
settings
• Gadolinium needed for CE
MRA
• More hampered by artifacts
• Inferior sensitivity for
intracranial occlusion and
stenosis

62. • T2* GRE- Intraarterial thrombus can sometimes be detected
as “blooming” hypointensity on T2* (GRE, SWI).
• Gradient-echo and susceptibility-weightedsequences are the
most sensitive sequences for depicting hemorrhagic
transformation in patients with ischemic stroke.
• Hemorrhagic transformation is rare in the first 12 hours after
stroke onset (the hyperacute stage), particularly within the
first 6 hours. When it occurs, it is usually occurs within the
first 24–48 hours and, in almost all cases, is present 4–5 days
after stroke.

63. T2* GRE
shows “blooming” of
the right M1/proximal
M2 MCA thrombus .
Compare to normal
signal intensity in the
left MCA genu .

64. MR PERFUSION;
• 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.
• Maps of CBF are taken to assess mismatch with DWI
• Mismatch basically mean that DWI abnormality is smaller
than PWI abnormality (mis-match) which suggest presence of penumbra.
➢PWI abnormality=core + penumbra
➢DWI abnormality=core

65. • CBF reduction and MTT prolongation are more
sensitive indicator of potentially viable
tissue(penumbra)
• CBV reduction marker of infarct core as it
decreses only in infarcted tissue
• In patients with diffusion-perfusion mismatch,
infarct growth and final infarct size is smaller if
treated with t PA than those who are not.
• Different studies done concluded that CT
perfusion and DWI-PWI MRI are equivalent in
identification of penumbra and prediction of
infarct size.

66. • On the DWI there is a large area with restricted
diffusion in the territory of the right middle
cerebral artery.
Notice also the involvementof the basal
ganglia.
There is a perfect match with the perfusion
images showing infarctedtissue with no
salvageabletissue, so this patient should not
undergo any form of thrombolytic therapy.

67. • On the left we first have a diffusion
image indicatingthe area with
irreversible changes (dead tissue).
In the middle there is a large area with
hypoperfusion.
On the right the diffusion-perfusion
mismatch is indicatedin blue.
This is the tissue at risk.
This is the brain tissue that maybe can be
saved with therapy.

68. Pattern of mismatch;
• PW more than DW –ischemic penumbra
• PW equals to DW-infarct
• PW less than DW-early reperfusion

70. Angiography;
• Digitalsubstraction angiographyis done mainly when endovasculartheraphyis being
considered.
• Also done to evaluatethe carotids
✓ To look for degree of stenosis
✓ To look for tendom lesions(horizontal MCA,carotidsiphon).
✓ Evaluatecollateral circulation.
• Findingsinclude abrupt vessel “cut-off,” a “meniscus” sign, tapered or “rat-tail”narrowing,
or tram-track appearance(contrast aroundintraluminalthrombus).
• Others are “bare” or “naked” area(s) of nonperfused brain, slow antegrade fillingwith
intraarterialcontrastpersisting into the capillaryor venous phase, and pialcollateralswith
retrograde filling across the cortical watershed.
• Less common signs are hyperemia with a vascular“blush” aroundthe infarctedzone (so-
called “luxury perfusion”) and “early draining”veins.

71. A 55-year-oldwoman with a stroke. a DSA shows severe stenosis (about 90 %) in
the M1 portion of the right MCA, b The BES is positioned at the lesion, c DSA
shows excellent recanalizationof the diseased segment immediate post-
procedural, d- 36 months later, DSA shows a perfect result.

72. Role of Doppler
• CAROTID DOPPLER
➢ Systemic atherosclerosis and atherosclerosis of extracranial and intracranial arteries have
been identified as the major cause of ischemic stroke.
➢ Doppler imaging of the extracranial atherosclerosis is routinely performed to assess the
atherosclerotic burden
➢ One of the indications for extracranial carotid doppler ultrasound include hemispheric or
nonhemispheric neurologic symptoms.
➢The technique is built on the principle of the Doppler effect, with measurementof the
change in the frequency and wavelength of a sound wave transmitted and reflected by
moving red blood cells within the vessel, termed as Doppler frequency shift.Velocity is
calculated using the Doppler formula.This allows the determination of the speed and
direction of the flow.

73. • B-mode imaging evaluates the course and caliber of the vessel
with the evaluation of intimal-media thicknessand quality of
plaque.
• The morphology of plaque is associated with the severity of
atherosclerotic disease. The vulnerable plaques are more prone
to rupture and acute thrombosis. The plaque echogenicity,
surface characteristic (i.e., regular vs. irregular), and presence of
calcification should be assessed and reported.
• The degrees of stenosisderived above are expressed as
percentage as per North American SymptomaticCarotid
EndarterectomyTrial (NASCET) criteria.

74. • A-Homogenous plaque
• B-heterogenous plaque

75. A,B-. Near occlusion (95-99% stenosis) with
homogeneous plaque

76. TRANSCRANIAL DOPPLER
• Transcranial doppler is non-invasive,non-ionising,portable,safe
technique for the assessment of intracranial blood flow.
• The three main windows for accessing the intracranial arteries
1-Transtemporal window
2-Transorbital window
3-Transforaminal window

77. The three main
windows for
accessing the
intracranial arteries.

79. A typical transcranial Doppler
spectra with velocity and
intensity scale on the left and
right axis, respectively. The wave
above baseline reflects flow
towards the probe (normal
middle cerebral artery (MCA)
tracing at depth 50 mm—
transtemporal window).

81. • Flow chart shows an acute
stroke imaging protocol

82. Summary;
• ACUTE STROKE IMAGING
✓NECT - Hyperdense vessel ± “dot” sign •
✓“Blurred,” effaced GM-WM borders “Insular ribbon” sign “Disappearing”
basal ganglia
✓Wedge-shaped hypodensity Involves both cortex, WM
✓ Look for Ca ++ emboli (≈ 50% risk future stroke)
• CECT - ± enhancing vessels (slow flow, collaterals)
• CTA -
✓Shows site, length of major vessel thrombus
✓ASVD Extracranial: Aorta, carotid bifurcation
✓Intracranial: Cavernous ICA, circle of Willis + branches

83. PCT-
✓ Infarct core (irreversibly damaged brain) Matched perfusion (CBV, CBF
both ↓) ↑ MTT
✓Ischemic penumbra Perfusion “mismatch” (↓ CBF but normal CBV)
• MRI-
✓T1WI -Usually normal in first 4-6 hours • ± loss of expected “flow void”
✓ T2WI -Usually normal in first 4-6 hours FLAIR (use narrow windows) • 50%
positive in first 4-6 hours Cortical swelling, gyral hyperintensity Intraarterial
hyperintensity (usually slow flow, not thrombus).
✓T2* (GRE, SWI) • Thrombus may “bloom” • Large infarcts may show
prominent hypointense medullary veins • Microbleeds (chronic
hypertension, amyloid)

84. • DWI and DTI • > 95% restriction within minutes Hyperintense on DWI
Hypointense on ADC map
• • “Diffusion-negative” acute strokes- Small (lacunar) infarcts Brainstem
lesions Rapid clot lysis/recanalization Transient/fluctuating hypoperfusion
• pMR
• DWI-PWI “mismatch” estimates penumbra • CBV-CBF, DWI-FLAIR
mismatches estimate penumbra
• DSA -
• Vessel “cut-off,” “meniscus” sign, tapered/“rat-tail” narrowing • “Bare”
area of unperfused brain • Slow antegrade or retrograde filling • Delayed
intraarterial contrast washout • Luxury perfusion “Blush” around “bare
area”

85. Lacunar stroke;
• Small vessel disease represents 15-30%of all strokes. Small artery occlusions(lenticulostriate,
thalamoperforating, and pontine perforating arteries, recurrent artery of Heubner). , also called
lacunar infarcts, are defined as lesions measuring < 15 mm in diameter.
• Many are clinically silent, although a strategically located lesion (e.g., in the internal capsule) can
cause significant neurologic impairment.
• Lacunar infarcts can be embolic, atheromatous, or thrombotic. Most involve penetrating arteries
in the basal ganglia/thalami, internal capsule, pons, and deep cerebral white matter.
• These small infarcts are frequently not appreciable at computed tomography (CT) scan and can
even be missedat autopsy, whereas they are clearly evident at 1,5 Tesla magnetic resonance
imaging (MRI). In 80% of cases they lack clinical signs or symptoms and can easily be
misdiagnosed.

86. • This is explained because even the most modern CT devices cannot
visualize lacunae smaller than 2 mm in the internal capsule, or most
of those localized in the thalamus and brain stem, due to artefacts
caused by the posterior cranial fossa bones.
• In the acute setting on CT, lacunar infarcts appear as ill-defined
hypodensities.

87. • CT image showing
hypointensities,lacunar
stroke of left lentiform
nucleus.

88. A-T2 FLAIR image showing
periventricular white matter
hyperintensities,and small
cavited lacunae with peripheral
gliosis,B-enlrged perivascular
space,and lentiform
hyperintensities.C-DWI showing
capsular lacunar infarct.

89. Thank you