Stroke is a suuden onset neurologic deficit. Imaging plays an important role in early diagnosis and timely treatment.

1. IMAGING IN ISCHEMIC STROKE
DR. NAVNI GARG

2. Definition
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 >24 hours

3. Functional loss of cell
Reduced blood flow
Autoregulation
CYTOTOXIC EDEMA,
CELL DEATH
Increased water content
VASOGENIC EDEMA
MASS EFFECT
GLIOSIS
MINUTES
12-24 hrs
24hrs-2wks
PATHOPHYSIOLOGY

4. Role of imaging in ischemic stroke
 To rule out mimics esp hemorrhage
 To suggest the therapeutic role
 To establish the etiology

5. Ischemic stroke mimics
 Hemorrhage
Intraparenchymal
Subarachnoid
Extra, Subdural
 Tumor
 Demyelination disorders
 Migraine

6. Stroke – Temporal phases
 Hyperacute - < 12hrs
 Acute-12hrs- 2days
 Subacute- 2days to two weeks
 Chronic- > 2wks
Radiol Clin N Am 44 (2006) 41–62

7. NCCT in stroke
 Very sensitive in detecting hemorrhage
 Other mimics ruled out-
ISCHEMIA SUSPECTED

8. Early CT findings
A) Hypoattenuating grey matter structures
B) Presence of one or more hyperattenuating
arteries
C)Early Mass effect

9. Obscuration of lentiform
nucleus
 Proximal MCA occlusion
Lenticulostriate Perforator
arteries

10. Insular ribbon sign
 Hypoattenuation of insular cortex

11. NCCT in acute stroke
 OTHER EARLY SIGNS
Loss of grey white matter differentiation
Early mass effect-
Narrowing of sylvian fissure
Loss of cortical sulci

12. Hyperdense MCA sign
 MCA occluded by fresh thrombus
 -specificity- 100%, sensitivity -30%
 Hyperdense MCA can also be seen
ONLY REVERSIBLE EARLY SIGN
high hematocrit
level
 calcification
in such cases –
usually bilateral

13. Hyperdense artery sign
 Hyperedense basilar artery sign
 MCA dash sign

14. NCCT
 Importance of window settings
Normal settings- w80 HU, C- 20HU
W- 8HU- C-32 HU SENSITIVITY
INCREASED

15. NCCT
 Advantages
very useful to exclude hemorrhage
widely accessible
convenient
short imaging time
 Disadvantages
findings are subtle
not useful for ischemic penumbra
Not useful for posterior fossa infarcts

16. Conventional MRI
 Can image only vasogenic edema, necrosis
 T1, T2 , FLAIR, GRE/susceptibility weighted
 FLAIR- detection of infarctions in
periventricular and cortical regions,
brainstem
 GRE/susceptibility weighted- for detection of
hemorrhage( IN INFARCTION)

17. Conventional MRI in acute
stroke
 Hyperacute phase-
loss of grey white matter
differentiation,
loss of flow voids
sulcal effacement
mass effect
 Acute infarct
lesion in arterial
distribution(Hypo-T1, Hyper –
T2)

18. Conventional MRI in stroke
 Chronic – secondary signs-
Wallerian degeneration
Cortical atrophy
Negative mass effect
T1 T2 FLAIR
Sub acute Iso or
Chronic

19. Post contrast techniques
 Immediate
Stagnation of contrast in vessels
 Acute- Meningeal enhancement adjacent to
infarct
 Subacute -Gyriform enhancement
 Intravascular, Meningeal enhancement
decrease by 1 wk

20. Conventional MR imaging
Hyperacute infarct Subacute infarct

21. DW- principles
 Use of STRONG GRADIENT PULSES
SENSITIVE TO MOLECULAR MOTION in long
TR( T2 weighted)
 Tissues with higher diffusion show greater
signal loss
 To reduce motion artifacts scan time is reduced
by EPI in place of conventional SE
( EPI is fast imaging technique)
 Less diffusion- bright –
diffusion restriction

22. DWI-b value
 DWI quality-
 B valueα Diffusion weighting
 B value range from 0- 1500
 Optimum b value is 1000
T2 Vs diffusion properties

23. DWI- stroke
 Hyperacute stroke- Cytotoxic edema
 Lesion appears bright

24. Temporal sensitivity
Spacial sensitivity
After 55 min
After 5 hrs

25. DWI- ADC value
 Quantitative measurement of diffusion
property
 Varies with time
Nadir 4-5 days
Pseudonormalization-1-4wks

26. DWI- stroke
persistent brightness – T2
shine through
DWI ADC
Subacute Moderately bright Towards normal
Chronic Mildly bright increased

27. DWI importance
 DWI- 100% sensitivity within minutes
 Most sensitive technique of all for hyperacute
stroke
 Essential part of MR evaluation of penumbra
 Useful in detecting new hyperacute , acute
lesions among the chronic lesions –
therapeutic significance

28. False positive Diffusion
 Causes of diffusion brightness
Cerebral abscess
Tumor
 DWI+ conventional MRI useful
False negative
small lacunar brainstem infarction
deep gray nuclei infarction

30. CEREBRAL INFARCTION (80%)CEREBRAL INFARCTION (80%)
PERCENT(%)
LARGEVESSEL OCCLUSION (ICA, MCA,PCA) 40-50
LACUNAR INFARCTS 25
CARDIAC EMBOLI 15
BLOOD DISORDER,VASCULITIS 10
<
PRIMARY INTRACRANIAL HEMORRHAGE (20%)
NONTRAUMATIC SAH 5%

31. Types of infarcts
 Large artery occlusions
 Lacunar infarcts
 Watershed infarcts
 Embolic infarcts
 Venous infarcts

33. Territorial blood supply

36. Rt MCA infarct

37. Territorial blood
supply

38. Lt PCA I territory

39. Rt PICA
infarct

40. SCA infarct

41. Lacunar infarcts
 Upto 1.5 cm in size
 Occlusion of perforating arteries
 Deep grey matter , deep white
matter,brainstem
 Multiple
 MR is useful to differentiate from VRS,focal
areas of gliosis

42. Lacunar infarcts
VRS

43. Lacunar infarct Virchow Robin
Spaces
Location Ant. To ant. comm
Size 1.5 cm 2 mm
DWI bright dark
FLAIR Peripheral
hyperintense
suppressed

44. Watershed infarcts
 Junction of large arterial territories
 Chronic large vessel stenosis precipitated by
hypotension
 DWI , PW helpful in etiology
MORE COMMONLY HEMORRHAGIC
EARLIER ENHANCEMENT

45. WATERSHED INFARCTS

46. Embolic infarcts

47. Venous infarction
 Common-SSS
 Less common- ICV
 Causes
Dural sinus thrombosis
Cortical venous thrombosis
Deep venous thrombosis
Pregnancy,Post partum
Dehydration
Infection
OC pills
Hypercoaguble states

48. Venous infarction
 Clinical presentation may not very suggestive
& underdiagnosed
 Findings
Vascular Parenchymal
MRV
CTV
Axial MRI
DSA
MRI
CT

49. Vascular findings
 NCCT- Hyperdense thrombus
Cord sign
 CECT-
Empty Delta sign

50. MRI findings
 Axial images-Dural sinus
Early acute-Isointense sinus(T1)
Late acute- Hyperintense(T1)
Subacute- Hyperintense (T1,T2)
Cord sign- Hyperintense cortical veins

51. Venous infarction
 Parenchymal findings
Edematous infarcts
Hemorrhagic infarcts
Site-
Grey white matter junction,
White matter,
No typical territorial distribution

54. Transcranial doppler USG
 TCD
2 MHz ,pulsed range gated device
Low band width, large less defined volume
 TCCS
B mode+Frequency based color coding
1.8to 3.6 MHz
Rapid reliable vessel identification
Can also image parenchyma

55. Transcranial doppler USG-
M1 and M2 of MCA
C1 of ICA
A1 of ACA
P1 and P2 of PCA
Vertebral arteries
Basilar artery
Temporal approach Suboccipital approach

57. Transcranial doppler USG
 Indications
Intracranial stenosis or occlusion
Secondary effects of extra cranial occlusion
Monitoring of vessel recanalization in stroke
Detection of microemboli
 Accuracy and pitfalls
sensitive and specific if stenosis > 50%
Accurate in detecting M1 lesions
Poor window in 10% - 20% of patients

58. Conventional angiography-
Indications
 DSA IS USUALLY PERFORMED ONLYDSA IS USUALLY PERFORMED ONLY
WHEN ENDOVASCULAR THERAPY ISWHEN ENDOVASCULAR THERAPY IS
BEING CONSIDEREDBEING CONSIDERED
evaluation of carotidsevaluation of carotids
 To determine degree of stenosis
 To look for tandem lesions( carotid siphon,
horizontal MCA)
 Evaluate collateral circulation

60. Conventional angiography-
acute infarcts
 Vessel occlusion- most specific
 Slow antegrade flow
 Retrograde filling
 Bare areas
 Mass effect
 Vascular blush

61. Conventional angiography-
Images

62. CTA
 Fast, thin section,volumetric spiral CT
examination performed with a time-
optimized bolus of contrast material for the
opacification of vessels.

63. CTA- data aquisition
Coverage Aortic arch to circle of Willis
Scanning parameters 120 kV, 260 mAs
Scanning delay Dependent on ROI placed
(empiric delay of 25 sec)
Contrast medium dose 100–120 mL 3–4 mL/sec
Section thickness 2.5 mm
Section reconstruction 1.25 mm

64. CTA- Source images
 Occlusion ,stenosis or
significant calcification
of an Extracranial
internal carotid artery
 Detection of hyperacute
infarct
 Substraction perfusion

66. CTA- post processing
techniques
 MIP
 single layer of the
brightest voxels in a
given plane
 Attenuation
information preserved,
 Depth information is
completely lost
 SSD
 first layer of voxels
within defined
thresholds
 Depth information is
preserved
 Attenuation information
is lost.
 Arteries vary in caliber
depending on the
thresholds selected

67. CTA- adv
 Volume rendering.
 Groups of voxels within defined attenuation
thresholds are selected,and a color as well as
an “opacity” is assigned

68. MIP
SSD
VRT
Basilar artery
calcifications

69. CTA- comparison
 Degree of stenosis- Axial, VR images
 Calcification- axial, MIP
 Anatomical, spacial relationship-axial, VRT

70. MR ANGIOGRAPHYMR ANGIOGRAPHY
TYPESTYPES
Non–CE MRANon–CE MRA CE MRACE MRA
TOF PCTOF PC
2D2D 3D 2D3D 2D 3D3D

71. MRA - techniques
 TOF techniques
use of gradient pulses with TRshorter than
background tissue– Flow related
enhancement of inflowing nuclei
 2D technique- individual slices
useful in slow flow states
 3D techniques-A volume of slab
useful in high flow states
Better spacial resolution

72. PROTOCOL 3D TOF
 TR 39ms
 TE 7ms
 FLIP ANGLE 25
 FOV 200mm
 SLAB THICKNESS 32mm
 MATRIX 512
 NO OF ACQ 1
 ORIENTATION TRANSVERSE
ADVANTAGESADVANTAGES
 BETTER SPATIAL RESOLUTION AND VESSEL CONTRAST
 QUICKER ACQUISITION

73. CE MRA
RAPID 3D GRADIENT ECHO (GRE) SEQUENCE FIRST PASS MRA USING A
SELECTIVELY LARGE BOLUS OF GADOLINIUM BASED CONTRAST.
ADVANTAGESADVANTAGES ::
 NOT SUSCEPTIBLE TO SIGNAL LOSS FROM TURBULENCE OR SLOW FLOW
COMPARED WITH TOF OR PC TECHNIQUE
 ALLOWS BETTER VESSEL TO BACKGROUND CONTRAST COMPARED WITH
TOF /PC
 SHORTER IMAGING TIME
 LESS SUSCEPTIBLE TO MOTION ARTIFACTS
 ALLOWS IDENTIFICATION OF SLOW FLOW IN NEARLY OCCLUDED VESSEL
 ALLOWS MORE ACCURATE ASSESSMENT OF STENOSIS & VISUALIZATION
OF ULCERATED PLAGUE

74. Evaluation of etiology

75. Ischemic penumbra
 Functionally impaired, morphologically intact
 Between thresholds of electrophysiological
dysfunction and tissue damage

76. Normal blood flow
parametres
Tissue CBF(ML/100g/mn)
Normal 50-60
Oligaemic 35
Penumbra( salvagable) 2o
Infarct <10

77. Imaging - ischemic penumbra
 Functional studies
Xenon CT
SPECT
PET
CT perfusion
MR perfusion

78. CT perfusion principles
CBF
CBV
MTT
TTP

79. CT- perfusion parameters
 CEREBRAL BLOOD VOLUME the volume of blood
per unit of brain tissue
 CEREBRAL BLOOD FLOW the volume of blood
flow per unitof brain tissue per minute
 MEAN TRANSIT TIME, the time difference
between the arterial inflow and venous
outflow
 TIME TO PEAK ENHANCEMENT the time from the
beginning of contrast material injection to
peak enhancement

80. CT perfusion - principles
 Early cerebral ischemia
 Later, CBV and CBF both decrease
Central volume principle
CBF= CBV/ MTT

81. CT perfusion – Data aquisition
 Coverage-- Four sections( of 5 mm thickness) chosen by the radiologist
( Depending on clinical presentation)
 LEVEL OF BASAL GANGLIA IS CHOSEN- ALL ARTERIAL TERRITORIES
REPRESENTED
Scanning
parameters
80 kV, 105 mAs
Section thickness
5 mm
Scanning delay
5 sec
Scanning duration
50sec
Contrast medium
Dose
50 mL rate of4–5
mL/sec

82. CT- perfusion –post
processing
 A total of 200 images are taken for post
processing( 50x 4)
 Two algorithms – Deconvolution technique
maximum slope method
 Time attenuation curves obtained from an
individual voxel and compared with
Artery( one of the ACA or MCA)
Vein (SSS)

83.  CBF calculated by central volume principle
ROI over artery ROI over vein
MTT is calculated
CBV calculated
ROI over parenchyma

84. CT perfusion - Interpretation

85. CT perfusion - Interpretation
M TT CBF CBV
Arterial stenosis normal normal
Oligaemia
(>60%)
near normal
Penumbra
(>30%) (<80%)
Infarct
(<30%) (<40%)

86. ACCORDING TO A STUDY AT PGI
CBF CBV MTT
Infarct o.19 0.49 3.15
Noninfarct
ischemic
0.58 1.18 2.5
Thresholds for salvagable tissue- CBF>0.37,CBV>0.83

87. CBV CBF
CBF-CBV= Penumbra

88. CBV CBF MTT
INFARCT WITH SALVAGABLE PENUMBRA

89. MTT CBF CBV
COMPLETED infarct

90. ISCHEMIC CORE
CT PERFUSION
CBF 30%
CBV 54%

91. PENUMBRA-
CT
PERFUSION
CBF 45%
CBV 67%

92. MR perfusion-Types
 Dynamic susceptibility contrast imaging
 Arterial spin labeling technique

93. MR perfusion –principles
First pass study
Change in SI in every voxel
is studied
The passage of an intravascular
MR contrast agent
transient loss of signal
( T2* effects)

94. MR perfusion interpretation
Parameters
CBF
CBV
MTT
Interpretation by Deconvolution
technique same as in CT perfusion
Maps of CBF are taken to assess mismatch
with DWI

95. DWI- perfusion mismatch

96. Patterns of mismatch
PW> DW Ischemic penumbra
PW=DW Infarct
PW<DW Early reperfusion

97. ASL method
 Alternative and emerging noninvasive method
 Water molecules in arterial blood -magnetically labelled
 Pair-wise comparison -Repeated measurements of
interleaved label and control acquisitions -
Control Labelled

98. ASL method
 Absolute CBF can be quantified
 No contrast agent
Disadvantages
 Relatively small labeling effect (<1% raw
signal). Low signal to noise ratio
 Very sensitive to transit effects

99. Ischemic penumbra - comparison
CT MR
Availability Good Fair
Examination time 5 min 15 min
Imaging volume 2-4 cms Entire brain
Contrast Iodine Gadolinium
Radiation present No
Parameter Mismatch- CBF,
CBV
DW- perfusion
mismatching

100. Comparison
 MODALITY SENSITIVITYMODALITY SENSITIVITY
SPECIFICITYSPECIFICITY
 CT PERFUSIONCT PERFUSION 88-95 98-100
(AJNR 2000)(AJNR 2000)
 MR PERFUSIONMR PERFUSION 74-84 96-
100
 Different studies have concluded that CT
perfusion and DWI-PWI MR are equivalentequivalent in
identification of penumbra and prediction of
infarct size.
(STROKE 2002) ( JCAT(STROKE 2002) ( JCAT
2003)2003)

101. Functional loss of cell
Reduced blood flow
Autoregulation
CYTOTOXIC EDEMA,
CELL DEATH
Increased water content
VASOGENIC EDEMA
MASS EFFECT
GLIOSIS
Perfusion
imaging
DWI
Conventional MRI
CT

103. Causes
 One of top ten causes of childhood death
 Presenting signs and symptoms variable
 Depends on age

104. Neonatal hypoxia - findings
 Neonatal injury
Central- Basal ganglia, Ventrolateral thalami, Brainstem
Peripheral-Peripheral cortex, adjacent whitematter

105. Central pattern

106. Peripheral Focal
FLAIR may not detect acute lesions
DWI, ADC values may be normal intially
Initial DWI , may not correspond to the final infarct volume
DELAYED CELL DEATH MECHANISMS

107. Imaging modality
Ultrasound- illdefined hyperechogenecity-
cystic degeneration
Conventional MR imaging
Neonate
Acute-isointense infarcted cortex
( missing cortex sign)
May not seen on FLAIR
Subacute stage-T1 hperintense, T2
hypointense

108. Imaging modality
 CEMR and CECT- Gyriform enhancement
from 5 days onwards
 Diffusion imaging
 Perfusion imaging- Moya-Moya disease for
surgical planning

109. Causes-Arterial stroke
 Cardiac causes
Cyanotic congenital heart disease
Vascular dissection
Mitral valve prolapse
 Hypercoaguble states
 Vasculopathies
 Infections
Posterior circulation-trauma to vertibrobasilar
system,MELAS
Thalamic infarcts-meningitis,CHD, migraine,
trauma

110. Moya- Moya Disease
 Progressive stenotic arteriopathy involving
proximal intracranial arteries
SUPRACLINOID ICA,
PROXIMAL ACA AND MCA
PCA RARELY, LATELY INVOLVED
HYPERTROPHY OF LENTICULOSTIATE
AND THALAMOPERFORATOR ARTERIES

111. Moya- Moya Disease
 Primary – bilateral, secondary- unilateral
Secondary(MoyaMoya syndrome)
NF-1
Down syndrome
Sickle cell disease
Radiation therapy
HIV
Glycogen storage disease

112. Moya- Moya disease- Imaging
Pial synangiosis- Dilated superficial
temporal and middle meningeal arteries
 Infarctions-
 Intense enhancementof basal ganglia
 Enhancement of dilated deep medullary veins in
centrum semiovale
 Pial collateral enhancement
 DSA- Puff of smoke appearance

115. Post pial synangiosis

117. Dissection
 Blood dissects through intimal defect- false
channel between intima and muscularis-
 Complications-

Obstruction of main lumen
Intramural thrombus
 Embolization- stroke
 Pseudoaneurysm

118. Dissection
 Imaging technique of choice
 MRA -2D TOF ,DSA-
Gradual irregular tapering,stenosis, Distal
emboli, psedoaneurysms
Non contrast fat supressed T1 sequence at base of skull and neck-
crescentic hyperintensity in vessel mura

119. CAROTID DISSECTION

120. VERTEBRAL ARTERY DISSECTION

121. NECT
HEMORRHAGE
CT PERFUSION
CTP- EVALUATION
COLOR MAPS OF TTP,CBF,CBV
CT ANGIOGRAPHY
VERTEBRAL BODY C5 TO VERTEX
END OF EXAMINATION
YES NO
CTA EVALUATION
EVALUATION & INTERPRETATION EARLY SIGNS OFISCHEMIC STROKE ?
REDUCED PERFUSION ?
STENOSIS OR OCCLUSION OF
MAJOR ARTERIES ?

122. ACUTE FOCAL NEUROLOGICAL DEFICIT WITHIN 6 HR
T2*GRE MRI ( OR CT)
NO ACUTE
HAEMORRHAGE
ACUTE HAEMORRHAGE
DWI/PWI/MRA
PWI >DWI
MCA BRANCH OCCLUSION DISTAL ICA OR
PROXIMAL MCA OCCLUSION
PWI <DWI
IV THROMBOLYSIS
IV/IA THROMBOLYSIS

123. CONCLUSION
 Stroke – No longer tragic medical event
But a medical emergency
 CT-initial investigation of choice
 Radiologist is the integral part of hyperacute
stroke management team,in evaluating the
ischemic penumbra and probable endovascular
therapy
 CTP, DW-PWI useful in evaluating penumbra
Comparable in sensitivity.Used according to the
availability

125. Modalities
 Intraarterial thrombolysis
 IA+I.V thrombolysis
 Mechanical thrombolysis
Probing with microguidewire
Concentric retriever
Balloon inflation techniques
Ultrasonic fibrinolysis catheter(EKOS)
Photoacoustic recanalization(EPAR)

126. I.A. thrombolysis
 Selective chemical thrombolysis at the site of
thrombus
Advantages
Higher conc. at site
Systemic exposure
Precise imaging
Monitoring of recanalization
Adj. mechanical thrombolysis
Disadvantages
Injury to vessels
Heparin use
Delay in thrombolysis
Logistic limitation

127. I.A. Thrombolysis-Materials
 Piccard catheter
 5-6 F guiding catheter
 Guidewire
 End hole microcatheter
 Thrombolytics

128. Thrombolytics
Thrombolytic Half
life(min)
Description
First generation
Urokinase
Streptokinase
14-20
18-23
Serine protease
Streptococcal protein
Second generation
(FIBRIN SPECIFIC)
Pro-urokinase
Alteplase(rt-PA)
20
3-5
Proenz. Of urokinase
Serine protease
Third generation
(FIBRIN SPECIFIC)
Tenecteplase
Reteplase
Desmoteplase
17
15-18
t-PA mutant
Deletion mutant of t-PA
Saliva of vampire bat,MOST POTENT

129. Thrombolytics-Dose
 Urokinase 2,50,000 units per vial
Diluted in 50 ml saline(5000U/ml)
10,000 units /min
( upto 1,25,000 U)
 6 mg-9 mg over 2hrs– prourokinase
 22 mg- t-PA

130. I.A. thrombolysis
indications
 Presentation 3 hours -6hrs
 Baseline NIHS score of >10
 Ineligibilty to I.V. thrombolysis

131. I.A. thrombolysis
contraindications
 > 6 hours from onset
 Baseline NIHS score <10
 Rapidly improving neurological status
 Intracranial hemorrhage,
 Parenchymal hypodensity in >1/3 of vascular
territory
 Stroke within previous 6 weeks
 Head trauma within 90 days
 INR > 1.7,aPTT >1.5,platelet counts< 100,000/l
 Uncontrolled hypertension

132. Combined thrombolysis
 Synergy of advantages
i.v. rt-PA (fast and easy to use)
 Improves the speed and frequency of recanalization
 t-PA dose-- 0.6mg/kg +20mg I.A
 Increased risk of hemorrhage
+IAT
 Titrated dose
Mechanical aids o recanalization
 Higher rates of recanalization

133. Mechanical thrombolysis
 Concentric Retriever

134. Mechanical thrombolysis
 Mechanical probing(Manipulation)

135. Mechanical thrombolysis
Balloon inflation

136. Mechanical thrombolysis
 Extends the tratment window
 Preclude use of thrombolytics
 Adjunctive treatment(Easens thrombolysis)
 Faster recanalization