This document outlines Dr. Sulav Pradhan's presentation on vascular territories of the brain and different types of strokes. It discusses the role of imaging modalities like CT, CT angiography, MRI, diffusion weighted imaging, and perfusion imaging in evaluating acute ischemic strokes. It describes the appearance of ischemic brain tissue on different sequences over time and how these modalities are used to distinguish irreversible infarcted tissue from potentially salvageable penumbra.

1. Dr Sulav Pradhan
Resident, MD Radiodiagnosis
NAMS, Bir hospital

2. Presentation outline
• Vascular territories of brain
• Stroke
• Hyperacute and acute ischemic stroke
• Role of Interventional radiology
• Subacute infarct
• Chronic infarct
• Lacunar infarct
• Multiple embolic infarct
• Watershed infarct
• Conclusion

4. Vascular territories of the brain.
1. Anterior circulation: consists of intradural internal
carotid artery with its branches and its terminal
branches viz middle cerebral artery and anterior
cerebral artery.
anterior communicating artery.
posterior communicating artery.
2. Posterior circulation : consists of vertebrobasilar
trunk including its terminal bifurcation into two
posterior cerebral arteries.

11. DEFINITION:
• Stroke is a syndrome caused by disruption of
the blood flow to part of the brain due to
either:
• (a) occlusion of a blood vessel (ischemic stroke,
seen in approximately 80% of cases); or
• (b) rupture of a blood vessel, resulting in injury
to cells and causing sudden loss of focal brain
functions.( Hemorraghic stroke).

12. 4 main etiologies
• Cerebral infarction – 80%
• Intraparenchymal haemorrhage – 15%
• Non traumatic subarachnoid haemorrhage –
5%
• Venous infarct (1%)

13. Ischemia Vs Infarction:
• Distinction between them is subtle but
important.
• Ischemia: viable brain tissue with inadequate
blood supply to sustain normal cellular
function.
• Infarction: cell death with loss of neurons, glia
or both.

14. Types:
• Hyperacute: <3hrs: golden hours, therapeutic
windows for IV rTPA.
• Acute: 3-6hrs important for intraarterial
thrombolysis.
• Subacute: 48hrs-2wks.
• Chronic: > 2wks.

15. Etiology:
• Atherosclerotic: 40-45%
• Small vessel disease( lacunar infarct):15-30%
• Cardioembolic disease:15-25% - MI, AF, valvular
disease.

16. • Pathogenesis:
cerebral blood flow(<15-18ml /100gm/min.)
O2 & glucose
ATP
Na –K ATPase
Na influx into cell
Cellular edema(cerebral edema)

17. Effect of Cerebral edema
Imaging changes:
• Hypodensity of overall brain tissue
• Loss of grey-white differentiation (obscuration
of basal ganglia, insular ribbon sign).
• Increased T1 & T2 relaxation time.

18. Effect of Cerebral edema
• Gyral swelling, sulcal effacement.
• Herniation of brain,compression of ventricles.
• Increased ICT.
• Neurological deficit,

20. • Is the stroke ischemic or hemorrhagic?
Non enhanced CT
• Is there a flow obstruction in a major vessel?
CT angiography
• Which tissue is already infarcted and which
is still salvageable?
Perfusion CT and CT angiography

21. • Non enhanced scanning must be performed as
soon as possible after the stroke code has been
activated .
• CT is highly sensitive for the depiction of
hemorrhagic lesions , and the key role of non
enhanced CT is the detection of hemorrhage or other
possible mimics of stroke (eg. neoplasm, AV
malformation) that could be the cause of the
neurologic deficit.

22. • The second role of non enhanced CT is the
detection of ischemic signs such as the
hyperdense vessel sign, the insular ribbon
sign, and obscuration of the lentiform
nucleus.
• The last two features are caused by a loss of
contrast between gray matter and white
matter on CT images

23.  Figure 2. Axial unenhanced CT
images in a proximal segment
of the left MCA in a 53-year-
old man (a) and a distal
segment of the left MCA in a
62-year-old woman (b),
obtained 2 hours after the
onset of right hemiparesis and
aphasia, show areas of
hyperattenuation (arrow)
suggestive of intravascular
thrombi

24.  Figure 3. Axial unenhanced CT
image obtained in a 53-year-
old man (same patient as in
Fig 2a) 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

25.  Figure 4. Axial unenhanced CT
image, obtained in a 73-year-old
woman 2 n 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.

26. • Lev et al showed sensitivity and specificity of 57% and
100%, respectively, for acute ischemic stroke detection
at unenhanced CT with the use of standard window
settings (width, 80 HU; center, 20HU).
• Sensitivity increased to 71% with a change of window
width and center level settings to 8 HU and 32 HU,
respectively, without a loss in specificity.
• Decrease the window width

27. Effect of window setting:
 Figure 5. Axial unenhanced CT
images, obtained in a 45-
year-old man 2 hours after
the onset of left hemiparesis,
show obscuration of the right
lentiform nucleus (arrow in b).
This feature is less visible with
the routine brain imaging
window used for a (window
width, 80 HU; center, 35
HU)than width the narrower
window used for b (window
width, 10 HU; center, 28 HU).

28. Figure . Drawings (top) illustrate the territories
(blue) of the ACA, middle cerebral artery (MCA), and
posterior cerebral artery. CT scans (bottom) show es-
tablished infarctions of these arteries

29. • European Cooperative Acute Stroke Study trial,
involvement of more than one-third of the MCA
territory depicted at unenhanced CT was a
criterion for the exclusion of patients from
thrombolytic therapy because of a potential
increase in the risk for hemorrhage .
• The Alberta Stroke Program Early CT Score
(ASPECTS) was proposed in 2001 as a means of
quantitatively assessing acute ischemia on CT
images by using a 10-point topographic scoring

30.  Figure 6. Schematic shows the 10
regions of the MCA distribution,
each of which accountsfor one
point in the ASPECTS system: M1,
M2, M3, M4, M5, M6, the
caudate nucleus (C), the lentiform
nucleus (L), the internal capsule
(IC), and the insular cortex (I).
 For each area involved in
ischemia depicted at
unenhanced CT, one point is
subtracted from the total score
of 10.

31. Figure 7. Unenhanced CT
images in a 56-year-old
man with right hemiparesis
(a at a lower level than b)
demonstrate involvement of
the M1region, insular cortex
(I), and lentiform nucleus
(L). Thus, three points are
subtracted from the 10-
point ASPECTS,and the final
score is seven points.
C caudate nucleus,
IC internal capsule.
Score of 7 or less –
poor prognosis

32. The main role of CT angiography is to:
• reveal the status of large cervical and
intracranial arteries and thereby help define
the occlusion site,
• depict arterial dissection,
• grade collateral blood flow, and
• characterize atherosclerotic disease

33. • is very useful in providing guidance for the interventional
neuroradiologist prior to intraarterial thrombolysis if
available.
• In intra-arterial thrombolysis higher chances of
recanalization is seen in the occlusion of ICA, MCA stem
and basilar artery.
• Thus, CT angiography is useful in detecting these
occlusions and differentiating them from more distal (M2
or M3) occlusions for intravenous, intraarterial, or mixed
(intravenous-intraarterial) treatment planning.

34. • In addition, CT angiography is especially
important for the detection of thrombosis of the
vertebro basilar system, since this entity is very
difficult to detect at non enhanced CT and the
brainstem is frequently not included in the
perfusion coverage.
• The main pitfalls is caused by basilar artery
occlusions that are missed because non
enhanced CT and perfusion CT are performed but
not CT angiography

37. CT perfusion imaging can be used to measure the
following perfusion parameters:
• cerebral blood volume (i.e, the volume of blood per unit of
brain tissue; normal range = 4–5 mL/100 g);
• Cerebral blood flow (i.e, the volume of blood flow per unit of
brain tissue per minute; normal range in gray matter = 50–60
mL/100 g/min);
• mean transit time, defined as the time difference between
the arterial inflow and venous outflow; and
• time to peak enhancement, which represents the time from
the beginning of contrast material injection to the maximum
concentration of contrast material within a region of interest

38. • The clinical application of CT perfusion imaging in acute stroke
is based on the hypothesis that the penumbra shows either:
(a) increased mean transit time with moderately decreased
cerebral blood flow (60%) and normal or increased cerebral
blood volume (80%–100% or higher) secondary to auto
regulatory mechanisms or
(b) increased mean transit time with markedly reduced cerebral
blood flow(30%) and moderately reduced cerebral blood
volume (60%),
• whereas infarcted tissue shows severely decreased cerebral
blood flow (30%) and cerebral blood volume (40%) with
increased mean transit time

39.  Figure 9. CT perfusion maps
of cerebral blood volume
(a)and cerebral blood flow (b)
show, in the left hemisphere,
a region of decreased blood
volume (white oval) that corresponds
to the ischemic core
and a larger region of decreased
blood flow (black oval
in b) that includes the ischemic
core and a peripheral
region of salvageable tissue.
The difference between the
two maps (black oval white
oval) is the penumbra.
Ischemic core Region of dec. blood
PenumbraWell perfused area

47. • A thorough evaluation of acute stroke can be
performed by using a combination of
Conventional MR imaging,
MR angiography, and
Diffusion- and perfusion-weighted MR
imaging techniques

48. • Conventional spin-echo MR imaging is more sensitive and
more specific than CT for the detection of acute cerebral
ischemia within the first few hours after the onset of stroke.
• It has the additional benefit of depicting the pathologic entity
(stroke and its mimics) in multiple planes.
• The MR sequences typically used in the evaluation of acute
stroke include T1-weighted spin-echo, T2- weighted fast spin-
echo, fluid-attenuated inversion recovery, T2*-weighted
gradient-echo, and gadolinium-enhanced T1-weighted spin-
echo sequences.

49. • hyperintense signal in white matter on T2W images
and FLAIR images, with a resultant loss of gray white
matter differentiation analogous to the loss at CT ;
• sulcal effacement and mass effect;
• loss of the arterial flow voids seen on T2-weighted
images; and
• stasis of contrast material within vessels in the affected
territories

50. • Like the hyper attenuated vessel sign seen at CT, a
low-signal-intensity or high-signal-intensity vessel
sign due to intravascular thrombus can be seen
on MR images obtained with a T2*-weighted
gradient-echo or FLAIR sequence, respectively.
• T2*-weighted gradient-echo images depict an
acute intracranial hemorrhage as an area of
abnormal blooming.

51. Figure 12. Acute stroke in the left medial
temporal lobe in a 44-year-old man.
(a, b) Axial T2-weighted (a) FLAIR (b) images
show areas with increased signal intensity.
(c) Gradient-echo image shows abnormal
low signal intensity in the same areas.
These findings are suggestive of hemorrhage.

52. • Conventional MR imaging is less sensitive than diffusion-
weighted MR imaging in the first few hours after a stroke
(hyperacute phase) and may result in false-negative
findings.
• Since the advent of diffusion MR imaging, conventional
MR imaging sequences play only a relatively minor role in
acute stroke imaging,
• Whereas diffusion-weighted sequences may be
appropriately included in any MR imaging protocol for
evaluation of acute stroke.

53. • Diffusion-weighted imaging sequences now
are incorporated into most MR imaging
protocols and are essential components of an
acute stroke evaluation

54. • The normal motion of water molecules within living
tissues is random (Brownian motion).
• In acute stroke, there is an alteration of homeostasis,
which normally maintains steady-state proportions of
intracellular and extracellular water.
• Acute stroke causes excess intracellular water
accumulation, or cytotoxic edema, with an overall
decreased rate of water molecular diffusion within the
affected tissue.

55. • Tissues with a higher rate of diffusion
undergo a greater loss of signal in a given
period of time than do tissues with a lower
diffusion rate.
• Therefore, areas of cytotoxic edema, in which
the motion of water molecules is restricted,
appear brighter on diffusion-weighted images
because of lesser signal losses.

56. • In humans, diffusion restriction with reduced ADC has been
observed as early as 30 minutes after the onset of ischemia.
• The ADC continues to decrease further and reaches a nadir at
approximately 3–5 days.
• Thereafter, the ADC starts to increase again, and it returns to
the baseline value at approximately 1–4 weeks.
• This is likely due to the development of vasogenic edema
along with the persistence of cytotoxic edema.
• In a few weeks to months, gliosis develops, with a resultant
increase in the quantity of extracellular water.

57. • This same pattern of change can be observed in the
diffusion-weighted MR imaging appearance of ischemic
human brain tissue during the evolution of acute stroke:
• Hyperintense signal is seen with reduced ADC values
from approximately 30 minutes to 5 days after the onset
of symptoms ;
• mildly hyperintense signal is seen with pseudonormal
ADC values at 1–4 weeks; and variable signal intensity
(because of T2 characteristics) is seen with increased
ADC values several weeks to months after symptom
onset

58. • The signal intensity in areas affected by acute
stroke on diffusion-weighted images, thus,
increases during the 1st week after symptom
onset and decreases thereafter; however, the
signal may remain hyperintense for a longer
period .
• Increased intensity of the diffusion-weighted
imaging signal in the initial few days is due to
restricted diffusion and thereafter is due to an
increase of the T2 signal (T2 shine-through) from
the infarcted tissue.

59. • Hence diffusion weighted imaging signal cannot
be used alone to reliably estimate infarct age;
• it is important to examine diffusion-weighted
images in comparison with ADC maps.
• Tissues in which ADC values are reduced almost
always undergo irreversible infarction; the
decrease in ADC values is only rarely reversible
with thrombolytic therapy.

60. • In contrast to unenhanced CT or conventional
MR imaging, which have low sensitivities
(50%) for acute ischemia detection within the
first 6 hours after onset, diffusion-weighted
imaging was reported to have had high
sensitivity and specificity, of 88%–100% and
86%–100%, respectively, in various studies.

61. • While diffusion-weighted MR imaging is most useful for
detecting irreversibly infarcted tissue, perfusion-
weighted imaging may be used to identify areas of
reversible ischemia as well
• typically susceptibility based and depend on T2*effects,
but they may be T1 weighted instead.
• Dynamic susceptibility-weighted (T2*-weighted)
sequences probably are most commonly used in acute
stroke evaluation, while the other MR perfusion imaging
techniques are more commonly used in tumor evaluation
or other applications

62. • The passage of an intravascular MR contrast agent
through the brain capillaries causes a transient loss of
signal because of the T2* effects of the contrast agent.
• The dynamic contrast-enhanced MR perfusion imaging
technique involves tracking of the tissue signal changes
caused by susceptibility (T2*) effects to create a
hemodynamic time–signal intensity curve.
• As in dynamic CT perfusion imaging, perfusion maps of
cerebral blood volume and mean transit time can be
calculated from this curve by using a deconvolution
technique.

63.  Figure . Time–signal intensity
curve illustrates the decrease
in signal intensity within an
ROI after the administration of
an MR contrast agent bolus.
The signal intensity decrease
is due to the T2* effect of the
contrast agent, an effect that
is exploited in dynamic
susceptibility-weighted MR
perfusion imaging to calculate
perfusion
parameters.

64. • 1. The lesion appears smaller on the diffusion weighted
images than on the perfusion-weighted images. This is
typically observed in large-vessel strokes.
• In the acute stroke setting, a region that shows both
diffusion and perfusion abnormalities is thought to
represent irreversibly infarcted tissue,
• while a region that shows only perfusion abnormalities
and has normal diffusion likely represents viable ischemic
tissue, or a penumbra

65. 2. The lesion has the same size on diffusion weighted
images and perfusion-weighted images. This occurs
when the tissue is ireversibly infarcted and there is no
penumbra.
3. The lesion appears larger on diffusion weighted images
than on perfusion-weighted images or is seen only on
diffusion-weighted images and not perfusion-weighted
images. These findings are usually associated with early
reperfusion of ischemic tissue, and the size of the lesion
on diffusion-weighted images does not usually change
substantially over time.

68. • Like CT angiography, MR angiography is useful
for detecting intravascular occlusion due to a
thrombus and for evaluating the carotid
bifurcation in patients with acute stroke.
• Time-of-flight MR angiography and contrast-
enhanced MR angiography are commonly
used to evaluate the intracranial and
extracranial circulation

72. • In future, the selection of patients for thrombolytic
therapy may be made more effective by performing
appropriate imaging studies rather than relying on the
time of onset as the sole determinant of selection.
• In a recent trial, intravenous desmoteplase
administration at 3–9 hours after the onset of acute
ischemia was associated with a higher rate of reperfusion
and a better clinical outcome than placebo in patients
selected because of a mismatch between findings on
diffusion and perfusion MR images

73. • Endovascular IA thrombolysis
• Endovascular catheter based thrombectomy
(clot removal using new-generation stent
retrievers and/or aspiration catheters)….with
distal tip balloon for proximal protection
during thrombus retrieval
• Carotid artery stenting
• Carotid dilatation balloons
Role of interventional radiology

74. Subacute infarct
• Strokes that are between 48 hrs to 2 wks duration.
• Characterized by marked edema and hemorrhagic transformation.
•Imaging findings are:
NCCT findings:
- more sharply defined wedge shaped decreased attenuation. Mass
effect initially increase and begins to decrease by 7- 10 days.
-Cases with hemorrhagic transformation shows gyriform cortical and
basal ganglia hyperdensity.
CECT shows: patchy gyriform enhancement appearing as early as two
days with peak at two weeks and disappearing by two month.

75. • MR findings :
1. T1 WI : non hemorrhagic infarct shows
hypointensity with moderate mass effect and sulcal
effacement. However, the hemorrhagic
transformation shows the iso signal intensity with
cortex initially followed by hyperintensity.
2. T2 WI : initially hyperintense, with time the signal
intensity decreases reaching iso at the one to two
weeks known as “T2 fogging effect”.

78. • These infarcts shows hyperintesity on FLAIR images. Final infarct volume
corresponds to FLAIR defined abnormality after one week.
• T2* gradient echo images show the hemorrhagic transformation as
petechial or gyriform blooming foci. However in basal ganglia it can be
petechial or confluent.
• DWI shows hyperintensity with hypointensity on ADC map for first several
days, which then gradually reverse subsequently.
• T1 contrast images shows intravascular enhancement in first 48 hrs which
is replaced by leptomemingeal enhacement caused by persisting pial
collateral blood flow after three to four days. Patchy and gyriform
enhancement occurs as early as two to three days and may persist for two
to three months.

80. Chronic cerebral infarct
• Also called post infarction encephalomalacia.
• Occurs two weeks after the onset.
Imaging findings:
1. NCCT : well defined hypodense area involving both grey and
white matter junction with enlargement of ipsilateral
ventricles and adjacent sulci. Small ipsilateral cerebral
peduncle . Atrophy of the contralateral cerebellar
hemisphere secondary to crossed cerebellar diachisis.
2. MR : shows cystic encephalomalcia with CSF equivalent
signal intensity on all sequences.

83. Multiple embolic infarct
• Simultaneous small infarct in multiple different vascular
distributions.
• This can be either cardiac which may be either aseptic or septic and
atheromatous from the ipsilateral atheromatous internal carotid
artery plaque.
Imaging features: involves the terminal cortical branches. GM- WM
interface most commonly affected.
NCCT shows the low attenuation foci in wedge shape distribution.
Atherosclerotic emboli occassionally demonstrate calcification. Septic
embolus are often hemorrhagic.
CECT shows multiple punctate or ring enhancing lesion.

84. • MRI : multifocal peripheral T2 and FLAIR
hyperintensites.
• Hemorhhagic foci show blooming on T2* GE
sequence.
• DWI shows small peripheral foci of restriction of
diffusion.
• T1 Contrast imaging shows multiple punctate
enhancing foci.
• Septic embolus demonstrate ring enhancement
resembling ,multiple microabscess.

86. Lacunar infarct
• Lacunae are < 15mm CSF filled spaces or holes.
• May be due to lipohyalinosis and atherosclerotic
occlusion of perforating arteries of circle of willis
and peripheral cortical branches or may be due to
embolic phenomenon.
• Location: most commonly involve basal ganglia ,
thalamus, internal capsule, pons and deep white
matter.

87. • Risk factors: age, HTN, diabetes.
• Lacunar infarcts are often asymptomatic but may sometime present
as clinically evident features attributed to small subcortical or brain
stem lesion known as lacunar stroke syndrome.
• Imaging features:
NECT: Acute lacunar infarct are usually not evident where as chronic
shows the well defined CSF like holes in the brain parenchyma.
MR : old infarct are hypointense on T1 and hyperintense in T2
weighted images. Suppressed on FLAIR with gliotic periphery remain
hyperintense. Acute lacunar infarct restrict on DWI and enhance on T1
contrast images.

89. Watershed or border zone infarct.
• Two types of vascular border zone:
external ( cortical ) : between ACA, MCA, PCA.
internal (deep white matter) : between perforating branches
and major arteries.
• Etiology : emboli ( cortical more common ).
regional hypoperfusion( deep WM )
global ( all three cortical WS zone)
• Imaging:
External – wedge and gyriform shaped.
internal – rosary like line of white matter hyperdensites.

91. • Current imaging techniques can be used to identify
hyperacute stroke and guide therapy by providing
information about the functional status of ischemic
brain tissue
• Both CT and MR imaging are useful for the
comprehensive evaluation of acute stroke and can
provide important and necessary information for
therapy planning.
• While the debate about which modality is best will
likely continue into the near future, it is important to
remember that both modalities currently have a role
in acute stroke evaluation.

92. Thank you

93. References
• Diagnostic Imaging Brain, Osborn, Salzman
and Jhaveri, 3rd edition
• CT and MRI of whole body, John R. Haaga, 6th
edition
• Fundamentals of imaging, Bryant and Helms