CT Imaging of Cerebral Ischemia and Infarction

Definition of stroke and cerebrovascular disorders and pathophysiology of cerebral infarct and CT imaging overview of acute-subacute and chronic infarcts and penumbra.
causes of cerebral edema , Radiological signs of acute infarct and hemorrhagic infarct and comparison of MRI and CT in the diagnosis of acute infarct
Role of diffusion weighted imaging (DWI) and diffusion perfusion mismatch

1. CT Imaging ofCT Imaging of
Cerebral Ischemia and Cerebral Ischemia and
InfarctionInfarction
DR SAKHER-ALKHADERI
CONSULTANT RADIOLOGIST
AMC

2. IntroductionIntroduction
Stroke is a lay term that encompasses a
heterogeneous group of cerebrovascular
disorders .
The four major types of stroke :
• Cerebral infarction (80%)
• Primary intracranial hemorrhage (15%)
• Nontraumatic subarachnoid hemorrhage (5%)
• Miscellaneous – vein occlusion (1%)

3. Cerebral InfarctionCerebral Infarction
•Large vessel occlusions ( ICA, MCA,
PCA) – 40-50%
•Small vessel (lacunar) infarcts – 25%
•Cardiac emboli – 15%
•Blood disorders – 5%
•Nonatheromatous occlusions – 5%

4. Table of contentTable of content
•Pathophysiology
•CT Imaging of Cerebral Infarcts:
Overview
•Acute Infarcts
•Subacute Infarcts
•Chronic Infarcts
•Lacunar Infarcts
•Hypoxic-Ischemic Encephalopathy

12. PathophysiologyPathophysiology

13. Physiology Physiology
of cerebral ischemia and infarctionof cerebral ischemia and infarction
**Most common situation**
Densely
ischemic
central
focus
Less
densely
ischemic
“penumbra”

14. Physiology Physiology
of cerebral ischemia and infarctionof cerebral ischemia and infarction

15. Physiology Physiology
of cerebral ischemia and infarctionof cerebral ischemia and infarction
**Ischemia produces**
Biochemical Reactions
Loss of ion homeostasis, Osmotically obligated
water, anaerobic glucolysis
Loss cell membrane function & Cytoskeletal integrity
Cell death

16. Physiology Physiology
of cerebral ischemia and infarctionof cerebral ischemia and infarction
**Selective vulnerability**
Most vulnerable = NeuronMost vulnerable = Neuron
Follow by Astrocytes, oligodendroglia, microglia
and endothelial cells

17. Physiology Physiology
of cerebral ischemia and infarctionof cerebral ischemia and infarction
**Collateral supply**
Dual or even triple interdigitating supplyDual or even triple interdigitating supply : : Subcortical
white matter U-fiber, external capsule, claustrum
Short arterioles from a single sourecShort arterioles from a single sourec : The cortex : The cortex
Large, long, single source vesselsLarge, long, single source vessels : Thalamus, basal : Thalamus, basal
ganglia, centrum semiovaleganglia, centrum semiovale

18. Physiology Physiology
of cerebral ischemia and infarctionof cerebral ischemia and infarction
Border zonesBorder zones / Vascular watershed/ Vascular watershed
• Arterial perfusion pressure is lowest in
these zone because of arteriolar
aborization
• The first to suffer ischemia and infarction
during generalized systemic hypotension

19. Border zones / Vascular watershedBorder zones / Vascular watershed
Adult, term infants
Fetus, preterm infant
Cortex and cerebellum Deep periventricular region

20. CT Imaging of Cerebral CT Imaging of Cerebral
InfarctsInfarcts

21. CT Imaging of Cerebral InfarctsCT Imaging of Cerebral Infarcts
The imaging The imaging
manifestations of manifestations of
cerebral ischemia cerebral ischemia
varyvary significantly significantly
with timewith time

22. Acute InfarctsAcute Infarcts

23. Acute InfarctsAcute Infarcts
The role of immediate CT The role of immediate CT
in the management of acute cerebral infarction is two foldin the management of acute cerebral infarction is two fold
1.1.Diagnose or exclude intracerebral Diagnose or exclude intracerebral
hemorhagehemorhage
2.2.Identify the presence of an Identify the presence of an
underlying structural lesion such as underlying structural lesion such as
tumor, vascular malformation.tumor, vascular malformation.

24. Acute InfarctsAcute Infarcts
First 12 hoursFirst 12 hours
• Almost 60 % = Normal
• Hyperdense artery (25 – 50%)
• Obscuration of lentiform nuclei
12 – 24 hours12 – 24 hours
• Loss of gray-white interfaces ( insular ribbon
sign)
• Sulcal effacement

25. Acute InfarctsAcute Infarcts
Hyperdense arteryHyperdense artery
• Usually the MCA –
hyperdense MCA sign
(25% of unselected
acute infarct)
• Hyperdense MCA sign
35-50% of MCA stroke
• Caused by acute
intraluminal thrombus

26. Dense MCA sign
This is a result of thrombus or embolus in the MCA.
On the left a patient with a dense MCA sign.
On CT-angiography occlusion of the MCA is visible.

27. Acute InfarctsAcute Infarcts
Hyperdense MCA

28. MCA infarction: on CT an area of hypoattenuation appearing within
six hours is highly specific for irreversible ischemic brain damage.
Hypo attenuating brain tissue

29. Hypo attenuating brain
tissue
The reason we see ischemia on CT is that in ischemia cytotoxic
edema develops as a result of failure of the ion-pumps.
These fail due to an inadequate supply of ATP.
An increase of brain water content by 1% will result in a CT
attenuation decrease of 2.5 HU.
On the left a patient with hypoattenuating brain tissue in the right
hemisphere.
The diagnosis is infarction, because of the location (vascular territory
of the middle cerebral artery (MCA) and because of the involvement
of gray and white matter, which is also very typical for infarction.

30. Hypoattenuation on CT is highly specific for irreversible ischemic
brain damage if it is detected within first 6 hours (1).
Patients who present with symptoms of stroke and who demonstrate
hypodensity on CT within first six hours were proven to have larger
infarct volumes, more severe symptoms, less favorable clinical
courses and they even have a higher risk of hemorrhage.
Therefore whenever you see hypodensity in a patient with stroke this
means bad news.
No hypodensity on CT is a good sign.
Hypo attenuating brain tissue

31. Obscuration of the lentiform
nucleus
Obscuration of the lentiform nucleus or blurred basal
ganglia

32. Acute InfarctsAcute Infarcts
Obscuration of lentiform nuclei

33. Obscuration of the lentiform
nucleus
Obscuration of the lentiform nucleus, also called blurred basal
ganglia, is an important sign of infarction.
It is seen in middle cerebral artery infarction and is one of the
earliest and most frequently seen signs (2).
The basal ganglia are almost always involved in MCA-infarction.

34. Insular Ribbon sign
Two patients with insular ribbon sign

35. Acute InfarctsAcute Infarcts
Loss of gray-white interfaces ( insular ribbon sign)

36. 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 removed from collateral flow.
It has to be differentiated from herpes encephalitis.

37. Acute InfarctsAcute Infarcts
Sulcal effacement

38. Acute InfarctsAcute Infarcts
Sulcal effacement

39. Subacute InfarctsSubacute Infarcts

40. Subacute InfarctsSubacute Infarcts
1-3 days1-3 days
• Increase mass effect
• Wedge-shaped low density area that involves
both gray and white matter
• Hemorrhagic transformation (basal ganglia and
cortex are common sites)
4-7 days4-7 days
• Gyral enhancement
• Mass effect, edema persist

41. Subacute InfarctsSubacute Infarcts

42. Subacute InfarctsSubacute Infarcts

43. Subacute InfarctsSubacute Infarcts

44. Hemorrhagic infarcts
•Petechial hemorrhage
•> 50%
•No effect on prognosis
•No mass effect
•Occurs at 4th day , rare in
the first 6 hrs
•Small foci of increased
attenuation in the infarcted
area
•Due to leaking blood from
high pressure vessels
•Secondary hematoma
•< 5%
•Affect prognosis
•mass effect
•Occurs after 4 days and in
the first 24 hr in the
thrombolysed patients
•Hematoma within the
infarcted area.
•Due to rupture vessels
because of rapid
reperfusion .

45. Hemorrhagic infarcts
15% of MCA infarcts
are initially
hemorrhagic.
Hemorrhage is most easily detected with CT, but it can also
be visualized with gradient echo MR-sequences.

46. Subacute InfarctsSubacute Infarcts
ECCT

48. Chronic InfarctsChronic Infarcts

49. Chronic InfarctsChronic Infarcts
Months to yearsMonths to years
• Encepholomalacic change, volume loss
• Calcification rare

50. Chronic InfarctsChronic Infarcts

51. Lacunar InfarctsLacunar Infarcts

52. Lacunar InfarctsLacunar Infarcts
• Small deep cerebral infarcts
• Typically located in the basal ganglia and
thalamus
• Small infarcts are often multiple
• Most true lacunar infarcts are not seen on CT
• Present they are usually seen as part of more
extensive white matter disease

53. Lacunar InfarctsLacunar Infarcts

54. Lacunar InfarctsLacunar Infarcts

55. Hypoxic-Ischemic Hypoxic-Ischemic
EncephalopathyEncephalopathy

56. Hypoxic-Ischemic Hypoxic-Ischemic
EncephalopathyEncephalopathy
• Consequence of global perfusion or
oxygenation disturbance
• Common causesCommon causes – severe prolonged
hypotension, cardiac arrest with successful
resuscitation, profound neonatal asphyxia,
cabonmonxide inhalation ( Decrease CBF)
• May be caused by RBC oxygenation is faulty
• Two basic patterns: “border zone infarcts” and
“generalized cortical necrosis”

58. Border zones / Vascular watershedBorder zones / Vascular watershed
Adult, term infants
Fetus, preterm infant
Cortex and cerebellum Deep periventricular region

59. Hypoxic-Ischemic Hypoxic-Ischemic
EncephalopathyEncephalopathy
• The most frequently and severely affected area is the
parietooccipital region at the confluence between the
ACA, MCA, and PCA territories.
• The basal ganglia are also common sites
• In premature infants HIE manifestations are those of
periventricular leukomalacia
• Most common observed on NECT is a low density band
at the interface between major vascular territories.
• The basal ganglia and parasagittal areas are the most
frequent sites.

65. CTA and CT Perfusion
Once you have diagnosed the
infarction, you want to know which
vessel is involved by performing a CTA.
Normal CTA

66. First look at the images on the left and try to detect the abnormality.
Then continue reading.
The findings in this case are very subtle.
There is some hypodensity in the insular cortex on the right, which is the area we always
look at first.
In this case it is suggestive for infarction, but sometimes in older patients with
leukencephalopathy it can be very difficult.
A CTA was performed (see next images).

67. Now we feel very comfortable with
the diagnosis of MCA infarction.

68. Studies were performed to compare CT
with MRI to see how much time it took
to perform all the CT studies that were
necessary to come to a diagnosis.
It was demonstrated that Plain CT,
CTP and CTA can provide
comprehensive diagnostic information
in less than 15 minutes, provided that
you have a good team.
In the case on the left first a non-
enhanced CT was performed.
If there is hemorrhage, then no further
studies are necessary.
In this case the CT was normal and a
CTP was performed, which
demonstrated a perfusion defect.
A CTA was subsequently performed
and a dissection of the left internal
carotid was demonstrated.

69. On PD/T2WI and FLAIR
infarction is seen as
high SI.
These sequences detect
80% of infarctions
before 24 hours.
They may be negative
up to 2-4 hours post-
ictus!
On the left T2WI and
FLAIR demonstrating
hyperintensity in the
territory of the middle
cerebral artery.
Notice the involvement
of the lentiform nucleus
and insular cortex.
MRI

70. High signal on conventional MR-sequences is
comparable to hypodensity on CT.
It is the result of irreversible injury with cell death.
So hyperintensity means BAD news: dead brain.

71. Diffusion Weighted Imaging (DWI)
DWI is the most sensitive sequence for stroke imaging.
DWI is sensitive to restriction of Brownian motion of extracellular
water due to imbalance caused by cytotoxic edema.
Normally water protons have the ability to diffuse extracellularly and
loose signal.
High intensity on DWI indicates restriction of the ability of water
protons to diffuse extracellularly.

72. First look at the images on the
left and try to detect the
abnormality.
Then continue reading.
The findings in this case are
very subtle.
There is some hypodensity
and swelling in the left frontal
region with effacement of sulci
compared with the
contralateral side.
You probably only notice
these findings because this is
an article about stroke and
you would normally read this
as 'no infarction'.
Now continue with the DWI
images of this patient.

73. When we look at the DWI-images it is very
easy and you don't have to be an expert
radiologist to notice the infarction.
This is why DWI is called 'the stroke
sequence'.

74. In the acute phase T2WI will be
normal, but in time the infarcted
area will become hyperintense.
The hyperintensity on T2WI reaches
its maximum between 7 and 30
days. After this it starts to fade.
DWI is already positive in the acute
phase and then becomes more
bright with a maximum at 7 days.
DWI in brain infarction will be
positive for approximately for 3
weeks after onset (in spinal cord
infarction DWI is only positive for
one week!).
ADC will be of low signal intensity
with a maximum at 24 hours and
then will increase in signal intensity
and finally becomes bright in the
chronic stage.
When we compare the findings on T2WI and
DWI in time we will notice the following:

75. First it was thought that everything that is bright on DWI is
dead tissue.
However now there are some papers suggesting that
probably some of it may be potentially reversible damage.
If you compare the DWI images in the acute phase with the
T2WI in the chronic phase, you will notice that the affected
brain volume in DWI is larger compared to the final infarcted
area (respectively 62cc and 17cc).

76. The area with abnormal perfusion can be
dead tissue or tissue at risk.
Combining the diffusion and perfusion
images helps us to define the tissue at risk,
i.e. the penumbra.

77. The ischemic penumbra denotes the part
of an acute ischaemic stroke which is at risk
of progressing to infarction, but is
still salvageable if re-perfused. It is usually
located around an infarct core which
represents the tissue which has or is going
to infarct regardless of re-perfusion.

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

79. On the left a patient with sudden onset of neurological symptoms.
MR was performed 1 hour after onset of symptoms.
First look at the images on the left and try to detect the abnormality.
Then continue reading.
These images are normal and we have to continue with DWI. See
next images.

80. On the DWI there is a large area with restricted
diffusion in the territory of the right middle cerebral
artery.
Notice also the involvement of the basal ganglia.
There is a perfect match with the perfusion images, so
this patient should not undergo any form of thrombolytic
therapy.

81. On the left another MCA infarction.
It is clearly visible on CT (i.e. irreversible changes).
There is a match of DWI and Perfusion, so no
therapy.

82. On the left another case.
The DWI and ADC map is shown.
Continue for the perfusion images

83. Now we can see that there is a severe mismatch.
Almost the whole left cerebral hemisphere is at risk
due to hypoperfusion.
This patient is an ideal candidate for therapy.

84. THE END