1. Radiological imaging of cerebral ischemia.
Dr/ ABD ALLAH NAZEER. MD.

2. Ischemic stroke results from a sudden cessation of adequate
amounts of blood reaching parts of the brain. Ischemic strokes can
be divided according to territory affected or mechanism.
Clinical presentation
An ischemic stroke typically presents with rapid onset neurological
deficit, which is determined by the area of brain that is involved. The
symptoms often evolve over hours, and may worsen or improve,
depending on the fate of the ischemic penumbra.
Pathophysiology
Interruption of blood flow through an intracranial artery leads to
deprivation of oxygen and glucose in the supplied vascular territory.
This initiates a cascade of events at a cellular level which, if
circulation is not re-established in time, will lead to cell death,
mostly through liquefactive necrosis.
The mechanism of vessel obstruction is important in addressing
therapeutic manoeuvres to both attempt to reverse or minimize the
effects and to prevent future infarcts.

3. Etiology of stroke
Stroke in adults:
• atherosclerosis of extracranial arteries that supply blood to the brain
• hypertension and atherosclerosis
• arterial embolism
• CNS vasculitis
Stroke in children and young adults:
• congenital or acquired heart conditions,
• hematologic and disorders,
• vasculopathies, and
• drug ingestion.
Neonatal stroke:
• Maternal causes: autoimmune disorders, coagulation disorders, congenital
heart disease, diabetes, trauma;
• Placental causes :thrombosis, placental abruption, placental infection,
chorioamnionitis;
• Congenital blood disorders;
• Systemic or CNS infection

7. TTP-time to peak; CBF- cerebral blood flow; CBV-cerebral blood volume;

8. Radiographic features.
The goals of CT in the acute setting are:
exclude intracranial hemorrhage, which would preclude thrombolysis;
look for any "early" features of infarction
exclude other intracranial pathologies that may mimic a stroke, such as tumour.
Immediate
The earliest CT sign visible is a hyperdense segment of a vessel, representing
direct visualization of the intravascular thrombus / embolus and as such is visible
immediately . Although this can be seen in any vessel, it is most often observed in
the middle cerebral artery.
Early (1-3 hours) (also known as hyperacute phase)
Within the first few hours a number of signs are visible depending on the site of
occlusion and the presence of collateral flow. Early features include:
loss of grey-white matter differentiation, and hypoattenuation of deep nuclei:
lentiform nucleus, changes seen as early as 1 hour after occlusion, visible in
75% of patients at 3 hours
cortical hypodensity with associated parenchymal swelling with resultant gyral
effacement.
cortex which has poor collateral supply (e.g. insular ribbon) is more
vulnerable .

9. First week
With time the hypo-attenuation and swelling become more marked
resulting in significant mass effect. This is a major cause of
secondary damage in large infarcts.
Second to third week
As time goes on the swelling starts to subside and small amounts of
cortical petechial hemorrhages (not to be confused with
hemorrhagic transformation) results in elevation of the attenuation
of the cortex. This is known as the CT fogging phenomenon .
Imaging a stroke at this time can be misleading as the affected
cortex will appear near normal.
Months
Later still the residual swelling passes, and gliosis sets in eventually
appearing as a region of low density with negative mass effect.
Cortical mineralization can also sometimes be seen appearing
hyperdense.

10. CT perfusion
CT perfusion has emerged as a critical tool in selecting patients for reperfusion
therapy as well as increasing the accurate diagnosis of ischemic stroke among non-
expert readers four fold compared to routine non-contrast CT .
It allows both the core of the infarct (that part destined to never recover regardless of
reperfusion) to be identified as well as the surrounding penumbra (the region which
although ischemic has yet to go on to infarct and can be potentially salvaged).
The key to interpretation is understanding a number of perfusion parameters:
cerebral blood volume (CBV)
cerebral blood flow (CBF)
mean transit time (MTT)
time to peak (TPP)
Areas which demonstrate matched defects in CBV and MTT represent the
unsalvageable infarct core, whereas areas which have prolonged MTT but preserved
CBV are considered to be the ischemic penumbra .
CT angiography
may identify thrombus within an intracranial vessel, and may guide intra-arterial
thrombolysis or clot retrieval.
evaluation of the carotid and vertebral arteries in the neck
establishing stroke etiology (eg. atherosclerosis, dissection)
access limitation for endovascular treatment (e.g. turtuosity, stenosis)

11. MRI
MRI is more time consuming and less available than CT, but has
significantly higher sensitivity and specificity in the diagnosis of acute
ischemic infarction in the first few hours after onset.
diffusion weighted imaging (DWI) / ADC:
diffusion restriction may be seen within minutes following the onset
of ischaemia
correlates well with infarct core
for detailed discussion of DWI and ADC in stroke see diffusion
weighted MRI in acute stroke
T2-weighted imaging and FLAIR:
less sensitive than DWI in the first few hours to parenchymal change
loss of normal signal void in large arteries may be visible immediately
after 6-12 hours infarcted tissue becomes high signal
sulcal effacement and mass effect develop and become maximal in the
first few days
fogging: between 1-4 weeks (peak 2-3 weeks) infiltration of
inflammatory cells may reduce T2 signal such that it becomes
relatively isointense to normal parenchyma.

12. T1:
low intensity roughly mirrors high T2 / FLAIR signal
cortical laminar necrosis or pseudolaminar necrosis may be seen as a ribbon
of intrinsic high T1 signal, usually after 2 weeks (although it can be seen
earlier).
T1 C+:
arterial enhancement (aka intravascular enhancement):
can be seen very early (0-2 hours) although it is more common at about
day 3
lasts approximately 1 week
seen in ~50% of cases
parenchymal enhancement:
usually begins towards the end of the first week
usually lasts less than 12 weeks; if longer than this the presence of an
underlying lesion should be considered
meningeal enhancement :
uncommon
seen in the first week, typically 1-3 days
usually fades by the start of the second week
GRE/SWI:
highly sensitive in the detection of hemorrhage

13. • DWI-MRI is the technique of choice for detection of
hyperacute cerebral ischemia (in the first six hours). In many
cases of hyperacute stroke in which hyperintense signal is
already present on T2-weighted images, DW sequence better
de#nes the size of the affected tissue
• Perfusion-weighted imaging (PWI) provides information on
the hemodynamic status of the affected tissue. In hyperacute
stroke, the tissue with abnormal perfusion is larger than the
DWI lesions, therefore, PWI help identify "tissue at risk"- the
so-called ischemic penumbra.
• Diffusion Tensor Imaging (DTI) has opened new possibilities
of imaging early stages of Wallerian Degeneration. DTI detects
changes of water diffusion in the fiber tracts within the first 2
weeks after stroke, at a time when T2-weighted images and
maps of the orientationally averaged diffusivity do not
reveal obvious changes

14. Early CT signs of ischemic stroke: there is loss of corpus striatum on the left side.

16. PICA recent infarcts.

17. Unenhanced CT images in a 56-year-old man with right hemiparesis (a at a lower level than
b) demonstrate involvement of the M1 region, insular cortex (I), and lentiform nucleus

18. Computer tomography (CT) in a patient with complete right middle cerebral artery
territory infarction (within arrows). Embolic infarctions involve a well-defined
vascular territory and characteristically have a triangular appearance on CT.

19. Axial unenhanced head CT demonstrating low attenuation suggestive of ischemia involving bilateral
thalami (A), portions of cerebellum bilaterally (B), and midbrain (C) as represented by the arrows.

20. Hyperdense MCA signals (a) and loss of corpus striatum (b) on the right.
On perfusion CT (MTT map), there is a large area of diminished perfusion
(c). DWI performed the next day shows a massive MCA infarction (d).

21. Slightly hyperdense MCA sign on the left (a). Angio–CT shows a
subocclusion at this level (b) that is also seen on the reconstructions (c).

22. Unenhanced axial CT image show infarction confined to the basal ganglia, Axial maximum-intensity-
projection image from CT angiogram shows occlusion (arrow) of right middle cerebral artery. Note
opacification of distal middle cerebral artery branches via collateral circulation from other arteries.

23. Unenhanced axial CT image of brain shows large infarction in essentially entire right middle
cerebral artery territory. CT angiogram shows occlusion (arrow) of right middle cerebral artery.

25. CT perfusion imaging of (A.) cerebral blood volume and (B.) mean transit time in a
patient with left-sided weakness and ischemic stroke in the right middle cerebral
artery territory. The prediction model in (C.) demonstrates areas of brain colored in
red that are likely irreversibly damaged (core infarction) and areas in green that are
ischemic (ischemic penumbra) but may be salvageable if blood flow is restored rapidly

26. a) From the perfusion-computed tomography raw data (first line), three parametric maps can be extracted, relating to mean
transit time (second row), regional cerebral blood flow (third row) and regional cerebral blood volume (fourth row),
respectively. Application of the concept of cerebral vascular autoregulation leads to a prognostic map (fifth row), in which the
infarct is shown in red and the penumbra in green, the latter being the target of thrombolytic drugs. (b, c) computed
tomography–angiography allows identification of the origin of the hemodynamic disturbance demonstrated by perfusion-
computed tomography. In this patient, it relates to an occlusion at the right M1–M2 junction (arrows). (d, e) Finally, computed
tomography–angiography reveals bilateral calcified atheromatous plaques at both carotid bifurcations (arrowheads

27. a) Nonenhanced CT
scans obtained 5 hours
after the onset of
symptoms in a 60-year-
old man with
motoric aphasia and
slight right hemiparesis
demonstrate normal
findings. (b) Perfusion
CT study shows a small,
wedge-shaped area of
nonperfused brain in
the left frontal lobe that
is best seen on the
lower images (arrow).
In addition,
there is a 3-second
prolongation of TTP
(measurement not
shown) within the entire
left hemisphere (green
area on TTP maps).

29. 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).
D, MTT map shows a
corresponding prolongation
within this same region
(arrows). C, CBV map
demonstrates no
abnormality, therefore,
representing a CBV/MTT
mismatch or ischemic
penumbra

30. An 87-year-old woman
presenting with acute
dysarthria, left facial droop,
and left-sided weakness.
On admission, NCCT and
CTP were performed
concurrently. A, NCCT
shows some microvascular
ischemic changes
posteriorly. B−D, CTP maps,
CBF (B), CBV (C), and MTT
(D), demonstrate a large
area of matched deficit on
CBV and MTT maps,
indicative of core infarct in
the right MCA territory.

31. Multimodal CT imaging in a
63-year-old female patient
with acute stroke obtained 4
h after symptom onset. NCT
scan shows subtle loss of the
gray–white matter interface
in the right parietal lobe. CTA
demonstrates a paucity of
MCA distal branches in the
affected brain area; no
proximal MCA occlusion was
found. PCT parametric maps
show a nearly complete
match between the MTT and
CBV parametric maps. The
patient was not treated with
rt-PA. CTA = CT angiography;
PCT = perfusion-CT; MTT =
mean transit time; CBV =
cerebral blood volume; rt-PA
= recombinant tissue
plasminogen activator.

32. Subacute left MCA infarction. CT perfusion shows hypoperfusion (a). On DWI, there is an
area of hyperintensity involving the basal ganglia on the left (b). Susceptibility-weighted
imaging (SWI) shows no hemorrhage (c), and there is a slight hyperperfusion due to
reperfusion a few days later, seen on arterial spin labeling (ASL) angiography (d).

33. Right-hemispheric stroke. There is disorganization of the
fibers on the reconstructed tractogram in the right hemisphere.

37. Acute stroke in the left medial temporal lobe.

38. Acute ischemia in the right posterior inferior cerebellar artery (PICA)
territory. DWI shows a bright lesion (a) with a decreased ADC (b), whereas
multivoxel spectroscopy shows a decrease in both NAA (c) and Cr (d).

39. DWI and ADC in acute stroke.

40. fMRI at the acute phase in a patient with a thalamic stroke. There is cortical activation on
the affected side, whereas a hypoperfused lesion is clearly visible in the left thalamus.

41. Penumbra model. The central ischemic core is seen as a hyperintensity on DWI (a). This area,
also visible on the ADC map (b), is surrounded by a larger area of hypoperfused tissue (c).

42. DWI in a patient with an acute left MCA infarction. On the T2-weighted
image, the lesion is visible (a). DWI shows a large hyperintensity on the
left MCA territory(b), with a decreased EDC in the corresponding area (c).

43. Multimodality imaging of a left middle cerebral artery (MCA) stroke. There is a large
hyperintensity on diffusion-weighted imaging (DWI), with a reduction in ADC; the lesion is
visible on the T2-weighted image (c), but there is no blood on the T2* images (d). The coronal
Flair image shows the extent of the infarct in the frontal and temporal lobes. Contrast-
enhanced (f) and intracranial time-of-flight MR angiography show a left MCA occlusion.

44. T2WI and FLAIR images in acute infarct.

46. (c) MIP images (left frontolateral view) and an SSD image (superior view) (far right) from CT
angiography show proximal occlusion of the left MCA (white arrow) as well as occlusion of the left ICA
(arrowhead). Note that the posterior cerebral arteries are predominantly supplied by the posterior
communicating arteries (black arrows). This is a common anatomic variant and explains why the
subtle TTP prolongation includes the territory of the posterior cerebral artery. (d) Nonenhanced CT
scans obtained 1 day later show hypoattenuating swelling in the left MCA territory.

47. (a) Nonenhanced CT scans
obtained 21⁄2 hours after
the onset of symptoms in a
73-year-old man with
right hemiplegia and
complete aphasia
demonstrate partial
obscuration of the lentiform
nucleus and subtle swelling
and hypoattenuation of the
left temporal lobe (arrows),
findings that indicate
infarction. (b) Perfusion CT
study demonstrates relative
values of 60% and 72% for
CBF and CBV, respectively
within the MCA territory,
findings that indicate tissue
at risk. In addition, a small
area of nonperfusion is seen
within the lentiform nucleus
(arrow).

48. Right MCA syndrome.

49. c) MIP images from CT
angiography show a
high-grade stenosis of
the left ICA (straight
arrow) that results in
narrowing of the distal
lumen of the ICA
(arrowheads) and of
the MCA (curved
arrow). The right
carotid artery and the
basilar artery are
normal. (d)
Nonenhanced CT scans
obtained 3 weeks after
the onset of
stroke demonstrate
infarction of the frontal
portion of the lentiform
nucleus (arrow) and a
small infarction in the
left frontal lobe
(arrowhead).

50. Subacute ischemic Stage
As time progresses, in the subacute phase, brain swelling and mass
effect will gradually build up within a week followed by gradual
improvement beginning from that 1 week onward. These are not
easily picked up by human eyes on CT. Initial hypodensity detected
by CT usually remains during this phase. However, an interesting
phenomena sometimes occurred during this phase known as “CT
fogging effect’ where hypodensed infarcted area disappear,
becoming isodense. This is probably dues to resolution of edema in
the infarcted area. This usually occurs between 2-6 weeks after the
onset of stroke. Such “disappeared infarct” will reappear in later
phase in a form of tissue cavitation (encephalomalcia). [
In addition to that, there is also a risk of hemorrhagic
transformation in 15-20% of the cases during this period of time.
Most of the time, this occurred within 4-6 days after onset of stroke.
Once happened, the hyperdensity CT image may persist up to 8-
10weeks.

51. CT result demonstrating the “fogging effect” occurs during subacute phase. Left
CT image is obtained at 36h with bilateral occipital hypodensities. Right image is
taken at 18 days showing the isodense appearance of previous infarct. Image

52. Cortical edema in a subacute infarct. a The axial FLAIR-weighted image shows
high signal, gyral swelling, and sulcal effacement. b There is subtle low signal
and gyral swelling (arrow) seen on the T1-weighted sagittal image

53. Enhancing infarcts. Postcontrast T1-weighted image shows gyriform enhancement at
the left insula and posterior parietal lobe from a subacute left MCA infarct

58. a) Ischemic penumbra and infarct core at acute time. Red shaded region represents the ischemic penumbra identified using an MTT perfusion
map while the blue one represents the infarct core manually delineated on the DWI image. A large area of perfusion/diffusion mismatch is
clearly distinguishable. (b) Swelling at acute time of stroke onset observed in a DWI image. A massive swollen infarct occupies most of the
MCA territory distorting the right ventricle. (c) An example of the influence of partial reperfusion in penumbra and core evolution patterns.
The acute DWI (left) and the acute perfusion TTP map (right) demonstrates the “reverse” mismatch revealing a partial reperfusion where the
TTP appears normal in the anterior portion of the MCA territory. (d) Scattered lesion at acute timepoint (3 h). The manually delineated lesion
in 3 different axial slices in a DWI image is composed of two topologically separate components. (e) Scattered lesion at a subacute timepoint
(6 days). For the same patient showed in (d), the evolution of the spatial boundaries of the manually delineated scattered lesion is shown at
a subacute timepoint. (f) Perfusion/diffusion mismatch and the influence of perfusion parameters on the boundary of the visible mismatch.
The red contour represents the DWI lesion depicted at an acute timepoint superimposed with both MTT (in blue) and CBF (in green) lesions
manually delineated at an acute timepoint.

59. Chronic ischemic Stage
In chronic stage, which has vaguely defined
period (weeks to months), the damaged
necrotic tissue is resorbed. This results in
formation of encephalomalcia accompanied
by gliosis of adjacent brain tissue. Associated
with this is dilation of ventricular system of
affected part, though usually found in
relatively large infarct. These pathological
finding could be picked up by non-enhanced
CT and MRI.

60. CT picture of various location of ischemic stroke at chronic
phase, demonstrating the encephalomalcia.

61. Wallerian degeneration. Coronal T2-weighted image shows encephalomalcia
of the right frontal and temporal lobes and T2 high signal extending into the
right cerebral peduncle (arrow) from Wallerian degeneration.

63. Laminar necrosis. This sagittal noncontrast T1-weighted image shows gyriform T1 high signal
in a chronic left MCA infarct. Mild enlargement of the sulci is consistent with encephalomalcia.

71. Deep cerebral vein thrombosis.

72. Thrombosis of deep cerebral veins.

74. Cortical venous thrombosis. This large edematous lesion in the right
hemisphere shows hypo-intensity on DWI (a), and hyperintensity on coronal
Flair imaging (b). MR phlebography shows a thrombosed cortical vein (c).

76. Conclusion:
MRI with a multimodality approach is highly sensitive to detect
early changes in stroke:
• DWI and SWI (T2*): detection of brain ischemia vs hemorrhage
• DWI and PWI: evaluation of the ischemic penumbra
• MRA: vessel occlusion
• SWI (T2*): hemorrhagic risk
Given the access-related limitations of MRI, unenhanced CT is
the most common imaging study used to exclude hemorrhage
in the acute patient, identify early signs seen after the ictus
onset and the vascular lesion responsible for the neurologic
deficit.
• CT perfusion allow to evaluate the ischemic core and the
ischemic penumbra
• CT angiography permit to evaluate the vessel status and the
occluded vessel

77. Thank You.