Cerebral Ischemia

Cerebral Ischemia

1. CT Imaging ofCT Imaging of
Cerebral Ischemia Cerebral Ischemia
and Infarctionand Infarction
Presented by EKKASIT SRITHAMMASIT, MD.Presented by EKKASIT SRITHAMMASIT, MD.
Ann G.Osborn
Diagnostic Neuroradiology; 11: 341-369

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

5. PathophysiologyPathophysiology

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

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

8. 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

9. 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

10. 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

11. 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

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

13. CT Imaging of Cerebral CT Imaging of Cerebral
InfarctsInfarcts

14. 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

15. Acute InfarctsAcute Infarcts

16. 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
2.2.Diagnose or exclude intracerebral Diagnose or exclude intracerebral
hemorhagehemorhage
3.3.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.

17. 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

18. 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

19. Acute InfarctsAcute Infarcts
Hyperdense MCA

20. Acute InfarctsAcute Infarcts
Obscuration of lentiform nuclei

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

22. Acute InfarctsAcute Infarcts
Sulcal effacement

23. Subacute InfarctsSubacute Infarcts

24. 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

25. Subacute InfarctsSubacute Infarcts

26. Subacute InfarctsSubacute Infarcts

27. Subacute InfarctsSubacute Infarcts

28. Subacute InfarctsSubacute Infarcts
ECCT

30. Chronic InfarctsChronic Infarcts

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

32. Chronic InfarctsChronic Infarcts

33. Lacunar InfarctsLacunar Infarcts

34. 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

35. Lacunar InfarctsLacunar Infarcts

36. Lacunar InfarctsLacunar Infarcts

37. Hypoxic-Ischemic Hypoxic-Ischemic
EncephalopathyEncephalopathy

38. 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”

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

41. 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.

46. At 2 months of age, T1-weighted brain MR imaging shows high-signal regions in the
periventricular area, atrophy of the white matter and serrated ventricular walls.