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CT Imaging of Cerebral Ischemia and Infarction

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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

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CT Imaging of Cerebral Ischemia and Infarction

  1. 1. CT Imaging ofCT Imaging of Cerebral Ischemia andCerebral Ischemia and InfarctionInfarction DR SAKHER-ALKHADERI CONSULTANT RADIOLOGIST AMC
  2. 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. 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. 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. 5. PathophysiologyPathophysiology
  6. 6. PhysiologyPhysiology of cerebral ischemia and infarctionof cerebral ischemia and infarction **Most common situation** Densely ischemic central focus Less densely ischemic “penumbra”
  7. 7. PhysiologyPhysiology of cerebral ischemia and infarctionof cerebral ischemia and infarction
  8. 8. PhysiologyPhysiology 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. 9. PhysiologyPhysiology 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. 10. PhysiologyPhysiology 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. 11. PhysiologyPhysiology 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. 12. Border zones / Vascular watershedBorder zones / Vascular watershed Adult, term infants Fetus, preterm infant Cortex and cerebellum Deep periventricular region
  13. 13. CT Imaging of CerebralCT Imaging of Cerebral InfarctsInfarcts
  14. 14. CT Imaging of Cerebral InfarctsCT Imaging of Cerebral Infarcts The imagingThe imaging manifestations ofmanifestations of cerebral ischemiacerebral ischemia varyvary significantlysignificantly with timewith time
  15. 15. Acute InfarctsAcute Infarcts
  16. 16. Acute InfarctsAcute Infarcts The role of immediate CTThe 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 intracerebralDiagnose or exclude intracerebral hemorhagehemorhage 2.2. Identify the presence of anIdentify the presence of an underlying structural lesion such asunderlying structural lesion such as tumor, vascular malformation.tumor, vascular malformation.
  17. 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. 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. 19. 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.
  20. 20. Acute InfarctsAcute Infarcts Hyperdense MCA
  21. 21. MCA infarction: on CT an area of hypoattenuation appearing within six hours is highly specific for irreversible ischemic brain damage. Hypo attenuating brain tissue
  22. 22. 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.
  23. 23. 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
  24. 24. Obscuration of the lentiform nucleus Obscuration of the lentiform nucleus or blurred basal ganglia
  25. 25. Acute InfarctsAcute Infarcts Obscuration of lentiform nuclei
  26. 26. 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.
  27. 27. Insular Ribbon sign Two patients with insular ribbon sign
  28. 28. Acute InfarctsAcute Infarcts Loss of gray-white interfaces ( insular ribbon sign)
  29. 29. 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.
  30. 30. Acute InfarctsAcute Infarcts Sulcal effacement
  31. 31. Acute InfarctsAcute Infarcts Sulcal effacement
  32. 32. Subacute InfarctsSubacute Infarcts
  33. 33. 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
  34. 34. Subacute InfarctsSubacute Infarcts
  35. 35. Subacute InfarctsSubacute Infarcts
  36. 36. Subacute InfarctsSubacute Infarcts
  37. 37. 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 .
  38. 38. 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.
  39. 39. Subacute InfarctsSubacute Infarcts ECCT
  40. 40. Chronic InfarctsChronic Infarcts
  41. 41. Chronic InfarctsChronic Infarcts Months to yearsMonths to years • Encepholomalacic change, volume loss • Calcification rare
  42. 42. Chronic InfarctsChronic Infarcts
  43. 43. Lacunar InfarctsLacunar Infarcts
  44. 44. 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
  45. 45. Lacunar InfarctsLacunar Infarcts
  46. 46. Lacunar InfarctsLacunar Infarcts
  47. 47. Hypoxic-IschemicHypoxic-Ischemic EncephalopathyEncephalopathy
  48. 48. Hypoxic-IschemicHypoxic-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”
  49. 49. Border zones / Vascular watershedBorder zones / Vascular watershed Adult, term infants Fetus, preterm infant Cortex and cerebellum Deep periventricular region
  50. 50. Hypoxic-IschemicHypoxic-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.
  51. 51. CTA and CT Perfusion Once you have diagnosed the infarction, you want to know which vessel is involved by performing a CTA. Normal CTA
  52. 52. 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).
  53. 53. Now we feel very comfortable with the diagnosis of MCA infarction.
  54. 54. 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.
  55. 55. 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
  56. 56. 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.
  57. 57. 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.
  58. 58. 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.
  59. 59. 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'.
  60. 60. 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:
  61. 61. 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).
  62. 62. 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.
  63. 63. 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.
  64. 64. 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.
  65. 65. 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.
  66. 66. 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.
  67. 67. 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.
  68. 68. On the left another case. The DWI and ADC map is shown. Continue for the perfusion images
  69. 69. 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.
  70. 70. THE END

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