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Imaging in acute stroke
This document discusses the use of various imaging modalities such as CT, MRI, CTA, and CTP in evaluating patients presenting with acute stroke. It outlines the goals of acute stroke imaging as establishing the diagnosis, obtaining information on vasculature, and guiding appropriate therapy. CT is described as the initial test to rule out hemorrhage and identify early signs of infarction. MRI sequences such as DWI, T2WI, and FLAIR are also summarized. The roles of CTA in evaluating vessels and CTP in identifying tissue at risk of infarction are covered. Imaging findings of ischemic and hemorrhagic stroke subtypes are presented.
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Introduction to imaging in acute stroke, types (ischemic and hemorrhagic), stroke mechanisms.
Summary of radiological tests like CT, MR, and their types for evaluating strokes.
Establish rapid diagnosis, evaluate intracranial vasculature, and guide therapy for infarction.
Four critical assessments: Parenchyma, Pipes, Perfusion, and Penumbra to evaluate stroke.
Defines penumbra in acute stroke as salvable tissue around irreversibly injured core.
Identification of early signs indicating ischemic strokes such as hypoattenuating brain tissue.
Details on CT imaging showing obscuration of the lentiform nucleus due to acute ischemia.
Describes CT imaging features of insular ribbon sign and dense MCA sign as indicators of stroke.
Incidence of hemorrhagic strokes and various conditions that may mimic stroke on NECT.
CTA's role in determining the involved vessel post-infarction diagnosis.
CT perfusion studies' significance in identifying ischemic penumbra and assessing risks.
Role of MRI in early detection of infarctions and its comparison to CT findings.
Emphasizes DWI's sensitivity in detecting strokes and its progression over time.
Describes DWI's pseudo-normalization and comparison of affected brain volume.
Explains the methodology of perfusion imaging with MRI for stroke evaluation.
Visuals of identifying irreversible changes and matching perfusion to guide therapy.
Criteria to determine suitability for t-PA treatment in stroke patients.
Identifies controversial relative contraindications for t-PA therapy based on imaging.
Defines various types of intracranial hemorrhage and the imaging approach for diagnosis.
Visual representations of different types of hemorrhagic strokes on CT imaging.Provides references used in the presentation and concludes with thanks.
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Imaging in acute stroke
- 1. Imaging In AcuteStroke Muhammad Bin Zulfiqar PGR New Radiology Department SHL/SIMS
- 2. Stroke Acute central nervoussystem injury with abrupt onset Mechanism: • Interruption of blood flow(Ischemic Stroke) or • Bleeding into or around the brain(Hemorrhagic stroke)
- 3. Stroke Types Most commonstroke etiologies: 1) Cerebral Infarction 80% 2) Primary Intracranial Hemorrhage 15% 3) Non traumatic subarachnoid hemorrhage 5%
- 4. Menu of RadiologicalTests CT: w/ or w/o contrast CT angiogram (CTA) MR: w/ or w/o contrast T1 or T2 weighted (T1WI, T2WI) FLAIR Diffusion weighted image (DWI) Susceptibility(very important) MR angiogram Cerebral Angiogram
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- 6. Goal of imaging •Establish diagnosis fast(exclude hemorrhage) • Obtain accurate information regarding intracranial vasculature and brain perfusion • Appropriate therapy(In case of infarction tPA inclusion)
- 7. 4 Ps ofAcute Stroke Imaging • Parenchyma: – Assess early sign of acute stroke, rule out hemorrhage (unenhanced CT) • Pipes: – Assess extracranial circulation (carotid and vertebral arteries of the neck) – Assess intracranial circulation for evidence of intravascular thrombus • Perfusion: – Assess Cerebral blood volume, cerebral blood flow, and mean transit time • Penumbra: – assess tissue at risk of dying if ischemia continues without recanalization of intravascular thrombus
- 8. PENUMBRA a core ofirreversibly infracted tissue surrounded by a peripheral region of ischemic but salvageable tissue referred to as a penumbra. Without early recanalization, the infarction gradually expands to include the penumbra.
- 9. CT EARLY SIGN •Hypo attenuating brain tissue • Obscuration of lentiform nucleus • Dense MCA sign • Insular ribbon sign • Loss of sulcal effacement
- 10. Hypo attenuating braintissue • MCA infarction: on CT an area of hypo attenuation appearing within six hours is highly specific for irreversible ischemic brain damage
- 11. Obscuration lentiform nucleus Axialunenhanced CT image shows hypo attenuation 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.
- 12. Obscuration lentiform nucleus Axialunenhanced CT images 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 with the narrower window used for b (window width, 10 HU; center, 28 HU).
- 13. Insular ribbon Sign Axialunenhanced CT image, shows hypo attenuation 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.
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- 15. Dense MCA sign Thisis 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.
- 16. Dense MCA sign (a)Unenhanced CT shows hyper attenuation in a proximal segment of the left MCA (arrows). (b, c) Axial (b) and coronal (c) reformatted images from CT angiography show the apparent absence of the same vessel segment(arrows
- 17. Hemorrhagic infarcts • 15%of MCA infarcts are initially hemorrhagic.
- 18. Stroke may Mimicson NECT • Tumor • Old Blood clot – EDH – SDH • Abscess • Brain Edema • Trauma
- 19. Tumor • Mets fromCA breast
- 20. Chronic Hemorrhage • CTaxial- left chronic frontoparietal subdural hematoma, hypo intense area. • Subacute hemorrhage
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- 24. CTA and CTPerfusion • Once we have diagnosed the infarction, we want to know which vessel is involved by performing a CTA.
- 25. CTA • Insular ribbonsign in right insular cortex • CTA disclose thrombus in rt. MCA
- 26. CT Perfusion (CTP) •With CT and MR imaging we can get a good impression of the area that is infracted. • but we cannot preclude a large ischemic penumbra (tissue at risk). With perfusion studies we monitor the first pass of an iodinated contrast agent bolus through the cerebral vasculature. Perfusion will tell us which area is at risk. Approximately 26% of patients will require a perfusion study to come to the proper diagnosis.
- 27. CT Perfusion (CTP) •The limitation of CT-perfusion is the limited coverage.
- 28. NECT, CTP andCTA • Study demonstrates that Plain CT, CTP and CTA can provide comprehensive diagnostic information in less than 15 minutes, provided that you have a good team.
- 29. NECT, CTP andCTA • CT is normal but patient is symptomatic • CTP shows a perfusion defect • CTA was subsequently performed and a dissection of the left internal carotid was demonstrated.
- 30. Role of MRI •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! • MR Hperintensity = CT Hypodensity
- 31. • T2WI andFLAIR demonstrating hyperintensity in the territory of the middle cerebral artery. • Notice the involvement of the lentiform nucleus and insular cortex.
- 32. Diffusion Weighted Imaging(DWI) • DWI is the most sensitive sequence for stroke imaging. • Also called Stroke sequence
- 33. DWI in posterior,anterior and middle cerebral infarction Diffusion Weighted Imaging (DWI)
- 34. Diffusion Weighted Imaging(DWI) • very subtle hypodensity and swelling in the left frontal region with effacement of sulci compared with the contralateral side. • DWI shows marked superiority in detecting infarct
- 35. Signal intensities onT2WI and DWI in time • In the acute phase T2WI will be normal, but in time the infracted 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. • 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.
- 36. Pseudo-normalization of DWI •This occurs between 10-15 days. • DWI is normal. • T2 WI shows subtle hyperintensity in rt. Occipital lobe. • GD T1 shows gyral enhancement which suggest infarct.
- 37. Pitfall in DWI •If we compare the DWI images in the acute phase with the T2WI in the chronic phase, we will notice that the affected brain volume in DWI is larger compared to the final infracted area (respectively 62cc and 17cc). • So everything bright on DWI might not be irreversibly dead.
- 38. Perfusion MR Imaging Technique •Perfusion with MR is comparable to perfusion CT. • A compact bolus of Gd-DTPA is delivered through a power injector. • Multiple echo-planar images are made with a high temporal resolution. • T2* gradient sequences are used to maximize the susceptibility signal changes.
- 39. Identification of PENUBRABY PMR • 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(PENUMBRA). • This is the brain tissue that maybe can be saved with therapy.
- 40. • Above imagesare normal and we have to continue with DWI. • On the DWI there is a large area with restricted diffusion in the territory of the right middle cerebral artery. • There is a perfect match with the perfusion images. • so this patient should not undergo any form of thrombolytic therapy.
- 41. • On theleft another MCA infarction. • It is clearly visible on CT (i.e. irreversible changes). • There is a match of DWI and Perfusion, so no therapy.
- 42. • The DWIand ADC map is shown which suggest infarct. • perfusion images show 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.
- 43. Selection for t-PA:Inclusion • No evidence of : – Hemorrhage • EDH/SDH • IPH • SAH – Non-stroke etiology • Tumor • Abscess • Trauma
- 44. Summary for t-PA:Relative Contraindications • Controversial – Evidence of a large MCA territory infarction • Gray-white de-differentiation > 1/3 of territory • Sulcal effacement/mass effect > 1/3 of territory
- 45. Hemorrhagic Stroke • Intracranialhaemorrhage is a collective term encompassing many different conditions characterized by the extra vascular accumulation of blood within different intracranial spaces.
- 46. Cranial CT Scanningand Hemorrhage • First line imaging study in suspected stroke patients – Exquisite sensitivity for the detection of blood – Ubiquitous in hospitals – So our focus is CT
- 47. Hemorrhagic Stroke • Intra-axialhaemorrhage – intracerebral haemorrhage – basal ganglia haemorrhage – lobar haemorrhage – pontine haemorrhage – cerebellar haemorrhage • Intraventricular haemorrhage (IVH) • extra-axial haemorrhage – extradural haemorrhage (EDH) – subdural haemorrhage (SDH) – subarachnoid haemorrhage (SAH)
- 48. Intracerebral Hemorrhage • Largeintracerebral hemorrhage with midline shift
- 49. ICH with IntraventricularExtension
- 50. Basal Ganglia Hemorrhagewith IC extension
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- 55. Non Traumatic SubduralHematoma • Acute subdural hematoma. Note the bright (white) image properties of the blood on this non contrast cranial CT scan. Note also the midline shift.
- 56. References • Acute stroke:usefulness of CT before starting thrombolytic therapy :by R von Kummer et al. Radiology 1997, Vol 205, 327-333, • Early CT findings in Lentiform Nucleusby N Tomura et al Radiology 1988, Vol 168, 463-467 • State of the art imaging of acute stroke by Ashok Srinivasan et al RadioGraphics 2006;26:S75-S95 • Radiopedia
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