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Neuroradiology 1a
- 1. NEURORADIOLOGY 1 SUBAHSHINI JEYABALAN SUPERVISOR: DR LEONG YUH YANG HUKM
- 2. OUTLINE : Cerebral ischemia: • Arterial Ischaemia : pathophysiology, evolution of stroke and radiopathological correlation. • Venous ischaemia : pathophysiology, radiopathological correlation. • Watershed area Cerebral hemorrhage : Evaluation of hematoma CNS vascular malformation Trauma : Herniation syndrome
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- 4. STROKE Definition**: A clinical syndromecharacterized by rapidly developing clinical symptoms and/or signs of focal, and at times global, loss of cerebral function, with symptoms lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin”. MOH statistic shows cerebrovascular accident is one of the top five leading cause of death since 2000’s; with mortality of 8.43 per 100 000 population. ** There is no incidence or prevalence data available for the country. **Malaysia Clinical Practice Guidelines Management of Ischemic Stroke 2nd Edition 2012
- 5. STROKE Divided into twobroads categories : Ischemic ( 85 % ) • Embolism • Thrombosis Hemorrhagic ( 15 % )
- 6. ISCHEMIC STROKE Pathophysiology Basis Interruption ofcerebral blood flow Ischemia at cellular level ( O2, glucose) ATP- dependent Na/K pump failure K+ Efflux Ca2+, Na+ and water influx Cellular swelling “Cytotoxic oedema” Liquefactive necrosis “Changes in brain water content are key to understanding signs of infarction in CT or MR”
- 7. ROLE OF IMAGINGIN A PATIENT WITH ACUTE STROKE 1. Cerebrovascular accident or not? Could it be tumour? 2. CVA : ? Ischaemic or ? Haemorrhagic = Exclude haemorrhage 3. To decide on management. u Differentiate between irreversibly affected brain tissue and reversibly impaired tissue (dead tissue versus tissue at risk) u Identify stenosis / occlusion of major extra- and intracranial arteries In this way we can select patients who are candidates for Medical thrombolysis? Neurointervention? Surgical intervention?
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- 9. ? CT ORMRI ? Imaging of acute stroke is performed either with CT or MRI, majority with CT CT u Widely available u Rapidly done u Exclude hemorrhage u 60% of infarcts are seen in CT within 3-6hours and all are seen in 24hours u Lesser sensitivity MRI u More time consuming u Less available u Significantly higher sensitivity and specificity à diagnosis of acute infarction in the first few hours after onset. Mainstay of imaging of acute ischemic stroke is non contrast CT but now it’s been supplemented by CT Angiography and CT Perfusion.
- 10. EVOLUTION OF ISCHEMIC STROKEAND ITS APPEARANCES
- 11. Immediate: Ø Dense arterysign • Earliest sign in CT visible hyperdense segment of a vessel (direct visualization of the clot) à Clot is hyperdense than normal flowing blood (40HU). • Depend on time of visualization / age of clot. Acute thrombus not much denser than flowing blood, however with time the clot contracts and become hyperdense (100HU). Ø MCA “Dot sign”
- 12. M1 segment ofright MCA is much denser than any other arteries CTA – hypoenhancement/ filling defect of the M1 segment of right MCA
- 13. This case demonstratesthe ‘DOT SIGN’ a typical appearance of a hyperdense MCA sign, more distally in M2/M3 branches. Dot sign represents a thromboembolism within the Sylvian fissure (M2,M3 segment). The sign appears when the high-attenuation MCA is viewed in axial section, since the occluded vessel courses in a plane perpendicular to the transverse plane of imaging.
- 14. Early/ Hyperacute phase(1-3 hours) Ø Hypoattenuating 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. An increase of brain water content by 1% will result in a CT attenuation decrease of 2.5 HU. • Loss of gray and white matter differentiation (typical for infarction) • Sulci effacement • Depend on the site of occlusion and presence of collateral flow. • Hypoattenuation on CT is highly specific for irreversible ischemic brain damage if it is detected within first 6 hours. • No hypodensity on CT is a good sign.
- 15. Hypoattenuating brain tissuein the right hemisphere: MCA infarction
- 16. Ø Obscuration ofthe lentiform nucleus • Also known as blurred basal ganglia • Is seen in middle cerebral artery infarction • Basal ganglia are almost always involved in MCA-infarction. Left lentiform nucleus appears hypoattenuated because of acute ischemic of the lenticulostriate territory resulting in obscuration of the lentiform nucleus. This features maybe seen on CT images within 2hours after the onset of stroke.
- 17. Ø Insular ribbonsign • Hypodensity and swelling of the insular cortex • Subtle early CT sign of infarction in MCA territory • This region is very sensitive to ischemic; furthest removed from collateral flow. Axial unenhanced CT image obtained in a 73years old woman 2 hours after the onset of left hemiparesis, shows hypoattenuation and obscuration of the lentiform nucleus (white arrow) and loss of gray white matter differentiation of the right insula (black arrows) – insula ribbon sign.
- 18. FIRST WEEK Ø Appearanceof mass effect at peak of 3-5days Day 3 : Axial unenhanced CT image obtained shows region of well demarcated low attenuation and in this case with some small hemorrhagic transformation and mass effect. Day 5: Mass effect was severe that decompression craniectomy done to reduce ICP and herniation.
- 19. SECOND TO THIRDWEEK Ø Swelling starts to subside; less mass effect Ø CT fogging phenomenon • transient return of infarcted cortex to a near normal appearance. Ø Seen in 50% of cases. Day 11: Axial unenhanced CT shows swelling and oedema reduced , increase density of infarcted region can mimic normal brain tissue.
- 20. CT Fogging Phenomenon ØAt 2 to 3 weeks following an infarct, the cortex regains near-normal density. Ø This is believed to occur as the result of: • migration of lipid-laden macrophages into the infarcted tissue • proliferation of capillaries • decrease in oedema Cortical laminar necrosis
- 21. CHRONIC STROKE (MONTHS) ØEncephalomalacia Ø Atrophy with enlargement of the adjacent sulci and ventricles Ø Cortical mineralization can also sometimes be seen appearing hyperdense. Axial unenhanced CT show well demarcated , very low density region at left parietal with no mass effect. Adjacent lateral ventricle is dilated.
- 23. Assessment of acutestroke Ø Alberta stroke program early CT score (ASPECTS) • Alberta Stroke Program Early CT score (ASPECTS) is a 10-point quantitative topographic CT scan score. • ASPECTS was developed to offer the reliability and utility of a standard CT examination with a reproducible grading system to assess early ischemic changes on pretreatment CT studies in patients with acute ischemic stroke of the anterior circulation.
- 24. ASPECT SCORE Ø Segmentalassessment of the MCA vascular territory is made and 1 point is deducted from the initial score of 10 for every region involved: § Caudate § Putamen § Internal capsule § Insular cortex § M1, M2, M3 are at the level of the basal ganglia § M4, M5, M6 are at the level of the ventricles immediately above the basal ganglia
- 25. • M1: "anteriorMCA cortex," corresponding to frontal operculum • M2: "MCA cortex lateral to insular ribbon" corresponding to anterior temporal lobe • M3: "posterior MCA cortex" corresponding to posterior temporal lobe • M4: "anterior MCA territory immediately superior to M1" • M5: "lateral MCA territory immediately superior to M2" • M6: "posterior MCA territory immediately superior to M3"
- 26. Ø A normalCT scan receives an ASPECTS of 10 points. Ø An ASPECTS of 0 indicates diffuse involvement throughout the MCA territory. Ø Patients with ASPECTS score less than 8 treated with thrombolysis have poorer clinical outcome. Ø Patients with scores ≥8 have a better chance for an independent outcome. Ø The score does not consistently predict treatment response or intracranial hemorrhage or offer prognostic information.
- 27. CT Angiography Ø CTangiography typically involve a volumetric helical acquisition that extends from the aortic arch to the circle of Willis. Ø CTA demonstrate a significant thrombus burden that can guide appropriate therapy in the form of intraarterial or mechanical thrombolysis. Ø Identification of carotid artery disease and visualization of the aortic arch may provide the cause of the ischemic event and guidance for interventional neuroradiologist.
- 28. • Intracranial majorvessel occlusion • Extracranial carotid arterial disease. Insular ribbon sign in right insular cortex Filling defect in keeping with thrombus in right MCA CT ANGIOGRAPHY
- 29. CT PERFUSION (CTP) ØCT perfusion in ischaemic stroke has become established in most centres with stroke services as an important adjunct, along with CT angiography (CTA), to conventional unenhanced CT brain imaging. Ø It enables differentiation of salvageable ischaemic brain tissue (the penumbra) from the irreversible damaged infarcted brain (the infarct core). This is useful when assessing a patient for treatment (thrombolysis or clot retrieval). Ø Monitoring the first pass of an iodinated contrast agent bolus through the cerebral vasculature. Ø The key to interpreting CT perfusion in the setting of acute ischaemic stroke is understanding and identifying the infarct core and the ischaemic penumbra, as a patient with a small core and a large penumbra is most likely to benefit from reperfusion therapies.
- 30. PARAMETERS ASSESSED Ø Meantransit time (MTT) = time difference between arterial inflow and venous outflow. Ø Time to peak (TTP): the time at which contrast concentration reaches its maximum (a delay > 4 s seems to indicate tissue at risk) Ø Cerebral blood flow (CBF) : defined as the volume of blood passing through a given amount of brain tissue per unit of time Ø Cerebral blood volume (CBV): defined as the volume of blood in a given amount of brain tissue Ø CBF = CBV / MTT
- 31. Core u increased MTT/Tmax umarkedly decreased CBF u markedly decreased CBV Penumbra u increased MTT/Tmax u moderately reduced CBF u near-normal or increased CBV u CBF/CBV ”mismatch” estimates penumbra
- 32. NECT, CTP ANDCTA u NECT is normal but patient is symptomatic u CTP shows a perfusion defect u CTA demonstrated a dissection of the left internal carotid artery.
- 33. ROLE OF MRI ØMore time consuming and less available Ø But has significant higher sensitivity and specificity diagnosis of acute ischemic infarction in the first few hours after onset Ø DWI/ ADC (stroke sequence) – High sensitivity (88-100%) and high specificity (86-100%) in the detection of small and early infarcts.
- 34. Acute (0-7 days) uWithin minutes of arterial occlusion, diffusion-weighted imaging demonstrates increased DWI signal and reduced ADC values. u ADC value decreases with maximal signal reduction at 1 to 4 days u Marked hyperintensity on DWI (a combination of T2 and diffusion weighting).
- 35. DIFFUSION WEIGHTED IMAGING(DWI) • Very subtle hypodensity and swelling in the left frontal region with effacement of sulci. • DWI shows marked superiority in detecting infarct
- 36. Subacute (1-3 weeks) ØADC pseudonormalization occurs in the second week (7-15 days) • ADC values rise and return to near baseline (infarcted tissue progressively gets brighter than normal parenchyma) • irreversible tissue necrosis is present despite normal ADC values • DWI remains hyperintense due to T2 shine through Ø After 2 weeks ADC values continue to rise above normal parenchyma and the region appears hyperintense
- 37. Chronic infarct (>3weeks) Ø ADC signal high Ø DWI signal low (as T2 hyperintensity and thus T2 shine through resolve)
- 38. T2WI / FLAIR ØOn T2WI and FLAIR infarction is seen as high signal intensity. Ø These sequences detect 80% of infarctions before 24 hours. Ø They may be negative up to 2-4 hours after onset of symptoms.
- 39. SIGNAL INTENSITIES ONT2WI AND DWI IN TIME • In 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 • 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
- 40. T1WI Ø T1 hypointensityis only seen after 16 hours and persists. Ø Acute: T1 signal remains low, although some cortical intrinsic high T1 signal may be seen as early as 3 days after infarction. After day 5 the cortex usually demonstrates contrast enhancement on T1 C+. Ø Subacute : T1 weighted sequences continue to show hypointensity with cortical intrinsic high T1 signal due to cortical lamina necrosis. Cortical enhancement is usually present throughout the subacute period. Ø Chronic : T1 signal remains low with intrinsic high T1 in the cortex if cortical necrosis is present. Cortical contrast enhancement usually persists for 2 to 4 months
- 41. Pre contrast T1WIshows mild effacement of sulci in the right MCA. A few subtle bright signal along the gyrus noted due to cortical laminar necrosis. Post contrast T1WI shows marked gyral enhancement, hallmark of subacute infarcts.
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- 43. Ø The ratesof haemorrhagic transformation of ischaemic strokes have been variably reported, but generally over half of all cerebral infarcts at some stage develop some haemorrhagic component. Ø The majority of haemorrhagic transformation after stroke (89%) is petechial haemorrhages; a minority (11%) haematomas. Ø Certain factors increase the risk of haemorrhagic transformation of stroke, including older age, larger stroke size, cardioembolic stroke, anticoagulant use, fever, hyperglycaemia, low serum cholesterol, elevated systolic blood pressure in the acute setting, thrombolytic therapy or other recanalization. Ø A commonly used classification system was developed for the European Cooperative Acute Stroke Study (ECASS II), which divides haemorrhagic transformation into four subtypes.
- 44. Pathophysiology Disruption of capillary endothelial cell Reperfusion intoinfarcted area Loss of vascular autoregulation Microscopic or gross leakage Receive anticoagulant/ thrombolysis therapy
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- 47. Ø Cerebral venousinfarction is an uncommon form of stroke. Ø Cerebral venous thrombosis is an important cause of stroke especially in children and young adults. Ø Most commonly secondary to cerebral venous thrombosis and manifests with or without haemorrhage. Other causes are trauma, infection (subdural empyema) and hypercoagulability disorders.
- 48. Pathophysiology Ø increased venouspressure • occlusion following thrombosis will increase local venous pressure and can lead to rupture of venules / capillaries • cerebral veins also lack valves so back pressure can be demonstrated Ø flow dynamics • the increased venous pressure reduces effective drainage of affected brain tissue, with increased cerebral blood volume and reduced perfusion pressures, with subsequent oxygen debt and eventual infarction Ø increased intracranial pressure • this is seen less frequently and in more severe cases due to the collaterals of the venous system Ø capillary recruitment • in the reperfusion phase of infarct, the recruitment of immature capillaries are themselves friable and prone to infarct/haemorrhage
- 50. Dense clot sign: Axial unenhanced CT images shows hyperattenuation within the superior sagittal sinus consistent with thrombus.
- 51. Visualization of athrombosed cortical vein that is seen as a linear or cord-like density, is also known as the cord sign.
- 52. Empty delta sign.Axial contrast- enhanced CT images shows a central region of low attenuation consistent with a thrombosis in the superior sagittal sinus.
- 53. The images onthe left show abnormal high signal on the T1- weighted images due to thrombosis. The thrombosis extends from the deep cerebral veins and straight sinus to the transverse and sigmoid sinus on the right. Notice the normal flow void in the left transverse sinus on the right lower image.
- 54. NECT shows hyperdenseinternal veins and bilateral (R > L) thalami hypodensities, compatible with dural vein thrombosis and venous infarction.
- 55. WATERSHED AREAS u Watershedcerebral infarctions, also known as border zone infarcts, occur at the border between cerebral vascular territories where the tissue is furthest from arterial supply and thus most vulnerable to reductions in perfusion. CORTICAL WATERSHED ZONE (EXTERNAL) DEEP WHITE MATTER WATHERSHED ZONE (INTERNAL) • Confluence of ACA/ MCA/ PCA territories • Typically at cortex, grey-white matter junction • Confluence of major territories and perforating branches • Typically at deep white matter
- 56. . ACA/MCA: in thefrontal cortex, extending from the anterior horn to the cortex MCA/PCA: in the parieto- occipital region, extending from the posterior horn to the cortex ≥3 lesions, each ≥3 mm in diameter, in a linear fashion parallel to the lateral ventricles in the centrum semiovale or corona radiata, which sometimes become more confluent and band-like
- 57. Ø Triple watershedzone: most vulnerable region where ACA, MCA, and PCA converge in the parieto-occipital region posterior to the lateral ventricles. The posterior confluence where all three vascular distributions meet together is especially vulnerable to cerebral hypoperfusion.
- 58. Axial view ofNECT shows in addition to bilateral chronic small vessel ischaemic change, on the left there is patchy cortical infarction in a border zone distribution
- 59. Axial view NECTshowing an old infarction of the cortex and adjacent subcortical white matter located at the right border zone of ACA and MCA.
- 60. References u Imaging inNeurology Osborn/Digre u Grainger&Allison’s Diagnostic Radiology Essential u Core Radiology, A Visual Approaching Diagnostic Imaging u Radiopedia.org u Radiology Assistant. nl