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MRI Stroke
- 13. FRONTAL LOBE –RED PARIETAL LOBE - BLUE
- 20. BASAL GANGLIA
- 22. Basal ganglia
- 23. HYPOTHALAMUS
- 26. PITUTARY FOSSA
- 28. CAVERNUS SINUS
- 38. HIPPOCAMPUS
- 42. BRAIN ARTERIES
- 46. VENOUS SYSTEM
- 49. Stroke Vascular pathology causing acute focal CNS injury leading to neurological deficit. Includes:- Cerebral infarct Intracerebral Hemorrhage Sub arachnoid hemorrhage
- 51. • Atherosclerotic stroke carotid bifurcation > cavernous ICA • Small vessel disease- • Cardioembolic disease • Others Undetermined etiology
- 52. PATHOPHYSIOLOGY OF ACUTE ISCHEMIC STROKE CEREBRAL BLOOD FLOW( in ml/min/100g ) NORMAL 50-60 OLIGEMIC STATE 35 ISCHEMIC STATE 20 INFARCTION <10
- 53. • It is the area at risk for infarction, if the blood flow is not restored to normal • It still has marginal blood supply from collateral sources and retains intact cellular metabolism.
- 54. ZONE OF OLIGEMIA ZONE OF PENUMBRA ZONE OF INFACRTION
- 68. GOALS OF NEUROIMAGING PRIMARYGOALS •To distinguish ischemic stroke from Intracranial Haemorrhage •Toselect patients for reperfusion therapies.
- 69. Give the answer
- 70. ACUTE STROKE
- 72. emergent NCCT
- 73. ANSWERED BY NCCT ANSWERED BY CTA
- 74. INTRACRANIAL HEMORRHAGE PRESENT No further imaging required,CTA can be done to evaluate for active bleeding RULEDOUT Now, Look whether major vessels is occluded CTA/MRA done immediately to depict potentially treatable major vessel occlusion
- 75. 3rd and 4th question of stroke 3.Is part of the brain irreversibly injured? 4.Is an ischemic PENUMBRA present ?
- 77. first 6 hours within 6-48 hours from onset HYPERACUTE INFARCT ACUTE INFARCT
- 78. MR STROKE PROTOCOL Fast stroke protocol (Expidited)……6 minutes Routene protocol………20-25 minutes includes:- parenchymal imaging MR Angiogram Perfusion imaging
- 80. • AlthoughCT is the most commonly used modality for stroke imaging, for hyperacute ischemia. • Absence of radiation
- 81. First 3-6 hours = normal BLURRINGOFGrey matter-White Matter INTERFACE LOSSOFTHE EXPECTED FLOWVOID
- 83. Nearly all stroke are FLAIR POSITIVE (cortical swelling and hyperintensity , intraarterial hyperintensity) by 7 hours T2 scans become positive by 12-24 hours
- 86. ADC value decrease (appears DARK)>>> high signal intensity on DWI = DWI POSITIVE Cytotoxic edema AQP4 ( astrocyte aquaporins ),
- 87. 2 b values
- 88. • DWI can detect ischemia within 20 minutes with 95% sensitivity signal intensity of DWI decreases after 3-4 days but persists for 10- 14 days. Hypointensity on ADC is maximum at 2-3 days, but persist for 7-10 days
- 90. Head of right caudate nucleus and lentiform nucleus show diffusion restriction
- 92. FLAIR- DWI MISMATCH DWI FLAIR viable ischemic penumbra eligibility for thrombolysis
- 93. BLOOMING hypointensity Large infarcts may show –prominent hypointense medullary veins haemoglobin deoxygenation
- 94. BLOOMING HYPOINTENSI TY IN LT. MCA – MRI CORRELATE OF HYPERDENSE MCA SIGN ON NCCT
- 95. FLAIR + PATCHY HYPERINTENSITY LINEAR HYPOINTENSITY IN LEFT MCA
- 96. DWI + DWI HYPERINTENSI TY LOSS OF FLOW IN LEFT MCA
- 97. T1 POST CONTRAST Intravascular (arterial) enhancement •Parenchymal enhancement is uncommon
- 98. densely ischemic core of the infarct DWI-PWI MISMATCH CBV-CBF, DWI –FLAIR MISMATCH
- 100. A negative DWI doesn’t exclude the diagnosis of stroke
- 101. Affects cortex in NONVASCULAR distribution
- 102. ABSCESS SHOWING DIFFUSION RESTRICTION
- 103. PRIMARY CNS LYMPHOMA showing diffusion restricti
- 104. STATUS EPILEPTICUS Affects cortex in NONVASCULAR distribution
- 105. IMAGING SEQUENCE HYPERACUTE INFARCT ACUTE INFARCT T1 WEIGHTED isointensity usually low signal intensity after 12- 24 hours, BLURRINGOF GW-WM INTERFACEcan be seen T2 WEIGHTED Isointensity after 12-24 hours ; may see loss of flow void in large arteries usually high signal intensity FLAIR usually positive after 7 hours high signal intensity DIFFUSIONWEIGHTED IMAGING high signal intensity high signal intensity ADC MAPPING low signal intensity low signal intensity CONTRAST ENHANCEDT1 WEIGHTED arterial enhancement may occur after 0-2 hours arterial enhancement may occur
- 107. 2D TOF MIP MRA 3D TOF VRT MRA
- 108. BILATERAL CAROTID MRA TOF MIP
- 109. LEFT ICA STENOSIS
- 110. ROLE OF PERFUSION MRI scale is graduated from red yellow green …… highest blue purple black…… lowest ischemic brain is blue purple infarct appears black
- 112. pMRI showing reduced CBF BLOOMININ G IN LEFT MCA
- 117. HEMORRHAGIC TRANSFORMATION (HT) 20-25% cases 2days to a week after ictus. Reperfusion either spontaneously / following treatment causes exudation of blood . HT Indicates favourable outcome
- 121. SWI PHASE
- 122. T1 C+ Arterial enhancement :- seen after 3 days, nonspecific Parenchymal enhancement :- after 5-7 days , remains for 2-3 months Laptomaningial enhancement :- or ring enhancement may be seen
- 123. DAY 2 DAY 0 DAY 7
- 126. •CHRONICCEREBRAL INFARCTS gliosis volume loss with anatomic vascular distribution. postinfarction encephalomalacia
- 127. MR IMAGING FEATURES T1WI- Hypointense , hyperintensity with cortical necrosis may be seen. T2WI- High signal intensity FLAIR - Low signal intensity in presence of cystic encephalomalacia , marginal gliosis around the old cavitated lesions shows hyperintensity.
- 129. T1 HYPOINTENSE FOCI
- 130. T2 HYPERINTENSE FOCI
- 134. ISCHEMIC STROKE, HYPOGLYCEMIA , STATUS EPILEPTICUS, CARDIACARREST in medial occipital cortex and perirolandic region • due to neuronal damage , reactive tissue change of glia and deposition of lipid laden macrophages. T1 hyperintensity – typically after 2 weeks to 1 month and fades over 3 months. But is seen for as long as 1.5 years
- 136. WATERSHED / BORDERZONE INFARCTS junction between two non- anastomosing distal arterial distributions.
- 139. 3-15mm CSF marker of cerebral small vessel disease. LACUNAR INFARCTS
- 141. FLAIR HYPERINTENSITY DWI HYPERINTENSITY ACUTE LACUNAR INFARCT
- 144. LACUNAR INFARCT IN RIGHT BASAL GANGLIA
- 145. VENOUS INFARCT
- 150. SPHENOPARIET AL AND CAVERNOUS SINUS DEEP CEREBRAL VEINS VOL AND TRANSVER SE SINUS CORTICAL VEINS AND SSS
- 152. DURAL SINUSTHROMBOSIS MR IMAGING FEATUR Acute DST T2* "blooms "empty delta"
- 155. Subacute DST Chronic DST "squiggly" parenchymal enhancement , thick enhancing dura
- 157. Thrombus in SSS FILLIN G DEFEC T IN SSS
- 158. FILLING DEFECT IN SSS FILLING DEFECT IN LEFT TS
- 159. ACUTE 0-5 DAYS SUBACUTE 6- 15DAYS CHRONIC>15 DAYS Isointense onT1 Hyperintense on bothT1 andT2 Isointense onT1 Hypointense on T2 Due to intracellular deoxyhemoglobin Due to methemoglobin In thrombus Iso -hyper onT2
- 160. SUPERFICIAL CEREBRALVEIN THROMBOSIS SuperficialThrombosisWith DST SuperficialThrombosis Without DST cause subarachnoid hemorrhage "cord" sign on CT which is called hyperintense vein sign MR shows thrombosed vein T2* GRE shows ○ Blooming …..thrombus in vein
- 161. SWI showing blooming in superficial cortical veins
- 162. SWI showing blooming in right VOT T1WI showing linear hyperintensi ty