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MR IMAGING IN STROKE
- 1. MR IMAGING INSTROKE MODERATOR DR RADHIKA BATRA PG DR SHIVALI ARYA DR SHUBHAM K.
- 2. DEFINITION Stroke is classicallycharacterized as a neurological deficit attributed to an acute focal injury of the central nervous system by a vascular cause , including cerebral infarction , intracerebral hemorrhage (ICH) and subarachanoid hemorrhage(SAH)”
- 3.
- 4. • Atherosclerotic stroke carotidbifurcation > cavernous ICA • Small vessel disease- • Cardioembolic disease • Others
- 5. PATHOPHYSIOLOGY OF ACUTEISCHEMIC STROKE CEREBRAL BLOOD FLOW( in ml/min/100g ) NORMAL 50-60 OLIGEMIC STATE 35 ISCHEMIC STATE 20 INFARCTION <10
- 6. • It isthe area at risk which is at the risk of infarction if the blood flow is not restored to normal • It still has marginal blood supply from collateral sources and retains intact cellular metabolism. Thus , it has potential to be restored under reperfusion conditions and is vital in
- 7. ZONE OF INFACRTION ZONEOF PENUMBRA ZONE OF OLIGEMIA
- 8. ISCHEMIA remains viable INFARCTION frankcell death
- 10.
- 13.
- 16.
- 18.
- 23. GOALS OF NEUROIMAGING PRIMARYGOALS •To distinguish ischemic stroke from Intracranial Haemorrhage •To select/triage patients for possible reperfusion therapies.
- 24. FOUR “MUST KNOW”QUESTIONS IN ACUTE STROKE TRIAGE
- 25.
- 27.
- 28.
- 29. INTRACRANIAL HEMORRHAGE PRESENT No further imaging required,CTAcan be done to evaluate for active bleeding RULED OUT Now, Look whether major vessels is occluded CTA/MRA done immediately to depict potentially treatable major vessel occlusion
- 30. 3rd and 4thquestion of stroke 3.Is part of the brain irreversibly injured? 4.Is an ischemic PENUMBRA present ?
- 31. UNSALVAGABLE INFARCTED CORE & POTENTIALLYSALVAGEABLE BRAIN
- 32. first 6 hours within6-48 hours from onset HYPERACUTE INFARCT ACUTE INFARCT
- 33. • A faststroke protocol / “Expedited” stroke protocol 6 minutes ) 20-25 minutes
- 35. • Although CTis the most commonly used modality for stroke imaging, partly because of its wide availability and faster acquisition time , some comprehensive stroke centres choose MRI rather than CT because of higher Sn and Sp of MRI for delineation of hyperacute ischemia. • Absence of radiation. delineating an ischemic penumbra discrepancy betweenCT/CTA and clinical stroke severity
- 36. First 3-6 hours= normal BLURRING OF Grey matter-White Matter INTERFACE LOSS OFTHE EXPECTED FLOWVOID
- 38. Nearly all strokeare FLAIR POSITIVE (cortical swelling and hyperintensity , intraarterial hyperintensity) by 7 hours T2 scans become positive by 12-24 hours
- 40.
- 41. ADC value decrease(appears DARK)>>> high signal intensity on DWI = DWI POSITIVE Cytotoxic edema AQP4 ( astrocyte aquaporins ),
- 42. DWI is basedonT2W sequence Diffusion is assessed quantitively by ADC 2 b values
- 43. within 20 min sensitivityof 90-95 % of DWI hyperintense signal intensity persist for about 10-14 days persists for 7-10 days
- 44.
- 45. Head of right caudate nucleusand lentiform nucleus show diffusion restriction
- 47. FLAIR- DWI MISMATCH viable ischemicpenumbra eligibility for thrombolysis DWI FLAIR
- 48. BLOOMING hypointensity Large infarcts mayshow –prominent hypointense medullary veins haemoglobin deoxygenation
- 49. BLOOMING HYPOINTENSI TY IN LEFT MCAARTERYSUSCEPTIBILTY SIGN – MRI CORRELATE OF HYPERDENSE MCA SIGN ON NCCT
- 50. FLAIR + PATCHY HYPERINTENSITY LINEARHYPOINTENSITY IN LEFT MCA
- 51. DWI + DWI HYPERINTENSI TY LOSS OFFLOW IN LEFT MCA
- 52. T1 POST CONTRAST Intravascular(arterial) enhancement •Parenchymal enhancement is uncommon
- 53. densely ischemic core ofthe infarct DWI-PWI MISMATCH CBV-CBF, DWI –FLAIR MISMATCH
- 55. A negative DWIdoesn’t exclude the diagnosis of stroke
- 56. Affects cortex inNONVASCULAR distribution
- 57. ABSCESS SHOWING DIFFUSIONRESTRICTION
- 58. PRIMARY CNS LYMPHOMAshowing diffusion restricti
- 59. STATUS EPILEPTICUS Affects cortexin NONVASCULAR distribution
- 60. IMAGING SEQUENCE HYPERACUTE INFARCT ACUTEINFARCT T1WEIGHTED isointensity usually low signal intensity after 12- 24 hours, BLURRINGOF GW-WM INTERFACE can 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
- 62. 2D TOF MIPMRA 3D TOF VRT MRA
- 63. BILATERAL CAROTID MRATOF MIP
- 64.
- 65. and is recommendedfor screening of aneurysm in asymptomatic patients. HIGH RESOLUTIONVESSEL WALL MRI
- 66. PROPERTIES T1 WIT2WI PDWI STIR C+T1WI Lipid rich necrotic core Iso/hyper Iso/hypo Iso/hyper Hypo Hypo Fibrous tissue iso iso iso Hyper Hyper Fresh Hemorrhage hyper Hypo Hypo Hypo Iso Recent Hemorrhage hyper hyper hyper hyper Iso calcification hypo hypo hypo hypo hypo
- 67. • Calcification • Recent/fresh haemorrhage • Lipid core • Fibrous component • Post gadolinium enhancement
- 69. red yellow green bluepurple black blue/purple
- 70. 1.CBV : cerebralblood volume 4-5 ml/100g 2.CBF : cerebral blood flow 50-60 ml/100g/min 3.MTT : Mean transit time
- 71.
- 72. PROPERTIES DYNAMIC SUSCEPTIBILTY CONTRAST(DSC) DYNAMIC CONTRAST ENHANCEMENT (DCE) ARTERIAL SPIN LABELLING (ASL) HANDLING OF BOLUS tracking of bolus technique Passage of bolus technique Tagging of bolus CONTRAST MEDIA intravenous gadolinium intravenous gadolinium No contrast MECHANISM OF RELAXATION t2/t2* relaxation Signal change due toT1 relaxation Signal change due to Magnetic labelled bloodT1 relaxation MECHANISM magnetic field is distorted by contrast agent by virtue of its paramagnetic property , leading to more susceptibility effect and causes reduction of t2 and t2* around the vessels Contrast agent cause dipole- dipole interaction between the protons in the water molecules leading toT1 shortening and production of signal Tagged blood by inversion flows into the capillary site followed by transcapillary exchange with the brain tissue and flows into the draining vein TYPES OF IMAGING SEQUENCES T2 /T2 *WI T1 WI Sequence with shortTE and longTR TOTAL DURATION OF SCAN Relatively short (< 2 min) Long (5-6 min) Long with multiple averaging SIGNALTO NOISE RATIO Very good good fair
- 73. • DSC injection ofa bolus of IV gadolinium T2 * contrast in the brain • DCE shortening ofT1 shortening IV gadolinium, outside the brain • ASL WITHOUT CONTRAST AGENT. It
- 75. pMRI showing reduced CBF BLOOMININ GIN LEFT MCA
- 76. MTT with prolongedtransit time
- 81.
- 82. T2WI Subacute infarct shows “T2FOGGING EFFECT” in which of lipid laden macrophages decrease in edema
- 83.
- 84.
- 85. Good rule ofthumb is , if infarct is low signal on ADC infarct is < 1week old. “T2 shine through” is seen DWI & ADC
- 88. T2* GRE •Petechial orgyriform “ blooming” foci •Prominent ipsilateral medullary veins on SWI
- 89. HEMORRHAGIC TRANSFORMATION (HT) 20-25%cases 2days to a week after ictus. Reperfusion either spontaneously or following treatment with tPA causes exudation of blood cells through damaged vascular endothelium and blood brain barrier. Petechial > lobar bleed HT Indicates favourable outcome
- 90.
- 93.
- 94. Arterial enhancement Parenchymal enhancement 2or 3 days 2-3 months Leptomeningeal enhancement-
- 95. DAY 0 DAY2 DAY 7
- 96.
- 97.
- 98. •CHRONIC CEREBRAL INFARCTS volumeloss with gliosis anatomic vascular distribution. postinfarction encephalomalacia
- 99. 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.
- 100. •DWI “T2 shine –through”cystic encephalomalacia •ADC – •SWI
- 101.
- 102.
- 103.
- 106. ISCHEMIC STROKE, HYPOGLYCEMIA, STATUS EPILEPTICUS, CARDIAC ARREST • Most frequently located in medial occipital cortex and perirolandic region • Occurs due to neuronal damage , reactive tissue change of glia and deposition of lipid laden macrophages. T1 hyperintensity – as early as 3-5 days , but typically after 2 weeks , with a peak at 1 month and fades over 3 months. But is seen for as long as 1.5 years
- 107.
- 108. WATER SHED /BORDER ZONE INFARCTS junction between two non- anastomosing distal arterial distributions.
- 109. ExternalWS(MC ,embolic): InternalWS(by regionalhypoperfusion)
- 110.
- 112. (often reffered toas “ man in the barrel distribution of weakness)
- 113. Differential diagnosis- • Lacunarinfarcts • Embolic infarcts • Posterior Reversible Encephalopathy Syndrome (PRES
- 114.
- 115. 3-15mm CSF marker ofcerebral small vessel disease. LACUNAR INFARCTS
- 116.
- 120. FLAIR HYPERINTENSITY DWIHYPERINTENSITY ACUTE LACUNAR INFARCT
- 121.
- 122.
- 124. LACUNAR INFARCT INRIGHT BASAL GANGLIA
- 125. Differential Diagnosis Forlacunar infarcts
- 126.
- 129. SPHENOPARIET AL AND CAVERNOUS SINUS DEEP CEREBRAL VEINS VOL AND TRANSVER SESINUS CORTICAL VEINS AND SSS
- 131. secondary to cerebralvenous thrombosis. reversible. •Timely intervention can reverse the disease process and long term sequelae.
- 132.
- 133. LOCAL SYSTEMIC Sinus traumaProtien s and c deficiency Regional infection Peripartum state Neoplastic invasion OCP use Hypercoagulable state secondary to malignancy Common Causes In 25% cases - no cause is identified Neonate shock , dehydration childrens Local infection such as mastoiditis Adults coaglulopathy Women Ocp , pregnancy Most common cause Presentation – Headache , seizure
- 134. DURAL SINUSTHROMBOSIS MR IMAGINGFEATURES Acute DST (Fat sinus) T2* "blooms "empty delta"
- 137. Subacute DST Chronic DST "squiggly"parenchymal enhancement , thick enhancing dura
- 140.
- 141. FILLING DEFECT INSSS FILLING DEFECT IN LEFT TS
- 142. ACUTE 0-5 DAYSSUBACUTE 6- 15DAYS CHRONIC>15 DAYS Isointense onT1 Hyperintense on bothT1 andT2 Isointense onT1 Hypointense onT2 Due to intracellular deoxyhemoglobin Due to methemoglobin In thrombus Iso -hyper onT2
- 143. SUPERFICIAL CEREBRALVEIN THROMBOSIS SuperficialThrombosis WithDST SuperficialThrombosis Without DST • Rare (5% of all CVTs) • May cause convexal subarachnoid hemorrhage • May see "cord" sign on CT which is called hyperintense vein sign on MR representing adj thrombosed vein •T2* (GRE, SWI) key to diagnosis ○ "Blooming" thrombus in vein(s)
- 144. SWI showing blooming in superficialcortical veins
- 145. SWI showing blooming inright VOT T1WI showing linear hyperintensi ty
- 149. DEEPVENOUSTHROMBOSIS IMAGING FEATURES Thalamic edemais the imaging hallmark , may extend to caudate region and deep white matter.
- 150. ICV HEMORRHAGE IN BOTH THALAMI SS ENGORGEMENTOF MEDULLARY VEINS VOG
- 151. BITHALAMIC EDEMA NON VISUALIZATION OFDEEP VENIS
- 152.
- 154. ARTERY OF PERCHERON(AOP) INFARCTION vascular variant P1 PCA segment midbrain and medial thalami
- 155.
- 156. Altered mental status Memoryimpairment When midbrain is also involved – hemiplegia , oculomotor disturbances may also be seen along with above triad. NCCT scans in early acute AOP occlusions are usually normal. T2/ FLAIR images shows round or ovoid hyperintensities in the medial thalami, just lateral to 3rd ventricle and midbrain. Vertical gaze palsy
- 158. TOP OF BASILARINFARCTION Locked in syndrome “dense basilar artery sign”
- 160. • It isImportant cause of stroke in the young patient and is
- 164. MULTIPLE EMBOLIC INFARCTS cardiacemboli GM-WM interface •MR- multifocal peripheral T2/FLAIR hyperintensities Differential diagnosis Hypotensive cerebral infarction – involve deep internal watershed zones Parenchymal mets – do not restrict on DWI
- 166. CHARACTERISTIC CT MRIMAGING Avaliablity GOOD FAIR Examination time (min) 5 min 15 min Imaging volume for perfusion study 2-4cm Entire brain Risk to the patient Radiation Contrast material Ionizing radiation a/w potential risk fgor cancers Iodinated contrast medium is mandatory , and pateints incur higher risks for anaphylaxis and toxic effect on kidney No ionizing radiation Minimally increased risks for toxic effects on the kidney
Editor's Notes
- #4 Stroke is categorized mainly into two types , in which ischemic stroke consists of 85 % of the cases and rest 15% is caused by the hemorrhagic stroke
- #5 Athero sclerotic vascular disease
- #6 Normal cerebral blood flow is 50-60 ml /min /100 g of brain tissue in infarction it goes even below 10 ml
- #8 Here is pictorial representation of 3 territories associated with stroke, in center there is zone of ischemic core. Surrounding it, is the penumbra. Outside penumbra there is zone of focal oligemia
- #9 In ischemia …………….. However in infarction
- #10 Anatomy of vascular territories
- #11 Aca vascular territory includes anterior two thirds of the medial surface . A thin strip of cortex over the top of the hemisphere and a small wedge along the inferomedial frontal lobe
- #12 Here is an example. In the given AXIAL T1 Weighted image . There is hypointense area extending anteroposteriorly till 2/3 rd of interhemispheric fissure on left side with Corresponding hyperintensity on T2 Weighted image
- #13 On DWI and corresponding ADC map , the area shows diffusion restriction s/o acute ACA territory infarct
- #14 MCA supplies most of the lateral surface of the hemisphere, the anterior tip of the temporal lobe and the inferolateral frontal lobe. MCA is the most frequently occluded intracranial vessel
- #15 In this example, there is e/o altered signal intensity area following CSF signal intensity noted in anterolateral part of right temporal region and right fronto-parietal, appearing hyperintense on T2 Weighted images, hypointense in T1 and FLAIR images with exvacuo dilatation of right lateral ventricle s/o volume loss.
- #16 DWI and corresponding ADC map do not show any diffusion restriction . On the right is MR angiogram showing non visualization of right MCA
- #17 PCA territory involves the occipital lobe and posterior third of the medial surface and posterolateral surfaces of the hemisphere as well as almost the entire inferior surface of the temporal lobe
- #18 In this example of acute PCA territory infarct, AXIAL FLAIR image shows hyperintensity in right temporo-occipital region.DWI shows hyperintensity in the right temporo-occipital region with low ADC values on ADC map s/o diffusion restriction
- #19 2 VA unite near the pontomedullary junction to form BA. BA courses superiorly into the prepontine cistern to terminate into 2 POSTERIOR CEREBRAL ARTERIES. Numerous small basilar perforating branches arise from the dorsal surface of the BA to supply the pons and midbrain. First major named BA branch is AICA .2 superior cerebellar arteries arise from each side of the distal BA that curve posterolaterally around the midbrain
- #20 Graphic shows the posterior circulation vascular territories of PICA in orange, AICA in sky blue, SCA in yellow, MEDULLARY perforating brances of VA, PONTINE PERFORATING branches of BA, thalamic perforating branches from the top of BA and PCOM ARTERIES
- #21 Here is an example. T2 axial and T1 Saggital image show focal altered signal intensity area on the left side of the medulla appearing hyperintense on T2 and hypointense on T1
- #22 Corresponding FLAIR coronal image show hyperintense area on the left side of the medulla
- #23 DWI and corresponding ADC map show diffusion restriction s/o acute medullary infarct
- #27 Warning signs of stroke can be remembered as the abbreviation BEFAST where B stands for loss of balance, E for eye symptoms, F for facial drooping, A stands for ARM nad leg weakness and S stands for speech difficulty. When all these symptoms are present it’s the time to call for ambulance
- #34 Generally there are two types of protocol
- #37 In first 3-6 hours, TWI shows normal study
- #38 Here is the T1 SAGITTAL image of a patient showing hypointensity in right FRONTOPARIETAL REGION
- #39 On t2/flair images, ……………………..
- #40 Here is the T2 Axial image of the same patient showing hyperintensity in right FRONTOPARIETAL REGION WITH BLURRING OF GREY WHITE MATTER JUNCTION
- #41 FLAIR CORONAL images show HYPERintensitY in RIGHT FRONTOPARIETAL REGION
- #42 On DWI ….. ADC value decrease and appears DARK with high signal intensity on DWI
- #46 Here is the example of the same patient shown before. DWI shows hyperintensity in the right frontoparietal region with hypointensity on corresponding ADC map s/o diffusion restriction
- #47 MR 2D ANGIO and 3D TOF MIP images show loss of flow related signals in right MCA. RIGHT ICA appear decreased in calibre as compared to left ICA
- #50 Here is an example of abnormal linear hypointensity noted in left MCA in the axial SWI image consistent with thrombus. This is called artery susceptibility sign which is considered as MRI correlate of hyperdense MCA seen on NCCT
- #51 Here is another example of 47y old male. FLAIR axial images show shows patchy hyperintensity in left caudate nucleus , lateral putamen and parietal cortex. T2* GRE shows several linear hypointensities in the affected MCA branches, consistent with haemoglobin deoxygenation caused by slow stagnating arterial blood flow.
- #52 DWI of the same patient shows multiple patchy foci of diffusion restriction consistent with ACUTE CEREBRAL INFARCTION. AXIAL 2D MRA shows no flow in the left MCA
- #55 Here is a CBF perfusion map showing perfusion abnormality in left frontoparietal region which appears blue on perfsuion map. DWI shows a smaller diffusion abnormality in left corona radiata. So the mismatched area shows ischemic penumbra. Areas that show matched diffusion and perfusion abnormality is the infarcted tissue
- #58 Right occipital pyogenic abscess showing marked diffusion restriction within the core on DWI and ADC maps and a peripheral enhancing pattern on T1 post gadolinium
- #59 HERE is an example of primary CNs LYMPHOMA showing Left frontal periventricular lesion showing prominent diffusion restriction presenting with hyperintensity on DWI and low ADC value
- #60 This is an example of MRI of patient with status epilepticus showing normal T1 and T2 WI . DWI and corresponding ADC map show diffusion restriction in non vascular distribution sparing white matter
- #61 Here is the summary of hyperacute and acute infarcts HYPERACUTE AND ACUTE INFARCTS show high signal intensity on DWI and corresponding low signal intensity on ADC map On c+ t1wi , arterial enhancement may occur in hyperacute and acute infarct.
- #63 Here is TOF MIP and VRT MRA showing excellent angiogram due to background suppression and better flow related signal leading to better distal small vessel visibilty
- #64 here is an example of AP VIEW of normal MR angiogram of cervicocranial arterial system
- #65 In this MR angiography of bilateral carotid system there is e/o short segment narrowing of Left ICA s/o left ICA stenosis
- #67 These are the sequences we take while characterizing plaque components . These are the things we look to characterize plaque
- #69 MRI of a plaque in the right common carotid artery demonstrating fibrous cap rupture with ulcer formation The crescent-shaped high signal region in the PDW, T2W, and CE-T1W) images corresponding to a region of thrombus formation, shown on the matched histology section
- #72 CBF is taken at the height of the curve. CBV is measured by area under the curve. T MAX is the time it takes for the tissue residue function to reach its maximum value.it is not influenced by the scan duration. Hence is the most widely accepted parameter to measure the penumbra
- #73 Mainly 3 perfusion techniques are used in perfusion MRA
- #75 This is an example of 51y woman with sudden onset of speech difficulties and right side weakness, FAST FLAIR sequence shows left MCA cortical hyperintensity . DWI shows restricted diffusion in the corresponding areas
- #76 T2* GRE in the same case shows blooming thrombus in the left M1 segment till bifurcation. Perfusion MR shows markedly reduced cerebral blood flow in the densely ischemic core infarct which appears smaller than the corresponding DWI and FLAIR abnormality
- #77 CBV is markedly reduced in the densely ischemic core infarct (SO there is matched reduction in both CBV and CBF), however there is a penumbra of well maintained CBV . Hence there is CBV-CBF MISMATCH in this area. MTT shows prolonged transit time therefore CBV/MTT MISMATCH in the large ischemic penumbra
- #82 THIS IS THE SAGGITAL T1 W MRI BRAIN IMAGE SHOWING area of T1 HYPOINTENSITY IN CORONA RADIATA REGION
- #83 This is the Axial t2wi of the same pt showing hyperintense signal corresponds to the right corona radiate region
- #84 These are the axial T2WI taken at sequential intervals of a patient with R MCA territory infarct showing T2 fogging phenomenon with decrease in the the signal intensity over the period of time almost reaching to isointensity in 3rd image
- #85 CORONAL FLAIR IMAGE OF THE SAME PT SHOWS HYPERINTENSE SIGNAL
- #87 Axial T1 WI, t2 and flair SHOWS ill defined hypointense signal, apeearing hyperintense on T2/FLAIR in left mca territory ,
- #88 DWI shows hyperintense signal and corresponding ADC map also shows hyperintense signal confirming that the high signal on DWI is not due to restricted diffudion and is due to T2 shine through.
- #91 Sagital T1 and axial T2 wi showing areas of altered signal intensity appearing heterogeneously hypointense with hyperintense foci within on T1 and ,Heterogenously hypERintense on T2 in left frontoparietal lobe with loss of grey white matter differenciation
- #92 FLAIR also shows high signal intensity
- #93 Showing few areas of restricted diffusion in the periphery on DWI and ADC
- #94 Extensive blooming is also seen within APPEARING white on phase images s/o large subacute infarct withj hemoorhagic transformation
- #96 These are the T1 post contrast axial images of a 75 year women with right sided weakness and left MCA terriortory infarct taken at DAY 0 , 2 AND DAY 7. Scan at D0 reveals mild intravascular enhancement , increasing on day 2 . Parenchymal enhancement is seen on day 7 scan .
- #97 this is an example showing Diffusion w and TTP perfusion images showing acute ischemic lesion in left thalamus with hypoperfusion in the corresponding location . In the cerebellum ,trace dwi is unremarkable while TTP demonstrate hypoperfusion in contralateral cerebellar hemisphere
- #100 Chronic infarct Follows CSF signal
- #102 This is the saggital T1WI of a showing multiple oval T1 hypointensities in left centrum semiovale and frontal white matter in a in a child with homocystinuria
- #103 Which apppeaer hyperintense on T2WI
- #104 And shows signal suppression on FLAIR in the centre with marginal hyperintensity
- #105 There is no diffusion restriction on DWI and ADC map s/o chronic infarcts with glioenccephalomalacic changes.
- #106 .MRA of the same pt reveals non visualization of left ICA with narrowing of M1 segment of left MCA and A1 segment of ACA .Thus metabolic disorders must be kept as defential in pediatric stroke
- #108 Flair coronal images showS gyriform hyperintensity in right parietal cortex Another case showing cortical laminar necrosis in occipital cortex on T1 saggital IMAGE
- #110 External –wedge or gyriform internal- rosary like line of WMHs
- #111 This is the diagram to show watershed zones .wedge shaped area between ACA , MCA and MCA – PCA represent external watershed zones. Curved blue line represent subcortical watershed zones. Yellow line indicate internal watershed zone b/w major vessels and perforating arteries.
- #112 here is case of watershed infarct FLAIR AXIAL MRI images shows bilateral areas of hyperintensity , most prominent are located posteriorly on the watershed b/w MCA –PCA and also bwtween ACA –MCA watershed in the last 2 images.
- #113 As we saw in THIS example. The image shows typical man in the barrel phenotype with atrophy of shoulder gilde muscles and arms hanging flaccidly .
- #116 Are characterized by……………………
- #118 Sag T1 and axial T2 wi showing T1 hypo and T2 hyperintense foci in left side of pons
- #119 Showing no signal suppression on FLAIR
- #120 With diffusion restriction on DWI and ADC map s/o acute lacunar infarct
- #121 this are the axial FLAIR and DWI images showing another example of acute lacunar infarct in left hemispheric white matter showing FLAIR AND DWI hyperintensity
- #122 Follow csf signal
- #123 C/o 75 y old men showing T1 hypointense and T2 hyperintense foci in mid pons
- #124 Showing signal suppression on FLAIR image with no enhancement on post contrast scan s/o chroniclacunar infarct. Also there are T2/FLAIR hyperintensities in subcortical and periventricular white matter b/l s/o ischemic demylination and glioenchephalomalcic changes in right parietal refgion
- #125 This is the another c/o CHRONIC LACUNAR infarct in right basal ganglia appearing hypointense on T1/ hyper on T2 with signal suppression on FLAIR
- #126 Pvs tends to be sharpely marginated , ovoid and linear with complete suppression on flair however lacunar infarcts are often irregular with FLAIR hyperintense rim.
- #129 MIP image from CE MR venography with color overlay shows Lateral MIP images from CE MR V shows veins from the lateral cerebral hemisphere that drains into the SSS 1 frontopolar , 2 anterior frontal , 3 posterior frontal , 4 vein ot tolard , 5 anterior parietal 6 SMCV which drain into sphwenopartietal snus or cavernous sinus , 7 is the vein of labbe that drains into transverse sinus
- #130 These are the Axial color coded diag demonstrating venous draignage pattern. As we can see Most of the Superficial part of the brain ie. Cortex , subcortical white matter shown in green color atre drained by cortical vein ( including VOT) and sss. Central core brain structures ie basal ganglia , thalami , lat and 3rd ventricles and most of corona radiate are drained by deep venous system ie. ICB , VOG & SS. Transverse sinus and vein of labbe drain the posterior temporal and inferior parietal lobe as shown in yellow color . Sp and cv
- #131 Lateral MIP image from CE MRV shows major component of deep venous system. 1 is the thalamostraite vein , 2 is septal vein 3rd is the internal cerebral vein , 4 is the basal vein of Rosenthal 5 th is the VOG
- #136 c/o 35 year old women presented with severe headache for 5 days . Axial T1 wi shows isointense thrombus in left sigmoid sinus Which appears hypointense on T2wi s/o acute left sigmoid sinus thrombusis
- #137 Frontal mip image from coronal TOF MR venography shows lack of flow in distal portion of left transverse sinusand sigmoid sinius
- #138 Subacute thrombus appears hyper on all sequences….. Clot signal in chronic dst is variable and depends on organization of clot….. LONG STANDING DST MAY DEVELOP SIGNIFICANT COLLATERAL FORMATION THROUGHT MEDULLARY VEINS WHICH IS SEEN AS SQIGGLY PARENCHYMAL
- #139 T2 * SWI shows innumerable prominent tortuous corkscrew squiggly medullary veins throughout both cerebral hemisphers . Venous DSA shows that distal SSS is occluded while proximal and mid seg are patent . Numourous enlarged medullary veins appears to hang in space . This is chronic SSS thrombosis with medullary collateral draingae
- #140 c/o Long standing chronic sss showing thick dural enhancement alonmg tentorium.
- #141 These IS THE axial T2shows absence of normal flow void and hyperintense thrombus in SSS and TOF3d multislab image shows filling defect in SSS
- #142 On post contrast axial image, there is filling defect in the left transverse sinus as well …and in SSS as visible in this coronal secttion
- #144 In cases of DST ,IT IS THE dst THAT extends
- #145 Here is a c/o superficial venous thrombosis. T2* GRE image shows lineaer hypointensity in right paracentral sulcus ( short arrow)due to magnatic succeptility effect at the site of thrombosed vein. Hypointense area shows corresponding AREAS OF cortical hemorrhage ( long arrow). On T1 wi only swollen gyri are seen.
- #146 This is a c/o VOT thrombosis.Axial T1wi Mri BRAIN shows T1 hyperintensity in post central gyrus , typical site for VOT s/o thrombosis and SWI shows blooming in the region of thrombosed vdein
- #147 Saggital view MR venography image shows non visualization of vein of tolard
- #148 Case of young women presented with seizure and altered mental status .T1 wi shows sublte “ dot sign” of T1 hyperintensity within a small cortical vein , within expected location of vein of labbe. T2 hyperintense area of mass effect involving left temporal lobe grey and white matter
- #149 T1 post contrast image show heterogenous enhancement within . AXIAL MR VENOGRPAHY confirms suspicioun of left transverse sinus thrombosis . No vein of labbe is visible on left and see the normal vein of labbe on right.
- #151 Axial graphic depicts deep venous occlusion with thrombosis of ICV , VOG and hemorrhage in both the rthalamus. Note the engorgement of medullarty veins
- #152 AXIAL FLAIR image show extensive signal abnormalities within both thalaMI extending into caudate nuclei . Saggital 2d phase contrastt MR venogram shows no signal from the portion of deep venous system s/o thrombosis
- #156 This image shows a single dominant perforating artery fromP1 segment as compared to normal in which multiple small perforating branches supply the thamus and midbrain
- #158 This is a c/o AOP INFARCTION . Axial DWI images shows diffusion restriction in bilateral paramedian thalamic and midbrain region – consistent with acute infarct.
- #159 LOCKED IN SYNDROME IS ALSO CALLED PSEUDOCOMA IN WHICH THE AFFECTED PT IS AWAKE AND CONCIOUS BUT IS PARALYZED AND VOICELESS .
- #160 Reformatted 3DMRA image demonstrate occlusion of the basilar artry in A pt with acute bilateral central infarct.
- #162 Here is an example of a young patient presenting with severe acute neck pain SHOWING left ICA dissection ON T2wi AS crescentric shaped hyperintense intramural hematoma causing expansion of the artery. However there is no narrowing of ICA lumen
- #163 Another example showing circumferential intramural hematoma seen bilaterally causing expansion of the bilateral ICA . There is narrowed lumen of the right ICA and open lumen of the left ICA
- #164 Here is MR Angiography of cervical region showing narrowing & abnormal contour of the of the left vertebral artery causing cerebellar tonsilar infarction on left side.
- #165 Simultaneous small acute infarcts in multiple different vascular distribution…………..most commonly emboli is cardiac in origin Clinically silent , they convey risk of subsequent stroke
- #166 Diffusion wi shows multiple foci od hyperintensities in both the cerebral hemisphere and in multiple vascular territories..cortical , subcortical and deep regions are affected. Restriction is confirmed on ADC maps , indicating this represents acute infarcts. The distribution raises concern for central embolic source such as cardiac source.