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Information about BRAIN INFARCTION part 1

Published on July 14, 2016

Author: neelammalik33


BRAIN INFARCTION. part 1: BRAIN INFARCTION. part 1 Dr Neelam Common causes of stroke: Common causes of stroke older patient younger patients child Atherosclerosis Emboli emboli from congenital heart disease cardiac emboli Arterial dissections,vasculopathy,drug abuse venous thrombosis blood dyscrasias i.e sickle cell disease Goals of Acute Stroke Imaging: Goals of Acute Stroke Imaging Imaging features: Imaging features 1) Angiographic signs of cerebral infarction Vessel occlusion50% Slow antegrade flow,delayed arterial emptying15% Collateral filling20% Nonperfused areas5% Vascular blush(luxury perfusion)20% AV shunting10% Mass effect 40% Slide7: 2)Cross sectional imaging CT is the first study of choice in acute stroke to exclude hemorrhage or any underlying mass/AVM Most CT examinations are normal in early stroke Slide8: Early CT signs include Loss of gray-white interfaces (insular ribbon sign) sulcal effacement Hyperdense clot in artery on non contrast CT( dense MCA sign) Slide11: An acute thrombus in an intracranial vessel typically has high attenuation. This feature is referred to as the hyperdense vessel sign (or, in cases of middle cerebral artery [MCA] involvement, hyperdense MCA sign) (Fig 2). Although this sign is highly specific, its sensitivity is poor (9). A hyperdense MCA sign also may be seen in the presence of a high hematocrit level or MCA calcification, but in such cases the hyperattenuation is usually bilateral (10–13). Rarely, fat emboli appear hypoattenuated when compared with attenuation in the contralateral vessel Slide12: Axial unenhanced CT images in a proximal segment of the left MCA in a 53-year-old man (a) Slide13: and a distal segment of the left MCA in a 62-year-old woman (b), obtained 2 hours after the onset of right hemiparesis and aphasia, show areas of hyperattenuation (arrow) suggestive of intravascular thrombi. Slide14: MCA infarction: on CT an area of hypoattenuation appearing within six hours is highly specific for irreversible ischemic brain damage. Slide15: 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. Slide16: Cytotoxic edema of the insular cortex, which is susceptible to early and irreversible ischemic damage, also causes local hypoattenuation, which results in the so-called insular ribbon sign Slide17: Axial unenhanced CT image, obtained in a 73-year-old woman 21/2 hours after the onset of left hemiparesis, shows hypoattenuation 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. Slide18: 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. Slide19: 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. Slide20: Edema, C ytotoxic edema develops in 6 hours detected by MRI. .Vasogenic edema develops later(detectable on CT at 12 to 24 hrs) Slide21: Characteristic differences between distribution of infarcts Emboli are peripheral wedge shaped In hypoperfusion there are watershed infarcts Basal ganglia infarcts Slide22: Reperfusion hemorrhage is not uncommon after 48 hrs, Most hemorrhages are petechial or gyral. Slide23: Hemorrhagic infarcts 15% of MCA infarcts are initially hemorrhagic. Slide24: Hemorrhage is most easily detected with CT, but it can also be visualized with gradient echo MR-sequences. Slide25: Mass effect in acute infarction. ..sulcal effacement ,ventricular compression Chronic infarcts Focal tissue loss, atrophy, porencephaly,cavitation,focal ventricular dilatatation Wallerian degeneration ..distal axon breakdown along white matter tracts Slide26: Acute versus chronic ischaemic stroke Dr Andrew Dixon et al. Differentiating between acute and chronic infarction on a CT brain is an important skill for many health professionals particularly in the emergency setting. pathology acute: cytotoxic oedema chronic: encephalomalacia hypoatt en uation acute: more dense than CSF chronic: CSF density mass effect acute: positive (volume gain) sulcal / ventricular effacement midline shift / herniation chronic: negative (volume loss) widened sulci exvaccuo dilatation of ipsilateral ventricle CT and MRI appearances of infarcts: CT and MRI appearances of infarcts Factor 1stday 1stweek 1st month >1month Stage acute early subacute late subacute chronic CT density subtle decrease decrease hypodense hypodense MRI T2W,edema T2W edema varied T1Wdark,T2W bright Mass effect mild Maximun resolving encephalomalacia Hemorrhage no most likely here variable MRI detectable Enhancement no Yes decreasing NO Slide28: Negative CT doesnot exclude cerebral infarcts MRI with diffusion wighted imaging (DWI) and perfusion weighted imaging (PWI) are imaging studies of choice in immediate infarct. STROKE EVOLUTION ON MRI: STROKE EVOLUTION ON MRI sequence Hyperacute<6hrs Acute>6hrs Subacute days to weeks Chronic DWI high high high(decrease with time) isointeense to bright ADC low low low to isointense isointense to bright T2W/FLAIR isointense slightly bright Bright Bright Slide31: 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. Slide32: 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. DWI: DWI Slide35: Pseudo-normalization of DWI This occurs between 10-15 days. The case on the left shows a normal DWI. On T2WI there is may be some subtle hyperintensity in the right occipital lobe in the vascular territory of the posterior cerebral artery. The T1WI after the administration of Gadolinium shows gyral enhancement indicating infarction. Slide36: The goal of imaging in a patient with acute stroke is: Exclude hemorrhage Differentiate between irreversibly affected brain tissue and reversibly impaired tissue (dead tissue versus tissue at risk) Identify stenosis or occlusion of major extra- and intracranial arteries In this way we can select patients who are candidates for thrombolytic therapy. Slide37: CT Perfusion (CTP) With CT and MR-diffusion we can get a good impression of the area that is infarcted, 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. The limitation of CT-perfusion is the limited coverage. Slide39: 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. Slide41: 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. Slide42: Perfusion MR Imaging 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. Slide44: 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. Slide45: 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. Slide46: 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. Slide47: 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. Slide48: another MCA infarction. It is clearly visible on CT (i.e. irreversible changes). There is a match of DWI and Perfusion, so no therapy. Slide49: The DWI and ADC map is shown. Continue for the perfusion images Slide50: 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. Slide53: Nonenhanced CT scan obtained 5 hours after the onset of stroke in a 65-year-old woman with MCA occlusion demonstrates obscuration of the lentiform nucleus (long white arrow) and of the head of the caudate nucleus (arrowhead) as well as hypoattenuation of the insular ribbon (short white arrow) and effacement of the sulci of the temporoparietal MCA territory (black arrows) Slide54: THANKYOU

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