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205 Cards in this Set
- Front
- Back
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Define "stroke":
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Stroke is a clinical term applied to any abrupt nontraumatic brain insult—literally “a blow from an unseen hand.” Strokes are caused by either brain infarction (75%) or hemorrhage (25%) and must be distinguished from other conditions that cause abrupt neurologic deficits.
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Define infarction:
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Infarction is a permanent injury that occurs when tissue perfusion is decreased long enough to cause necrosis, typically as the result of occlusion of the feeding artery.
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Define TIA:
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Transient ischemic attacks (TIAs) are defined as transient neurologic symptoms or signs lasting less than 24 hours, which may serve as a “warning sign” of an infarction occurring in the next few weeks or months. TIAs are often caused by temporary occlusion of a feeding artery.
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Define intracranial hemorrhage:
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Hemorrhage is seen when blood ruptures through the arterial wall, spilling into the surrounding parenchyma, subarachnoid space, or ventricles.
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How many brain infarcts are caused by emboli vs. thrombus?
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Among those with an established mechanism, about two thirds of infarcts are caused by thrombi and one third are caused by emboli.
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Where do thrombi tend to occur?
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Thrombi are formed at sites of abnormal vascular endothelium, typically over an area of atherosclerotic plaque or ulcer.
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What factors determine whether or not occlusion of a neck artery will cause an infarct?
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A large-artery thrombosis in the neck may or may not cause distal infarction, depending on the time course of occlusion and available collateral supply.
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What are lacunes?
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Small-vessel thrombi frequently occur in end arteries of the brain, accounting for about one fifth of infarcts (“lacunes”).
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Where do emboli arise?
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Emboli may arise from the heart, aortic arch, carotid arteries, or vertebral arteries, causing infarction by distal migration and occlusion. Also, don't forget about parodoxical emboli going through PFO's.
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What's your differential for a stroke in a pediatric patient?
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Congenital heart disease
Blood dyscrasias Meningitis Arterial dissection Trauma ECMO Venous thrombosis |
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What's your differential for a stroke in a young adult patient?
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Cardiac emboli
Atherosclerosis Drug abuse Arterial dissection Coagulopathy Vasculitis Venous thrombosis |
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What's your differential for a stroke in an elderly adult patient?
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Atherosclerosis
Cardiac emboli Coagulopathy Amyloid Vasculitis Venous thrombosis |
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What percent of the cardiac output does the brain consume?
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The brain consumes 20% of the total cardiac output to maintain its minute-to-minute delivery of glucose and oxygen.
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Why can the brain not survive very long without bloodflow?
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Because the brain holds no significant long-term energy stores (e.g., glycogen, fat), disruption of blood flow for even a few minutes will lead to neuronal death. Minor reduction in perfusion is initially compensated for by increased extraction of substrate, but injury becomes inevitable below a critical flow threshold.
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Which nerve cells are more susceptible to ischemia?
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-Gray matter normally receives 3 to 4 times more blood flow than white matter and is therefore more likely to suffer under conditions of oligemia.
-Some subsets of neurons (e.g., cerebellar Purkinje cells, hippocampal CA-1 neurons) are injured more readily than others, possibly because of their greater concentrations of receptors for excitatory amino acids. -The slower-metabolizing capillary endothelial cells and white matter oligodendrocytes are more resistant to ischemia than gray matter but will also die when deprived of nutrients. -Cells served by penetrating end arteries or those residing in the watershed zone between major territories have no alternate route for perfusion and are therefore more prone to infarction. -Damage will likely be more severe in a patient with an incomplete circle of Willis than in one with a complete arterial collateral pathway. |
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When does cytotoxic edema from infarction peak?
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This edema peaks 3 to 7 days postinfarction and is maximal in the gray matter. A smaller component of vasogenic edema also develops as the more resistant capillary endothelial cells lose integrity.
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What are some hyperacute signs of infarction on CT and MR?
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These “hyperacute” signs primarily relate to morphologic changes in the vessels rather than density or signal changes in the parenchyma. On CT, the actual thrombus may occasionally be seen in larger intracranial branches, resulting in the “hyperdense artery sign”. On MR, the normal black signal of flowing blood within the lumen (“flow void”) is immediately lost and may be replaced by abnormal signal representing clotting or slow flow. Loss of the flow void is best seen acutely in the large vessels (carotid siphon, vertebrobasilar vessels, middle cerebral artery [MCA] branches).
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What are some early signs of MCA infarction on CT?
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CT scans done within 6 hours of MCA occlusion will commonly exhibit the “insular ribbon sign,” a subtle but important blurring of the gray–white layers of the insula caused by early edema. Early edema may also be most conspicuous in the putamen in proximal middle cerebral artery occlusions (lentiform nucleus edema sign).
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What are some early signs of MCA infarction on MR?
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However, the most sensitive imaging sequence for detection of brain ischemia is diffusion-weighted MR imaging (DWI), which may turn positive minutes after infarction begins, well before a CT would show even subtle signs. Hyperintense signal on DWIs (“light-bulb sign”) precedes T2 hyperintensity, which typically develops at 6 to 12 hours postictal.
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How long after an infarct does it take for T2 hyperintensity to show up.
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It typically develops at 6 to 12 hours post-infarct
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How long after an infarct does it take for DWI to become positive?
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It may turn positive minutes after infarction begins
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Aside from hemorrhage, mass, or other structural abnormalities, what other findings on screening CT can be contraindications for thrombolytics?
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Patients with extensive edema on their initial CT scan may be at particularly high risk for reperfusion hemorrhage, so these patients should be excluded from thrombolytic treatment. Although universal guidelines are not agreed upon, patients with edema affecting more than one third of the MCA territory should generally be excluded.
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What's the physics behind DWI sequences?
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DWIs are acquired by applying a strong gradient pair that sensitizes the images to microscopic (brownian) water motion.
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Other than finding acute infarcts, what can DWI be useful for in stroke patients?
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This can also be a useful way to distinguish new ischemic areas (high signal on DWIs) from older lesions (normal or low signal on DWIs).
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What is seen on ADC mapping?
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The ADC reflects “pure” diffusion behavior, free of any underlying T2 contributions (“shine through” or “dark through”).
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Describe the FLAIR sequence. What is it useful for?
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FLAIR allows heavy T2 weighting of the parenchyma while simultaneously suppressing free water signal from the CSF. These techniques increase the conspicuity of T2 changes in ischemia. FLAIR is not inherently better than T2 MR for early detection of ischemia, but it may be particularly helpful in detecting small lesions in the cortex and for exclusion of acute subarachnoid hemorrhage.
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Describe the "fogging effect":
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One potential imaging pitfall, the “fogging effect,” may be encountered on CTs obtained during the second week after infarction, while edema and mass effect are subsiding. At this stage, decrease in edema and accumulation of proteins from cell lysis balance one another such that brain morphology and density in the injured region can appear nearly normal by CT. Fogging effects are much less of a problem on MR because of its greater tissue sensitivity, particularly when contrast is used.
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What should you think of if you see edema continuing one month after an infarct?
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Edema or mass effect that persists beyond 1 month effectively rules out simple ischemia and should raise the possibility of recurrent infarction or an underlying tumor.
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What are some signs of remote infarct?
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In the weeks and months following infarction, macrophages remove dead tissue, leaving a small amount of gliotic scar and encephalomalacia behind. CSF takes up the space previously occupied by brain. The affected corticospinal tract atrophies (wallerian degeneration), leading to a shrunken appearance of the ipsilateral cerebral peduncle. If hemorrhage accompanied the infarct, hemosiderin may be seen grossly or detected as signal hypointensity by T2WIs. Widening of adjacent sulci and “ex vacuo” dilatation of the ventricle occurs adjacent to the infarcted area.
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Describe hemorrhagic transformation of infarction. Why does it happen? What are the symptoms? Where is it seen?
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Reperfusion into infarcted capillary beds may lead secondarily to gross or microscopic hemorrhage, seen in up to half of infarcts. In most cases this takes the form of microscopic leakage (diapedesis) of red blood cells, but on rare occasions a frank hematoma will form. Physical disruption of the capillary endothelial cells, loss of vascular autoregulation, and anticoagulation or use of thrombolytics may all contribute to the development of these hemorrhages. Patients may develop headaches at the time of bleeding but commonly have no new symptoms, presumably because the hemorrhage occurs within brain areas that are already dead or dysfunctional. Hemorrhagic infarction is confined to the territory of the infarcted vessel, whereas primary hemorrhage does not necessarily respect vascular boundaries.
View Figure FIGURE 4.8. Petechial Hemorrhage and Gyral Enhancement in Subacute Infarction. A. Precontrast T1WI shows mild effacement of sulci in the right middle cerebral artery territory. A few subtle areas of bright signal intensity scattered along the cortex indicate areas of petechial hemorrhage or laminar necrosis (arrows). B. Postcontrast T1WI demonstrates marked gyral enhancement, a hallmark of subacute infarction. The peak time for hemorrhagic transformation is at about 1 to 2 weeks postinfarction. |
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What should you think of if you see intraventricular hemorrhage with hemorrhagic transformation of an infarct?
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Intraventricular extension is uncommonly seen with hemorrhagic transformation and should raise the possibility of another process (such as hypertensive bleed or a ruptured arteriovenous malformation [AVM]).
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What does hemorrhagic transformation of an infarct look like on CT and MR?
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-It is usually manifested as a serpiginous line of petechial blood following the gyral contours of the infarcted cortex.
-These dots of hemorrhage are often patchy and discontinuous. -On CT a faint line of high attenuation is observed, and on MR bright signal is seen along the affected gyrus on the unenhanced T1WI because of methemoglobin. -The petechial gyral pattern is not seen in primary brain hemorrhage and can be helpful in confirming the underlying ischemic etiology of a suspicious lesion. -More extensive hemorrhagic transformation of the infarcted tissue may lead to the formation of a gross parenchymal hematoma. -Here, the blood does not conform to a gyrus and may form a clot that is indistinguishable from a primary hematoma. -Gross parenchymal hematomas tend to occur earlier and are more commonly associated with clinical deterioration. -Confluent hematomas seen on infarct follow-up studies should be reported promptly since anticoagulation therapy is contraindicated, even when the finding is incidental. |
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How is hemorrhagic transformation of an infarct managed?
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Management in the presence of petechial hemorrhage is controversial, but many neurologists continue anticoagulation if there is a well-documented embolic source.
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What are Elster's "rule of three"?
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MR parenchymal enhancement of infarction peaks at 3 days to 3 weeks and resolves by 3 months.
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When does an infarct enhance on MR? Where is this seen?
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Intravascular enhancement on MR is commonly seen in the infarcted territory during the first week. This may be caused by slow flow or vasodilatation leading to stasis of gadolinium, likely in both arteries and veins. The proximal trunks of more distally occluded arteries and leptomeningeal cortical channels are most prominently involved. The area of vascular enhancement may extend beyond the T2 hyperintensity, possibly indicating recruitment of collateral supply at the ischemic border.
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Why do infarcts start enhancing?
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An intact blood-brain barrier normally excludes contrast from the brain. Leakage of macromolecular contrast agents through damaged vessels leads to local accumulation of iodine, seen as high attenuation (enhancement) of infarcted parenchyma. Breakdown of the blood-brain barrier underlies both hemorrhagic transformation and contrast enhancement of infarctions.
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How does management change for anterior territory (carotid territory) infarcts versus posterior territory (vertebrobasilar territory)infarcts?
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Patients with anterior circulation ischemia have been shown to benefit from carotid endarterectomy when the carotid is narrowed by at least 70% compared to its normal diameter. Surgery has not been proven beneficial for patients with lesser degrees of carotid stenosis or for those with posterior territory TIAs, who therefore usually receive medical therapy (e.g., anticoagulation).
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Summarize the findings seen on CT and MR minutes after an infarct:
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CT:
No changes MR: Absent flow void Arterial enhancement (days 1–10) DWI: high signal |
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Summarize the findings seen on CT and MR 2-6 hours after an infarct:
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CT:
Hyperdense artery sign Insular ribbon sign MR: Brain swelling (T1) Subtle T2 hyperintensity |
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Summarize the findings seen on CT and MR 6-12 hours after an infarct:
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CT:
Sulcal effacement ±Decreased attenuation MR: T2 hyperintensity |
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Summarize the findings seen on CT and MR 12–24 hours after an infarct:
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CT:
Decreased attenuation MR: T1 hypointensity |
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Summarize the findings seen on CT and MR 3–7 days after an infarct:
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CT:
Maximal swelling MR: Maximal swelling |
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Summarize the findings seen on CT and MR 3–21 days after an infarct:
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CT:
Gyral enhancement (peak: 7–14 days) MR: Gyral enhancement (peak: 3–21 days) Petechial methemoglobin |
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Summarize the findings seen on CT and MR 30–90 days after an infarct:
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CT:
Encephalomalacia Loss of enhancement Resolution of petechial blood MR: Encephalomalacia Loss of enhancement Resolution of petechial blood |
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What causes amaurosis fugax?
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Embolic occlusion of the ophthalmic branch of the ICA may cause transient monocular blindness (amaurosis fugax).
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What types of things cause narrowing of the carotid artery?
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Atherosclerotic disease near the carotid bifurcation is responsible for the majority of ischemic events in the ICA territory. Arterial dissection, trauma, fibromuscular dysplasia, tumor encasement, prior neck radiotherapy, and connective tissue diseases may also cause significant carotid narrowing.
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How narrow does the carotid artery need to be to cause symptoms?
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Hemodynamic effects begin to be seen when there is >80% reduction in area or >60% decrease in diameter. Lesions causing less severe narrowing may nonetheless become symptomatic when they serve as a nidus for thrombus formation or are unmasked by hypotension. Studies have shown a clear benefit of endarterectomy in symptomatic patients with >70% stenosis but not for those with <30% narrowing.
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Why is evaluation of the entire internal carotid artery important?
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Evaluation of the surgically inaccessible cranial segments (petrous, cavernous, and supraclinoid) is necessary to exclude high-grade intracranial stenoses or “tandem” lesions that might contraindicate endarterectomy.
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What are the three divisions of the ACA's?
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The ACA is divided into three subgroups: medial lenticulostriate branches serve the rostral portions of the basal ganglia, pericallosal branches supply the corpus callosum, and hemispheric branches serve the medial aspects of the frontal and parietal lobes
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What is the recurrent artery of Heubner?
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The medial lenticulostriate branches of the ACA penetrate the anterior perforating substance to give variable supply to the anteroinferior aspect of the internal capsule, putamen, globus pallidus, caudate head, and portions of the hypothalamus and optic chiasm. The largest of these vessels supplies the caudate head/anterior internal capsule region and is recognized as the recurrent artery of Heubner.
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Describe the course of the ACA after it gives of the medial lenticulostriate brances:
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Above the takeoff of the lenticulostriate branches, the ACAs are interconnected by the anterior communicating artery. Each ACA ascends further, giving off branches to the frontal pole (orbitofrontal and frontopolar arteries).The ACAs terminate as a bifurcation into the (lower) pericallosal and (upper) callosomarginal branches. These arteries run parallel to the corpus callosum from front to back, supplying the medial cortex of the frontal and parietal lobes.
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What is the most common variation of ACA anatomy?
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ACA branching patterns are quite variable from one patient to the next, with about 10% having only one pericallosal branch that supplies both hemispheres—an “azygos” ACA.
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What percent of patients have an azygous ACA?
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about 10%
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What are the branches of the MCA's?
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Its offspring are the lateral lenticulostriate branches, which supply most of the basal ganglia region, and the hemispheric branches, which serve the lateral cerebral surface
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What structures are supplied by the lateral lenticulostriate branches of the MCA?
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The lateral lenticulostriate branches arise from the proximal MCA as numerous small perforating end arteries distributed to the putamen, lateral globus pallidus, superior half of the internal capsule and adjacent corona radiata, and majority of the caudate.
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Can you explain why the insular ribbon sign happens?
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When the proximal MCA is occluded, this insular region is furthest from any potential collateral supply, probably explaining the early appearance of the edema that gives rise to the “insular ribbon sign”
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Describe the course of the vertebral arteries:
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The vertebral arteries usually originate from the subclavian arteries, ascend straight upward in the transverse foramina of C6–C3, turn sharply through the C2–C1 foramen magnum levels, and unite anterior to the low medulla to form the basilar artery.
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Where does atherosclerosis usually affect the vertebral arteries?
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Atherosclerotic narrowing commonly affects the vertebral arteries at their origins and may affect the basilar artery over variable lengths.
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Where does arthritis usually affect the vertebral arteries?
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Narrowing of the cervical portion of the vertebrals may be caused by compressive uncovertebral osteophytes.
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Where would trauma most likely affect the vertebral arteries?
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Rapid head turning (e.g., motor vehicle accidents) may stretch the vertebral arteries at the C1–C2 level, leading to arterial dissection.
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How is vertebrobasilar ischemia treated??
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Anticoagulation and antiplatelet agents remain the mainstay of treatment for vertebrobasilar ischemia. Angioplasty and stenting are sometimes feasible for correction of atherosclerotic lesions but are usually reserved for severe medically refractory cases.
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How does the basilar artery terminate?
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The basilar ends at its bifurcation into the posterior cerebral arteries, just above the tentorium cerebelli.
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What are the main branches off the PCA's?
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The major branches of the PCA include the midbrain and thalamic perforating vessels, the posterior choroidal arteries, and the cortical branches to the medial temporal and occipital lobes.
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What structures does the posterior choroidal artery supply?
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The posterior choroidal arteries arise from the proximal PCA to supply the choroid plexus of the third and lateral ventricles, pineal gland, and regions contiguous with the third ventricle.
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What is a fetal PCA? What percent of pts have this?
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In about 20% of patients, one or both of the proximal PCA segments may be hypoplastic or absent. In these cases, flow is derived from the ICA system via a prominent posterior communicating artery. This is commonly referred to as “fetal origin” of the PCA, since embryologically the PCA develops with the ICA. Because this is a fairly common variation, both vertebral and carotid disease should be considered when evaluating PCA infarctions.
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What should you immediately think of when you see a cerebellar hemorrhage or large infarction?
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Cerebellar hemorrhages and any infarctions with significant mass effect are neurosurgical emergencies requiring posterior fossa decompression.
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What are the branches of the cerebellar arteries called?
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Cerebellar arteries come off the basilar artery. The correct order of cerebellar branches going from top to bottom can be remembered using the acronym SAP: the superior, anterior inferior, and posterior inferior cerebellar arteries.
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What does the SCA supply?
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The upper parts of the cerebellum are supplied by the SCA. These arise from the distal basilar artery as the last large branches beneath the tentorium cerebelli. The SCA territory includes the superior vermis, middle and superior cerebellar peduncles, and superolateral aspects of the cerebellar hemispheres (i.e., the “roof” of the cerebellum).
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What does the PICA supply?
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The bottom of the cerebellum is supplied by the PICA. The PICA is the first major intracranial branch of the vertebrobasilar system, usually arising from the distal vertebral artery 1 to 2 cm below the basilar origin. Its territory is variable but often includes the dorsolateral medulla, inferior vermis, and posterolateral cerebellar hemisphere.
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What is the relationship between the size of the AICA and PICA?
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The PICA maintains a reciprocal relation with the AICA above it: If the PICA is large, then the ipsilateral AICA is usually small, and vice versa. This arrangement is sometimes referred to as the AICA-PICA loop.
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Which cerebellar artery is the most commonly infarcted?
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The PICA is usually the largest cerebellar hemispheric branch and the most commonly infarcted.
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Describe watershed infarction:
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An episode of transient global hypoperfusion may result in bilateral infarctions in the watershed regions. Typical triggering events include cardiac arrest, massive bleeding, anaphylaxis, and surgery under general anesthesia. The border zones are regions perfused by terminal branches of two adjacent arterial territories. When flow in one or both of the parent vessels falls below a critical level, the brain tissue in the watershed zone is the first to suffer.
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When would a watershed infarct be unilateral?
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Unilateral watershed damage may be seen when carotid occlusion or stenosis is unmasked by global hypotension.
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What does a watershed infarct look like?
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They are typically bilatearl. Images show a string of small deep white matter lesions (“rosary bead sign”) or damage extending out from the “corners” of the lateral ventricles on higher sections.
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Define lacune:
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Lacunes are the cavities (literally, “little lakes”; 2 to 5 mm3) left in the brain as the result of occlusion of a penetrating artery, causing infarction and ensuing encephalomalacia.
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What is the etiology behind lacunes?
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Patients usually have a history of long-standing hypertension, which leads to lipohyalinosis of the vessels and eventual thrombosis.
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What arteries supply the internal capsule?
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Its contributors include the ACA and MCA lenticulostriate branches, the ICA anterior choroidal branch, and the PCA thalamogeniculate branches.
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Define Etat lacunaire:
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“Etat lacunaire” refers to a state of multiple lacunar infarctions.
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Define etat crible:
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“etat crible,” refers to the enlarged perivascular spaces (Virchow-Robin spaces) that may develop around perforating vessels. These normal spaces may simulate lacunes but have no associated neurologic deficit or other clinical relevance.
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Define Virchow-Robin spaces:
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Enlarged perivascular spaces that may develop around perforating vessels. These normal spaces may simulate lacunes but have no associated neurologic deficit or other clinical relevance.
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What do enlarged perivascualr spaces (Virchow-Robin spaces) look like on imaging?
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By definition, Virchow-Robin spaces should follow CSF intensity on all MR sequences, have no associated mass effect, and occur along the path of a penetrating vessel. Common locations include the medial temporal lobes and inferior third of the putamen and thalamus. Occasionally they may be seen along the course of small medullary veins near the vertex. Most perivascular spaces seen on MR are between 1 and 3 mm in diameter, but some may be 5 mm or larger.
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What are UBO's?
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Small foci of T2 hyperintensity are commonly seen scattered throughout the brains of older patients, with or without clinical symptoms. These “UBOs” (unidentified bright objects) can cause considerable consternation. They are commonly associated with patchy or diffuse T2 hyperintensity in the centrum semiovale. Pages could be filled with different authors’ terms for related processes: small-vessel ischemic disease, senescent change, Binswanger disease, multi-infarct dementia, and leukoaraiosis, to name a few. There is no consensus on when these imaging changes should be considered abnormal, and when they simply represent a normal part of the aging process.
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What do infarcts from vasculitis look like on imaging?
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Vasculitic infarcts are often scattered across multiple vascular territories and therefore may produce atypical patterns of damage. Varying stages of inflammation, necrosis, fibrosis, and aneurysms may be seen simultaneously.
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How are vasculitides evaluated?
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Cases of suspected vasculitis are evaluated by conventional angiography, which provides the highest possible resolution. Views of the intracranial circulation and the external carotid artery are reviewed in search of irregular focal narrowing. Positive sites may then be selected for biopsy confirmation. Sometimes the vessels affected are so small that the angiogram is normal. In these cases, skin, nerve, muscle, or random temporal artery biopsy may be required to make the diagnosis. Diagnostic confirmation is important, since many of the vasculitides respond to steroids or cytotoxic drugs.
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What things predispose to venous infarcts?
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Predisposing factors include hypercoagulable states; pregnancy; infection (spread from contiguous scalp, face, middle ear, or sinus); dehydration; meningitis; and direct invasion by tumor.
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How do pts with venous occlusion present?
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Characteristically, venous infarcts occur in younger patients, who present with headache, sudden focal deficits, and often seizures.
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How does venous occlusion cause infarction?
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Although the arterial supply is intact, blockage of the outflow leads to stasis, deoxygenation of blood, and neuronal death. Continued perfusion into damaged, occluded vessels frequently leads to hemorrhage.
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Where are venous occlusion infarcts usually located?
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Any dural sinus or cortical vein may be affected, but the most common are transverse (lateral), superior sagittal, and cavernous sinus occlusions.
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What do venous occlusion infarcts look like on CT?
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A pattern of hemorrhagic infarction in the deep cortical or subcortical regions is usually present. These lesions tend to be rounded and may spare some overlying cortex, as opposed to the classic wedge-shaped arterial occlusions that grow larger toward the surface. Venous infarctions may also be suspected when there is an apparent infarct that does not conform to a known arterial territory.
The venous clot responsible may be seen indirectly as a filling defect in the superior sagittal sinus on contrast-enhanced CT, i.e., the “empty delta” sign. |
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When is the "empty delta sign" most likely to be seen?
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The empty delta sign is usually present 1 to 4 weeks after sinus occlusion, but it may not be seen in the acute and chronic phases of the disease.
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What can mimic an empty delta sign?
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An appearance that mimics the empty delta sign has also been described in up to 10% of normal patients when CT scanning is delayed for more than 30 minutes after contrast infusion. This is probably a result of differential blood pool clearance and dural absorption of contrast, effectively highlighting the dural margins of a normal venous sinus.
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What imaging best evaluates for venous occlusion?
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A combination of spin-echo MR and MR venography probably provides the best imaging evaluation for dural sinus occlusion. MR venography can be very helpful in equivocal cases. Whole-brain CTA protocols, modified to add a slightly longer scan delay after injection, also offer excellent noninvasive evaluation of venous disease. Conventional angiography is now reserved mostly for difficult diagnostic cases or when endovascular intervention is considered.
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What does venous thrombosis look like on MR? What is a potential pitfall?
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On MR, venous sinus thrombosis is suspected when venous flow voids are lost and confirmed when an actual clot is observed. Normal but slowly flowing blood can sometimes cause high signal within veins, a potential MR pitfall in the diagnosis of venous occlusion.
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Define hemorrhage:
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Hemorrhage occurs when an artery or vein ruptures, allowing blood to burst forth into the brain parenchyma or subarachnoid spaces.
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Two main types of hemorrhage:
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Although mixed patterns occur, hemorrhages are most conveniently divided into subarachnoid and parenchymal categories.
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Why is hemorrhage bright on CT?
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Because of the formation of “clot,” which has far less serum and (therefore less water) than whole blood.
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How well does MR detect acute hemorrhage?
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Although acute blood can sometimes be challenging to detect on routine MR, sensitivity is excellent when FLAIR is used for subarachnoid hemorrhage and gradient-echo T2* sequences are used for parenchymal bleeding. MR is better than CT for detection and characterization of subacute or chronic hemorrhage.
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What are the four oxygenation states of hemoglobin?
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Oxygenated hemoglobin is sequentially converted to deoxyhemoglobin, methemoglobin, and then hemosiderin over time.
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What does oxyhemoglobin look like on T2WI?
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Oxyhemoglobin is a diamagnetic compound containing ferrous (Fe+2) ions, detected as high signal intensity on T2WIs (particularly first echo).
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What does oxyhemoglobin look like on T1WI?
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Iso/dark (same as deoxyhemoglobin)
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What does Deoxyhemoglobin look like on T1WI?
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Iso/dark (same as oxyhemoglobin)
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What does deoxyhemoglobin look like on T2WI?
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Dark (opposite of oxyhemoglobin)
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What does Methemoglobin (intracellular) look like on T1WI?
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Bright (same as extracellular methemoglobin)
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What does Methemoglobin (intracellular) look like on T2WI?
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Dark (opposite of extracellular methemoglobin)
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What does Methemoglobin (extracellular) look like on T1WI?
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Bright (same as intracellular methemoglobin)
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What does Methemoglobin (extracellular) look like on T2WI?
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Bright (opposite of intracellular methemoglobin)
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What does hemosiderin/ferritin look like on T1WI?
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Iso/dark
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What does hemosiderin/ferritin look like on T2WI?
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Dark
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How fast is oxyhemoglobin converted to deoxyhemoglobin in a hemorrhage?
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This takes place over hours for parenchymal hematomas but can be delayed considerably when oxygen-containing CSF surrounds subarachnoid blood.
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How long does it take for deoxyhemoglobin to be converted to methemoglobin in a hemorrhage?
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In parenchymal or extra-axial hematomas, further oxidation of deoxyhemoglobin leads to formation of methemoglobin, a ferric (Fe+3) paramagnetic substance. This occurs over several days or longer—parallel in time course to lysis of red blood cells.
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What types of cells are layering in a hemorrhage with hematocrit effect on MR?
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T2WIs of subacute hematomas therefore show a “hematocrit effect”: a dependent layer of intact cells exhibiting dark signal (intracellular methemoglobin) and a plasma supernatant showing bright signal (extracellular methemoglobin released after cell lysis).
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What do remote hemorrhages look like on CT and MR?
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An area of remote hemorrhage will commonly be seen as atrophy alone on CT or T1WIs, but a dark rim along the cleft on a T2WI implicates a prior bleed.
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How long does it take for methemoglobin to be converted to hemosiderin/ferritin in a hemorrhage?
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Further oxidation of hemoglobin and breakdown of the globin molecule lead to accumulation of hemosiderin in the lysosomes of macrophages. This takes place greater than 21 days after the hemorrhage.
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What are some causes of subarachnoid hemorrhage?
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Subarachnoid hemorrhage (SAH) is most commonly the result of aneurysm rupture. AVMs of the brain or spinal cord and vascular malformations involving the dura may also cause SAH but usually in combination with parenchymal or subdural bleeding, respectively. Previously normal vessels may rupture into the subarachnoid space when damaged by drugs, trauma, or dissection. SAH may also occasionally be seen in patients with marked thrombocytopenia or other severe coagulopathies.
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What percent of the population has an intracranial aneurysm?
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One percent to 2% of the population has aneurysms, thought to occur because of a congenital absence of the arterial media.
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At what diameter is an intracranial aneurysm at increased risk of rupture?
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Those larger than 3 to 5 mm are at increased risk for rupture.
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What percent of intracranial aneurysms are found in the anterior circulation vs. the posterior circulation?
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About 85% sprout from the anterior part of the circle of Willis, while 15% arise in the vertebrobasilar territory.
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What should you think of when you see an aneurysm of a distal branch?
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When distal branch aneurysms are seen, an episode of prior trauma or systemic infection should be considered (e.g., bacterial endocarditis with “mycotic” aneurysm).
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What conditions are associated with intracranial aneurysms?
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Conditions associated with aneurysms include atherosclerosis, fibromuscular disease, and polycystic kidney disease.
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Which is better for detecting subarachnoid hemorrhage, CT or MR?
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Even large acute SAHs easily seen with CT may be entirely missed on routine spin-echo MR. CT is more than 90% sensitive for the detection of acute SAH, probably because of the increased density of clotted blood. The use of FLAIR sequences on MR can improve conspicuity of acute blood, but CT is still considered the imaging method of choice when clinical findings suggest the possibility of SAH.
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What things would make detection of SAH more difficult?
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SAHs may be quite difficult to detect, even by CT, when the patient's hematocrit is low, the amount of hemorrhage is small, or there is a delay in scanning. In these cases, detection of red blood cells or xanthochromia by lumbar puncture may be the only way to confirm a suspected SAH.
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Where are the most sensitive places to look for SAH?
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most sensitive places to look for SAH on CT are the dependent portions of the subarachnoid space where gravity causes the blood to settle: the interpeduncular fossa and the far posterior aspects of the occipital horns
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Why is prompt scanning important in the detection of SAH?
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Prompt scanning is important, because dissolution of subarachnoid blood reduces CT sensitivity to 66% by day 3.
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What percent of pts will have multiple intracranial aneurysms?
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About 15% to 20% of patients with subarachnoid bleeding will have multiple aneurysms.
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If a pt has multiple intracranial aneurysms, how can you tell which one caused the SAH?
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When multiple aneurysms are present, the one that is largest or most irregular, has focal mass effect, is intra-aneurysmal, or shows a change on serial exams is likely to be the culprit.
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How long does it take for SAH to no longer be detected by CT?
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Unless there has been a massive SAH or rebleeding, subarachnoid blood is generally inconspicuous on CT at 1 week.
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Define intraparenchymal hemorrhage:
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Primary intraparenchymal hemorrhage occurs as a result of bleeding directly into the brain substance.
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Which has a higher mortality and morbidity, a hemorrhage or an infarct? Why?
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Parenchymal bleeds generally have a higher initial mortality than infarcts, but on recovery they show fewer deficits than a similar-sized infarct. This is because hemorrhage tends to tear through and displace brain tissue but can be resorbed. A similar-sized infarct is made up of dead rather than merely displaced neurons.
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What sorts of things cause parenchymal hemorrhage?
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The main differential considerations are hypertensive hemorrhage, vascular malformations, drug effects, amyloid angiopathy, and bloody tumors.
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Where are hypertensive hemorrhages usually located?
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Hypertensive hemorrhages are seen in the putamen (35% to 50%), the subcortical white matter (30%), the cerebellum (15%), the thalamus (10% to 15%), and the pons (5% to 10%)
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What is thought to cause hypertensive hemorrhages?
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As with lacunes, lipohyalinosis of vessels is thought to be the primary predisposing pathologic feature, although miliary aneurysms in the vessel wall may also play a role.
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Which hypertensive bleeds tend to have a poor prognosis?
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Bleeds in the posterior fossa, those with a large amount of mass effect, or those that extend into the ventricular system have a relatively poor prognosis.
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What are the four main types of vascular malformations?
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There are four main subtypes: AVMs, cavernous malformations, telangiectasias, and venous malformations.
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Define AVM:
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AVMs are an abnormal tangle of arteries directly connected to veins without an intervening capillary network.
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How do intracranial AVMs present?
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Most patients present with hemorrhage or seizures.
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What is the annual risk of an AVM bleeding?
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AVMs have a 2% to 3% annual risk of bleeding, but the risk may double or triple in the first year after an initial bleed.
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What do AVMs look like on CT?
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Unruptured AVMs typically appear as a jumble of enlarged vessels without mass effect (Fig. 4.37). Noncontrast CT will show a mixed-attenuation lesion, sometimes with evidence of calcification.
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What do AVMs look like on MR?
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MR demonstrates flow voids or complex flow patterns, sometimes leading to artifacts in the phase-encoding direction. T2W or T2*W images may show dark signal intensity related to the AVM, a sign of prior hemorrhage with hemosiderin deposition.
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What AVM's look like on enhanced studies?
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Intravenous contrast usually results in marked enhancement and therefore increased conspicuity of the AVM on both CT and MR studies. Feeding arteries and draining veins may show impressive enlargement well beyond the center (nidus) of the AVM.
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What percent of AVM's are associated with an aneurysm? Where is it usually located?
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About 10% of AVMs will develop an associated aneurysm, generally on a feeding artery.
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What do hemorrhagic AVM's look like on imaging?
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AVMs can be difficult to detect soon after hemorrhage. Occasionally, the AVM will obliterate itself at the time of rupture, but more commonly the resultant hematoma compresses and obscures many of the remaining vessels. Contrast studies may identify an enhancing portion of a vascular malformation adjacent to a hemorrhage. Normally, acute hemorrhage will not take up contrast unless there is an associated vascular malformation.
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Do parenchymal hemorrhages enhance?
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Normally, acute hemorrhage will not take up contrast unless there is an associated vascular malformation. A subacute hematoma of any cause may enhance because of a surrounding vascular capsule and should not be mistaken for an AVM.
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Describe cavernous malformation:
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Cavernous malformations are thin-walled sinusoidal vessels (neither arteries nor veins) that may present with seizures or small parenchymal hemorrhages. These lesions may be asymptomatic and can occur on a familial basis.
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What do cavernous malformations look like on imaging?
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CT scans and angiography are usually normal. MR will show a reticulated, often enhancing lesion with dark rim (hemosiderin) on T2.
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Define venous malformation:
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Venous malformations (also called developmental venous anomalies or venous angiomas) are congenitally anomalous veins that drain normal brain.
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What percent of pts have a venous malformation?
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They are seen in 1% to 2% of patients studied by contrast MR but may easily be missed on CT or noncontrast MR.
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What do venous malformations look like on MR?
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The classic appearance is of an enlarged enhancing stellate venous complex that extends to the ventricular or cortical surface. The contrast-enhanced MR appearance is usually diagnostic, such that angiography is rarely needed.
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What is the treatment of venous malformations?
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Although these may bleed, treatment is somewhat controversial because they are commonly seen in asymptomatic patients and are often the only venous drainage for a brain region.
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Describe intracranial telangiectasias:
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Telangiectasias are dilated capillary-sized vessels and are usually diagnosed at autopsy. These are generally small, solitary lesions found incidentally by MR. No treatment is necessary.
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What generic term can you use to describe a small cerebrovascular malformation?
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The generic term occult cerebrovascular malformation is used to describe telangiectasias, cavernous malformations, and small thrombosed AVMs.
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What do occult cerebrovascular malformations look like on imaging?
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Occult cerebrovascular malformations are usually inconspicuous on CT but may be detected as a small area of calcification. On MR, an occult cerebrovascular malformation should be suspected when focal heterogeneous signal (acute/subacute blood) is seen with a surrounding ring of hypointensity (hemosiderin). Unless it has recently ruptured, an occult cerebrovascular malformation should show no mass effect or edema. If all these criteria are met, conventional angiography may be unnecessary.
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Describe drug-associated intracranial hemorrhage:
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Sympathomimetic drugs seem to provide an effective (if unintended) stress test for the presence of brain vascular anomalies (Fig. 4.33). Drugs such as amphetamines and cocaine have been commonly associated with intracranial hemorrhage. Symptoms develop within minutes to hours following use of the drug. The genesis may be related to transient hypertension or arteritis-like vascular change similar to periarteritis nodosa. Up to 50% of drug abusers who suffer an intracranial hemorrhage have a demonstrable underlying structural cause, such as an aneurysm or AVM.
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Describe amyloid angiopathy:
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Amyloid angiopathy or “congophilic” angiopathy is an increasingly recognized cause of intracranial hemorrhage and is frequently lobar in nature. It is characterized by amyloid deposits in the media and adventitia of medium size and small cortical leptomeningeal arteries. It is not associated with systemic vascular amyloidosis. This angiopathy characteristically affects elderly individuals. Cerebral amyloid angiopathy is associated with progressive senile dementia in about 30% of cases. Systemic hypertension is common in this age group but is not directly related to cerebral amyloid angiopathy. Widespread, multifocal involvement can be seen in some cases, particularly when T2*W MR sequences are used to make old hemorrhages more conspicuous. Amyloid angiopathy should come to mind when an elderly, frequently demented patient presents with new or recurrent superficial hemorrhages.
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How is amyloid angiopathy associted with post-thrombolytic hemorrhage?
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Pre-existing amyloid “microbleeds” may also be an underlying source for some cases of postthrombolytic hemorrhage.
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Why do some brain tumors cause hemorrhage?
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Tumor necrosis, vascular invasion, and neovascularity may contribute to the pathogenesis of hemorrhagic neoplasms.
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What is the most likely primary brain tumor to cause hemorrhage? What types of metastatic tumors tend to cause hemorrhage?
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Glioblastomas are the most common primary brain tumors to hemorrhage, while in the metastatic category, bronchogenic carcinoma, thyroid, melanoma, choriocarcinoma, and renal cell carcinoma often bleed.
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What imaging features suggest that a hemorrhage is from a malignancy?
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-Intratumoral bleeds tend to be more complex and heterogeneous than benign hematomas.
-The expected evolution of blood products is commonly delayed with tumors, possibly because of profound intratumoral hypoxia. -If a patient is scanned during the acute phase, lack of enhancement beyond the hematoma strongly supports a primary intracranial hemorrhage. -If there is an enhancing component, then lesions such as tumor or AVM must be considered. -In the subacute phase, however, a resolving hematoma may develop a thin area of ring enhancement of its own. -Both acute hemorrhage and hemorrhagic neoplasms may cause an edematous reaction, although with tumors, edema is more predominant. -In a benign intracranial hypertensive bleed, the edema should begin to substantially resolve within a week, while in the presence of a neoplasm it should persist. -With a resolving benign hematoma, a fully circumferential hemosiderin ring begins to develop at about 2 to 3 weeks on MR. -In the hematoma associated with tumor, this hemosiderin ring may be absent or incomplete. |
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How can the evolution of blood products help you determine if a hemorrhage is from a malignancy versus something else?
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Malignancies tend to have irregular and complex evolution of blood products, while non-malignant hemorrhages have a predictable evolution of blood products from peripheral to central.
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How can the hemosiderin rim help you determine if a hemorrhage is from a malignancy versus something else?
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The hemosiderin ring will be complete with non-malignant causes of hemorrhage, while malignancies can cause delayed and incomplete formation of a hemosiderin ring.
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How can the surrounding edema help you determine if a hemorrhage is from a malignancy versus something else?
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Surrounding edema is usually minimal to mild in non-malignant causes of hemorrhages, while malignancies tend to have moderate to severe surrounding edema.
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How can the acute enhancement pattern help you determine if a hemorrhage is from a malignancy versus something else?
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Non-malignant causes of hemorrhages do not enhance (unless there's an AVM), while malignancies will always enhance.
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What is your differential for a hemorrhage with enhancing components?
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Hemorrhagic tumor versus AVM versus hemorrhagic infarct (because of the breakdown of the blood brain barrier)
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What should you do if you can't tell if a hemorrhage was caused by a tumor or not?
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Sometimes when the findings are ambiguous, a follow-up exam in 3 to 6 weeks will clarify the diagnosis, avoiding the need for a biopsy.
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Describe how an infarct can become hemorrhagic:
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In hemorrhagic infarction, arterial occlusion causes infarction of the parent vessel itself, along with its brain territory. If clot dissolution occurs or if collateral flow ensues, blood may then be extruded from the damaged vessel wall.
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How can you tell a hemorrhagic infarct from a primary hemorrhage?
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Hemorrhagic infarctions therefore tend to be in classic vascular distributions and infrequently show much mass effect. They are less confluent than hematomas and usually exhibit some degree of contrast enhancement, since breakdown of the blood-brain barrier is present by definition. They are not associated with intraventricular blood, which may accompany a primary bleed. Primary hemorrhage is characterized by disruption of the blood vessel wall, leading to extravasation of blood into the surrounding tissues, sometimes at a distance from the damaged vessel. Unlike hemorrhagic infarcts, primary hemorrhages may therefore cross vascular boundaries.
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