483 lines
35 KiB
Markdown
483 lines
35 KiB
Markdown
---
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title: "Acute Ischemic Stroke"
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docid: "69a7a1f7-9c78-4ad1-82dd-9b13f2e717b3"
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authors:
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- key: "07a2c087-6202-49e7-870b-7aa162d18f06"
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value: "Bronwyn E. Hamilton, MD"
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breadcrumbs:
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-
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name: "Vasculature"
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slug: "vasculature"
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treeNodeId: "9d3db335-364f-44ec-b2e2-30b03ce93228"
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-
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name: "Diagnosis"
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slug: "diagnosis"
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treeNodeId: "4a210126-9f87-404e-b419-a73f44d0e94c"
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-
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name: "Extracranial Cerebral Arteries"
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slug: "extracranial-cerebral-arteries"
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treeNodeId: "593e17de-cd84-4587-8349-872ed33d28c4"
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-
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name: "Acute Ischemic Stroke"
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slug: "acute-ischemic-stroke"
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treeNodeId: null
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category: "Vasculature"
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cmeTopicId: "269a1301-f57a-4247-b62a-de2d927ea3bf"
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documentVersionId: "90d363cc-bb77-48d7-ae31-85fefda3de0c"
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imageCount: 32
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lastUpdated: "04/18/16"
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pageDescription: "Acute Ischemic Stroke"
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pageKeywords: "Vasculature, Diagnosis, Extracranial Cerebral Arteries, Acute Ischemic Stroke"
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pageTitle: "Acute Ischemic Stroke | STATdx"
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enhancedTitle: "Acute Ischemic Stroke"
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type: "DX"
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references: true
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breadcrumbs:
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- "Vasculature"
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- "Diagnosis"
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- "Extracranial Cerebral Arteries"
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- "Acute Ischemic Stroke"
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---
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# KEY FACTS
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- ## Terminology
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- Interrupted blood flow to brain resulting in cerebral ischemia/infarction with variable neurologic deficit
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- ## Imaging
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- Major artery (territorial) infarct
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- Generally wedge-shaped; both GM & WM involved
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- Embolic infarcts
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- Often focal/small, at GM-WM interface
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- NECT
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- Hyperdense vessel (high specificity, low sensitivity)
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- "Dense MCA" sign: Acute thrombus in middle cerebral artery
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- Loss of GM-WM distinction in 1st 3 hours (50-70%)
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- "Insular ribbon" sign: Loss of GM-WM differentiation of insular cortex
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- MR
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- Best diagnostic clue is high signal on DWI with corresponding low signal on ADC
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- ↓ CBF and ↓ CBV on perfusion MR (or CT)
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- ## Top Differential Diagnoses
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- Hyperdense vessel mimics
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- Parenchymal hypodensity (nonvascular causes)
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- ## Pathology
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- Severely ischemic core
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- CBF < (6-8 mL)/(100 g/min)
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- Peripheral penumbra
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- CBF = (10-20 mL)/(100 g/min)
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- ## Clinical Issues
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- 2nd most common cause of death worldwide
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- Leading cause of morbidity in USA
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- Treatment
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- IV thrombolysis (< 3 hours of symptom onset)
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- IA thrombolysis (selected acute strokes < 6 hours)
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- Clinical diagnosis inaccurate in 15-20% of strokes
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# TERMINOLOGY
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- ## Synonyms
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- Stroke, brain attack, cerebrovascular accident
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- ## Definitions
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- Interrupted blood flow to brain resulting in cerebral ischemia/infarction with variable neurologic deficit
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# IMAGING
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- ## General Features
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- ### Best diagnostic clue
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- High signal on DWI with corresponding low signal on ADC
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- Decreased cerebral blood flow (CBF) and cerebral blood volume (CBV) on CT or MR perfusion
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- ### Location
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- 1 or more vascular territories or at border zones (watershed)
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- ### Size
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- Dependent on degree of compromise and collateral circulation
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- ### Morphology
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- Territorial infarct
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- Conforms to arterial territory
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- Generally wedge-shaped
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- Both gray matter (GM) and white matter (WM) are involved
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- Embolic infarcts (often focal, at GM-WM interface)
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- ## CT Findings
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- ### NECT
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- Hyperdense vessel (high specificity, low sensitivity)
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- Represents acute thrombus in cerebral vessel(s)
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- Hyperdense M1 segment of middle cerebral artery (MCA) in 35-50%; most common vessel involved
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- "Dot" sign: Occluded MCA branches in sylvian fissure (16-17%)
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- Loss of gray-white matter (GM-WM) distinction in 1st 3 hours (50-70%)
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- Obscuration of deep gray nuclei
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- Loss of cortical "ribbon"
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- Parenchymal hypodensity
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- If > 1/3 MCA territory initially hypodense, then larger lesion usually develops later
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- Temporary transition to isodensity (up to 54%) at 2-3 weeks post ictus (CT "fogging")
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- Gyral swelling, sulcal effacement 12-24 hours
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- "Hemorrhagic transformation" in 15-45%
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- Delayed onset (24-48 hours) most typical
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- Can be gross (parenchymal) or petechial
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- ### CECT
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- Enhancing cortical vessels: Slow flow or collateralization acutely
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- Absent vessels: Occlusion
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- Perfusion CT (pCT): Assess ischemic core vs. penumbra; identify patients who benefit most from revascularization
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- pCT calculates CBF, CBV, time to peak (TTP)
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- Deconvolution can give mean transit time (MTT)
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- Cortical/gyral enhancement after 48-72 hours
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- CTA: Identify occlusions, dissections, stenoses, collaterals
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- ## MR Findings
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- ### T1WI
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- Early cortical swelling and hypointensity, loss of GM-WM borders
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- ### T2WI
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- Cortical swelling, hyperintensity after 12-24 hours
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- May normalize 2-3 weeks post ictus (MR "fogging")
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- ### FLAIR
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- Parenchymal hyperintensity appears (6 hours post ictus) while other sequences normal
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- Intraarterial FLAIR hyperintensity is early sign of major vessel occlusion or slow flow
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- ### T2* GRE
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- Detection of acute blood products
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- Arterial "blooming" (thrombosed vessel) from clot susceptibility
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- ### DWI
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- Hyperintense restriction from cytotoxic edema
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- Improves hyperacute stroke detection to 95%
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- Best correlates with "ischemic core" (final infarct size); some diffusion abnormalities reverse
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- May have reduced sensitivity in brainstem and medulla during 1st 24 hours
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- Restriction typically lasts 7-10 days
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- High signal can persist up to 2 months post ictus
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- After 10 days, T2 effect may predominate over low ADC: T2 "shine-through"
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- Corresponding low signal on ADC maps
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- May normalize after tissue reperfusion
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- Hyper- or isointensity on ADC map (T2 "shine-through") may mimic diffusion restriction
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- Distinguish cytotoxic from vasogenic edema in complicated cases
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- May be helpful to evaluate new deficits after tumor resection
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- ### PWI
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- Dynamic contrast bolus or arterial spin-labeling techniques
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- Maximum slope gives relative CBF and CBV
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- Deconvolution gives absolute values
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- Bolus-tracking T2* gadolinium PWI with CBV map
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- ↓ perfusion; 75% larger than DWI abnormality
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- DWI/PWI mismatch may identify penumbra (potentially viable but at-risk tissue)
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- ### T1WI C+
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- Variable enhancement patterns evolve over time
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- Hyperacute: Intravascular enhancement (stasis from slow antegrade or retrograde collateral flow)
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- Acute: Meningeal enhancement (pial collateral flow appears in 24-48 hours, resolves over 3-4 days)
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- Subacute: Parenchymal enhancement (appears after 24-48 hours, can persist for weeks/months)
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- MRA: Major vessel occlusions, stenoses, status of collaterals
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- MRS: Elevated lactate, decreased NAA
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- Conventional MR sequences positive in 70-80%
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- Restricted diffusion improves accuracy to 95%
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- Diffusion tensor imaging (DTI)
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- Multidirectional diffusion-weighted images; at least 6 directions can be used to calculate DTI trace and generate ADC maps
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- Higher spatial resolution
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- May be more sensitive for small ischemic foci, emboli, cortical strokes
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- ## Angiographic Findings
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- Conventional: Vessel occlusion (cut off, tapered, "tram track")
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- Slow antegrade flow and slow retrograde collateral flow
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- Intraluminal thrombus = filling defect
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- Neurointerventional: Intraarterial (IA) fibrinolytic therapy for treatment of selected acute nonhemorrhagic stroke within 6-hour window
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- IA mechanical clot removal with retriever device
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- ## Imaging Recommendations
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- ### Best imaging tool
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- MR + DWI; T2* GRE
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- ### Protocol advice
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- NECT as initial study to exclude hemorrhage/mass
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- CT perfusion and CTA if available
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- MR using DWI/FLAIR/GRE ± MRA, PWI
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- DSA with thrombolysis in selected patients
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# DIFFERENTIAL DIAGNOSIS
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- ## Hyperdense Vessel Mimics
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- High hematocrit (polycythemia)
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- Microcalcification in vessel wall
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- Diffuse cerebral edema makes vessels appear relatively hyperdense
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- Normal circulating blood always slightly hyperdense to normal brain
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- ## Parenchymal Hypodensity (Nonvascular Causes)
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- Infiltrating neoplasm (e.g., astrocytoma)
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- Cerebral contusion
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- Inflammation (cerebritis, encephalitis)
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- Evolving encephalomalacia
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- Dural venous thrombosis with parenchymal venous congestion and edema
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# PATHOLOGY
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- ## General Features
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- ### Etiology
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- Common causes
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- Thrombotic vs. embolic, dissection, vasculitis, hypoperfusion
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- Unusual causes
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- Complicated vasculopathy, including posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome; venous stroke
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- Early: Critical disturbance in CBF
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- Severely ischemic core: CBF < (6-8 mL)/(100 g/min)
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- Normal CBF ~ (60 mL)/(100 g/min)
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- Oxygen depletion, energy failure, terminal depolarization, ion homeostasis failure
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- Bulk of final infarct → cytotoxic edema, cell death
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- Later: Evolution from ischemia to infarction depends on many factors (e.g., hyperglycemia influences "destiny" of ischemic brain tissue)
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- Ischemic penumbra: CBF = (10-20 mL)/(100 g/min)
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- Theoretically salvageable tissue
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- Target of thrombolysis, neuroprotective agents
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- ### Associated abnormalities
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- Cardiac disease, prothrombotic states
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- Additional stroke risk factors: C-reactive protein, homocysteine
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- ## Gross Pathologic & Surgical Features
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- Acute thrombosis of major vessel
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- Pale, swollen brain; GM-WM boundaries blurred
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- ## Microscopic Features
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- After 4 hours: Eosinophilic neurons with pyknotic nuclei
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- 15-24 hours: Neutrophils invade, and necrotic nuclei look like "eosinophilic ghosts"
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- 2-3 days: Blood-derived phagocytes
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- 1 week: Reactive astrocytosis, ↑ capillary density
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- End result: Fluid-filled cavity lined by astrocytes
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# CLINICAL ISSUES
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- ## Presentation
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- ### Most common signs/symptoms
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- Focal acute neurologic deficit
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- Paresis, aphasia, decreased mental status
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- ## Demographics
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- ### Age
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- Usually older adults
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- ### Gender
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- No gender predilection
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- ### Epidemiology
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- 2nd most common cause of death worldwide
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- Among leading causes of morbidity in USA
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- ## Natural History & Prognosis
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- Clinical diagnosis inaccurate in 15-20% of strokes
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- Malignant MCA infarct (coma, death)
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- Up to 10% of all stroke patients
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- Fatal brain swelling with increased ICP
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- ## Treatment
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- "Time is brain": IV thrombolytic therapy window < 3 hours
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- IA window < 6 hours except for vertebrobasilar thrombosis (up to 24 hours because of high morbidity and mortality)
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- Patient selection most important factor in outcome
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- Symptom onset < 6 hours
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- No parenchymal hematoma on CT
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- < 1/3 MCA territory hypodensity
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# DIAGNOSTIC CHECKLIST
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- ## Consider
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- DWI positive for acute stroke only if ADC correlates
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- Rarely, ischemia may mimic tumor or encephalitis
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ba323bb3-7781-4789-81b2-774e4fcadb49
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## References
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# Selected References
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1. [Parrilla G et al: Hemorrhage/contrast staining areas after mechanical intra-arterial thrombectomy in acute ischemic stroke: imaging findings and clinical significance. AJNR Am J Neuroradiol. 33(9):1791-6, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22538076%5Bpmid%5D)
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1. [Wang DJ et al: The value of arterial spin-labeled perfusion imaging in acute ischemic stroke: comparison with dynamic susceptibility contrast-enhanced MRI. Stroke. 43(4):1018-24, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22328551%5Bpmid%5D)
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1. [Harris AD et al: Diffusion and perfusion MR imaging of acute ischemic stroke. Magn Reson Imaging Clin N Am. 17(2):291-313, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19406360%5Bpmid%5D)
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1. [Kranz PG et al: Does diffusion-weighted imaging represent the ischemic core? An evidence-based systematic review. AJNR Am J Neuroradiol. 30(6):1206-12, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19357385%5Bpmid%5D)
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1. [Lee KY et al: Distal hyperintense vessels on FLAIR: an MRI marker for collateral circulation in acute stroke? Neurology. 72(13):1134-9, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19211928%5Bpmid%5D)
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1. [Sanossian N et al: Angiography reveals that fluid-attenuated inversion recovery vascular hyperintensities are due to slow flow, not thrombus. AJNR Am J Neuroradiol. 30(3):564-8, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19022866%5Bpmid%5D)
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1. [Soares BP, Chien JD, Wintermark M. MR and CT monitoring of recanalization, reperfusion, and penumbra salvage: everything that recanalizes does not necessarily reperfuse! Stroke. 40(3 Suppl):S24-7, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19064812%5Bpmid%5D)
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1. [Chen Z et al: Evaluating ischemic stroke with diffusion tensor imaging. Neurol Res. 30(7):720-6, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18513464%5Bpmid%5D)
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1. [Provenzale JM et al: Optimization of perfusion imaging for acute cerebral ischemia: review of recent clinical trials and recommendations for future studies. AJR Am J Roentgenol. 191(4):1263-70, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18806174%5Bpmid%5D)
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1. [Lell MM et al: New techniques in CT angiography. Radiographics. 26 Suppl 1:S45-62, 2006](http://www.ncbi.nlm.nih.gov/pubmed/?term=17050518%5Bpmid%5D)
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1. [Bourekas EC et al: Intraarterial thrombolytic therapy within 3 hours of the onset of stroke. Neurosurgery. 54(1):39-44; discussion 44-6, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14683539%5Bpmid%5D)
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1. [Diaz J et al: Cerebral ischemia: new risk factors. Cerebrovasc Dis. 17 Suppl 1:43-50, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14694279%5Bpmid%5D)
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1. [Fiebach JB et al: Stroke magnetic resonance imaging is accurate in hyperacute intracerebral hemorrhage: a multicenter study on the validity of stroke imaging. Stroke. 35(2):502-6, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14739410%5Bpmid%5D)
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1. [Fiehler J et al: Predictors of apparent diffusion coefficient normalization in stroke patients. Stroke. 35(2):514-9, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14739409%5Bpmid%5D)
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1. [Gass A et al: Diffusion-weighted MRI for the "small stuff": the details of acute cerebral ischaemia. Lancet Neurol. 3(1):39-45, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14693110%5Bpmid%5D)
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1. [Kelly PJ et al: Inflammation, homocysteine, and vitamin B6 status after ischemic stroke. Stroke. 35(1):12-5, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14657454%5Bpmid%5D)
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1. [Kidwell CS et al: Comparison of MRI and CT for detection of acute intracerebral hemorrhage. JAMA. 292(15):1823-30, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15494579%5Bpmid%5D)
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1. [Mahagne MH et al: Voxel-based mapping of cortical ischemic damage using Tc 99m L,L-ethyl cysteinate dimer SPECT in acute stroke. J Neuroimaging. 14(1):23-32, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14748205%5Bpmid%5D)
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1. [Nakajima M et al: Relationships between angiographic findings and National Institutes of Health stroke scale score in cases of hyperacute carotid ischemic stroke. AJNR Am J Neuroradiol. 25(2):238-41, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14970023%5Bpmid%5D)
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1. [Borisch I et al: Preoperative evaluation of carotid artery stenosis: comparison of contrast-enhanced MR angiography and duplex sonography with digital subtraction angiography. AJNR Am J Neuroradiol. 24(6):1117-22, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12812936%5Bpmid%5D)
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1. [Eastwood JD et al: Quantitative assessment of the time course of infarct signal intensity on diffusion-weighted images. AJNR Am J Neuroradiol. 24(4):680-7, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12695203%5Bpmid%5D)
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1. [Leary MC et al: Validation of computed tomographic middle cerebral artery "dot"sign: an angiographic correlation study. Stroke. 34(11):2636-40, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=14593125%5Bpmid%5D)
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1. [Tomandl BF et al: Comprehensive imaging of ischemic stroke with multisection CT. Radiographics. 23(3):565-92, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12740462%5Bpmid%5D)
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1. [Toyoda K et al: Fluid-attenuated inversion recovery intraarterial signal: an early sign of hyperacute cerebral ischemia. AJNR Am J Neuroradiol. 22(6):1021-9, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11415892%5Bpmid%5D)
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## Images
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### Selected Images
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*Coronal graphic illustrates a left M1 occlusion. A proximal occlusion affects the entire middle cerebral artery (MCA) territory, including the basal ganglia, which are perfused by lenticulostriate (perforating) arteries <img src='img/arrows/BS.png'/>. Acute ischemia is often identified by subtle loss of the gray-white matter interfaces with blurring of the basal ganglia and an "insular ribbon" sign on the initial CT.*
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*Coronal graphic illustrates a left M1 occlusion. A proximal occlusion affects the entire middle cerebral artery (MCA) territory, including the basal ganglia, which are perfused by lenticulostriate (perforating) arteries <img src='img/arrows/BS.png'/>. Acute ischemia is often identified by subtle loss of the gray-white matter interfaces with blurring of the basal ganglia and an "insular ribbon" sign on the initial CT.*
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*Axial NECT demonstrates a hyperdense MCA sign representing acute thrombus <img src='img/arrows/WS.png'/> in a patient with acute stroke symptoms.*
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*Axial NECT shows subtle loss of the right temporal gray-white matter interfaces <img src='img/arrows/WS.png'/> representing an "insular ribbon" sign.*
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*Axial pCT (CBF) shows decreased blood flow <img src='img/arrows/BO.png'/> in the right hemisphere related to hyperacute MCA ischemia. The CBF and CBV color maps cephalad to this slice showed a large MCA wedge-shaped defect. There was a similar perfusion abnormality on the TTP maps (not shown). Lack of a mismatch between CBV and TTP maps suggests that no ischemic penumbra is present.*
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*Axial DWI MR shows a large wedge-shaped hyperintensity related to restricted diffusion <img src='img/arrows/WO.png'/> representing acute ischemia in a left MCA distribution. There is sparing of the basal ganglia, consistent with distal M1 occlusion.*
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*Axial NECT shows a hypodense wedge-shaped region of acute infarct <img src='img/arrows/WS.png'/> with mild mass effect and sulcal effacement related to a right M1 embolic occlusion due to a calcified thrombus <img src='img/arrows/WO.png'/>.*
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*Axial NECT demonstrates bilateral posterior circulation hypodensities <img src='img/arrows/WS.png'/> in a 20-month-old boy presenting with seizures after recent circumcision complicated by hematoma.*
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*Axial NECT shows hyperdense thrombus <img src='img/arrows/WS.png'/> in the distal basilar artery of a 66-year-old woman with altered sensorium. Percutaneous thrombolysis is usually considered at later time points, up to 24 hours, because of the high morbidity and mortality associated with basilar thrombosis.*
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*Axial DWI MR shows hyperintensity related to restricted diffusion in a patient with vertebrobasilar disease and a posterior inferior cerebellar artery acute infarct. MR is superior to CT in evaluation of a posterior fossa stroke.*
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*Coronal CTA MIP reconstruction shows a focal filling defect within the proximal M1 segment <img src='img/arrows/WS.png'/> in a patient with acute MCA ischemia. Intraarterial thrombolysis may be helpful if the patient presents to the emergency department within 6 hours of symptoms onset.*
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*Angiography in a 27-year-old man with a history of methamphetamine and tobacco use shows focal tight stenosis within the distal right M1 segment <img src='img/arrows/WS.png'/>. He presented with stuttering symptoms of left-sided weakness and face droop.*
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*Sagittal T2WI MR shows multiple watershed ischemic foci in the deep white matter <img src='img/arrows/WS.png'/> in a "string of pearls" configuration.*
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*Axial T2* GRE MR shows multifocal hemorrhages <img src='img/arrows/WS.png'/> within an ischemic infarct in a 13-year-old boy with 3 weeks of fatigue, epistaxis, and acute loss of consciousness. He was found to have leukemia complicated by disseminated intravascular coagulation.*
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*Axial NECT shows cerebellar infarcts <img src='img/arrows/WS.png'/> in a 34-year-old woman with bilateral vertebral artery dissections. Note effacement of basal cisterns <img src='img/arrows/WO.png'/> and temporal horn dilation <img src='img/arrows/WC.png'/> indicating upward transtentorial herniation.*
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*Axial T2WI MR shows bilateral wedge-shaped occipital areas of hyperintensity <img src='img/arrows/WS.png'/> in a 77-year-old woman, which do not allow for a reliable distinction between chronic and acute ischemia.*
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*Axial DWI MR in the same patient accurately reflects the acute area of left occipital ischemia <img src='img/arrows/WS.png'/>, while encephalomalacia is apparent in the right occipital lobe <img src='img/arrows/WO.png'/>.*
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*Axial NECT shows multifocal hypodensities in the left cerebellum <img src='img/arrows/WS.png'/>, consistent with embolic infarction within the left PICA distribution in this 40-year-old man with longstanding insulin-dependent diabetes and chronic renal failure. He presented with acute severe headache, nausea, and vomiting without localizing neurological finding.*
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*Axial CTA shows occlusion of the left vertebral artery <img src='img/arrows/WS.png'/>. Compare with a normal dominant right vertebral artery <img src='img/arrows/WO.png'/>.*
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*Axial CTA shows intimal flap <img src='img/arrows/WS.png'/> in a 47-year-old woman with bilateral internal carotid artery dissections.*
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*Axial NECT shows hyperdense left deep nuclei <img src='img/arrows/WS.png'/> in a patient post recent IV thrombolytic therapy followed by mechanical thrombectomy for left MCA occlusion. These may reflect contrast staining &/or hemorrhage. Contrast gradually fades over time and does not imply worse prognosis. Matching hypointensity on GRE suggests hemorrhage.*
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*Axial T1 C+ MR shows heterogeneous gyriform enhancement in right MCA territory due to breakdown of BBB in subacute infarction. This appearance can mimic glioblastoma. Follow-up imaging may be important in patients without available imaging at the time of ictus to ensure appropriate evolution.*
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*Anteroposterior angiography shows left M1 occlusion <img src='img/arrows/BO.png'/> and associated prominent lenticulostriate vessels <img src='img/arrows/BC.png'/>.*
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### Additional Images
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*Axial DWI MR in a patient 2 hours after stroke onset shows restricted diffusion. Correlative ADC hypointensity was also demonstrated within the same geographic area (not shown).*
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*Axial CECT shows abrupt right MCA cut-off <img src='img/arrows/WC.png'/> in a patient with hyperacute stroke symptoms. (Courtesy J. Eastwood, MD.)*
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*Axial DWI MR shows small emboli infarcts <img src='img/arrows/WS.png'/> in the left hemisphere.*
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*Axial CT perfusion map in the same patient reveals significantly prolonged mean transit time within the MCA distribution (red region).*
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*Axial DWI MR shows restricted diffusion within the right occipital lobe in a patient with sudden onset of visual symptoms.*
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*Axial FLAIR MR shows multiple foci of intraarterial high signal <img src='img/arrows/WS.png'/> suggesting slow flow in this patient with left internal carotid artery dissection.*
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*Coronal CTA shows slight irregularity within the reconstituted left vertebral artery segment <img src='img/arrows/BS.png'/>, consistent with dissection in this symptomatic patient.*
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*Axial single-phase arterial spin-labeling (ASL) perfusion shows hemispheric asymmetry, decreased on the left <img src='img/arrows/WS.png'/>, in a patient with acute left internal carotid artery dissection.*
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*Axial FLAIR MR shows classic deep white matter watershed ischemic foci <img src='img/arrows/WS.png'/> in a "string of pearls" appearance.*
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*Axial DWI MR in a 35-year-old woman post transsphenoidal surgery for Cushing disease shows multifocal infarctions <img src='img/arrows/WS.png'/> as a complication of Enterobacter meningitis.*
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