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KEY FACTS

Terminology
- Interrupted blood flow to brain resulting in cerebral ischemia/infarction with variable neurologic deficit
Imaging
- Major artery (territorial) infarct - Generally wedge-shaped; both GM & WM involved
- Embolic infarcts - Often focal/small, at GM-WM interface
- NECT - Hyperdense vessel (high specificity, low sensitivity) - "Dense MCA" sign: Acute thrombus in middle cerebral artery - Loss of GM-WM distinction in 1st 3 hours (50-70%) - "Insular ribbon" sign: Loss of GM-WM differentiation of insular cortex
- MR - Best diagnostic clue is high signal on DWI with corresponding low signal on ADC - ↓ CBF and ↓ CBV on perfusion MR (or CT)
Top Differential Diagnoses
- Hyperdense vessel mimics
- Parenchymal hypodensity (nonvascular causes)
Pathology
- Severely ischemic core - CBF < (6-8 mL)/(100 g/min)
- Peripheral penumbra - CBF = (10-20 mL)/(100 g/min)
Clinical Issues
- 2nd most common cause of death worldwide
- Leading cause of morbidity in USA
- Treatment - IV thrombolysis (< 3 hours of symptom onset) - IA thrombolysis (selected acute strokes < 6 hours)
- Clinical diagnosis inaccurate in 15-20% of strokes

TERMINOLOGY

Synonyms
- Stroke, brain attack, cerebrovascular accident
Definitions
- Interrupted blood flow to brain resulting in cerebral ischemia/infarction with variable neurologic deficit

IMAGING

General Features

Best diagnostic clue

- High signal on DWI with corresponding low signal on ADC
- Decreased cerebral blood flow (CBF) and cerebral blood volume (CBV) on CT or MR perfusion

Location

- 1 or more vascular territories or at border zones (watershed)

Size

- Dependent on degree of compromise and collateral circulation

Morphology

- Territorial infarct
        - Conforms to arterial territory
        - Generally wedge-shaped
        - Both gray matter (GM) and white matter (WM) are involved
- Embolic infarcts (often focal, at GM-WM interface)

CT Findings

NECT

- Hyperdense vessel (high specificity, low sensitivity)
        - Represents acute thrombus in cerebral vessel(s)
        - Hyperdense M1 segment of middle cerebral artery (MCA) in 35-50%; most common vessel involved
        - "Dot" sign: Occluded MCA branches in sylvian fissure (16-17%)
- Loss of gray-white matter (GM-WM) distinction in 1st 3 hours (50-70%)
        - Obscuration of deep gray nuclei
        - Loss of cortical "ribbon"
- Parenchymal hypodensity
        - If > 1/3 MCA territory initially hypodense, then larger lesion usually develops later
        - Temporary transition to isodensity (up to 54%) at 2-3 weeks post ictus (CT "fogging")
- Gyral swelling, sulcal effacement 12-24 hours
- "Hemorrhagic transformation" in 15-45%
        - Delayed onset (24-48 hours) most typical
        - Can be gross (parenchymal) or petechial

CECT

- Enhancing cortical vessels: Slow flow or collateralization acutely
- Absent vessels: Occlusion
- Perfusion CT (pCT): Assess ischemic core vs. penumbra; identify patients who benefit most from revascularization
        - pCT calculates CBF, CBV, time to peak (TTP)
        - Deconvolution can give mean transit time (MTT)
- Cortical/gyral enhancement after 48-72 hours

CTA: Identify occlusions, dissections, stenoses, collaterals

MR Findings

T1WI

- Early cortical swelling and hypointensity, loss of GM-WM borders

T2WI

- Cortical swelling, hyperintensity after 12-24 hours
- May normalize 2-3 weeks post ictus (MR "fogging")

FLAIR

- Parenchymal hyperintensity appears (6 hours post ictus) while other sequences normal
- Intraarterial FLAIR hyperintensity is early sign of major vessel occlusion or slow flow

T2* GRE

- Detection of acute blood products
- Arterial "blooming" (thrombosed vessel) from clot susceptibility

DWI

- Hyperintense restriction from cytotoxic edema
        - Improves hyperacute stroke detection to 95%
        - Best correlates with "ischemic core" (final infarct size); some diffusion abnormalities reverse
        - May have reduced sensitivity in brainstem and medulla during 1st 24 hours
        - Restriction typically lasts 7-10 days
                  - High signal can persist up to 2 months post ictus
                  - After 10 days, T2 effect may predominate over low ADC: T2 "shine-through"
- Corresponding low signal on ADC maps
        - May normalize after tissue reperfusion
        - Hyper- or isointensity on ADC map (T2 "shine-through") may mimic diffusion restriction
- Distinguish cytotoxic from vasogenic edema in complicated cases
        - May be helpful to evaluate new deficits after tumor resection

PWI

- Dynamic contrast bolus or arterial spin-labeling techniques
        - Maximum slope gives relative CBF and CBV
        - Deconvolution gives absolute values
- Bolus-tracking T2* gadolinium PWI with CBV map
        - ↓ perfusion; 75% larger than DWI abnormality
        - DWI/PWI mismatch may identify penumbra (potentially viable but at-risk tissue)

T1WI C+

- Variable enhancement patterns evolve over time
        - Hyperacute: Intravascular enhancement (stasis from slow antegrade or retrograde collateral flow)
        - Acute: Meningeal enhancement (pial collateral flow appears in 24-48 hours, resolves over 3-4 days)
        - Subacute: Parenchymal enhancement (appears after 24-48 hours, can persist for weeks/months)

MRA: Major vessel occlusions, stenoses, status of collaterals
MRS: Elevated lactate, decreased NAA
Conventional MR sequences positive in 70-80% - Restricted diffusion improves accuracy to 95%
Diffusion tensor imaging (DTI) - Multidirectional diffusion-weighted images; at least 6 directions can be used to calculate DTI trace and generate ADC maps - Higher spatial resolution - May be more sensitive for small ischemic foci, emboli, cortical strokes

Angiographic Findings
- Conventional: Vessel occlusion (cut off, tapered, "tram track") - Slow antegrade flow and slow retrograde collateral flow - Intraluminal thrombus = filling defect
- Neurointerventional: Intraarterial (IA) fibrinolytic therapy for treatment of selected acute nonhemorrhagic stroke within 6-hour window - IA mechanical clot removal with retriever device

Imaging Recommendations

Best imaging tool
```
- MR + DWI; T2* GRE
```

Protocol advice

- NECT as initial study to exclude hemorrhage/mass
        - CT perfusion and CTA if available
- MR using DWI/FLAIR/GRE ± MRA, PWI
- DSA with thrombolysis in selected patients

DIFFERENTIAL DIAGNOSIS

Hyperdense Vessel Mimics
- High hematocrit (polycythemia)
- Microcalcification in vessel wall
- Diffuse cerebral edema makes vessels appear relatively hyperdense
- Normal circulating blood always slightly hyperdense to normal brain
Parenchymal Hypodensity (Nonvascular Causes)
- Infiltrating neoplasm (e.g., astrocytoma)
- Cerebral contusion
- Inflammation (cerebritis, encephalitis)
- Evolving encephalomalacia
- Dural venous thrombosis with parenchymal venous congestion and edema

PATHOLOGY

General Features

Etiology

- Common causes
        - Thrombotic vs. embolic, dissection, vasculitis, hypoperfusion
- Unusual causes
        - Complicated vasculopathy, including posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome; venous stroke
- Early: Critical disturbance in CBF
        - Severely ischemic core: CBF < (6-8 mL)/(100 g/min)
                  - Normal CBF ~ (60 mL)/(100 g/min)
        - Oxygen depletion, energy failure, terminal depolarization, ion homeostasis failure
        - Bulk of final infarct → cytotoxic edema, cell death
- Later: Evolution from ischemia to infarction depends on many factors (e.g., hyperglycemia influences "destiny" of ischemic brain tissue)
- Ischemic penumbra: CBF = (10-20 mL)/(100 g/min)
        - Theoretically salvageable tissue
        - Target of thrombolysis, neuroprotective agents

Associated abnormalities

- Cardiac disease, prothrombotic states
- Additional stroke risk factors: C-reactive protein, homocysteine

Gross Pathologic & Surgical Features
- Acute thrombosis of major vessel
- Pale, swollen brain; GM-WM boundaries blurred
Microscopic Features
- After 4 hours: Eosinophilic neurons with pyknotic nuclei
- 15-24 hours: Neutrophils invade, and necrotic nuclei look like "eosinophilic ghosts"
- 2-3 days: Blood-derived phagocytes
- 1 week: Reactive astrocytosis, ↑ capillary density
- End result: Fluid-filled cavity lined by astrocytes

CLINICAL ISSUES

Presentation

Most common signs/symptoms

- Focal acute neurologic deficit
- Paresis, aphasia, decreased mental status

Demographics

Age
```
- Usually older adults
```
Gender
```
- No gender predilection
```

Epidemiology

- 2nd most common cause of death worldwide
- Among leading causes of morbidity in USA

Natural History & Prognosis
- Clinical diagnosis inaccurate in 15-20% of strokes
- Malignant MCA infarct (coma, death) - Up to 10% of all stroke patients - Fatal brain swelling with increased ICP
Treatment
- "Time is brain": IV thrombolytic therapy window < 3 hours - IA window < 6 hours except for vertebrobasilar thrombosis (up to 24 hours because of high morbidity and mortality)
- Patient selection most important factor in outcome - Symptom onset < 6 hours - No parenchymal hematoma on CT - < 1/3 MCA territory hypodensity

DIAGNOSTIC CHECKLIST

Consider
- DWI positive for acute stroke only if ADC correlates
- Rarely, ischemia may mimic tumor or encephalitis

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References

Selected References

Images

Selected Images

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 . 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.

Axial NECT demonstrates a hyperdense MCA sign representing acute thrombus in a patient with acute stroke symptoms.

Axial NECT shows subtle loss of the right temporal gray-white matter interfaces representing an "insular ribbon" sign.

Axial pCT (CBF) shows decreased blood flow 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.

Axial DWI MR shows a large wedge-shaped hyperintensity related to restricted diffusion representing acute ischemia in a left MCA distribution. There is sparing of the basal ganglia, consistent with distal M1 occlusion.

Axial NECT shows a hypodense wedge-shaped region of acute infarct with mild mass effect and sulcal effacement related to a right M1 embolic occlusion due to a calcified thrombus .

Axial NECT demonstrates bilateral posterior circulation hypodensities in a 20-month-old boy presenting with seizures after recent circumcision complicated by hematoma.

Axial NECT shows hyperdense thrombus 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.

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.

Coronal CTA MIP reconstruction shows a focal filling defect within the proximal M1 segment 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.

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 . He presented with stuttering symptoms of left-sided weakness and face droop.

Sagittal T2WI MR shows multiple watershed ischemic foci in the deep white matter in a "string of pearls" configuration.

Axial T2 GRE MR shows multifocal hemorrhages 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.*

Axial NECT shows cerebellar infarcts in a 34-year-old woman with bilateral vertebral artery dissections. Note effacement of basal cisterns and temporal horn dilation indicating upward transtentorial herniation.

Axial T2WI MR shows bilateral wedge-shaped occipital areas of hyperintensity in a 77-year-old woman, which do not allow for a reliable distinction between chronic and acute ischemia.

Axial DWI MR in the same patient accurately reflects the acute area of left occipital ischemia , while encephalomalacia is apparent in the right occipital lobe .

Axial NECT shows multifocal hypodensities in the left cerebellum , 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.

Axial CTA shows occlusion of the left vertebral artery . Compare with a normal dominant right vertebral artery .

Axial CTA shows intimal flap in a 47-year-old woman with bilateral internal carotid artery dissections.

Axial NECT shows hyperdense left deep nuclei 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.

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.

Anteroposterior angiography shows left M1 occlusion and associated prominent lenticulostriate vessels .

Additional Images

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).

Axial CECT shows abrupt right MCA cut-off in a patient with hyperacute stroke symptoms. (Courtesy J. Eastwood, MD.)

Axial DWI MR shows small emboli infarcts in the left hemisphere.

Axial CT perfusion map in the same patient reveals significantly prolonged mean transit time within the MCA distribution (red region).

Axial DWI MR shows restricted diffusion within the right occipital lobe in a patient with sudden onset of visual symptoms.

Axial FLAIR MR shows multiple foci of intraarterial high signal suggesting slow flow in this patient with left internal carotid artery dissection.

Coronal CTA shows slight irregularity within the reconstituted left vertebral artery segment , consistent with dissection in this symptomatic patient.

Axial single-phase arterial spin-labeling (ASL) perfusion shows hemispheric asymmetry, decreased on the left , in a patient with acute left internal carotid artery dissection.

Axial FLAIR MR shows classic deep white matter watershed ischemic foci in a "string of pearls" appearance.

Axial DWI MR in a 35-year-old woman post transsphenoidal surgery for Cushing disease shows multifocal infarctions as a complication of Enterobacter meningitis.

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KEY FACTS

Terminology

Imaging

Top Differential Diagnoses

Pathology

Clinical Issues

TERMINOLOGY

Synonyms

Definitions

IMAGING

General Features

Best diagnostic clue

Location

Size

Morphology

CT Findings

NECT

CECT

MR Findings

T1WI

T2WI

FLAIR

T2* GRE

DWI

PWI

T1WI C+

Angiographic Findings

Imaging Recommendations

Best imaging tool

Protocol advice

DIFFERENTIAL DIAGNOSIS

Hyperdense Vessel Mimics

Parenchymal Hypodensity (Nonvascular Causes)

PATHOLOGY

General Features

Etiology

Associated abnormalities

Gross Pathologic & Surgical Features

Microscopic Features

CLINICAL ISSUES

Presentation

Most common signs/symptoms

Demographics

Age

Gender

Epidemiology

Natural History & Prognosis

Treatment

DIAGNOSTIC CHECKLIST

Consider

References

Selected References

Images

Selected Images

Additional Images

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