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KEY FACTS

Terminology
- Subacute infarction ~ 2-14 days following initial ischemic event
Imaging
- Best diagnostic clue: Gyral edema and enhancement within basal ganglia and cortex
- Typically wedge-shaped abnormality involving gray and white matter within vascular distribution
- Hemorrhagic transformation of initial ischemic infarction occurs in 20-25% of middle cerebral artery (MCA) occlusions, usually by 48-72 hours
- "2-2-2" rule = enhancement begins at 2 days, peaks at 2 weeks, disappears by 2 months
- MRS: ↑ lactate, ↓ NAA within infarcted tissue
- DWI: ↑ diffusion restriction, ↓ ADC initially, reversing as it proceeds into/through subacute stage
- "Fogging" effect = normal T2WI with striking enhancement on T1WI C+ 1-2 weeks following ictus
Top Differential Diagnoses
- Neoplasm
- Venous infarction
- Encephalitis/cerebritis
Clinical Issues
- Acute-onset focal neurologic deficit
- Elderly patient with typical risk factors: Hypertension, diabetes, smoking history, obesity, hypercholesterolemia
- 1st month after infarction, mortality predominantly from neurologic complications; 1:4 die of recurrent stroke event
- Acute anticoagulation after 1st infarction reduces mortality
Diagnostic Checklist
- Enhancement is key to defining subacute stage of cerebral infarction
- Subacute ischemia often mimics neoplasm - Recommend short-term follow-up to ensure expected course of evolution

TERMINOLOGY

Abbreviations
- Subacute stroke, subacute cerebrovascular accident (CVA)
Definitions
- Focal brain necrosis following obstruction of blood flow to localized area of brain
- Subacute infarct ~ 2-14 days following initial ischemic event
- May occur ± hemorrhagic transformation (HT)

IMAGING

General Features

Best diagnostic clue

- Gyral edema, enhancement in basal ganglia/cortex
- Look for HT
        - Typically occurs in 20-25% of cases 2-7 days after acute event
        - Related to reperfusion, spontaneous or following therapy

Location

- Cerebral hemispheres, brainstem, cerebellum in territorial vascular distribution

Size

- Extremely variable
- Ranges from focal ("lacunes") to global (hemispheric)

Morphology

- Variable depending on location, size, etiology
- Typically wedge-shaped; involves both gray and white matter
        - Recognizable vascular distribution

CT Findings

NECT

- Wedge-shaped area of ↓ attenuation involving gray and white matter
- Mass effect initially ↑, then ↓ by 7-10 days; often less than expected given lesion size as acuity resolves
- HT of ischemic infarct occurs in 20-25% of middle cerebral artery (MCA) occlusions, usually by 48-72 hours
        - Common locations are basal ganglia and cortex
        - Hemorrhagic foci detected in majority of medium/large subacute infarcts

CECT

- Enhancement typically patchy or gyral
- May appear as early as 2-3 days after ictus; persists up to 8-10 weeks
- "2-2-2" rule = enhancement begins at 2 days, peaks at 2 weeks, disappears by 2 months

CTA

- Evidence of subacute occlusion correlates strongly, independently with poor clinical outcome
        - Significantly worse discharge National Institutes of Health Stroke Scale (NIHSS) score

CT perfusion - More useful in acute > subacute stroke - Helpful in predicting tissue outcome - Significant difference between infarct and periinfarct tissue for both relative cerebral blood flow (rCBF), relative cerebral blood volume (rCBV)

MR Findings

T1WI

- Hypointense edema with mass effect
- HT: Signal changes of hemorrhage
- May see gyriform ↑ signal (pseudolaminar necrosis)

T2WI

- Hyperintense edema with mass effect
- "Fogging" effect = normal T2WI with striking enhancement on T1WI C+ 1-2 weeks following ictus
- HT: Signal changes of evolving hemorrhage
- Early wallerian degeneration can occur
        - Look for well-defined hyperintense band in corticospinal tract

FLAIR

- Hyperintense edema with mass effect
- Hyperintensity (dot sign) in slow-flowing/occluded vessels
- By 1 week, final infarct volume corresponds to FLAIR-defined abnormality
- May see "fogging" effect, similar to T2WI

T2* GRE
```
- May see blooming if HT has occurred
```

DWI

- ↑ diffusion restriction, ↓ ADC initially, reversing as it proceeds into/through subacute stage
- DWI, T1WI C+ complement each other in detecting subacute infarcts
        - Early subacute can be ↑ DWI and ↓ T1WI C+

T1WI C+

- Intravascular enhancement in initial 48 hours; disappears at 3-4 days as vessels recanalize
- Parenchymal enhancement (typically patchy or gyral)
        - May appear as early as 2-3 days after ictus
        - Can persist up to 8-10 weeks

MRA
```
- Vessel occlusion (large vessel)
```

MRS

- ↑ lactate, ↓ NAA within infarcted tissue
- In subacute and chronic infarction, lactate/choline and NAA/choline ratios correlate with outcome
        - Positive correlation between NAA and Scandinavian Stroke Scale (SSS) scores
        - Positive correlation between NAA reduction and Barthel index scores
        - Lactate presence correlates with lower SSS scores

MR T2* perfusion - ↓ rCBV of acute infarct ↑ in subacute stage, reflecting reperfusion hyperemia - ↓ again in chronic stage
SWI: May see hypointensity related to microhemorrhage

Angiographic Findings
- Conventional - May see intraluminal thrombus &/or vessel occlusion - Slow antegrade flow with delayed arterial emptying - Slow retrograde filling through collateral vessels - "Bare" areas = regions of nonperfused or slowly perfused brain tissue
Nuclear Medicine Findings
- Diminished/absence of perfusion with SPECT or PET
- HMPAO SPECT may show reflow hyperemia after reperfusion in acute and subacute stages

Imaging Recommendations

Best imaging tool

- MR with DWI, T2*, T1WI C+
- Consider CT or MR perfusion (more helpful in acute stroke)

Protocol advice

- CT and MR: C+ for assessing subacute age

DIFFERENTIAL DIAGNOSIS

Neoplasm
- DWI: Vasogenic ("tumoral") edema instead of cytotoxic edema
- Enhancing mass instead of patchy, gyral enhancement
- Will not regress on follow-up imaging
Venous Infarction
- Nonarterial distribution
- Venous instead of arterial occlusion, typically major dural sinus
- More commonly hemorrhagic, primarily affecting white matter instead of cortex
- Different clinical presentation/setting (trauma, hypercoagulable states, pregnancy, dehydration)
Encephalitis/Cerebritis
- DWI: Strong restriction
- Nonvascular distribution
- Gyriform, ring-enhancing patterns (late cerebritis)
- Different clinical presentation

PATHOLOGY

General Features

Etiology

- Prolonged cerebral ischemia
- Duration and severity of ischemic insult determines cellular viability
- Less commonly, may be result of infectious etiologies
        - Sequelae of meningitis (bacterial, mycobacterial, etc.)
- May also be result of inflammatory diseases, such as vasculopathy, angiitis, etc.
- Uncontrolled, unilateral, supratentorial expanding lesions can cause descending tentorial herniation → ischemic infarction of occipital lobe
- Ischemia/infarction involves typical vascular territories or watershed (border zone) distributions depending on etiology
- Sequelae of infarction vary with sensitivity of individual cell types to ischemia
- Other factors: Adequacy of collateral blood supply, degree, duration, and distribution of flow reduction

Genetics

- Hypercholesterolemia, diabetes, hypertension, and homocysteine ↑ stroke risk

Gross Pathologic & Surgical Features
- Blurring of gray-white demarcation
- Mass effect with narrowing of sulci, displacement of adjacent structures
- Softening of ischemic tissues from water retention
Microscopic Features
- Fragmentation of axons and early disintegration of myelin sheaths; loss of oligodendrocytes, astrocytes
- 48 hours: Neutrophils begin to pass through vessel walls into brain tissue
- 72-96 hours: Macrophages aggregate around vessels
- 2 weeks: Macrophages are predominate reactive cells

CLINICAL ISSUES

Presentation

Most common signs/symptoms

- Acute-onset focal neurologic deficit
- ~ 50% of patients with infarction → permanent neurologic deficits have preceding TIAs

Clinical profile

- Elderly patient with typical risk factors: Hypertension, diabetes, smoking history, obesity, hypercholesterolemia, etc.

Demographics

Age

- Usually > 55 years
- Women often slightly older than men at presentation

Sex

- Females often more disabled after age adjustment
- Fatality rates similar

Epidemiology

- Highest cause of USA adult morbidity
- 3rd cause of USA adult mortality

Natural History & Prognosis
- 1st month after infarction, mortality predominantly from neurologic complications - 1:4 die of recurrent stroke event
- Later mortality from respiratory, cardiovascular causes
- Survival after 1st infarction: 1 week (92%), 30 days (83%), 6 months (77%), 1 year (71%), 5 years (46%), 10 years (28%)
Treatment
- To improve long-term survival, aggressive management of pulmonary and cardiac disease is critical
- Acute anticoagulation after 1st infarction reduces mortality
- Current research: Therapeutic hypothermia and gene therapy (antiapoptotic protein BCL-2) during acute stroke event

DIAGNOSTIC CHECKLIST

Consider
- Is affected area another space-occupying pathology (i.e., tumor)?
- Recommend short-term follow-up to ensure expected course of evolution
Image Interpretation Pearls
- Enhancement is key to defining subacute stage of cerebral infarction
- Appearance on DWI/ADC often helpful

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References

Selected References

Images

Selected Images

Axial CT at 3 days after initial onset of weakness and speech difficulties shows the classic appearance of an early subacute cerebral infarct. Note the wedge-shaped, low-density area involving both the gray and white matter in the MCA distribution with blood products in the right basal ganglia.

Axial FLAIR MR in a 58-year-old man 1 week after onset of visual changes shows classic imaging of a subacute infarct with hyperintensity in the cortex and subcortical white matter of the occipital lobe in a PCA distribution.

Axial DWI MR in the same patient shows hyperintensity within the left PCA distribution. The hyperintensity represents a combination of true diffusion restriction and T2 shine-through.

Axial T1 C+ MR in the same patient shows gyriform enhancement along the cortex of the occipital lobe . This enhancement may be seen as early as 2 days and may last up to 2 months after the patient's initial ischemic event. Without clinical history, imaging may mimic a tumor, venous infarct, or cerebritis.

Axial T1 C+ MR shows well-defined gyriform enhancement in the PCA distribution in a subacute infarct patient who was sent to a neurosurgeon for concerns of a cortical "tumor."

Axial FLAIR MR in the same patient shows the "fogging" effect with near-normal signal on T2/FLAIR MR with striking enhancement on T1WI C+ MR. This "fogging" effect typically occurs 1-2 weeks following the acute stroke. Initially, the infarct shows hyperintensity, which decreases over time, with isointensity at 1-2 weeks.

Axial DWI MR in a 45-year-old woman with an abnormal cardiac valve resulting in embolic disease in multiple vascular distributions 5 days after a posterior circulation infarct shows high signal due to restricted diffusion in bilateral cerebellar hemispheres. DWI scans can be hyperintense up to 7-10 days following acute stroke onset.

Axial T1 C+ MR in the same patient shows patchy enhancement in the right cerebellar hemisphere . Cardioembolic disease represents 15-25% of major strokes.

Axial DWI trace MR in a 61-year-old patient 3 days after symptoms shows DWI restriction. True restricted diffusion persists several days after stroke onset and gradually reverses with DWI hypointensity and ADC hyperintensity.

Axial T1 C+ MR shows gyriform enhancement in the MCA distribution. Note lack of mass effect in this late subacute infarct. The major differential considerations for a subacute infarct include neoplasm and cerebritis. Repeat imaging may be necessary to exclude neoplasm.

Additional Images

Axial T1 C+ MR in the same patient shows striking curvilinear enhancement within the sulci and over the gyri of the affected area . This represents collateral flow in small vessels over and within the pia ("leptomeningeal collaterals"), adjacent to the infarcted brain.

Axial DWI MR demonstrates diffusion restriction in the right PCA distribution.

Axial T1 MR shows swollen gyri in the left PCA distribution , findings typical for subacute cerebral infarction.

Axial T2 MR shows gyral swelling and extensive hyperintensity involving both the gray and white matter of the right temporal lobe.

Axial T1 C+ MR demonstrates classic gyriform enhancement of a subacute cerebral infarction. Some underlying T1-hyperintense hemorrhage is masked by extensive enhancement.

Axial NECT shows a wedge-shaped, nonhemorrhagic infarct. Lack of mass effect and CSF-like hypodensity aid in diagnosing subacute age.

Axial DWI MR demonstrates hyperintense restricted diffusion of cytotoxic edema within both the right ACA and MCA vascular territories.

Axial NECT shows a classic nonhemorrhagic left MCA territory infarction involving the basal ganglia. Note the relatively mild ventricular and sulcal mass effect given the size of the lesion during subacute stage.

Axial T1 MR shows a hemorrhagic subacute infarction involving gray matter as well as a small portion of subcortical white matter. Gyriform enhancement was also present.

Axial CECT demonstrates extensive gyral subacute infarct enhancement 6 weeks after ictus. Note the absence of mass effect given the lesion size as acuity diminishes.

Axial NECT demonstrates cortical hemorrhage of a subacute left MCA distribution infarction. Note the lack of mass effect given the lesion size.

Axial collapsed view MRA reveals the lack of flow in the right PCA .

Axial CECT demonstrates gyriform enhancement in the left MCA territory, a finding seen in subacute infarcts.

Axial T2 MR shows almost no abnormality except for minimal hyperintensity on the T2 . Occasionally, subacute cerebral infarcts may be difficult to visualize on standard MR scans because of the so-called "fogging" effect.

Axial T1 C+ MR in the same patient demonstrates striking gyriform enhancement .

Sagittal T1 C+ MR shows well-defined gyriform enhancement in the right MCA distribution. Note the lack of mass effect in this late subacute infarct. The major differential considerations for a subacute infarct include neoplasm and cerebritis. Repeat imaging may be necessary to exclude neoplasm.

Axial NECT demonstrates gyriform hyperdensity related to cortical hemorrhagic transformation in a right hemispheric watershed infarct. Note the surrounding low-density edema.

Axial CT obtained 48 hours after initial onset of weakness and speech difficulties shows the classic appearance of a late acute/early subacute cerebral infarct. Note the wedge-shaped, low-density area involving both the gray and white matter in the left MCA distribution.

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KEY FACTS

Terminology

Imaging

Top Differential Diagnoses

Clinical Issues

Diagnostic Checklist

TERMINOLOGY

Abbreviations

Definitions

IMAGING

General Features

Best diagnostic clue

Location

Size

Morphology

CT Findings

NECT

CECT

CTA

MR Findings

T1WI

T2WI

FLAIR

T2* GRE

DWI

T1WI C+

MRA

MRS

Angiographic Findings

Nuclear Medicine Findings

Imaging Recommendations

Best imaging tool

Protocol advice

DIFFERENTIAL DIAGNOSIS

PATHOLOGY

General Features

Etiology

Genetics

Gross Pathologic & Surgical Features

Microscopic Features

CLINICAL ISSUES

Presentation

Most common signs/symptoms

Clinical profile

Demographics

Age

Sex

Epidemiology

Natural History & Prognosis

Treatment

DIAGNOSTIC CHECKLIST

Consider

Image Interpretation Pearls

References

Selected References

Images

Selected Images

Additional Images

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