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title: "Subacute Cerebral Infarction"
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docid: "0109f4c0-c84a-4d85-97cb-afe437b9cc43"
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authors:
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- key: "8d5254e9-8dda-478b-8f08-bdee97a32c79"
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value: "Karen L. Salzman, MD, FACR"
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breadcrumbs:
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-
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name: "Brain"
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slug: "brain"
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treeNodeId: "6d8829f1-14d7-45af-8675-255189aa526a"
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-
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name: "Diagnosis"
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slug: "diagnosis"
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treeNodeId: "51c00394-446e-4a38-94af-d3b1d14d34e8"
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||||
-
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name: "Pathology-Based Diagnoses"
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slug: "pathology-based-diagnoses"
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treeNodeId: "d9d3a8ed-f21b-4831-8c77-591a3500ef77"
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-
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name: "Stroke"
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slug: "stroke"
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treeNodeId: "12307683-f1ff-4823-a7d3-b10b40f9fd82"
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-
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name: "Cerebral Ischemia and Infarction"
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slug: "cerebral-ischemia-and-infarction"
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treeNodeId: "51051846-a223-42f7-b626-2a5a26cf6c44"
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-
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name: "Subacute Cerebral Infarction"
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slug: "subacute-cerebral-infarction"
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treeNodeId: null
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category: "Brain"
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cmeTopicId: "56146806-ca6e-440e-a0cf-9c7a446b1906"
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documentVersionId: "3dccb47d-0565-41ae-855b-a166b848e50f"
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imageCount: 28
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lastUpdated: "08/10/20"
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pageDescription: "Subacute Cerebral Infarction"
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pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Stroke, Cerebral Ischemia and Infarction, Subacute Cerebral Infarction"
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pageTitle: "Subacute Cerebral Infarction | STATdx"
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enhancedTitle: "Subacute Cerebral Infarction"
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type: "DX"
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references: true
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breadcrumbs:
|
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- "Brain"
|
||||
- "Diagnosis"
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||||
- "Pathology-Based Diagnoses"
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- "Stroke"
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- "Cerebral Ischemia and Infarction"
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- "Subacute Cerebral Infarction"
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---
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# KEY FACTS
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- ## Terminology
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- Subacute infarction ~ 2-14 days following initial ischemic event
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- ## Imaging
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- Best diagnostic clue: Gyral edema and enhancement within basal ganglia and cortex
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- Typically wedge-shaped abnormality involving gray and white matter within vascular distribution
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- Hemorrhagic transformation of initial ischemic infarction occurs in 20-25% of middle cerebral artery (MCA) occlusions, usually by 48-72 hours
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- "2-2-2" rule = enhancement begins at 2 days, peaks at 2 weeks, disappears by 2 months
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- MRS: ↑ lactate, ↓ NAA within infarcted tissue
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- DWI: ↑ diffusion restriction, ↓ ADC initially, reversing as it proceeds into/through subacute stage
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- "Fogging" effect = normal T2WI with striking enhancement on T1WI C+ 1-2 weeks following ictus
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- ## Top Differential Diagnoses
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- Neoplasm
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- Venous infarction
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- Encephalitis/cerebritis
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- ## Clinical Issues
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- Acute-onset focal neurologic deficit
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- Elderly patient with typical risk factors: Hypertension, diabetes, smoking history, obesity, hypercholesterolemia
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- 1st month after infarction, mortality predominantly from neurologic complications; 1:4 die of recurrent stroke event
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- Acute anticoagulation after 1st infarction reduces mortality
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- ## Diagnostic Checklist
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- Enhancement is key to defining subacute stage of cerebral infarction
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- Subacute ischemia often mimics neoplasm
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- Recommend short-term follow-up to ensure expected course of evolution
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# TERMINOLOGY
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- ## Abbreviations
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- Subacute stroke, subacute cerebrovascular accident (CVA)
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- ## Definitions
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- Focal brain necrosis following obstruction of blood flow to localized area of brain
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- Subacute infarct ~ 2-14 days following initial ischemic event
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- May occur ± hemorrhagic transformation (HT)
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# IMAGING
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- ## General Features
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- ### Best diagnostic clue
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- Gyral edema, enhancement in basal ganglia/cortex
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- Look for HT
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- Typically occurs in 20-25% of cases 2-7 days after acute event
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- Related to reperfusion, spontaneous or following therapy
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- ### Location
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- Cerebral hemispheres, brainstem, cerebellum in territorial vascular distribution
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- ### Size
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- Extremely variable
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- Ranges from focal ("lacunes") to global (hemispheric)
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- ### Morphology
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- Variable depending on location, size, etiology
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- Typically wedge-shaped; involves both gray and white matter
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- Recognizable vascular distribution
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- ## CT Findings
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- ### NECT
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- Wedge-shaped area of ↓ attenuation involving gray and white matter
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- Mass effect initially ↑, then ↓ by 7-10 days; often less than expected given lesion size as acuity resolves
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- HT of ischemic infarct occurs in 20-25% of middle cerebral artery (MCA) occlusions, usually by 48-72 hours
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- Common locations are basal ganglia and cortex
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- Hemorrhagic foci detected in majority of medium/large subacute infarcts
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- ### CECT
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- Enhancement typically patchy or gyral
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- May appear as early as 2-3 days after ictus; persists up to 8-10 weeks
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- "2-2-2" rule = enhancement begins at 2 days, peaks at 2 weeks, disappears by 2 months
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- ### CTA
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- Evidence of subacute occlusion correlates strongly, independently with poor clinical outcome
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- Significantly worse discharge National Institutes of Health Stroke Scale (NIHSS) score
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- CT perfusion
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- More useful in acute > subacute stroke
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- Helpful in predicting tissue outcome
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- Significant difference between infarct and periinfarct tissue for both relative cerebral blood flow (rCBF), relative cerebral blood volume (rCBV)
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- ## MR Findings
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- ### T1WI
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- Hypointense edema with mass effect
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- HT: Signal changes of hemorrhage
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- May see gyriform ↑ signal (pseudolaminar necrosis)
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- ### T2WI
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- Hyperintense edema with mass effect
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- "Fogging" effect = normal T2WI with striking enhancement on T1WI C+ 1-2 weeks following ictus
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- HT: Signal changes of evolving hemorrhage
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- Early wallerian degeneration can occur
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- Look for well-defined hyperintense band in corticospinal tract
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- ### FLAIR
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- Hyperintense edema with mass effect
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- Hyperintensity (dot sign) in slow-flowing/occluded vessels
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- By 1 week, final infarct volume corresponds to FLAIR-defined abnormality
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- May see "fogging" effect, similar to T2WI
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- ### T2* GRE
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- May see blooming if HT has occurred
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- ### DWI
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- ↑ diffusion restriction, ↓ ADC initially, reversing as it proceeds into/through subacute stage
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- DWI, T1WI C+ complement each other in detecting subacute infarcts
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- Early subacute can be ↑ DWI and ↓ T1WI C+
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- ### T1WI C+
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- Intravascular enhancement in initial 48 hours; disappears at 3-4 days as vessels recanalize
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- Parenchymal enhancement (typically patchy or gyral)
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- May appear as early as 2-3 days after ictus
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- Can persist up to 8-10 weeks
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- ### MRA
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- Vessel occlusion (large vessel)
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- ### MRS
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- ↑ lactate, ↓ NAA within infarcted tissue
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- In subacute and chronic infarction, lactate/choline and NAA/choline ratios correlate with outcome
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- Positive correlation between NAA and Scandinavian Stroke Scale (SSS) scores
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- Positive correlation between NAA reduction and Barthel index scores
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- Lactate presence correlates with lower SSS scores
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- MR T2* perfusion
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- ↓ rCBV of acute infarct ↑ in subacute stage, reflecting reperfusion hyperemia
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- ↓ again in chronic stage
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- SWI: May see hypointensity related to microhemorrhage
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- ## Angiographic Findings
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- Conventional
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- May see intraluminal thrombus &/or vessel occlusion
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- Slow antegrade flow with delayed arterial emptying
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- Slow retrograde filling through collateral vessels
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- "Bare" areas = regions of nonperfused or slowly perfused brain tissue
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- ## Nuclear Medicine Findings
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- Diminished/absence of perfusion with SPECT or PET
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- HMPAO SPECT may show reflow hyperemia after reperfusion in acute and subacute stages
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- ## Imaging Recommendations
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- ### Best imaging tool
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- MR with DWI, T2*, T1WI C+
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- Consider CT or MR perfusion (more helpful in acute stroke)
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- ### Protocol advice
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- CT and MR: C+ for assessing subacute age
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# DIFFERENTIAL DIAGNOSIS
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- [Neoplasm](/document/glioblastoma/45c3147e-3a1b-4fbf-a626-ed6e99a02ac2)
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- DWI: Vasogenic ("tumoral") edema instead of cytotoxic edema
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- Enhancing mass instead of patchy, gyral enhancement
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- Will not regress on follow-up imaging
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- [Venous Infarction](/document/cortical-venous-thrombosis/d314f5f7-21b6-46d1-a51c-e796cacc012c)
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- Nonarterial distribution
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- Venous instead of arterial occlusion, typically major dural sinus
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- More commonly hemorrhagic, primarily affecting white matter instead of cortex
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- Different clinical presentation/setting (trauma, hypercoagulable states, pregnancy, dehydration)
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- [Encephalitis/Cerebritis](/document/abscess/552b58e6-aa5e-49b4-b9aa-e0413c07bf3c)
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- DWI: Strong restriction
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- Nonvascular distribution
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- Gyriform, ring-enhancing patterns (late cerebritis)
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- Different clinical presentation
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# PATHOLOGY
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- ## General Features
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- ### Etiology
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- Prolonged cerebral ischemia
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- Duration and severity of ischemic insult determines cellular viability
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- Less commonly, may be result of infectious etiologies
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- Sequelae of meningitis (bacterial, mycobacterial, etc.)
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- May also be result of inflammatory diseases, such as vasculopathy, angiitis, etc.
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- Uncontrolled, unilateral, supratentorial expanding lesions can cause descending tentorial herniation → ischemic infarction of occipital lobe
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- Ischemia/infarction involves typical vascular territories or watershed (border zone) distributions depending on etiology
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- Sequelae of infarction vary with sensitivity of individual cell types to ischemia
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- Other factors: Adequacy of collateral blood supply, degree, duration, and distribution of flow reduction
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- ### Genetics
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- Hypercholesterolemia, diabetes, hypertension, and homocysteine ↑ stroke risk
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- ## Gross Pathologic & Surgical Features
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- Blurring of gray-white demarcation
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- Mass effect with narrowing of sulci, displacement of adjacent structures
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- Softening of ischemic tissues from water retention
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- ## Microscopic Features
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- Fragmentation of axons and early disintegration of myelin sheaths; loss of oligodendrocytes, astrocytes
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- 48 hours: Neutrophils begin to pass through vessel walls into brain tissue
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- 72-96 hours: Macrophages aggregate around vessels
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- 2 weeks: Macrophages are predominate reactive cells
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# CLINICAL ISSUES
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- ## Presentation
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- ### Most common signs/symptoms
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- Acute-onset focal neurologic deficit
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- ~ 50% of patients with infarction → permanent neurologic deficits have preceding TIAs
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- ### Clinical profile
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- Elderly patient with typical risk factors: Hypertension, diabetes, smoking history, obesity, hypercholesterolemia, etc.
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- ## Demographics
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- ### Age
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- Usually > 55 years
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- Women often slightly older than men at presentation
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- ### Sex
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- Females often more disabled after age adjustment
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- Fatality rates similar
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- ### Epidemiology
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- Highest cause of USA adult morbidity
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- 3rd cause of USA adult mortality
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- ## Natural History & Prognosis
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- 1st month after infarction, mortality predominantly from neurologic complications
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- 1:4 die of recurrent stroke event
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- Later mortality from respiratory, cardiovascular causes
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- Survival after 1st infarction: 1 week (92%), 30 days (83%), 6 months (77%), 1 year (71%), 5 years (46%), 10 years (28%)
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- ## Treatment
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- To improve long-term survival, aggressive management of pulmonary and cardiac disease is critical
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- Acute anticoagulation after 1st infarction reduces mortality
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- Current research: Therapeutic hypothermia and gene therapy (antiapoptotic protein BCL-2) during acute stroke event
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# DIAGNOSTIC CHECKLIST
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- ## Consider
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- Is affected area another space-occupying pathology (i.e., tumor)?
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- Recommend short-term follow-up to ensure expected course of evolution
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- ## Image Interpretation Pearls
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- Enhancement is key to defining subacute stage of cerebral infarction
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- Appearance on DWI/ADC often helpful
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62b91377-75c2-40c0-8e3d-3e9ff4f24cbd
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## References
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# Selected References
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1. [Mistry EA et al: White matter disease and outcomes of mechanical thrombectomy for acute ischemic stroke. AJNR Am J Neuroradiol. 41(4):639-44, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32165366%5Bpmid%5D)
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1. [Wessell AP et al: A critical assessment of the golden hour and the impact of procedural timing in stroke thrombectomy. AJNR Am J Neuroradiol. 41(5):822-7, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32414902%5Bpmid%5D)
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1. [Bill O et al: Focal hypoperfusion in acute ischemic stroke perfusion CT: clinical and radiologic predictors and accuracy for infarct prediction. AJNR Am J Neuroradiol. 40(3):483-9, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30792249%5Bpmid%5D)
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1. [Majidi S et al: MRI-based thrombolytic therapy in patients with acute ischemic stroke presenting with a low NIHSS. Neurology. 93(16):e1507-13, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31519779%5Bpmid%5D)
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1. [Sotoudeh H et al: Misleading CT perfusion in subacute ischemic stroke. Emerg Radiol. 26(5):581-6, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31432350%5Bpmid%5D)
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1. [Arnold Fiebelkorn C et al: Frequency of acute and subacute infarcts in a population-based study. Mayo Clin Proc. 93(3):300-6, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29426582%5Bpmid%5D)
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1. [Yang YM et al: Normalization of T2 relaxation time and apparent diffusion coefficient in relation to the inflammatory changes in the substantia nigra of rats with focal cerebral ischemia. Acta Radiol. 56(7):837-43, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25260416%5Bpmid%5D)
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1. [Zöllner JP et al: Changes of pH and energy state in subacute human ischemia assessed by multinuclear magnetic resonance spectroscopy. Stroke. 46(2):441-6, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25503553%5Bpmid%5D)
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1. [Brunner IC et al: Plasticity and response to action observation: a longitudinal FMRI study of potential mirror neurons in patients with subacute stroke. Neurorehabil Neural Repair. 28(9):874-84, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24642381%5Bpmid%5D)
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1. [Ntaios G et al: Acute imaging does not improve ASTRAL score's accuracy despite having a prognostic value. Int J Stroke. 9(7):926-31, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24894405%5Bpmid%5D)
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1. [Qiao Y et al: Intracranial plaque enhancement in patients with cerebrovascular events on high-spatial-resolution MR images. Radiology. 271(2):534-42, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24475850%5Bpmid%5D)
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1. [Drier A et al: Prediction of subacute infarct size in acute middle cerebral artery stroke: comparison of perfusion-weighted imaging and apparent diffusion coefficient maps. Radiology. 265(2):511-7, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22923715%5Bpmid%5D)
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1. [Kamalian S et al: CT perfusion mean transit time maps optimally distinguish benign oligemia from true "at-risk" ischemic penumbra, but thresholds vary by postprocessing technique. AJNR Am J Neuroradiol. 33(3):545-9, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22194372%5Bpmid%5D)
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1. [Donnan GA et al: Penumbral selection of patients for trials of acute stroke therapy. Lancet Neurol. 8(3):261-9, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19233036%5Bpmid%5D)
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1. [Elkind MS: Outcomes after stroke: risk of recurrent ischemic stroke and other events. Am J Med. 122(4 Suppl 2):S7-13, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19332241%5Bpmid%5D)
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1. [Olivot JM et al: Perfusion MRI (Tmax and MTT) correlation with xenon CT cerebral blood flow in stroke patients. Neurology. 72(13):1140-5, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19332690%5Bpmid%5D)
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1. [Muñoz Maniega S et al: Changes in NAA and lactate following ischemic stroke: a serial MR spectroscopic imaging study. Neurology. 71(24):1993-9, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=19064881%5Bpmid%5D)
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1. [Vernino S et al: Cause-specific mortality after first cerebral infarction: a population-based study. Stroke. 34(8):1828-32, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12855836%5Bpmid%5D)
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## Images
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### Selected Images
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||||
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*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 <img src='img/arrows/WS.png'/> involving both the gray and white matter in the MCA distribution with blood products <img src='img/arrows/CS.png'/> in the right basal ganglia.*
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||||
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||||
*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 <img src='img/arrows/WS.png'/> involving both the gray and white matter in the MCA distribution with blood products <img src='img/arrows/CS.png'/> in the right basal ganglia.*
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*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 <img src='img/arrows/WO.png'/> in a PCA distribution.*
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||||
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||||
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||||
*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.*
|
||||
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||||
|
||||
*Axial T1 C+ MR in the same patient shows gyriform enhancement along the cortex of the occipital lobe <img src='img/arrows/WO.png'/>. 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.*
|
||||
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||||
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||||
*Axial T1 C+ MR shows well-defined gyriform enhancement <img src='img/arrows/CC.png'/> in the PCA distribution in a subacute infarct patient who was sent to a neurosurgeon for concerns of a cortical "tumor."*
|
||||
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||||
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||||
*Axial FLAIR MR in the same patient shows the "fogging" effect <img src='img/arrows/CC.png'/> 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.*
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||||
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||||
*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 <img src='img/arrows/WO.png'/> 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 <img src='img/arrows/WS.png'/>. 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 <img src='img/arrows/CC.png'/> 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 <img src='img/arrows/CS.png'/>. 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 <img src='img/arrows/BS.png'/>, 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 <img src='img/arrows/WS.png'/> and MCA <img src='img/arrows/WO.png'/> 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 <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
*Axial CECT demonstrates gyriform enhancement <img src='img/arrows/WO.png'/> 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 <img src='img/arrows/WS.png'/>. 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 <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
*Sagittal T1 C+ MR shows well-defined gyriform enhancement <img src='img/arrows/CC.png'/> 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 <img src='img/arrows/CS.png'/> 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 <img src='img/arrows/WS.png'/> involving both the gray and white matter in the left MCA distribution.*
|
||||
|
||||
Reference in New Issue
Block a user