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---
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title: "Adult Hypoxic-Ischemic Injury"
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docid: "91ac293f-161c-4b3b-81e5-740f831eaa5d"
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authors:
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value: "Kelly A. Dahlstrom, DO"
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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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name: "Brain"
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slug: "brain"
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treeNodeId: "0361042c-9c90-48e4-864e-a2e6428ee9c9"
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name: "Diagnosis"
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slug: "diagnosis"
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treeNodeId: "948c6f1e-8e18-45f3-bd9d-7a04ab0b8708"
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name: "Pathology-Based Diagnoses"
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slug: "pathology-based-diagnoses"
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treeNodeId: "d60fe914-7897-46a0-9cd2-f88ffb322f16"
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slug: "stroke"
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treeNodeId: "7a135176-0a69-4fc9-b200-59569fbf5166"
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name: "Cerebral Ischemia and Infarction"
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slug: "cerebral-ischemia-and-infarction"
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treeNodeId: "11d50e7d-f3e9-4071-b2b7-26b11ab40ea6"
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name: "Adult Hypoxic-Ischemic Injury"
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slug: "adult-hypoxic-ischemic-injury"
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treeNodeId: null
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category: "Brain"
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documentVersionId: "bc630553-154e-43a7-9d97-716b627c4c2d"
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imageCount: 26
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lastUpdated: "08/19/25"
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pageDescription: "Adult Hypoxic-Ischemic Injury"
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pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Stroke, Cerebral Ischemia and Infarction, Adult Hypoxic-Ischemic Injury"
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pageTitle: "Adult Hypoxic-Ischemic Injury | STATdx"
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enhancedTitle: "Adult Hypoxic-Ischemic Injury"
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type: "DX"
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references: true
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cases: 2
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breadcrumbs:
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- "Brain"
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- "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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- "Adult Hypoxic-Ischemic Injury"
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---
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## KEY FACTS
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- ### Terminology
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- Hypoxic-ischemic injury (HII) includes global HII, global anoxic injury, cerebral hypoperfusion injury
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- Etiologies: Cardiac arrest, cerebrovascular disease, drowning, asphyxiation
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- ### Imaging
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- Injury patterns highly variable depending on brain maturity, severity and length of insult
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- Mild to moderate: Watershed zone infarcts
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- Severe: Gray matter structures (basal ganglia, thalami, cortex, cerebellum, hippocampi)
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- MR best to assess overall extent of injury within hours after HII event
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- DWI: 1st modality to be positive (within hours)
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- DWI: Restriction in deep nuclei ± cortex
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- T2/FLAIR: ↑ signal in cerebellum, basal ganglia, cortex
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- Acute changes not reliably identified with T2
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- MRS: More sensitive and indicative of severity of injury in first 24 hours after HII
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- ↑ lactate, ↑ glutamine-glutamate
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- ### Top Differential Diagnoses
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- Ischemic territorial infarction
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- Traumatic cerebral edema
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- Toxic/metabolic disorder
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- Posterior reversible encephalopathy syndrome (PRES)
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- Creutzfeldt-Jakob disease
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- MELAS
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- ### Pathology
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- Common underlying process regardless of cause
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- ↓ cerebral blood flow (CBF) and ↓ blood oxygenation
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- Switch from oxidative phosphorylation to anaerobic metabolism
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- Glutamate-related cytotoxic processes
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## TERMINOLOGY
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- ### Synonyms
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- Hypoxic-ischemic injury (HII), hypoxic-ischemic encephalopathy (HIE)
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- ### Definitions
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- Includes various etiologies of injury: Global HII, global anoxic injury, cerebral hypoperfusion injury
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## IMAGING
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- ### General Features
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- #### Best diagnostic clue
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- Symmetric T2/FLAIR hyperintensity in deep gray nuclei ± cortex
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- DWI restriction in acute phase
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- #### Location
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- Mild to moderate: Watershed zone infarcts
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- Severe: Gray matter (GM) structures: Basal ganglia (BG), thalami, cerebral cortex (sensorimotor and visual), cerebellum, hippocampi
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- Cerebellar injury tends to be more common in older patients; Purkinje cells are sensitive to ischemia
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- Brainstem may rarely be involved
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- Injury patterns are highly variable depending on brain maturity, severity and length of insult
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- ### CT Findings
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- #### NECT
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- Diffuse cerebral edema with effacement of CSF containing spaces
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- ↓ cortical GM and BG attenuation; loss of normal gray-white differentiation
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- Indicators of poor prognosis
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- White cerebellum sign: Apparent high attenuation of cerebellum/brainstem relative to cerebral hypodensity
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- Reversal sign: Inversion of normal gray and white matter (WM) attenuation
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- Pseudosubarachnoid hemorrhage sign: ↑ intracranial pressure → CSF displacement and engorgement of pial venous structures; in combination with hypodense parenchyma, subarachnoid spaces appear hyperdense
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- ### MR Findings
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- #### T1WI
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- Normal to very subtle abnormalities
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- BG may show T1 hyperintensity
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- GM signal abnormalities may persist into end of 2nd week
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- Chronic stages show cortical pseudolaminar necrosis
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- #### T2WI
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- Normal to very subtle abnormalities in first 24 hours
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- BG typically shows T2 hyperintensity
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- GM signal abnormalities may persist into end of 2nd week
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- Chronic stages show residual BG hyperintensity
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- #### FLAIR
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- Symmetric hyperintensity in deep gray nuclei ± cortex
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- Subtle abnormalities (hyperintensity) in first 24 hours
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||||
- #### DWI
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- 1st imaging modality to become positive, within hours after HII event
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- ↑ signal in cerebellar hemispheres, BG, cerebral cortex
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- Often perirolandic and occipital cortex
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- DWI abnormalities pseudonormalize by end of 1st week
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||||
- ADC is reduced in hyperacute phase following HII event due to influx of water from extra- to intracellular space
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- ADC values are reduced in severe WM and in some severe BG and thalamic injury
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- ADC values may pseudonormalize or even be high initially in some less severe but clinically significant injuries
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- Abnormal ADC values pseudonormalize during 2nd week, whereas fractional anisotropy (FA) values continue to ↓
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||||
- DTI: FA may be abnormal
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- Low FA may reflect breakdown in WM organization
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||||
- Moderate BG/thalamic injury may result in atrophy but not overt infarct due to delayed apoptosis (may account for normal early ADC values)
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- Accompanying low FA within some severe and all moderate GM lesions → associated with significant later impairment
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||||
- #### PWI
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||||
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- Typically global hyperperfusion after anoxic event, due to loss of vascular resistance
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||||
- #### MRS
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||||
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||||
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- More sensitive and more indicative of injury severity in first 24 hours after HII
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- ↑ lactate at 1.3 ppm, ↑ glutamine-glutamate peak at 2.3 ppm
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- ↑ lactate after 24 hours portends poor neurologic outcome
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||||
- NAA is usually normal in acute setting and declines 48 hours after acute injury
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||||
- ### Imaging Recommendations
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||||
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||||
- #### Best imaging tool
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- MR, particularly DWI/DTI, is most sensitive modality to show abnormalities after ictus
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- Portable MR may be of benefit for prognostication in critically ill ICU patients (not widely available)
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- #### Protocol advice
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- DTI/DWI are most sensitive
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- Acute ischemic cerebral changes cannot be reliably identified with T2/FLAIR sequences
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- T2*GRE/SWI helpful to detect petechial or subarachnoid hemorrhage
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||||
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||||
## DIFFERENTIAL DIAGNOSIS
|
||||
|
||||
- [Acute Cerebral Ischemia-Infarction](/document/acute-cerebral-ischemiainfarction/7a3ed4a9-ae05-4d64-ae8e-6a30105501e1)
|
||||
- Wedge-shaped T2 hyperintensity in vascular distribution
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||||
- DWI positive acutely
|
||||
- [Traumatic Cerebral Edema/Ischemia](/document/posttraumatic-brain-swelling/21a74d44-6e0c-40c6-b865-a4267453d629)
|
||||
- Compressed ventricles and effaced sulci due to combination of vasogenic edema in WM and cytotoxic edema in GM → herniation of brain
|
||||
- Vascular compression can lead to infarction
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||||
- [Toxic/Metabolic Disorder](/document/carbon-monoxide-poisoning/827ae14b-3d0f-4c3a-937a-e450a7eec716)
|
||||
- Selective vulnerability of GM to energy depletion
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||||
- Carbon monoxide: T2-hyperintense globi pallidi (GP) ± subcortical WM
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||||
- Methanol: Hyperintense putamen ± hemorrhagic necrosis
|
||||
- Mitochondrial encephalopathy: Symmetric BG abnormality
|
||||
- Drugs [heroin; methylenedioxymethamphetamine (MDMA), a.k.a. ecstasy]: T2-hyperintense GP
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||||
- Osmotic demyelination: T2 hyperintense BG, central pons, thalami, WM
|
||||
- [Posterior Reversible Encephalopathy Syndrome (PRES)](/document/posterior-reversible-encephalopath-/84176f2c-fc9d-4497-8af9-1430b9f0187c)
|
||||
- Predominantly vasogenic edema in subcortical WM of bilateral parietooccipital regions
|
||||
- May involve deep gray nuclei
|
||||
- DWI classically negative
|
||||
- [Creutzfeldt-Jakob Disease](/document/creutzfeldt-jakob-disease-cjd/30a88a01-b24d-476d-a933-48aabcdb6f95)
|
||||
- Progressive T2 hyperintensity in BG, thalamus, and cortex
|
||||
- FLAIR hyperintensity in cortex in sporadic disease
|
||||
- DWI: Restriction in deep gray nuclei and cortex; may resolve late in disease
|
||||
- ### MELAS
|
||||
|
||||
|
||||
- **M**itochondrial myopathy, **e**ncephalopathy with **l**actic **a**cidosis, and **s**troke-like episodes
|
||||
- Uncommon cause of childhood stroke
|
||||
- T2-hyperintense gyral edema; crosses vascular distributions
|
||||
- Spares subcortical and deep WM
|
||||
|
||||
## PATHOLOGY
|
||||
|
||||
- ### Staging, Grading, & Classification
|
||||
|
||||
|
||||
- Common underlying process regardless of cause of injury
|
||||
- Diminished cerebral blood flow and reduced blood oxygenation
|
||||
- Brain ischemia due to cardiac arrest or cerebrovascular disease and 2° to hypoxia due to ↓ blood flow
|
||||
- Switch from oxidative phosphorylation to anaerobic metabolism: ↓ ATP, ↑ lactate
|
||||
- Release of presynaptic glutamate → activation of NMDA receptors → triggers cytotoxic processes
|
||||
- Severe energy depletion → cell necrosis; lesser energy depletion → apoptosis
|
||||
- Sites of brain injury determined by maturity of brain, severity and duration of hypoxic-ischemic insult
|
||||
- Selective vulnerability: Patterns of injury reflect dysfunction of selected excitatory neuronal circuits depleted most rapidly
|
||||
- Areas with highest concentrations of glutamate or excitatory amino acid receptors (GM) are more susceptible to injury
|
||||
- Areas with greatest energy demands become energy deficient
|
||||
- Cell death may not be evident until days after initial insult
|
||||
- Delayed WM injury: Postanoxic leukoencephalopathy
|
||||
- 2-3 weeks after HII event in 2-3% of patients
|
||||
- Clinical stability followed by acute neurologic decline, most (75%) recover
|
||||
- Brain-damaging effects of HII are age dependent but do not ↑ linearly with advancing age and development
|
||||
- Immature brain is less resistant to HII than its adult counterpart
|
||||
- Intermediate age groups are more tolerant to HII than either very young or more mature ages
|
||||
- Mechanism behind reduced diffusion during ischemia is thought to be caused by cytotoxic edema, which results from breakdown of cellular membrane Na/K pump system
|
||||
- As cytotoxic edema develops → shift of water from extracellular to intracellular space
|
||||
- Cell membrane remains intact, no overall ↑ in tissue water; **initially**: ↑ FA, ↓ ADC, normal T2
|
||||
- Shorter intervals of HII primarily damage cerebral cortex and hippocampus, while longer periods result in more extensive damage and can be associated with cavitary lesions of cerebral hemispheres
|
||||
- Cavitary lesions, vertical band-like distribution of noncavitary lesions, mineralization more common in immature brain
|
||||
- Patterns associated with poor clinical outcome: Diffuse cortical and deep GM pattern, medial occipital with perirolandic involvement, precentral gyrus involvement, diffuse WM involvement, brainstem, cerebellar &/or hippocampal involvement
|
||||
|
||||
## CLINICAL ISSUES
|
||||
|
||||
- ### Presentation
|
||||
|
||||
|
||||
- #### Most common signs/symptoms
|
||||
|
||||
|
||||
- Etiologies: Cardiac arrest, cerebrovascular disease, drowning, asphyxiation
|
||||
- Hypoxia in cases of near drowning involves putamen and caudate nucleus
|
||||
- ### Natural History & Prognosis
|
||||
|
||||
|
||||
- Death or profound long-term neurologic disability
|
||||
- Neurologic sequela, such as cerebral palsy and epilepsy
|
||||
- BG involvement often leads to movement disorders
|
||||
- ### Treatment
|
||||
|
||||
|
||||
- Supportive care; however, this does not prevent ongoing injury following causative insult
|
||||
- Hypothermia; excitatory amino acid antagonists
|
||||
|
||||
## DIAGNOSTIC CHECKLIST
|
||||
|
||||
- ### Image Interpretation Pearls
|
||||
|
||||
|
||||
- If MR is negative in first 24 hours, repeat exam at 2-4 days to exclude delayed injury
|
||||
- ### Reporting Tips
|
||||
|
||||
|
||||
- Important to describe extent of cortical and deep GM involvement
|
||||
|
||||
67df9962-d618-43f5-959e-bc75df719946
|
||||
|
||||
## References
|
||||
|
||||
## Selected References
|
||||
|
||||
1. [Diamanti S et al: Prognostic value of signal abnormalities on brain MRI in post-anoxic super-refractory status epilepticus: a single-center retrospective study. Eur J Neurol. 32(1):e70045, 2025](http://www.ncbi.nlm.nih.gov/pubmed/?term=39817609%5Bpmid%5D)
|
||||
1. [Shih JJ et al: Neurological injury in comatose patients following substance-use-related out-of-hospital cardiac arrest: a retrospective cohort study in a safety net hospital. Neurocrit Care. ePub, 2025](http://www.ncbi.nlm.nih.gov/pubmed/?term=40082337%5Bpmid%5D)
|
||||
1. [Faraj C et al: The white cerebellum sign: classic but under recognized sign of brain injury. Radiol Case Rep. 19(6):2408-10, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=38585389%5Bpmid%5D)
|
||||
1. [Merhav G et al: Exploring the thalamus L-sign: initial findings and associations with white matter injury in premature infants. Pediatr Radiol. 54(9):1532-9, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=38970707%5Bpmid%5D)
|
||||
1. [Calabrese E et al: Parieto-occipital injury on diffusion MRI correlates with poor neurologic outcome following cardiac arrest. AJNR Am J Neuroradiol. 44(3):254-60, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=36797027%5Bpmid%5D)
|
||||
1. [Bambach S et al: Arterial spin labeling applications in pediatric and adult neurologic disorders. J Magn Reson Imaging. 55(3):698-719, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=33314349%5Bpmid%5D)
|
||||
1. [Beekman R et al: Bedside monitoring of hypoxic ischemic brain injury using low-field, portable brain magnetic resonance imaging after cardiac arrest. Resuscitation. 176:150-8, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35562094%5Bpmid%5D)
|
||||
1. [Hoiland RL et al: Neurologic prognostication after cardiac arrest using brain biomarkers: a systematic review and meta-analysis. JAMA Neurol. 79(4):390-8, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35226054%5Bpmid%5D)
|
||||
1. [Schick A et al: Association of hypoxic ischemic brain injury on early CT after out of hospital cardiac arrest with neurologic outcome. Am J Emerg Med. 54:257-62, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35219011%5Bpmid%5D)
|
||||
1. [Kirsch K et al: Prognostication of neurologic outcome using gray-white-matter-ratio in comatose patients after cardiac arrest. BMC Neurol. 21(1):456, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=34809608%5Bpmid%5D)
|
||||
1. [Endisch C et al: Hypoxic-ischemic encephalopathy evaluated by brain autopsy and neuroprognostication after cardiac arrest. JAMA Neurol. 77(11):1430-9, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32687592%5Bpmid%5D)
|
||||
1. [Jiang W et al: Gray matter nuclei damage in acute carbon monoxide intoxication assessed in vivo using diffusion tensor MR imaging. Radiol Med. 125(1):80-6, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31529401%5Bpmid%5D)
|
||||
1. [León-Lozano MZ et al: Cerebrospinal fluid levels of neuron-specific enolase predict the severity of brain damage in newborns with neonatal hypoxic-ischemic encephalopathy treated with hypothermia. PLoS One. 15(6):e0234082, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32479533%5Bpmid%5D)
|
||||
1. [Narayanan S et al: Arterial spin labeling in pediatric neuroimaging. Semin Pediatr Neurol. 33:100799, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32331614%5Bpmid%5D)
|
||||
1. [Scheibe F et al: Movement disorders after hypoxic brain injury following cardiac arrest in adults. Eur J Neurol. 27(10):1937-47, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32416613%5Bpmid%5D)
|
||||
1. [Sheth KN et al: Assessment of brain injury using portable, low-field magnetic resonance imaging at the bedside of critically ill patients. JAMA Neurol. 78(1):41-7, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32897296%5Bpmid%5D)
|
||||
1. [Wright JN et al: Cerebellar watershed injury in children. AJNR Am J Neuroradiol. 41(5):923-8, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32327437%5Bpmid%5D)
|
||||
1. [de Oliveira AM et al: Imaging patterns of toxic and metabolic brain disorders. Radiographics. 39(6):1672-95, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31589567%5Bpmid%5D)
|
||||
1. [Peckham ME et al: Low b-value diffusion weighted imaging is promising in the diagnosis of brain death and hypoxic-ischemic injury secondary to cardiopulmonary arrest. Crit Care. 22(1):165, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29925413%5Bpmid%5D)
|
||||
1. [Fragoso DC et al: Imaging of Creutzfeldt-Jakob disease: imaging patterns and their differential diagnosis. Radiographics. 37(1):234-57, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28076012%5Bpmid%5D)
|
||||
1. [Lee BK et al: "Pseudo-subarachnoid hemorrhage sign" on early brain computed tomography in out-of-hospital cardiac arrest survivors receiving targeted temperature management. J Crit Care. 40:36-40, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28314170%5Bpmid%5D)
|
||||
1. [McKnight CD et al: A simplified approach to encephalitis and its mimics: key clinical decision points in the setting of specific imaging abnormalities. Acad Radiol. 24(6):667-76, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28258904%5Bpmid%5D)
|
||||
1. [Finelli PF et al: Three-territory DWI acute infarcts: diagnostic value in cancer-associated hypercoagulation Stroke (Trousseau Syndrome). AJNR Am J Neuroradiol. 37(11):2033-6, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=27365322%5Bpmid%5D)
|
||||
1. [de Havenon A et al: Medial occipital lobe hyperperfusion identified by arterial spin-labeling: a poor prognostic sign in patients with hypoxic-ischemic encephalopathy. AJNR Am J Neuroradiol. 36(12):2292-5, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=26338917%5Bpmid%5D)
|
||||
1. [Tekes A et al: Apparent diffusion coefficient scalars correlate with near-infrared spectroscopy markers of cerebrovascular autoregulation in neonates cooled for perinatal hypoxic-ischemic injury. AJNR Am J Neuroradiol. 36(1):188-93, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25169927%5Bpmid%5D)
|
||||
1. [Ghei SK et al: MR imaging of hypoxic-ischemic injury in term neonates: pearls and pitfalls. Radiographics. 34(4):1047-61, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25019441%5Bpmid%5D)
|
||||
1. [Muttikkal TJ et al: MRI patterns of global hypoxic-ischemic injury in adults. J Neuroradiol. 40(3):164-71, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23433904%5Bpmid%5D)
|
||||
1. [White ML et al: Anatomical patterns and correlated MRI findings of non-perinatal hypoxic-ischaemic encephalopathy. Br J Radiol. 86(1021):20120464, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23255548%5Bpmid%5D)
|
||||
1. [Wu O et al: Comatose patients with cardiac arrest: predicting clinical outcome with diffusion-weighted MR imaging. Radiology. 252(1):173-81, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19420318%5Bpmid%5D)
|
||||
1. [Huang BY et al: Hypoxic-ischemic brain injury: imaging findings from birth to adulthood. Radiographics. 28(2):417-39; quiz 617, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18349449%5Bpmid%5D)
|
||||
1. [Pollock JM et al: Anoxic injury-associated cerebral hyperperfusion identified with arterial spin-labeled MR imaging. AJNR Am J Neuroradiol. 29(7):1302-7, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18451089%5Bpmid%5D)
|
||||
1. [Kavanagh EC: The reversal sign. Radiology. 245(3):914-5, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=18024460%5Bpmid%5D)
|
||||
1. [Grant PE et al: Acute injury to the immature brain with hypoxia with or without hypoperfusion. Radiol Clin North Am. 44(1):63-77, viii, 2006](http://www.ncbi.nlm.nih.gov/pubmed/?term=16297682%5Bpmid%5D)
|
||||
1. Schaefer P. Stroke and cerebral ischemia. In Edelman R: Clinical Magnetic Resonance Imaging. 3rd ed.Saunders Elsevier. 1454–98, 2006
|
||||
1. [van Pul C et al: Selecting the best index for following the temporal evolution of apparent diffusion coefficient and diffusion anisotropy after hypoxic-ischemic white matter injury in neonates. AJNR Am J Neuroradiol. 26(3):469-81, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=15760851%5Bpmid%5D)
|
||||
1. [Mutlu H et al: Cranial MR imaging findings of potassium chlorate intoxication. AJNR Am J Neuroradiol. 24(7):1396-8, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12917136%5Bpmid%5D)
|
||||
1. [Dijkhuizen RM et al: Dynamics of cerebral tissue injury and perfusion after temporary hypoxia-ischemia in the rat: evidence for region-specific sensitivity and delayed damage. Stroke. 29(3):695-704, 1998](http://www.ncbi.nlm.nih.gov/pubmed/?term=9506615%5Bpmid%5D)
|
||||
1. [Hantson P et al: Neurotoxicity to the basal ganglia shown by magnetic resonance imaging (MRI) following poisoning by methanol and other substances. J Toxicol Clin Toxicol. 35(2):151-61, 1997](http://www.ncbi.nlm.nih.gov/pubmed/?term=9120884%5Bpmid%5D)
|
||||
1. [Yager JY et al: The effect of age on susceptibility to hypoxic-ischemic brain damage. Neurosci Biobehav Rev. 21(2):167-74, 1997](http://www.ncbi.nlm.nih.gov/pubmed/?term=9062939%5Bpmid%5D)
|
||||
|
||||
## Anatomy
|
||||
|
||||
### Default Mode Network
|
||||
Brain/ANATOMY:a29f7551-d39d-4deb-933e-b8d2816168c3
|
||||
|
||||
### Basal Ganglia
|
||||
Brain/ANATOMY:a9de3815-ec59-4c78-adf0-94974065a7e3
|
||||
|
||||
### Limbic System
|
||||
Brain/ANATOMY:f2a117ed-9429-441d-baa0-5e99e05722ac
|
||||
|
||||
### Language Overview
|
||||
Brain/ANATOMY:40f2ed79-0d31-4943-aaa2-7c3244a7e87b
|
||||
|
||||
### Functional Network Overview
|
||||
Brain/ANATOMY:ef0be4c8-3d36-4ca9-b4c5-f22f66d2b367
|
||||
|
||||
### Attention Control Network
|
||||
Brain/ANATOMY:a1bedda5-6478-40b2-98e7-6c5f5363b06f
|
||||
|
||||
### Limbic Network
|
||||
Brain/ANATOMY:e1a20b61-b2c1-44c5-ba04-59843855bfef
|
||||
|
||||
### Memory Overview
|
||||
Brain/ANATOMY:40e2e25f-421b-4653-94e3-641b09b47e4d
|
||||
|
||||
### Social Brain Anatomy
|
||||
Brain/ANATOMY:0352d34a-5966-494e-b9c3-c26bde257bca
|
||||
|
||||
### Gyral/Sulcal Anatomy
|
||||
Brain/ANATOMY:849da2a0-4a32-4a07-8f00-c69291e59434
|
||||
|
||||
### Gyral/Sulcal Anatomy
|
||||
Brain/ANATOMY:299a5990-1805-4018-85b5-191d8416385b
|
||||
|
||||
### Functional Network Overview
|
||||
Brain/ANATOMY:7b97f239-0f6f-4809-ac44-594cdf4842d5
|
||||
|
||||
### Brain
|
||||
Ultrasound/ANATOMY:080771c2-02f3-408d-ad70-04a80d849500
|
||||
|
||||
## Cases
|
||||
|
||||
- {'cases': [{'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'ca9f024c-9776-4a18-9eaf-f05089f35008', 'description': 'Single image from the outside NECT scan shows low-density brain caused by diffuse brain swelling and cerebral edema. This makes blood in normal vessels (arrows) seem unusually dense. Notice that the suprasellar subarachnoid space (curved arrow) is not filled with blood, as it would be if this were aneurysmal subarachnoid hemorrhage. The cerebellum (open arrow) appears more dense than the supratentorial brain, the so-called "white cerebellum" or "cerebellar reversal sign" caused by maintenance of blood flow in the vertebrobasilar circulation while the internal carotid circulation is severely compromised.', 'history': 'Middle-aged patient "found down," taken to local hospital where NECT scan was read as "aneurysmal subarachnoid hemorrhage". Patient was transferred and urgent cerebral angiogram recommended.', 'imagePoolId': '8fa06920-70bb-4627-9c19-a3132d2b9ed6', 'name': 'Mimic', 'teachingPoint': 'Diffusely swollen, edematous brain makes {b|all} vessels (veins as well as arteries) and dura appear hyperdense. This should not be mistaken for aneurysmal subarachnoid hemorrhage!'}], 'caseType': 'Other', 'name': 'OTHER'}
|
||||
- {'cases': [{'authors': [{'key': 'cef7db60-9956-4bc0-95ed-6dea14b493ed', 'value': 'Brian Chin, MD'}], 'caseVersionId': '1886e72b-ec58-4e29-9d14-3457a928609c', 'description': 'Typical CT and MR example of globi pallidi hypoxic-ischemic injury in an adult after narcotic abuse/overdose.\n\nAxial NECT (#1-2) at presentation shows hypoattenuation within the globi pallidi bilaterally (open arrows). The caudate heads (arrows) and putamen (curved arrows) are normal in attenuation.\n\nMR obtained 3 days later shows infarction of the globi pallidi, with hyperintense DWI (#3), hypointense ADC (#4) and FLAIR (#5), and T2WI (#6-7) hyperintense signal (open arrows) related to hypoxic-ischemic injury. There are small foci of T2* gradient echo susceptibility (curved arrows, #8), likely representing small areas of hemorrhagic necrosis. The T1WI (#9) and T1 C+ (#10-11) sequences show hypointense signal without enhancement (open arrows).', 'history': 'Former alcohol dependency; patient found unresponsive in morning after injecting Oxycontin.', 'imagePoolId': '3f1ad7c9-2b2c-4a4a-9d52-f2bb37f01deb', 'name': 'Globi pallidi infarction', 'teachingPoint': None, 'demographics': '46 Years old female'}, {'authors': [{'key': 'a25c450b-3d34-4f64-bba3-cc0834813df6', 'value': 'Miral D. Jhaveri, MD, MBA'}], 'caseVersionId': 'a99caaad-531d-4eb3-86fb-237be778a577', 'description': 'Axial NECT (#1) demonstrates low-density changes in the caudate (curved arrows), lentiform nuclei (arrows), and in the temporooccipital regions (open arrows) bilaterally.\n\nAxial DW images (#2-3) show restricted diffusion in the basal ganglia (arrows, #2-6) and frontal and temporooccipital cortex (open arrows, #2-6). On the axial FLAIR images (#4-5) and axial T2 image (#6), these corresponding areas show high signal. There is symmetric distribution of the abnormality, suggesting a metabolic cause.', 'history': 'Patient was unresponsive after cardiac arrest.', 'imagePoolId': 'a165351e-ceec-4d39-aa1f-4e9165a64021', 'name': 'Hypoxic ischemic encephalopathy', 'teachingPoint': 'In view of the history of cardiac arrest, the findings are consist with severe hypoxic ischemic encephalopathy. In severe hypoxic encephalopathy, the gray matter structures (basal ganglia, thalami, cortex) are preferentially involved, as these structures have the greatest energy demands.', 'demographics': '30 Years old female'}, {'authors': [{'key': '8d5254e9-8dda-478b-8f08-bdee97a32c79', 'value': 'Karen L. Salzman, MD, FACR'}], 'caseVersionId': '92dc12e0-88be-4d5e-a0a6-44fe27d1cd97', 'description': 'CT example of severe hypoxic-ischemic injury after hanging.\n\nAxial CT images (#1-4) show extensive low density representing hypoxic ischemic injury involving the basal ganglia (curved white arrows, #2-3), thalami (open arrows, #2), and cortex (arrows, #1-4) throughout the supratentorial brain. There is effacement of the sulci related to diffuse cerebral edema (curved black arrows, #4). There is also hyperdensity of the superior cerebellum (open black arrow, #1) related to a reversal sign or white cerebellar sign, indicating severe injury with a poor prognosis.', 'history': 'Patient found after hanging.', 'imagePoolId': 'dbce6bbb-ca7f-42e7-b00f-722df1313f4b', 'name': 'Hanging injury', 'teachingPoint': 'Involvement of the gray matter structures and a cerebellar reversal sign in this case indicates severe injury.', 'demographics': '47 Years old female'}], 'caseType': 'typical', 'name': 'TYPICAL'}
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
*Axial NECT of a 33-year-old patient found down with severe HII is shown. There is diffuse cerebral edema and loss of gray-white differentiation. Cisternal CSF effacement and vascular engorgement contribute to the pseudosubarachnoid hemorrhage appearance <img src='img/arrows/CC.png' alt='cyan curved arrow'/> of the suprasellar and ambient cisterns.*
|
||||
|
||||
|
||||
*Axial NECT of a 33-year-old patient found down with severe HII is shown. There is diffuse cerebral edema and loss of gray-white differentiation. Cisternal CSF effacement and vascular engorgement contribute to the pseudosubarachnoid hemorrhage appearance <img src='img/arrows/CC.png' alt='cyan curved arrow'/> of the suprasellar and ambient cisterns.*
|
||||
|
||||
|
||||
*Coronal NECT is after asphyxiation. The white cerebellar sign with diffuse cerebral hypoattenuation <img src='img/arrows/BC.png' alt='black curved arrow'/> and relative ↑ density <img src='img/arrows/WO.png' alt='white open arrow'/> of the cerebellum indicates severe injury and poorer prognosis.*
|
||||
|
||||
|
||||
*Symmetric FLAIR hyperintensity of the basal ganglia <img src='img/arrows/CS.png' alt='cyan solid arrow'/> and thalami <img src='img/arrows/WS.png' alt='white solid arrow'/> status post cardiac arrest is shown. T2 and FLAIR MR typically become positive in early subacute period (> 24 hours to 2 weeks).*
|
||||
|
||||
|
||||
*Postanoxic axial DWI MR shows ↑ signal in the bilateral hippocampi <img src='img/arrows/WC.png' alt='white curved arrow'/>. HII results in excessive presynaptic release of glutamate, which has a high affinity for NMDA receptors (located abundantly in the hippocampus). Persistent binding of glutamate has excitotoxic effects, causing cell death.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a confused patient shows symmetric hyperintensity in the globi pallidi <img src='img/arrows/WS.png' alt='white solid arrow'/>. Imaging differential considerations in this patient include HII, carbon monoxide poisoning and drugs of abuse, such as heroin and methylenedioxymethamphetamine (MDMA), a.k.a. ecstasy.*
|
||||
|
||||
|
||||
*Axial T2 MR shows the chronic sequelae of severe HII in this 26-year-old with hyperintensity and atrophy of the basal ganglia, including the caudate heads <img src='img/arrows/CS.png' alt='cyan solid arrow'/>, putamina <img src='img/arrows/WO.png' alt='white open arrow'/>, and globi pallidi <img src='img/arrows/BS.png' alt='black solid arrow'/>.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a 76-year-old 2 days post CPR with ROSC shows diffuse signal abnormality throughout the cerebellum. Severe HII can affect the cerebellum in the adult population. Purkinje cells are exquisitely sensitive to ischemic damage. Immature Purkinje cells protect the cerebellar cortex in the neonatal population.*
|
||||
|
||||
|
||||
*Axial DWI in the same patient shows signal hyperintensity in the bilateral cerebellar hemispheres related to cytotoxic edema. Involvement of the cerebellum typically indicates a poor prognosis.*
|
||||
|
||||
|
||||
*Axial DWI MR after anoxic event with confluent hyperintense signal abnormality <img src='img/arrows/BO.png' alt='black open arrow'/> in the cerebral white matter is shown. DWI signal abnormalities may pseudonormalize by the end of the 1st week.*
|
||||
|
||||
|
||||
*Axial DTI trace MR shows extensive hyperintensity related to cytotoxic edema throughout cortex <img src='img/arrows/WS.png' alt='white solid arrow'/> in this 63-year-old unresponsive man with severe HII. Sensorimotor and visual cortex is most commonly involved.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
*Axial FLAIR MR demonstrates hyperintense signal in bilateral hippocampi <img src='img/arrows/WC.png' alt='white curved arrow'/>.*
|
||||
|
||||
|
||||
*Axial DWI MR shows symmetrically ↑ signal in bilateral globi pallidi <img src='img/arrows/WS.png' alt='white solid arrow'/>. DWI is the earliest modality to become positive (within the 1st few hours after a hypoxic-ischemic event). DWI abnormalities may pseudonormalize by the end of the 1st week.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows symmetric hyperintensity in the basal ganglia <img src='img/arrows/WS.png' alt='white solid arrow'/> and occipital cortex <img src='img/arrows/BO.png' alt='black open arrow'/> in this patient with hypoperfusion injury.*
|
||||
|
||||
|
||||
*Axial DTI trace MR in a 21-year-old unresponsive man shows extensive hyperintensity related to cytotoxic edema throughout the cortex and subcortical white matter <img src='img/arrows/WS.png' alt='white solid arrow'/> as well as the external capsules <img src='img/arrows/WO.png' alt='white open arrow'/> in this patient with severe HII.*
|
||||
|
||||
|
||||
*Axial T2 MR in the same patient shows hyperintensity throughout the cortex, subcortical white matter <img src='img/arrows/WS.png' alt='white solid arrow'/>, and the external capsules <img src='img/arrows/WO.png' alt='white open arrow'/>. Complete effacement of the sulci is related to gyral swelling. Involvement of the visual and sensorimotor cortex is common in severe HII.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows symmetric hyperintensity in the basal ganglia bilaterally <img src='img/arrows/WS.png' alt='white solid arrow'/> in a patient with a history of chronic anoxic injury. These deep gray nuclei are also atrophic. Subtle cortical thinning and hyperintensity are also seen in bilateral occipital lobes <img src='img/arrows/WO.png' alt='white open arrow'/>.*
|
||||
|
||||
|
||||
*Axial NECT shows diffuse cerebral parenchymal hypodensity with obscuration of the gray-white interfaces <img src='img/arrows/WC.png' alt='white curved arrow'/>. There is poor delineation of the deep gray nuclei <img src='img/arrows/WO.png' alt='white open arrow'/>. The sulci and gyri are completely effaced. When hyperdensity of the cerebellum is seen, this indicates severe injury and a poorer prognosis.*
|
||||
|
||||
|
||||
*Axial DWI MR shows symmetric restricted diffusion in the caudate heads, putamina <img src='img/arrows/WS.png' alt='white solid arrow'/>, and cortex in a comatose patient status post cardiac arrest. The cortical involvement is most prominent in the occipital lobes <img src='img/arrows/WO.png' alt='white open arrow'/>.*
|
||||
|
||||
|
||||
*Axial 3D FLAIR 2 days after cardiac arrest with symmetric hyperintensity within the hippocampi <img src='img/arrows/WC.png' alt='white curved arrow'/> in this patient with severe HII is shown.*
|
||||
|
||||
|
||||
*Axial FLAIR 4 days after cardiac arrest with markedly abnormal signal hyperintensity with the deep gray nuclei and cerebral cortices is shown.*
|
||||
|
||||
|
||||
*Axial NECT shows diffuse cerebral parenchymal hypodensity with loss of the gray-white interfaces <img src='img/arrows/BC.png' alt='black curved arrow'/> in this young adult following asphyxiation. There is poor delineation of the deep gray nuclei <img src='img/arrows/WO.png' alt='white open arrow'/>. The sulci and gyri are completely effaced related to diffuse cerebral edema.*
|
||||
|
||||
|
||||
*Axial T2 MR shows symmetric hyperintensity of the basal ganglia <img src='img/arrows/CS.png' alt='cyan solid arrow'/> in this 73-year-old with severe anoxic injury. Imaging differential considerations include both toxic metabolic disorders, such as osmotic demyelination and Creutzfeldt-Jakob disease (CJD).*
|
||||
|
||||
|
||||
*Axial DWI MR shows diffusely increased signal in bilateral cerebellar hemispheres <img src='img/arrows/WS.png' alt='white solid arrow'/>. Severe HII can affect the cerebellum in the adult population. The Purkinje cells are exquisitely sensitive to ischemic damage. Immature Purkinje cells protect the cerebellar cortex in the neonatal population.*
|
||||
|
||||
|
||||
*Axial ADC map shows corresponding ↓ signal in bilateral cerebellar hemispheres related to cytotoxic edema. Involvement of the cerebellum typically indicates a poor prognosis.*
|
||||
|
||||
|
||||
*Axial DTI MR shows symmetric ↑ signal in the globi pallidi <img src='img/arrows/WS.png' alt='white solid arrow'/> in this patient with severe anoxic injury. DTI is the earliest modality to become positive within the 1st few hours after a hypoxic-ischemic event.*
|
||||
|
||||
|
||||
*Axial DTI trace MR shows extensive white matter hyperintensity <img src='img/arrows/WO.png' alt='white open arrow'/> related to cytotoxic edema in this 43-year-old woman with mild to moderate HII. DWI signal abnormalities may pseudonormalize by the end of the 1st week.*
|
||||
|
||||
+459
@@ -0,0 +1,459 @@
|
||||
---
|
||||
title: "Cerebral Hyperperfusion Syndrome"
|
||||
docid: "2c495cde-3ebe-494c-8987-d0a6dd61a065"
|
||||
authors:
|
||||
- key: "2bca6b86-1eca-4e93-b997-4e18913686a7"
|
||||
value: "Hediyeh Baradaran, MD, MS"
|
||||
- key: "5cff4116-3654-4b3a-bb75-5ebe0b8c9850"
|
||||
value: "Anne G. Osborn, MD, FACR"
|
||||
breadcrumbs:
|
||||
-
|
||||
name: "Brain"
|
||||
slug: "brain"
|
||||
treeNodeId: "0361042c-9c90-48e4-864e-a2e6428ee9c9"
|
||||
-
|
||||
name: "Diagnosis"
|
||||
slug: "diagnosis"
|
||||
treeNodeId: "948c6f1e-8e18-45f3-bd9d-7a04ab0b8708"
|
||||
-
|
||||
name: "Pathology-Based Diagnoses"
|
||||
slug: "pathology-based-diagnoses"
|
||||
treeNodeId: "d60fe914-7897-46a0-9cd2-f88ffb322f16"
|
||||
-
|
||||
name: "Stroke"
|
||||
slug: "stroke"
|
||||
treeNodeId: "7a135176-0a69-4fc9-b200-59569fbf5166"
|
||||
-
|
||||
name: "Cerebral Ischemia and Infarction"
|
||||
slug: "cerebral-ischemia-and-infarction"
|
||||
treeNodeId: "11d50e7d-f3e9-4071-b2b7-26b11ab40ea6"
|
||||
-
|
||||
name: "Cerebral Hyperperfusion Syndrome"
|
||||
slug: "cerebral-hyperperfusion-syndrome"
|
||||
treeNodeId: null
|
||||
category: "Brain"
|
||||
documentVersionId: "b154b4e4-2720-4a8a-8501-f658bfaf930d"
|
||||
imageCount: 19
|
||||
lastUpdated: "08/19/25"
|
||||
pageDescription: "Cerebral Hyperperfusion Syndrome"
|
||||
pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Stroke, Cerebral Ischemia and Infarction, Cerebral Hyperperfusion Syndrome"
|
||||
pageTitle: "Cerebral Hyperperfusion Syndrome | STATdx"
|
||||
enhancedTitle: "Cerebral Hyperperfusion Syndrome"
|
||||
type: "DX"
|
||||
references: true
|
||||
breadcrumbs:
|
||||
- "Brain"
|
||||
- "Diagnosis"
|
||||
- "Pathology-Based Diagnoses"
|
||||
- "Stroke"
|
||||
- "Cerebral Ischemia and Infarction"
|
||||
- "Cerebral Hyperperfusion Syndrome"
|
||||
---
|
||||
## KEY FACTS
|
||||
|
||||
- ### Terminology
|
||||
|
||||
|
||||
- Rare disorder most commonly occurring as complication of cerebral revascularization
|
||||
- Other etiologies less common
|
||||
- Status epilepticus
|
||||
- MELAS
|
||||
- Major ↑ in ipsilateral cerebral blood flow (CBF) well above normal metabolic demands
|
||||
- ### Imaging
|
||||
|
||||
|
||||
- Ipsilateral gyral swelling, sulcal effacement in post carotid endarterectomy (CEA) patient
|
||||
- ↑ CBF, cerebral blood volume (CBV) on perfusion MR (pMR), perfusion CT (pCT)
|
||||
- Early draining vein, capillary blush on DSA after revascularization
|
||||
- ### Top Differential Diagnoses
|
||||
|
||||
|
||||
- Acute cerebral ischemia-infarction
|
||||
- Status epilepticus
|
||||
- MELAS
|
||||
- Posterior reversible encephalopathy syndrome (PRES)
|
||||
- Hypercapnia
|
||||
- ### Pathology
|
||||
|
||||
|
||||
- Cerebral hyperperfusion syndrome (CHS) probably caused by maladaptive autoregulatory mechanisms, altered cerebral hemodynamics
|
||||
- "Normal perfusion pressure breakthrough"
|
||||
- Rapid restoration of normal perfusion following revascularization → hyperperfusion in previously underperfused brain
|
||||
- ### Clinical Issues
|
||||
|
||||
|
||||
- ~ 3% of post-CEA patients develop CHS
|
||||
- Triad of unilateral headache, neurologic deficit, seizures
|
||||
- Variable cognitive impairment
|
||||
- Ipsilateral face, eye pain
|
||||
- ### Diagnostic Checklist
|
||||
|
||||
|
||||
- Need to distinguish stroke/TIA from CHS
|
||||
|
||||
## TERMINOLOGY
|
||||
|
||||
- ### Abbreviations
|
||||
|
||||
|
||||
- Cerebral hyperperfusion syndrome (CHS)
|
||||
- ### Synonyms
|
||||
|
||||
|
||||
- Post-CEA hyperperfusion
|
||||
- Luxury perfusion
|
||||
- ### Definitions
|
||||
|
||||
|
||||
- Rare (3.5%) disorder most commonly occurring as complication of cerebral revascularization
|
||||
- Mildly ↑ cerebral blood flow (CBF) common after carotid endarterectomy (CEA), typically asymptomatic
|
||||
- CHS defined as ≥ 100% ↑ in rCBF compared to preoperative values
|
||||
- Major ↑ in ipsilateral CBF well above normal metabolic demands
|
||||
- Usually following carotid revascularization procedure
|
||||
- CEA
|
||||
- Angioplasty with stenting
|
||||
- Thrombolysis
|
||||
- May occur in other settings [e.g., status epilepticus, mitochondrial encephalopathy lactic acidosis and stroke-like episodes (MELAS)]
|
||||
- After drainage of chronic subdural hematomas
|
||||
|
||||
## IMAGING
|
||||
|
||||
- ### General Features
|
||||
|
||||
|
||||
- #### Best diagnostic clue
|
||||
|
||||
|
||||
- Ipsilateral subcortical edema, gyral swelling, sulcal effacement in post-CEA patient
|
||||
- ↑ CBF, cerebral blood volume (CBV) on perfusion MR (pMR), perfusion CT (pCT)
|
||||
- #### Size
|
||||
|
||||
|
||||
- Variable
|
||||
- #### Morphology
|
||||
|
||||
|
||||
- Follows vascular distribution
|
||||
- ### Angiographic Findings
|
||||
|
||||
|
||||
- Sentinel signs suggestive of maximal arteriolar dilation, disrupted cerebral autoregulation
|
||||
- Early draining vein in treated ischemic territory
|
||||
- Early contrast filling vein(s) in late arterial or capillary phase
|
||||
- Prominent capillary blush (luxury perfusion) denser than rest of arterial territory
|
||||
- Persists late into venous phase
|
||||
- ### Imaging Recommendations
|
||||
|
||||
|
||||
- #### Best imaging tool
|
||||
|
||||
|
||||
- MR with DWI, SWI, PWI
|
||||
- SPECT
|
||||
- #### Protocol advice
|
||||
|
||||
|
||||
- Add T2* (GRE or SWI) to look for hemorrhage
|
||||
- ### CT Findings
|
||||
|
||||
|
||||
- #### NECT
|
||||
|
||||
|
||||
- Gyral swelling
|
||||
- Cortical effacement
|
||||
- Patchy or diffuse white matter (WM) edema
|
||||
- Posterior parietooccipital lobe most common
|
||||
- ± hypodensity (may occur without attenuation alterations)
|
||||
- Frank hemorrhage in < 1%
|
||||
- #### CECT
|
||||
|
||||
|
||||
- Prominent vessels with ↑ intravascular enhancement
|
||||
- May demonstrate contrast extravasation in severe cases (rare)
|
||||
- CT perfusion
|
||||
- Elevated CBF, ↓ TTP
|
||||
- ### MR Findings
|
||||
|
||||
|
||||
- #### T1WI
|
||||
|
||||
|
||||
- Cortical swelling
|
||||
- ± mild hypointensity
|
||||
- Sulci effaced
|
||||
- #### T2WI
|
||||
|
||||
|
||||
- Gyral swelling, patchy hyperintensity
|
||||
- #### FLAIR
|
||||
|
||||
|
||||
- Hyperintense cortex, patchy subcortical hyperintensity
|
||||
- Hyperintensity in subarachnoid spaces on postcontrast FLAIR reported 2° to blood-brain barrier (BBB) disruption
|
||||
- #### T2* GRE
|
||||
|
||||
|
||||
- Frank hemorrhage in < 1%
|
||||
- Blooming on GRE or SWI
|
||||
- #### DWI
|
||||
|
||||
|
||||
- Usually normal, as edema is vasogenic, not cytotoxic
|
||||
- ~ 25% show small foci of restricted diffusion compared to preoperative DWI
|
||||
- #### PWI
|
||||
|
||||
|
||||
- Elevated CBV, CBF
|
||||
- Shortened MTT
|
||||
- Side-to-side difference of 3 seconds predictive of CHS
|
||||
- #### T1WI C+
|
||||
|
||||
|
||||
- May be normal
|
||||
- May show slightly ↑ prominence of cerebral vessels
|
||||
- Parenchymal enhancement in severe cases
|
||||
- #### MRA
|
||||
|
||||
|
||||
- Preoperative ↓ signal intensity in middle cerebral artery (MCA) may identify patients at risk for CHS
|
||||
- ### Other Modality Findings
|
||||
|
||||
|
||||
- SPECT
|
||||
- N-isopropyl-p-I-123-iodoamphetamine or I-123-iomazenil SPECT
|
||||
- Shows hyperperfusion in ipsilateral cerebral hemisphere after surgery
|
||||
- CBF ≥ 100% in revascularized territory from baseline
|
||||
- Can be detected even in asymptomatic patients
|
||||
- May be correlated with long-term neuronal damage that CT, MR do not detect
|
||||
- May be associated with crossed cerebellar diaschisis
|
||||
- ### Ultrasonographic Findings
|
||||
|
||||
|
||||
- Transcranial color duplex (TCD)
|
||||
- 1.5-2x ↑ in MCA flow velocity
|
||||
|
||||
## DIFFERENTIAL DIAGNOSIS
|
||||
|
||||
- [Acute Cerebral Ischemia-Infarction](/document/acute-cerebral-ischemiainfarction/7a3ed4a9-ae05-4d64-ae8e-6a30105501e1)
|
||||
- TTP/MTT prolonged (not ↓)
|
||||
- Typically shows restriction on DWI (CHS often negative)
|
||||
- [Status Epilepticus](/document/status-epilepticus/bb0430ba-9933-40b4-a95b-97ca85070486)
|
||||
- Metabolic hyperperfusion in affected brain
|
||||
- History of seizure helpful but may not be available
|
||||
- [Posterior Reversible Encephalopathy Syndrome](/document/posterior-reversible-encephalopath-/84176f2c-fc9d-4497-8af9-1430b9f0187c)
|
||||
- Failed autoregulation → hyperperfusion → endothelial injury/vasogenic edema
|
||||
- Predilection for posterior circulation
|
||||
- Markedly elevated blood pressure (many etiologies)
|
||||
- Eclampsia, preeclampsia
|
||||
- Chemotherapy
|
||||
- Renal failure
|
||||
- Hemolytic uremic syndrome/thrombotic thrombocytopenic purpura
|
||||
- Drug abuse (especially cocaine)
|
||||
- ### MELAS
|
||||
|
||||
|
||||
- Acute oxidative phosphorylation defect
|
||||
- Stroke-like episodes related to vasogenic edema, hyperperfusion, neuronal damage
|
||||
- Cortical hyperintensity, enhancement
|
||||
- Perform MRS in unaffected region, look for lactate
|
||||
- ### Hypercapnia
|
||||
|
||||
|
||||
- Carbon dioxide is potent stimulator of CBF
|
||||
- Vasodilatory effect on cerebral vasculature
|
||||
|
||||
## PATHOLOGY
|
||||
|
||||
- ### General Features
|
||||
|
||||
|
||||
- #### Etiology
|
||||
|
||||
|
||||
- Theories
|
||||
- Impaired cerebral autoregulation
|
||||
- Damage from free radicals causing vasodilation with ↑ vascular permeability
|
||||
- Baroreceptor reflex breakdown limiting ability to respond to changes in blood pressure
|
||||
- Trigeminovascular reflex (vasoactive neuropeptide release)
|
||||
- CHS probably caused by maladaptive autoregulatory mechanisms, altered cerebral hemodynamics
|
||||
- "Normal perfusion pressure breakthrough"
|
||||
- Chronic ischemia → impaired autoregulation
|
||||
- Loss of normal vasoconstriction
|
||||
- "Resistance" vessels become chronically dilated
|
||||
- Rapid restoration of normal perfusion following revascularization → hyperperfusion in previously underperfused brain
|
||||
- Cognitive impairment after CEA or angioplasty/stenting may result from
|
||||
- Cerebral embolization during dissection, stenting
|
||||
- Global cerebral hypoperfusion during carotid cross-clamping
|
||||
- CHS
|
||||
|
||||
## CLINICAL ISSUES
|
||||
|
||||
- ### Presentation
|
||||
|
||||
|
||||
- #### Most common signs/symptoms
|
||||
|
||||
|
||||
- Symptoms range from mild to severe/life-threatening
|
||||
- Ipsilateral headache, eye and facial pain
|
||||
- Other signs/symptoms
|
||||
- Neurologic deficit and seizures
|
||||
- Variable cognitive impairment
|
||||
- Timing
|
||||
- Peaks at 12 hours after carotid angioplasty/stenting (CAS)
|
||||
- 6 days after CEA
|
||||
- Can be delayed by up to 1 month
|
||||
- ### Demographics
|
||||
|
||||
|
||||
- #### Age
|
||||
|
||||
|
||||
- For postendarterectomy CHS, generally older patients
|
||||
- For other etiologies (e.g., seizure, MELAS), any age
|
||||
- #### Epidemiology
|
||||
|
||||
|
||||
- ~ 3-4% of post-CEA patients develop mild CHS
|
||||
- Highest risk = impaired cerebrovascular reserve, asymptomatic stenosis
|
||||
- > 100% ↑ in CBF after treatment
|
||||
- Covariate clinical risk factors
|
||||
- Age
|
||||
- Hypertension (especially postoperative)
|
||||
- Diabetes
|
||||
- Bilateral lesions
|
||||
- Extent of ICA stenosis
|
||||
- High grade > low grade
|
||||
- Presence of contralateral carotid occlusion or high-grade stenosis
|
||||
- Duration of cross-clamping
|
||||
- Diminished carotid reserve
|
||||
- Poor collateral blood flow
|
||||
- ↓ cerebrovascular reactivity to acetazolamide challenge
|
||||
- ### Natural History & Prognosis
|
||||
|
||||
|
||||
- Neurologic emergency
|
||||
- If not treated promptly/adequately, can cause death or severe disability
|
||||
- If no intracranial hemorrhage
|
||||
- Usually reversible
|
||||
- No major tissue destruction
|
||||
- May result in persistent mild cognitive impairment
|
||||
- 1% of CHS with intracranial hemorrhage
|
||||
- Poor prognosis
|
||||
- ### Treatment
|
||||
|
||||
|
||||
- Prevention
|
||||
- Minimize intraoperative cerebral ischemia
|
||||
- Consider continuing postoperative anesthesia/continuous sedation
|
||||
- Strict postoperative blood pressure control
|
||||
- Staged angioplasty in at-risk patients can ↓
|
||||
- Efficacious for patients with severe impairment of hemodynamic reserve in I-123 IMP SPECT
|
||||
- Can treat with antihypertensives; antiseizure medications in those with seizures
|
||||
|
||||
## DIAGNOSTIC CHECKLIST
|
||||
|
||||
- ### Consider
|
||||
|
||||
|
||||
- Post-CEA/carotid artery stenting patient with neurologic deficit with asymmetric imaging findings
|
||||
- Need to distinguish stroke/transient ischemic attack from CHS
|
||||
|
||||
c93b3d99-3fd1-4665-a469-c99ef0079d4e
|
||||
|
||||
## References
|
||||
|
||||
## Selected References
|
||||
|
||||
1. [Abdelkarim A et al: Cerebral hyperperfusion syndrome after carotid revascularization; predictors and complications. Ann Vasc Surg. 115:13-22, 2025](http://www.ncbi.nlm.nih.gov/pubmed/?term=40044075%5Bpmid%5D)
|
||||
1. [Araya S et al: Impact of postoperative cerebral hyperperfusion on 2-year cognitive outcomes of patients undergoing carotid endarterectomy. J Neurosurg. 142(1):70-7, 2025](http://www.ncbi.nlm.nih.gov/pubmed/?term=39126727%5Bpmid%5D)
|
||||
1. [Chow CY et al: Cerebral hyperperfusion syndrome risk comparison between transcarotid artery revascularization and carotid artery stenting with distal embolic protection. Ann Vasc Surg. 113:112-9, 2025](http://www.ncbi.nlm.nih.gov/pubmed/?term=39880283%5Bpmid%5D)
|
||||
1. [Jung MK et al: Prediction of cerebral hyperperfusion syndrome after combined bypass surgery in moyamoya disease using hemodynamic and clinical data. Clin Nucl Med. 50(7):588-95, 2025](http://www.ncbi.nlm.nih.gov/pubmed/?term=40173304%5Bpmid%5D)
|
||||
1. [Irizato N et al: Unexpected cerebral hyperperfusion after transient hypoperfusion associated with stroke-like migraine attacks after radiation therapy syndrome. NMC Case Rep J. 11:135-40, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=38863579%5Bpmid%5D)
|
||||
1. [Turpin J et al: Hyperperfusion syndrome after superficial temporal artery-middle cerebral artery bypass for non-moyamoya steno-occlusive disease. J Stroke Cerebrovasc Dis. 32(8):107222, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=37384979%5Bpmid%5D)
|
||||
1. [Lin YH et al: Update on cerebral hyperperfusion syndrome. J Neurointerv Surg. 50(7):588-95, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32414892%5Bpmid%5D)
|
||||
1. [Murai S et al: Safety and efficacy of staged angioplasty for patients at risk of hyperperfusion syndrome: a single-center retrospective study. Neuroradiology. 62(4):503-10, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31915841%5Bpmid%5D)
|
||||
1. [Pavlov O: Rapid evacuation of chronic subdural hematoma - a possible traumatic brain injury (TBI). Med Hypotheses. 137:109539, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31952019%5Bpmid%5D)
|
||||
1. [Sakata H et al: Symptomatic cerebral hyperperfusion after cerebral vasospasm associated with aneurysmal subarachnoid hemorrhage. World Neurosurg. 137:379-83, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32105869%5Bpmid%5D)
|
||||
1. [Fassaert LMM et al: Transcranial Doppler 24 hours after carotid endarterectomy accurately identifies patients not at risk of cerebral hyperperfusion syndrome. Eur J Vasc Endovasc Surg. 58(3):320-7, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31350134%5Bpmid%5D)
|
||||
1. [Ghuman M et al: Sentinel angiographic signs of cerebral hyperperfusion after angioplasty and stenting of intracranial atherosclerotic stenosis: a technical note. AJNR Am J Neuroradiol. 40(9):1523-5, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31345945%5Bpmid%5D)
|
||||
1. [Lin T et al: ASL perfusion features and type of circle of Willis as imaging markers for cerebral hyperperfusion after carotid revascularization: a preliminary study. Eur Radiol. 29(5):2651-8, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30443757%5Bpmid%5D)
|
||||
1. [Omura T et al: Cerebral hyperperfusion syndrome after a burr hole drainage surgery for chronic subdural hematoma. World Neurosurg. 50(7):588-95, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30610989%5Bpmid%5D)
|
||||
1. [Sharma P et al: Cerebral hyperperfusion syndrome after chronic subdural hematoma drainage. World Neurosurg. 126:694, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31546329%5Bpmid%5D)
|
||||
1. [Huibers AE et al: Editor's choice - cerebral hyperperfusion syndrome after carotid artery stenting: a systematic review and meta-analysis. Eur J Vasc Endovasc Surg. 56(3):322-33, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30196814%5Bpmid%5D)
|
||||
1. [Kirchoff-Torres KF et al: Cerebral hyperperfusion syndrome after carotid revascularization and acute ischemic stroke. Curr Pain Headache Rep. 22(4):24, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29556806%5Bpmid%5D)
|
||||
1. [Galyfos G et al: Cerebral hyperperfusion syndrome and intracranial hemorrhage after carotid endarterectomy or carotid stenting: A meta-analysis. J Neurol Sci. 381:74-82, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28991720%5Bpmid%5D)
|
||||
1. [Cano EJ et al: Asymmetric brain edema after cardiac transplantation: cerebroautoregulatory failure and relative hyperperfusion. Transplant Proc. 47(1):194-7, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25645802%5Bpmid%5D)
|
||||
1. [Horie N et al: De novo ivy sign indicates postoperative hyperperfusion in moyamoya disease. Stroke. 45(5):1488-91, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24713526%5Bpmid%5D)
|
||||
1. [van Mook WN et al: Cerebral hyperperfusion syndrome. Lancet Neurol. 4(12):877-88, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=16297845%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
*A 70-year-old woman with > 90% stenosis of her proximal left cervical internal carotid artery (ICA) underwent carotid endarterectomy. A few days after surgery, she developed acute face and neck pain. FLAIR MR demonstrates patchy subcortical hyperintensity <img src='img/arrows/WS.png' alt='white solid arrow'/>, compatible with reperfusion changes and sulcal failure of CSF suppression <img src='img/arrows/CS.png' alt='cyan solid arrow'/>, compatible with subarachnoid hemorrhage.*
|
||||
|
||||
|
||||
*A 70-year-old woman with > 90% stenosis of her proximal left cervical internal carotid artery (ICA) underwent carotid endarterectomy. A few days after surgery, she developed acute face and neck pain. FLAIR MR demonstrates patchy subcortical hyperintensity <img src='img/arrows/WS.png' alt='white solid arrow'/>, compatible with reperfusion changes and sulcal failure of CSF suppression <img src='img/arrows/CS.png' alt='cyan solid arrow'/>, compatible with subarachnoid hemorrhage.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient shows more evidence of reperfusion changes in the left cerebral hemisphere <img src='img/arrows/WO.png' alt='white open arrow'/>.*
|
||||
|
||||
|
||||
*Axial CTA MIP MR in a patient following a left CEA shows increased vascularity throughout the left posterior temporal and occipital region <img src='img/arrows/CO.png' alt='cyan open arrow'/>.*
|
||||
|
||||
|
||||
*Axial SWI in the same patient has evidence of subarachnoid <img src='img/arrows/BS.png' alt='black solid arrow'/> and parenchymal hemorrhage <img src='img/arrows/BO.png' alt='black open arrow'/> in the left occipital region. Cerebral hyperperfusion syndrome is rare, most commonly occurring as a complication of cerebral revascularization. Patients with hemorrhage have a worse prognosis.*
|
||||
|
||||
|
||||
*A 56-year-old man with > 70% stenosis of his proximal left cervical ICA underwent carotid endarterectomy. A few hours after surgery, he became acutely confused and developed right-sided weakness. Perfusion source image shows markedly increased vasculature in the left hemisphere <img src='img/arrows/BO.png' alt='black open arrow'/>.*
|
||||
|
||||
|
||||
*CT perfusion obtained in the same patient appears relatively normal, but cerebral blood flow (CBF) on the left (2a, 2b ROIs) is increased compared to the right side.*
|
||||
|
||||
|
||||
*TTP in the same patient is even more striking. The abnormal side is not the right middle cerebral artery (MCA) distribution (green) but is the left side (blue) where the TTP is markedly shortened.*
|
||||
|
||||
|
||||
*Axial T2 MR in the same patient shows gyral swelling, sulcal effacement, and hyperintensity in the left temporal and parietooccipital cortex/subcortical white matter <img src='img/arrows/WS.png' alt='white solid arrow'/>, basal ganglia <img src='img/arrows/WC.png' alt='white curved arrow'/>. DWI (not shown) was normal. This is a classic example of postcarotid endarterectomy hyperperfusion syndrome.*
|
||||
|
||||
|
||||
*Axial T1 C+ FS MR shows cerebral hyperperfusion in status epilepticus in a 52-year-old woman with left-sided weakness following prolonged seizure. Note the increased intravascular, sulcal enhancement in the right temporal lobe compared to the left hemisphere <img src='img/arrows/WS.png' alt='white solid arrow'/>.*
|
||||
|
||||
|
||||
*pMR in the same patient shows increased CBF in the right temporal lobe <img src='img/arrows/WO.png' alt='white open arrow'/>, corresponding to the increased intravascular enhancement noted on the previous image.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
*Axial NECT in a patient with confusion, right-sided weakness following left CEA shows subtle increased hypodensity <img src='img/arrows/WS.png' alt='white solid arrow'/> in the cortex and subcortical WM of the left parieto-occipital lobes.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient shows hyperintensity in the cortex <img src='img/arrows/WS.png' alt='white solid arrow'/> and basal ganglia <img src='img/arrows/WO.png' alt='white open arrow'/>.*
|
||||
|
||||
|
||||
*Axial DWI MR in the same patient shows no evidence of restricted diffusion.*
|
||||
|
||||
|
||||
*Axial T1 C+ FS MR in the same patient shows increased vascularity <img src='img/arrows/WS.png' alt='white solid arrow'/> in the left parieto-occipital region.*
|
||||
|
||||
|
||||
*Coronal T1 C+ FS MR in the same patient shows a faint capillary blush <img src='img/arrows/WS.png' alt='white solid arrow'/> in the same area. This was cerebral hyperperfusion syndrome.*
|
||||
|
||||
|
||||
*Anteroposterior view of DSA shows abrupt occlusion of the left MCA just distal to its origin <img src='img/arrows/BS.png' alt='black solid arrow'/> in a patient with a sudden onset of right-sided weakness and stroke-like symptoms. Little collateral filling of the distal MCA is seen.*
|
||||
|
||||
|
||||
*After superselective catheterization of the left MCA and infusion of tissue plasminogen activator for 2 hours, normal circulation was restored, as shown on this AP DSA.*
|
||||
|
||||
|
||||
*Following restoration of normal blood flow in the previously occluded left MCA, the patient experienced worsening right-sided weakness and throbbing headache. Axial MR perfusion study shows elevated (red area <img src='img/arrows/WS.png' alt='white solid arrow'/>), not decreased, CBF in the left temporal and parietal lobes.*
|
||||
|
||||
|
||||
*Axial MR perfusion in the same patient shows elevated cerebral blood volume <img src='img/arrows/BS.png' alt='black solid arrow'/>.*
|
||||
|
||||
@@ -0,0 +1,488 @@
|
||||
---
|
||||
title: "Childhood Stroke"
|
||||
docid: "fbfddb67-5d7e-4979-9a22-85ff72665a91"
|
||||
authors:
|
||||
- key: "b2e6dabb-ee1c-42a4-a332-9f0814c1c607"
|
||||
value: "Surjith Vattoth, MD"
|
||||
- key: "47381de4-c9fd-4999-8dd0-1808cd72db6b"
|
||||
value: "Luke L. Linscott, MD"
|
||||
breadcrumbs:
|
||||
-
|
||||
name: "Brain"
|
||||
slug: "brain"
|
||||
treeNodeId: "0361042c-9c90-48e4-864e-a2e6428ee9c9"
|
||||
-
|
||||
name: "Diagnosis"
|
||||
slug: "diagnosis"
|
||||
treeNodeId: "948c6f1e-8e18-45f3-bd9d-7a04ab0b8708"
|
||||
-
|
||||
name: "Pathology-Based Diagnoses"
|
||||
slug: "pathology-based-diagnoses"
|
||||
treeNodeId: "d60fe914-7897-46a0-9cd2-f88ffb322f16"
|
||||
-
|
||||
name: "Stroke"
|
||||
slug: "stroke"
|
||||
treeNodeId: "7a135176-0a69-4fc9-b200-59569fbf5166"
|
||||
-
|
||||
name: "Cerebral Ischemia and Infarction"
|
||||
slug: "cerebral-ischemia-and-infarction"
|
||||
treeNodeId: "11d50e7d-f3e9-4071-b2b7-26b11ab40ea6"
|
||||
-
|
||||
name: "Childhood Stroke"
|
||||
slug: "childhood-stroke"
|
||||
treeNodeId: null
|
||||
category: "Brain"
|
||||
documentVersionId: "af997e1d-decf-4c8a-84d5-7ea6839f5613"
|
||||
imageCount: 35
|
||||
lastUpdated: "07/21/25"
|
||||
pageDescription: "Childhood Stroke"
|
||||
pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Stroke, Cerebral Ischemia and Infarction, Childhood Stroke"
|
||||
pageTitle: "Childhood Stroke | STATdx"
|
||||
enhancedTitle: "Childhood Stroke"
|
||||
type: "DX"
|
||||
references: true
|
||||
breadcrumbs:
|
||||
- "Brain"
|
||||
- "Diagnosis"
|
||||
- "Pathology-Based Diagnoses"
|
||||
- "Stroke"
|
||||
- "Cerebral Ischemia and Infarction"
|
||||
- "Childhood Stroke"
|
||||
---
|
||||
## KEY FACTS
|
||||
|
||||
- ### Terminology
|
||||
|
||||
|
||||
- Acute neurologic dysfunction due to loss of vascular integrity
|
||||
- ### Imaging
|
||||
|
||||
|
||||
- NECT: ↓ attenuation of affected gray matter
|
||||
- Insular ribbon sign → loss of distinct insular cortex
|
||||
- Hyperdense MCA sign → thrombosed MCA
|
||||
- MR: ↓ diffusion within ~ 30 minutes of arterial occlusion
|
||||
- Cytotoxic edema evident in affected territory on FLAIR/T2 by 4-6 hours after arterial occlusion
|
||||
- Enhancement of infarct typically occurs after 5-7 days
|
||||
- CTA/MRA: Critical for early evaluation & identification of possible etiology (e.g., dissection, arteriopathy)
|
||||
- CTA 1st line for rapid identification of large vessel occlusion amenable to catheter-directed thrombectomy
|
||||
- MR perfusion imaging can provide valuable information regarding region at risk in setting of acute stroke
|
||||
- Arterial spin labeling (ASL) can provide useful perfusion information without contrast administration
|
||||
- ### Top Differential Diagnoses
|
||||
|
||||
|
||||
- Seizure-related injury
|
||||
- Acute encephalitis
|
||||
- Mitochondrial encephalopathies
|
||||
- Posterior reversible encephalopathy syndrome (PRES)
|
||||
- ### Pathology
|
||||
|
||||
|
||||
- Major causes: Cardiac disease (~ 25%), moyamoya, dissection, vasculitis, RCVS, hematologic
|
||||
- No underlying cause discovered in ~ 25% of cases
|
||||
- ### Clinical Issues
|
||||
|
||||
|
||||
- Incidence: 2-3/100,000 per year in USA
|
||||
- Mortality: 0.6/100,000
|
||||
- Children typically present later than adults (> 24 hours)
|
||||
- Focal deficit may be masked by lethargy, coma, irritability
|
||||
- Catheter-based thrombectomy increasingly used in children
|
||||
- Capacity for recovery in children > > adults
|
||||
- ### Diagnostic Checklist
|
||||
|
||||
|
||||
- When stroke is suspected clinically or by imaging, do not hesitate to perform vessel imaging
|
||||
|
||||
## TERMINOLOGY
|
||||
|
||||
- ### Synonyms
|
||||
|
||||
|
||||
- Cerebrovascular accident, cerebral infarct, cerebral ischemia
|
||||
- ### Definitions
|
||||
|
||||
|
||||
- Acute alteration of neurologic function due to loss of vascular integrity
|
||||
- This document specifically addresses arterial ischemia beyond perinatal period to 18 years age
|
||||
|
||||
## IMAGING
|
||||
|
||||
- ### General Features
|
||||
|
||||
|
||||
- #### Best diagnostic clue
|
||||
|
||||
|
||||
- Cytotoxic edema & restricted diffusion (acutely) in affected vascular territory
|
||||
- #### Location
|
||||
|
||||
|
||||
- Proximal & distal middle cerebral artery (MCA) territory most commonly affected
|
||||
- #### Morphology
|
||||
|
||||
|
||||
- Stroke caused by arterial occlusion typically conforms to 1 arterial territory
|
||||
- ### CT Findings
|
||||
|
||||
|
||||
- #### NECT
|
||||
|
||||
|
||||
- ↓ attenuation of affected gray matter with loss of normal gray matter-white matter differentiation
|
||||
- ↓ in white matter attenuation less pronounced
|
||||
- Often wedge-shaped & localized to 1 arterial territory
|
||||
- Diffuse ischemic injury can lead to reversal sign with gray matter diffusely ↓ in attenuation relative to white matter
|
||||
- Insular ribbon sign → loss of distinct of insular cortex
|
||||
- Hyperdense MCA sign → ↑ density of acutely thrombosed MCA
|
||||
- Hemorrhagic transformation (HT)
|
||||
- Symptomatic HT in 3%; asymptomatic HT in 30%
|
||||
- Asymptomatic HT usually parenchymal
|
||||
- White matter or deep nuclear hemorrhage often mass-like → hematoma within infarcted tissue
|
||||
- #### CECT
|
||||
|
||||
|
||||
- Enhancement of infarcted territory typically occurs after 5-7 days
|
||||
- #### CTA
|
||||
|
||||
|
||||
- Invaluable for demonstrating focal vascular abnormalities in acute setting
|
||||
- CTA 1st line for rapid identification of large vessel occlusion amenable to catheter-directed thrombectomy
|
||||
- Intimal flap in acutely dissected vessel
|
||||
- ### MR Findings
|
||||
|
||||
|
||||
- **T1WI**:**** Acute: ↓ signal with gyral swelling
|
||||
- Chronic: ± ↑ signal in cortical laminar necrosis
|
||||
- **T1WI FS**: Allows identification of mural hematoma (↑ signal) in dissected vessel
|
||||
- **T2WI**: Loss of flow void in thrombosed vessel
|
||||
- **FLAIR**: ↑ signal with gyral swelling (within ~ 4-6 hours)
|
||||
- Abnormal sulcal ↑ signal (climbing ivy sign) of chronic, slow-flow collaterals in setting of longstanding proximal vascular occlusion
|
||||
- **DWI**: Most sensitive for early detection of ischemia
|
||||
- Acute: Restricted diffusion (↑ DWI, ↓ ADC signal) ≤ 30 minutes after ischemic insult
|
||||
- Subacute (7-14 days): Pseudonormalization of signal
|
||||
- ↑ DWI, ADC ~ brain parenchyma
|
||||
- Chronic: Facilitated diffusion in gliotic brain
|
||||
- ↑/~ DWI, ↑ ADC
|
||||
- **SWI/T2* GRE**: May see ↑ size & number of cortical vessels****
|
||||
- ↑ extraction fraction & possibly recoverable brain
|
||||
- **T1WI C+**: Cortical & leptomeningeal enhancement seen after ~5-7 days following acute infarct
|
||||
- Enhancing climbing ivy sign
|
||||
- **MRA**: Can detect arterial occlusion & stenosis in large- & medium-sized cerebral vessels
|
||||
- Look for underlying dissection or arteriopathy
|
||||
- **PWI**: Provides valuable information about affected brain
|
||||
- Ischemic penumbra: ↓ perfusion, no DWI change (PWI-DWI mismatch)
|
||||
- May define brain salvageable with acute stroke therapy
|
||||
- Arterial spin labeling can provide useful perfusion information without contrast administration
|
||||
- **MRS**: ↑ lactate hallmark of ischemia/infarct
|
||||
- Not specific
|
||||
- **Vessel wall imaging**: Vessel wall enhancement patterns improve discrimination of underlying stroke etiology
|
||||
- ### Ultrasonographic Findings
|
||||
|
||||
|
||||
- #### Grayscale ultrasound
|
||||
|
||||
|
||||
- Affected territory hyperechoic in acute/subacute stage
|
||||
- #### Color Doppler
|
||||
|
||||
|
||||
- Direct Doppler evaluation ideal for surveillance of vascular occlusion in neonate with open sutures
|
||||
- Transcranial Doppler evaluation of circle of Willis through temporal squamosa
|
||||
- ↑ velocities can predict stenoses detectable by MRA
|
||||
- Used as screening tool in children with sickle cell anemia
|
||||
- ### Angiographic Findings
|
||||
|
||||
|
||||
- Catheter angiography rarely necessary in acute evaluation of childhood stroke
|
||||
- Justified if contemplating endovascular therapy
|
||||
- Best modality for detailed evaluation of primary arteriopathies
|
||||
- ### Nuclear Medicine Findings
|
||||
|
||||
|
||||
- PET & SPECT techniques can be used to
|
||||
- Identify salvageable regions at risk (ischemic penumbra)
|
||||
- Demonstrate effects of synangiosis surgery in moyamoya-type vasculopathies
|
||||
- ### Imaging Recommendations
|
||||
|
||||
|
||||
- #### Best imaging tool
|
||||
|
||||
|
||||
- CT initial imaging test for signs/symptoms of stroke; excellent for excluding hemorrhagic stroke (more common in children vs. adults)
|
||||
- MR with DWI, MRA, PWI
|
||||
- #### Protocol advice
|
||||
|
||||
|
||||
- Contrast can help in assessing timing of injury & performing perfusion imaging
|
||||
- Dedicated vessel wall MR imaging to define underlying etiology [e.g. focal cerebral arteriopathy (FCA)]
|
||||
|
||||
## DIFFERENTIAL DIAGNOSIS
|
||||
|
||||
- ### Seizure-Related Injury
|
||||
|
||||
|
||||
- Swelling & restricted diffusion secondary to persistent seizure activity
|
||||
- Differentiation by clinical presentation & EEG
|
||||
- [Acute Encephalitis](/document/acute-encephalitis/a45f63bb-c25b-481d-a001-9c520c58060b)
|
||||
- Acute parenchymal inflammation secondary to infectious agents, typically viral
|
||||
- Slower onset with encephalopathy
|
||||
- [Mitochondrial Encephalopathies](/document/mitochondrial-encephalopathies/88524348-177d-4b8f-8029-5d065a2349f0)
|
||||
- Symmetric basal ganglia involvement common
|
||||
- Usually have manifestations beyond CNS
|
||||
- [Posterior Reversible Encephalopathy Syndrome (PRES)](/document/posterior-reversible-encephalopath-/84176f2c-fc9d-4497-8af9-1430b9f0187c)
|
||||
- Patchy cortical/subcortical edema most common in parietal & occipital lobes, typically in setting of hypertension
|
||||
- Diffusion restriction uncommon
|
||||
- [Neonatal Herpes Encephalitis](/document/herpes-encephalitis/1a126429-d4c6-4bbf-9181-1a6e0093e5f9)
|
||||
- Infant with seizures 2-5 weeks after birth
|
||||
- DWI most sensitive for detection in early disease
|
||||
- Often bilateral with temporal predominance but can occur anywhere
|
||||
- ### MELAS
|
||||
|
||||
|
||||
- **M**itochondrial **e**ncephomyopathy, **l**actic acidosis, **s**troke-like episodes
|
||||
- Areas of ischemia crossing arterial territories, often parietal
|
||||
- MRS: ↑ lactate in normal-appearing brain
|
||||
- [Group B Strep Meningitis](/document/group-b-streptococcal-meningitis/8656e127-afc7-4bca-82dc-589d0a9b5093)
|
||||
- Associated vasculitis causes ischemia in small perforating arteries
|
||||
- Unilateral or bilateral deep gray nuclei ischemia
|
||||
|
||||
## PATHOLOGY
|
||||
|
||||
- ### General Features
|
||||
|
||||
|
||||
- Cardiac disease (~ 25%)
|
||||
- Congenital heart disease, valvular heart disease, arrhythmias, & cardiomyopathies
|
||||
- Moyamoya-type arteriopathy
|
||||
- Sickle cell disease, neurofibromatosis type 1, radiation therapy, trisomy 21, Alagille syndrome
|
||||
- Arterial dissection (e.g., trauma)
|
||||
- FCA of childhood
|
||||
- Reversible cerebral vasoconstriction syndrome (RCVS)
|
||||
- Hematologic/metabolic (e.g., coagulopathy)
|
||||
- Hereditary Vasculopathies
|
||||
- *COL4A1*/*A2*mutations: Small vessel ischemia/infarct, microhemorrhages, porencephaly, epilepsy
|
||||
- *ACTA2*-associated disorders: Arg179His & Arg179Cys mutations in *ACTA2*gene
|
||||
- Straight, dilated proximal ICAs, occlusive disease of terminal ICAs, absent basal moyamoya collaterals
|
||||
- Hypoplasia & bending of anterior corpus callosum
|
||||
- V-shaped anterior corpus callosum on axial MR
|
||||
- Deficient anterior cingulate gyrus & abnormal radial gyration of frontal lobes
|
||||
- Horizontal thick fornix, perisylvian & frontal dysgyria
|
||||
- Twin peaks pons: Flattening of midline pons with ↓AP diameter & midline basilar artery impression
|
||||
- Multiple indentations on parasagittal surface of pons probably from straightened pontine arterial branches
|
||||
- Apparent squeezing of cerebral peduncles
|
||||
- Idiopathic (~ 25%)
|
||||
|
||||
## CLINICAL ISSUES
|
||||
|
||||
- ### Presentation
|
||||
|
||||
|
||||
- #### Most common signs/symptoms
|
||||
|
||||
|
||||
- Depends on patient age, etiology, & involved artery
|
||||
- < 1 year: Seizures, encephalopathy > focal neurologic
|
||||
- > 1 year: Usually focal neurologic (e.g., hemiplegia, early hand preference)
|
||||
- Speech difficulties, gait abnormality, seizure
|
||||
- Seizure → deficit often attributed to postictal state (Jacksonian paralysis)
|
||||
- Embolic cause: Sudden onset of symptoms
|
||||
- Stenoocclusive cause: Gradual/intermittent (e.g., TIA)
|
||||
- Focal deficit may be masked by lethargy, coma, irritability
|
||||
- Children typically present later than adults (> 24 hours)
|
||||
- Poor recognition/understanding of symptoms by child, caregiver, physician
|
||||
- Uncommon diagnosis in children, requires high degree of suspicion
|
||||
- ### Demographics
|
||||
|
||||
|
||||
- #### Age
|
||||
|
||||
|
||||
- Incidence/mortality greatest < 1 year
|
||||
- Large percentage occur in perinatal period
|
||||
- Perinatal arterial ischemic stroke (PAIS)
|
||||
- #### Epidemiology
|
||||
|
||||
|
||||
- Incidence: 2-3/100,000 per year in USA
|
||||
- Mortality: 0.6/100,000
|
||||
- Underrecognized as significant source of morbidity in pediatric population
|
||||
- ### Natural History & Prognosis
|
||||
|
||||
|
||||
- Capacity for recovery better than in adults, due to
|
||||
- Better compensatory mechanisms, collateral recruitment, neuronal plasticity
|
||||
- Fewer concomitant risk factors
|
||||
- ### Treatment
|
||||
|
||||
|
||||
- Clinical window of opportunity/benefit not as well understood in children as compared to adults
|
||||
- Mechanical thrombectomy frequently employed for acute large vessel occlusion
|
||||
- Mainstay of chronic therapy for fixed vascular lesions & vasculopathies: Aspirin
|
||||
- Transfusion therapy for at-risk children with sickle cell
|
||||
- Dissection: Anticoagulation, vessel occlusion, or stenting
|
||||
|
||||
## DIAGNOSTIC CHECKLIST
|
||||
|
||||
- ### Image Interpretation Pearls
|
||||
|
||||
|
||||
- Use same imaging signs as adults
|
||||
- Have low threshold for use of CTA
|
||||
- Vessel wall MR to identify underlying etiology
|
||||
|
||||
b4043ca8-e8d7-4e84-8dde-8de4e7f04908
|
||||
|
||||
## References
|
||||
|
||||
## Selected References
|
||||
|
||||
1. [Askarova AE et al: Hemorrhagic stroke in children. J Cent Nerv Syst Dis. 16:11795735241289913, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=39493255%5Bpmid%5D)
|
||||
1. [Sporns PB et al: Endovascular thrombectomy for childhood stroke (Save ChildS Pro): an international, multicentre, prospective registry study. Lancet Child Adolesc Health. 8(12):882-890, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=39401507%5Bpmid%5D)
|
||||
1. [Treves B et al: Can Hemorrhagic Stroke Genetics Help Forensic Diagnosis in Pediatric Age (<5 Years Old)? Genes (Basel). 15(5), 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=38790247%5Bpmid%5D)
|
||||
1. [Jiang B et al: Neuroimaging in pediatric stroke. Semin Pediatr Neurol. 43:100989, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=36344022%5Bpmid%5D)
|
||||
1. [Subramanian S et al: ACTA2-Related Dysgyria: An Under-Recognized Malformation of Cortical Development. AJNR Am J Neuroradiol. 43(1):146-150, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=34857515%5Bpmid%5D)
|
||||
1. [Chabrier S et al: Hyperacute recanalization strategies and childhood stroke in the evidence age. Stroke. 52(1):381-4, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=33349018%5Bpmid%5D)
|
||||
1. [Oesch G et al: Focal cerebral arteriopathy of childhood: clinical and imaging correlates. Stroke. 52(7):2258-65, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=34039030%5Bpmid%5D)
|
||||
1. [Visser MJ et al: Automated perfusion-diffusion magnetic resonance imaging in childhood arterial ischemic stroke. Stroke. 52(10):3296-304, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=34404238%5Bpmid%5D)
|
||||
1. [Fearn ND et al: Focal cerebral arteriopathy and childhood stroke. Curr Opin Neurol. 33(1):37-46, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31815778%5Bpmid%5D)
|
||||
1. [Donahue MJ et al: Neuroimaging advances in pediatric stroke. Stroke. 50(2):240-8, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30661496%5Bpmid%5D)
|
||||
1. [D'Arco F et al: Expanding the Distinctive Neuroimaging Phenotype of ACTA2 Mutations. AJNR Am J Neuroradiol. 39(11):2126-2131, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30262641%5Bpmid%5D)
|
||||
1. [Dlamini N et al: Arterial wall imaging in pediatric stroke. Stroke. 49(4):891-8, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29581340%5Bpmid%5D)
|
||||
1. [Khalaf A et al: Pediatric stroke imaging. Pediatr Neurol. 86:5-18, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30122281%5Bpmid%5D)
|
||||
1. [Zagaglia S et al: Neurologic phenotypes associated with COL4A1/2 mutations: expanding the spectrum of disease. Neurology. 91(22):e2078-88, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30413629%5Bpmid%5D)
|
||||
1. [Beslow LA: Stroke Diagnosis in the pediatric emergency department: an ongoing challenge. Stroke. 48(5):1132-33, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28336680%5Bpmid%5D)
|
||||
1. [Satti S et al: Mechanical thrombectomy for pediatric acute ischemic stroke: review of the literature. J Neurointerv Surg. 9(8):732-7, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=27448827%5Bpmid%5D)
|
||||
1. [Wilson JL et al: Endovascular therapy in pediatric stroke: utilization, patient characteristics, and outcomes. Pediatr Neurol. 69:87-92.e2, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28233666%5Bpmid%5D)
|
||||
1. [Madaelil TP et al: Mechanical thrombectomy in pediatric acute ischemic stroke: clinical outcomes and literature review. Interv Neuroradiol. 22(4):426-31, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=26945589%5Bpmid%5D)
|
||||
1. [Polan RM et al: Susceptibility-weighted imaging in pediatric arterial ischemic stroke: a valuable alternative for the noninvasive evaluation of altered cerebral hemodynamics. AJNR Am J Neuroradiol. 36(4):783-8, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25477354%5Bpmid%5D)
|
||||
1. [Bernard TJ et al: Emergence of the primary pediatric stroke center: impact of the thrombolysis in pediatric stroke trial. Stroke. 45(7):2018-23, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24916908%5Bpmid%5D)
|
||||
1. [Gemmete JJ et al: Arterial ischemic stroke in children. Neuroimaging Clin N Am. 23(4):781-98, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=24156865%5Bpmid%5D)
|
||||
1. [Freundlich CL et al: Pediatric stroke. Emerg Med Clin North Am. 30(3):805-28, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22974650%5Bpmid%5D)
|
||||
1. [Kitchen L et al: The pediatric stroke outcome measure: a validation and reliability study. Stroke. 43(6):1602-8, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22474056%5Bpmid%5D)
|
||||
1. [Beslow LA et al: Hemorrhagic transformation of childhood arterial ischemic stroke. Stroke. 42(4):941-6, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21350202%5Bpmid%5D)
|
||||
1. [Cárdenas JF et al: Pediatric stroke. Childs Nerv Syst. 27(9):1375-90, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21336993%5Bpmid%5D)
|
||||
1. [Dowling MM et al: Intracardiac shunting and stroke in children: a systematic review. J Child Neurol. 26(1):72-82, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21212453%5Bpmid%5D)
|
||||
1. [Lanni G et al: Pediatric stroke: clinical findings and radiological approach. Stroke Res Treat. 2011:172168, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21603166%5Bpmid%5D)
|
||||
1. [Larrue V et al: Etiologic investigation of ischemic stroke in young adults. Neurology. 76(23):1983-8, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21646623%5Bpmid%5D)
|
||||
1. [Munot P et al: Characteristics of childhood arterial ischemic stroke with normal MR angiography. Stroke. 42(2):504-6, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21193747%5Bpmid%5D)
|
||||
1. [Sedney CL et al: Cervical abnormalities causing vertebral artery dissection in children. J Neurosurg Pediatr. 7(3):272-5, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21361766%5Bpmid%5D)
|
||||
1. [Shellhaas RA et al: Mimics of childhood stroke: characteristics of a prospective cohort. Pediatrics. 118(2):704-9, 2006](http://www.ncbi.nlm.nih.gov/pubmed/?term=16882826%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
*Axial CTA MIP in a 14-year-old with right-sided weakness and history of congenital heart disease shows abrupt cutoff <img src='img/arrows/CS.png' alt='cyan solid arrow'/> of the M1 segment of the left middle cerebral artery (MCA). MIP imaging is particularly helpful to identify vessel occlusion in stroke. This patient was treated with catheter-directed thrombectomy.*
|
||||
|
||||
|
||||
*Axial CTA MIP in a 14-year-old with right-sided weakness and history of congenital heart disease shows abrupt cutoff <img src='img/arrows/CS.png' alt='cyan solid arrow'/> of the M1 segment of the left middle cerebral artery (MCA). MIP imaging is particularly helpful to identify vessel occlusion in stroke. This patient was treated with catheter-directed thrombectomy.*
|
||||
|
||||
|
||||
*Axial DWI in the same patient after thrombectomy shows restricted diffusion <img src='img/arrows/CS.png' alt='cyan solid arrow'/> in the left basal ganglia, consistent with acute infarction. Note preservation of the remainder of the left MCA territory.*
|
||||
|
||||
|
||||
*Axial time-of-flight MRA in a 2-year-old with multiple infarcts of various ages shows multiple small areas of flow-related signal <img src='img/arrows/CS.png' alt='cyan solid arrow'/> in the bilateral thalami, consistent with lenticulostriate collaterals of moyamoya.*
|
||||
|
||||
|
||||
*Axial DWI MR in the same patient with moyamoya-type vasculopathy shows diffusion restriction in the right frontoparietal foci of signal abnormality <img src='img/arrows/CS.png' alt='cyan solid arrow'/>, suggesting an acute/subacute infarct. However, there is no diffusion restriction in the left parietal region <img src='img/arrows/WO.png' alt='white open arrow'/>, suggesting this infarct is of an older age.*
|
||||
|
||||
|
||||
*Axial DWI MR in a 6-year-old with imbalance and acute infarct of the left basal ganglia <img src='img/arrows/CS.png' alt='cyan solid arrow'/> shows diffusion restriction (↓ ADC not shown). Acute infarct in a child should prompt further evaluation with MRA or CTA to detect an underlying vessel abnormality.*
|
||||
|
||||
|
||||
*3D MRA of the circle of Willis in the same patient shows irregular narrowing of the left proximal <img src='img/arrows/CS.png' alt='cyan solid arrow'/> and distal <img src='img/arrows/CO.png' alt='cyan open arrow'/> segments of the MCA, consistent with vasculitis.*
|
||||
|
||||
|
||||
*Axial DWI MR in a 12-year-old with reversible cerebral vasoconstriction syndrome (RCVS) who recently started mycophenolate and presented with acute onset of left-sided weakness shows multifocal cortical <img src='img/arrows/CS.png' alt='cyan solid arrow'/> and subcortical <img src='img/arrows/CO.png' alt='cyan open arrow'/> infarcts.*
|
||||
|
||||
|
||||
*Lateral projection DSA from an internal carotid artery (ICA) injection in the same patient shows multifocal areas of medium vessel narrowing <img src='img/arrows/CS.png' alt='cyan solid arrow'/> and irregularity <img src='img/arrows/CO.png' alt='cyan open arrow'/>, a common feature of RCVS. The spectrum of underlying etiologies for childhood stroke is diverse.*
|
||||
|
||||
|
||||
*Axial DWI MR in a 16-year-old boy involved in a motor vehicle accident shows multiple small foci of diffusion restriction <img src='img/arrows/CS.png' alt='cyan solid arrow'/>, consistent with small infarcts. Multiple infarcts should raise concern for dissection, especially when confined to a single arterial territory.*
|
||||
|
||||
|
||||
*Axial CTA in the same patient shows vessel wall irregularity and an intimal flap in the left ICA <img src='img/arrows/WS.png' alt='white solid arrow'/>. The right ICA <img src='img/arrows/CS.png' alt='cyan solid arrow'/> is small and revealed areas of irregularity on other images (not shown). These findings are consistent with bilateral ICA dissections.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
*Axial NECT in a 15-year-old girl with dilated cardiomyopathy shows a large area of low attenuation in the right MCA territory <img src='img/arrows/CS.png' alt='cyan solid arrow'/>. Note the sulcal effacement and loss of gray matter-white matter differentiation.*
|
||||
|
||||
|
||||
*Axial DWI MR in the same patient confirms restricted diffusion in the right MCA territory <img src='img/arrows/CS.png' alt='cyan solid arrow'/>. Also note the focus of restricted diffusion in the left periventricular region <img src='img/arrows/WO.png' alt='white open arrow'/>. Multiple infarcts in multiple vascular territories should raise suspicion of a proximal embolic source.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR in a 1-year-old with arteriopathy and subacute infarction shows gyriform enhancement of the cortical ribbon. Enhancement is common in the subacute phase of infarction. Precontrast T1 is necessary to distinguish true enhancement from the intrinsic ↑ T1 seen in cortical laminar necrosis.*
|
||||
|
||||
|
||||
*Axial ADC map in the same patient shows modestly ↓ ADC <img src='img/arrows/CO.png' alt='cyan open arrow'/> within the affected cortex but resolution of acute gyral swelling, as evidenced by prominent sulci <img src='img/arrows/CS.png' alt='cyan solid arrow'/>, suggesting the infarct is in the subacute phase.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR in a 2-year-old girl shows cortical enhancement <img src='img/arrows/CS.png' alt='cyan solid arrow'/> in the region of a right frontoparietal infarct, suggesting that it is at least a week old.*
|
||||
|
||||
|
||||
*Axial time-of-flight MRA in a 2-year old with multiple infarcts of various ages shows multiple tiny foci of flow-related signal in the bilateral thalami <img src='img/arrows/CS.png' alt='cyan solid arrow'/>. This appearance is consistent with lenticulostriate collaterals of moyamoya-type vasculopathy in the setting of bilateral carotid terminus occlusions.*
|
||||
|
||||
|
||||
*Axial T2 MR in a high school football player who developed vomiting, confusion, and vertigo during a game shows gyral swelling and hyperintense signal in the medial temporal lobe <img src='img/arrows/WS.png' alt='white solid arrow'/>, which is in the vascular territory of the left posterior cerebral artery (PCA). Intracranial MRA acquired at the same time showed a small embolus in the left PCA.*
|
||||
|
||||
|
||||
*Axial CTA of the cervical arteries in the same patient shows a subtle linear filling defect <img src='img/arrows/WS.png' alt='white solid arrow'/> consistent with an intimal flap in the left vertebral artery.*
|
||||
|
||||
|
||||
*Axial NECT in a 2-day-old with congenital heart disease and seizures shows a well-defined, wedge-shaped region of ↓ attenuation <img src='img/arrows/WS.png' alt='white solid arrow'/> corresponding to the left MCA vascular territory, consistent with an acute/subacute arterial ischemic stroke.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR in an 8-year-old with a history of neurofibromatosis type 1 and known bilateral carotid terminus occlusions (resulting in a moyamoya-type vasculopathy pattern) shows abnormal sulcal enhancement (climbing ivy sign) <img src='img/arrows/CS.png' alt='cyan solid arrow'/> due to arterial collaterals distal to a proximal occlusion.*
|
||||
|
||||
|
||||
*Note the segment <img src='img/arrows/WO.png' alt='white open arrow'/> of the insular cortical ribbon that is no longer visible on this axial NECT in a 9-year-old with acute right hemiparesis. This subtle finding may be the 1st indicator of an acute stroke.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR shows the typical climbing ivy pattern of arterial collateral enhancement <img src='img/arrows/CS.png' alt='cyan solid arrow'/> in distal territories caused by proximal occlusion from a moyamoya-type vasculopathy. Note the white matter infarct on the left <img src='img/arrows/WS.png' alt='white solid arrow'/>.*
|
||||
|
||||
|
||||
*Axial DWI MR shows an acute infarct on the right <img src='img/arrows/WS.png' alt='white solid arrow'/> with T2 shine-through in an old left-sided stroke <img src='img/arrows/WO.png' alt='white open arrow'/>.*
|
||||
|
||||
|
||||
*Coronal T2 MR shows multiple areas of infarction <img src='img/arrows/WS.png' alt='white solid arrow'/> resulting from left hemisphere herniation. Secondary infarction from herniation can cause more morbidity than the initial insult.*
|
||||
|
||||
|
||||
*Axial DWI MR shows a characteristic "watershed" distribution of infarction in the right cerebral hemisphere. This infarct was the result of a carotid terminus stenosis that developed from bacterial meningitis and vasculitis.*
|
||||
|
||||
|
||||
*Axial NECT in a 14-year-old boy with acute right hemiparesis shows a hyperdense MCA sign <img src='img/arrows/WS.png' alt='white solid arrow'/>, indicating acute thrombus in a proximal MCA branch.*
|
||||
|
||||
|
||||
*Coronal FLAIR MR in the same patient shows edema in the insular cortex and frontal operculum supplied by the affected MCA branch <img src='img/arrows/WS.png' alt='white solid arrow'/>. The patient had complete recovery without direct treatment, and no etiology was found.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a 13-year-old girl with seizures after using ephedra shows foci of increased cortical and subcortical white matter signal in the right PCA and left superior cerebellar artery distributions <img src='img/arrows/WS.png' alt='white solid arrow'/>.*
|
||||
|
||||
|
||||
*Sagittal oblique volume-rendered MRA in the same patient shows multiple foci of arterial narrowing <img src='img/arrows/WS.png' alt='white solid arrow'/> and dilation <img src='img/arrows/WO.png' alt='white open arrow'/> due to a primary arteritis of the CNS.*
|
||||
|
||||
|
||||
*Axial CECT shows a subtle linear filling defect <img src='img/arrows/WC.png' alt='white curved arrow'/> in the left ICA of a child presenting with a left hemisphere infarct after mandibular surgery. The defect represents an arterial dissection.*
|
||||
|
||||
|
||||
*Axial T2 MR shows predominately cortical/subcortical swelling and abnormal signal <img src='img/arrows/WS.png' alt='white solid arrow'/> of the left parietal lobe, typical of a subacute left MCA territory infarct. Approximately 1/3 of childhood strokes will not have an underlying etiology diagnosed.*
|
||||
|
||||
|
||||
*Axial DWI MR in a 17-year-old girl shows a geographic area of diffusion restriction <img src='img/arrows/CS.png' alt='cyan solid arrow'/> in the right insular region, consistent with an infarct. Work-up revealed a hypercoagulable state (antiphospholipid antibody).*
|
||||
|
||||
|
||||
*Axial ADC map in a 17-year-old girl shows a geographic area of diffusion restriction <img src='img/arrows/CS.png' alt='cyan solid arrow'/> in the right insular region, consistent with an infarct. Work-up revealed a hypercoagulable state (antiphospholipid antibody).*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a 2-year-old girl shows multiple areas of cytotoxic edema <img src='img/arrows/CS.png' alt='cyan solid arrow'/> in both cerebral hemispheres in this patient with moyamoya-type vasculopathy.*
|
||||
|
||||
|
||||
*Axial T2WI MR shows a small periventricular infarct <img src='img/arrows/WS.png' alt='white solid arrow'/> in a 6-month-old. MRA revealed left carotid aneurysm. Proximal arterial pathology should always be investigated at presentation.*
|
||||
|
||||
@@ -0,0 +1,480 @@
|
||||
---
|
||||
title: "Chronic Cerebral Infarction"
|
||||
docid: "e318c9c0-0ba3-4966-8101-d24ac7ccc9b0"
|
||||
authors:
|
||||
- key: "a25c450b-3d34-4f64-bba3-cc0834813df6"
|
||||
value: "Miral D. Jhaveri, MD, MBA"
|
||||
- key: "5cff4116-3654-4b3a-bb75-5ebe0b8c9850"
|
||||
value: "Anne G. Osborn, MD, FACR"
|
||||
breadcrumbs:
|
||||
-
|
||||
name: "Brain"
|
||||
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|
||||
treeNodeId: "0361042c-9c90-48e4-864e-a2e6428ee9c9"
|
||||
-
|
||||
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|
||||
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|
||||
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|
||||
-
|
||||
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|
||||
slug: "pathology-based-diagnoses"
|
||||
treeNodeId: "d60fe914-7897-46a0-9cd2-f88ffb322f16"
|
||||
-
|
||||
name: "Stroke"
|
||||
slug: "stroke"
|
||||
treeNodeId: "7a135176-0a69-4fc9-b200-59569fbf5166"
|
||||
-
|
||||
name: "Cerebral Ischemia and Infarction"
|
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slug: "cerebral-ischemia-and-infarction"
|
||||
treeNodeId: "11d50e7d-f3e9-4071-b2b7-26b11ab40ea6"
|
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-
|
||||
name: "Chronic Cerebral Infarction"
|
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slug: "chronic-cerebral-infarction"
|
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treeNodeId: null
|
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category: "Brain"
|
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cmeTopicId: "cb7f2010-e24d-4f18-b265-6a9c7f37e858"
|
||||
documentVersionId: "c0049c96-3499-4457-8ee1-d93bc5202a4f"
|
||||
imageCount: 25
|
||||
lastUpdated: "10/02/25"
|
||||
pageDescription: "Chronic Cerebral Infarction"
|
||||
pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Stroke, Cerebral Ischemia and Infarction, Chronic Cerebral Infarction"
|
||||
pageTitle: "Chronic Cerebral Infarction | STATdx"
|
||||
enhancedTitle: "Chronic Cerebral Infarction"
|
||||
type: "DX"
|
||||
references: true
|
||||
ddx: true
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||||
cases: 2
|
||||
breadcrumbs:
|
||||
- "Brain"
|
||||
- "Diagnosis"
|
||||
- "Pathology-Based Diagnoses"
|
||||
- "Stroke"
|
||||
- "Cerebral Ischemia and Infarction"
|
||||
- "Chronic Cerebral Infarction"
|
||||
---
|
||||
## KEY FACTS
|
||||
|
||||
- ### Imaging
|
||||
|
||||
|
||||
- Cerebral infarction (CI): Volume loss with gliosis along affected margins
|
||||
- Classic: Wedge-shaped area of encephalomalacia
|
||||
- Territorial infarction
|
||||
- Involves brain supplied by major cerebral artery
|
||||
- Watershed infarction
|
||||
- Involves brain between main vascular territories
|
||||
- Lacunar infarction(s)
|
||||
- Most common in basal ganglia/thalami, deep white matter
|
||||
- ### Top Differential Diagnoses
|
||||
|
||||
|
||||
- Porencephalic cyst
|
||||
- Arachnoid cyst
|
||||
- Postsurgical/posttraumatic encephalomalacia
|
||||
- Low-attenuating tumors
|
||||
- ### Pathology
|
||||
|
||||
|
||||
- Volume loss, gliosis are pathological hallmarks
|
||||
- ### Clinical Issues
|
||||
|
||||
|
||||
- Older adult patients with typical risk factors
|
||||
- Focal neurologic deficit
|
||||
- Varies depending on size, location of CI
|
||||
- Stroke severity most consistent predictor of 30-day mortality after stroke
|
||||
- Lacunar stroke most common stroke subtype associated with vascular dementia
|
||||
- ### Diagnostic Checklist
|
||||
|
||||
|
||||
- Evaluate for associated acute infarcts in same or different vascular territory
|
||||
- Evaluate for underlying cause
|
||||
- CTA/MRA of extra-/intracranial vasculature
|
||||
- If negative, consider cardiac source
|
||||
- Evaluate for risk factors
|
||||
|
||||
## TERMINOLOGY
|
||||
|
||||
- ### Abbreviations
|
||||
|
||||
|
||||
- Cerebral infarction (CI)
|
||||
- ### Synonyms
|
||||
|
||||
|
||||
- Old ischemic stroke
|
||||
- Postinfarction encephalomalacia
|
||||
- ### Definitions
|
||||
|
||||
|
||||
- End result of prolonged cerebral ischemia
|
||||
|
||||
## IMAGING
|
||||
|
||||
- ### General Features
|
||||
|
||||
|
||||
- #### Best diagnostic clue
|
||||
|
||||
|
||||
- Volume loss with gliosis along affected margins
|
||||
- #### Location
|
||||
|
||||
|
||||
- Cerebral hemispheres, brainstem, cerebellum
|
||||
- **Territorial infarction**
|
||||
- Involves brain tissue supplied by major cerebral artery
|
||||
- Common sites
|
||||
- Supratentorial: Middle cerebral artery (MCA), anterior cerebral artery (ACA), posterior cerebral artery (PCA) distribution
|
||||
- Infratentorial: Basilar artery (BA), posterior inferior cerebellar artery (PICA) distribution
|
||||
- **Watershed (border zone) infarction** involves brain tissue between main vascular territories
|
||||
- Involves brain tissue between main vascular territories
|
||||
- **Lacunar infarctions**
|
||||
- Small infarcts in deep, penetrating artery distributions
|
||||
- Typically located in basal ganglia/thalami, white matter (WM)
|
||||
- #### Size
|
||||
|
||||
|
||||
- Extremely variable
|
||||
- Ranging from focal ("lacunes") to lobar or global (hemispheric)
|
||||
- #### Morphology
|
||||
|
||||
|
||||
- Extremely variable depending on location, size, etiology of vascular insult
|
||||
- Classic: Wedge-shaped area of encephalomalacia
|
||||
- Involves full-thickness of cortex, underlying WM
|
||||
- ### CT Findings
|
||||
|
||||
|
||||
- #### NECT
|
||||
|
||||
|
||||
- Focal, well-delineated, low-attenuation areas in affected vascular distribution
|
||||
- Adjacent sulci become prominent; ipsilateral ventricle enlarges
|
||||
- Wallerian degeneration may be present
|
||||
- Dystrophic Ca⁺⁺ may rarely occur in infarcted brain
|
||||
- Hyperdense cortical mineralization may be seen
|
||||
- #### CECT
|
||||
|
||||
|
||||
- No enhancement
|
||||
- #### CTA
|
||||
|
||||
|
||||
- May see lack of flow in affected vessel distribution
|
||||
- ### MR Findings
|
||||
|
||||
|
||||
- #### T1WI
|
||||
|
||||
|
||||
- Isointense to CSF in affected areas
|
||||
- High cortical T1 signal if cortical necrosis
|
||||
- Volume loss
|
||||
- Adjacent sulci become prominent
|
||||
- Ipsilateral ventricle enlarges
|
||||
- Wallerian degeneration may be present
|
||||
- Distribution of wallerian degeneration depends on primary region of injury
|
||||
- MCA infarct: Corticospinal tracts
|
||||
- Pontine infarct: Bilateral middle cerebellar peduncles
|
||||
- #### T2WI
|
||||
|
||||
|
||||
- Isointense to CSF in affected areas
|
||||
- Borders of infarction may show ↑ signal secondary to gliosis/spongiosis
|
||||
- Differentiation of subacute from chronic infarction on standard SE/FSE sequences may be difficult due to prolonged relaxation times in both
|
||||
- #### FLAIR
|
||||
|
||||
|
||||
- Low signal in encephalomalacic area
|
||||
- Hyperintense gliotic WM at margins
|
||||
- #### T2* GRE
|
||||
|
||||
|
||||
- May see hemosiderin staining in gliotic areas or along borders of infarction
|
||||
- May see cortical hemosiderin staining
|
||||
- #### DWI
|
||||
|
||||
|
||||
- No restriction
|
||||
- ↑ diffusivity (↑ signal on ADC)
|
||||
- Rare chronic infarcts with persistent high signal on diffusion
|
||||
- #### T1WI C+
|
||||
|
||||
|
||||
- No enhancement
|
||||
- #### MRA
|
||||
|
||||
|
||||
- May see lack of flow in affected vessel
|
||||
- #### MRS
|
||||
|
||||
|
||||
- Shows loss of NAA peak in affected area
|
||||
- ### Angiographic Findings
|
||||
|
||||
|
||||
- Conventional
|
||||
- May see lack of flow in affected vessel and its vascular territory
|
||||
- ### Imaging Recommendations
|
||||
|
||||
|
||||
- #### Best imaging tool
|
||||
|
||||
|
||||
- CT or MR
|
||||
- #### Protocol advice
|
||||
|
||||
|
||||
- No contrast necessary if imaging typical (i.e., lack of mass effect or volume loss)
|
||||
- Include T2* sequence (GRE, SWI) to evaluate for hemorrhage
|
||||
|
||||
## DIFFERENTIAL DIAGNOSIS
|
||||
|
||||
- [Porencephalic Cyst](/document/porencephalic-cyst/132b5c61-f762-46ad-853c-615f4117d010)
|
||||
- Congenital cyst typically seen in younger age groups
|
||||
- Thought to occur from focal encephalomalacia due to localized cerebral insult
|
||||
- Lined by gliotic WM
|
||||
- [Arachnoid Cyst](/document/arachnoid-cyst/8a848a6c-ad10-4533-b48c-3e9969cee55c)
|
||||
- No gliotic margins
|
||||
- Usually in locations atypical for vascular territory
|
||||
- Intact gray matter lining brain, displaced by cyst
|
||||
- ### Postoperative/Posttraumatic Encephalomalacia
|
||||
|
||||
|
||||
- History and associated findings help to distinguish
|
||||
- May see leptomeningeal cyst in posttraumatic setting
|
||||
- [Low-Attenuation Tumors](/document/oligodendroglioma-idh-mutant-and-1-/650c343e-cca8-484f-a93c-3961b57a30c4)
|
||||
- Typically shows mass effect
|
||||
- Usually slightly hyperdense/hyperintense compared to CSF
|
||||
|
||||
## PATHOLOGY
|
||||
|
||||
- ### General Features
|
||||
|
||||
|
||||
- #### Etiology
|
||||
|
||||
|
||||
- Prolonged cerebral ischemia
|
||||
- Duration and severity of ischemic insult determines cellular viability
|
||||
- Results of CI vary with sensitivity of individual cell types to ischemia
|
||||
- Other factors include adequacy of collateral blood supply and degree, duration, and distribution of flow reduction
|
||||
- Most CI caused by territorial, watershed, lacunar infarcts
|
||||
- Less commonly result of infectious/inflammatory etiologies
|
||||
- Sequelae of meningitis (bacterial, mycobacterial, etc.)
|
||||
- Vasculopathy, angiitis, etc.
|
||||
- Rare
|
||||
- Unilateral descending tentorial herniation
|
||||
- May cause secondary ischemic infarction of occipital lobe
|
||||
- #### Genetics
|
||||
|
||||
|
||||
- Hypercholesterolemia, diabetes, hypertension, homocysteine ↑ stroke risk
|
||||
- ### Gross Pathologic & Surgical Features
|
||||
|
||||
|
||||
- Volume loss and gliosis pathological hallmarks
|
||||
- Liquefaction resulting in cyst formation
|
||||
- Cystic areas traversed by trabeculations of blood vessels, surrounded by firm glial tissue
|
||||
- Typically in main vascular territories or watershed (border zone) distribution depending on etiology
|
||||
- ### Microscopic Features
|
||||
|
||||
|
||||
- Fibrillary gliosis along margin of infarction
|
||||
- Macrophages may persist in interstices of infarcts; some may contain hemosiderin
|
||||
|
||||
## CLINICAL ISSUES
|
||||
|
||||
- ### Presentation
|
||||
|
||||
|
||||
- #### Most common signs/symptoms
|
||||
|
||||
|
||||
- Focal neurologic deficit with history of acute onset
|
||||
- #### Clinical profile
|
||||
|
||||
|
||||
- Older adult with typical risk factors
|
||||
- Hypertension, diabetes, smoking history, obesity, hypercholesterolemia, etc.
|
||||
- ### Demographics
|
||||
|
||||
|
||||
- #### Age
|
||||
|
||||
|
||||
- Usually > 55 years
|
||||
- #### Sex
|
||||
|
||||
|
||||
- Women typically older than men
|
||||
- Female patients often more disabled after age adjustment
|
||||
- Fatality rates similar
|
||||
- #### Epidemiology
|
||||
|
||||
|
||||
- 2nd or 3rd leading cause of death in Western world (after noncerebral cardiovascular disease and cancer)
|
||||
- Major cause of long-term disability
|
||||
- 1 in 5 with 1st stroke will survive to 10 years
|
||||
- Estimates in USA range from 760,000-780,000 annually; contributes to ~ 150,000 deaths/year
|
||||
- Estimated 5,800,000 stroke survivors in USA
|
||||
- ### Natural History & Prognosis
|
||||
|
||||
|
||||
- Varies greatly depending on size of CI and degree of neurologic deficit
|
||||
- Stroke severity most consistent predictor of 30-day mortality after stroke
|
||||
- Mortality rates in USA declined dramatically in 1970s and 1980s, but plateaued by 1990s
|
||||
- Stroke mortality in USA predicted to ↑ 3x as fast as general population over next 30 years
|
||||
- Lacunar stroke most common stroke subtype associated with vascular dementia
|
||||
- ### Treatment
|
||||
|
||||
|
||||
- Acute anticoagulation after 1st infarction associated with reduced mortality
|
||||
- To improve long-term survival after CI, aggressive management of pulmonary and cardiac disease critical
|
||||
|
||||
## DIAGNOSTIC CHECKLIST
|
||||
|
||||
- ### Consider
|
||||
|
||||
|
||||
- Could lesion be arachnoid cyst or porencephalic cyst?
|
||||
- ### Image Interpretation Pearls
|
||||
|
||||
|
||||
- Look for signs of volume loss in vascular territory
|
||||
- Evaluate for associated acute infarcts in same or different vascular territory
|
||||
- ### Reporting Tips
|
||||
|
||||
|
||||
- Evaluate for underlying cause
|
||||
- Multiple infarcts in different vascular territories
|
||||
- Suggests cardioembolic source or vasculitis
|
||||
- Bilateral watershed infarcts
|
||||
- Hypoperfusion event
|
||||
- Unilateral watershed infarct
|
||||
- Hypoperfusion event and ipsilateral carotid stenosis
|
||||
- Infarct in setting of trauma
|
||||
- Evaluate for dissection
|
||||
|
||||
43ed5712-d15f-492e-9738-cf38489e1ae1
|
||||
|
||||
## References
|
||||
|
||||
## Selected References
|
||||
|
||||
1. [Nguyen TN et al: Endovascular management of acute stroke. Lancet. 404(10459):1265-78, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=39341645%5Bpmid%5D)
|
||||
1. [Shafaat O et al: Stroke imaging. StatPearls, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=31536242%5Bpmid%5D)
|
||||
1. [Salerno A et al: Patterns of ischemic posterior circulation strokes: a clinical, anatomical, and radiological review. Int J Stroke. 17(7):714-22, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=34581223%5Bpmid%5D)
|
||||
1. [Zhao Y et al: Neuronal injuries in cerebral infarction and ischemic stroke: from mechanisms to treatment (Review). Int J Mol Med. 49(2), 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=34878154%5Bpmid%5D)
|
||||
1. [Ciacciarelli A et al: Chronic cerebral hypoperfusion: an undefined, relevant entity. J Clin Neurosci. 73:8-12, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31948882%5Bpmid%5D)
|
||||
1. [Finsterer J et al: Metabolic stroke or stroke-like lesion: peculiarities of a phenomenon. J Neurol Sci. 412:116726, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32088469%5Bpmid%5D)
|
||||
1. [Rabinstein AA: Update on treatment of acute ischemic stroke. Continuum (Minneap Minn). 26(2):268-86, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32224752%5Bpmid%5D)
|
||||
1. [Sagnier S et al: The new insights into human brain imaging after stroke. J Neurosci Res. 100(5):1171-81, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31498491%5Bpmid%5D)
|
||||
1. [Yusof NNM et al: Non-invasive imaging techniques for the differentiation of acute and chronic thrombosis. Thromb Res. 177:161-71, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30921535%5Bpmid%5D)
|
||||
1. [Lake EM et al: Functional magnetic resonance imaging in chronic ischaemic stroke. Philos Trans R Soc Lond B Biol Sci. 371(1705), 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=27574307%5Bpmid%5D)
|
||||
1. [Allen LM et al: Sequence-specific MR imaging findings that are useful in dating ischemic stroke. Radiographics. 32(5):1285-97; discussion 1297-9, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22977018%5Bpmid%5D)
|
||||
|
||||
## Differential diagnosis
|
||||
|
||||
### Abnormal Shape/Configuration of Corpus Callosum
|
||||
DDX:c75baee2-7a4c-4fd8-9b3f-cc662d0f1c18
|
||||
|
||||
### Abnormal Shape/Configuration of Corpus Callosum
|
||||
DDX:238ca32d-6bc6-4f5a-81b1-6601dd605856
|
||||
|
||||
### Signal/Attenuation Abnormalities of Corpus Callosum
|
||||
DDX:578bd09b-da74-43a2-b068-2d4854a61254
|
||||
|
||||
## Cases
|
||||
|
||||
- {'cases': [{'authors': [{'key': '8d5254e9-8dda-478b-8f08-bdee97a32c79', 'value': 'Karen L. Salzman, MD, FACR'}], 'caseVersionId': '927ea197-d168-4c22-bfd0-30f36f6beac6', 'description': 'Typical MR example of brainstem atrophy related to chronic basilar perforating artery infarcts.\r\n\r\nSagittal T1 MR (#1) shows volume loss in the inferior pons (arrow) related to a chronic infarct in a pontine perforator distribution. Axial T2 MR images (#2-4) show volume loss in the left inferior pons (curved arrow, #2), mid pons level (curved arrow, #3), and midbrain (curved arrow, #4) related to chronic ischemia in a pontine perforator distribution. Note that the chronic ischemia respects the midline (arrow, #2).\r\n\r\nComment: A focal infarct in the pons or pontomedullary junction is typically secondary to a pontine perforator or basilar branch artery occlusion. The pontine perforator vessels arise from the basilar artery. When an infarct involves the rostral brainstem and occipital lobes, it is typically caused by a distal basilar artery occlusion.', 'history': 'Patient with a history of dysarthria, ataxia, and "clumsy hand" syndrome.', 'imagePoolId': '979d098e-63f9-4a13-a433-323cd5a42994', 'name': 'Chronic brainstem infarcts', 'teachingPoint': None, 'demographics': '68 Years old male'}, {'authors': [{'key': '8d5254e9-8dda-478b-8f08-bdee97a32c79', 'value': 'Karen L. Salzman, MD, FACR'}], 'caseVersionId': 'be1b4983-0316-4a56-8d4d-40aa96108de5', 'description': 'Typical CT and MR case of a right cerebellar chronic cerebral infarction in the posterior inferior cerebellar artery (PICA) distribution.\n\nAxial NECT images (#1-2) show focal low attenuation in the right cerebellar hemisphere representing encephalomalacia (arrows) in the PICA vascular distribution.\n\nAxial T2 MR image (#3) shows hyperintensity in the right cerebellar hemisphere, isointense to CSF related to the chronic infarct (arrow). Note the lack of mass effect and the mild increase in the adjacent sulci compared to the contralateral hemisphere (curved arrow). Axial FLAIR MR image (#4) shows central hypointense encephalomalacia surrounded by a thin rim of hyperintense gliosis (open arrow), characteristic of chronic cerebral infarction. Mild prominence of the adjacent sulci related to the volume loss is noted (curved arrow). DWI MR images (#5-6) show increased diffusion, hypointensity (arrows) of the encephalomalacic brain, confirming the chronic nature of the ischemia. ADC map shows the area is hyperintense (arrow).', 'history': 'Patient with dizziness for years and new onset weakness.', 'imagePoolId': 'bc68fa28-082c-433a-a219-e34ebd916209', 'name': 'PICA vascular distribution', 'teachingPoint': None, 'demographics': '58 Years old male'}, {'authors': [{'key': '8d5254e9-8dda-478b-8f08-bdee97a32c79', 'value': 'Karen L. Salzman, MD, FACR'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '613392b1-b4a7-40b6-85a7-90edc4eb3356', 'description': 'Typical MR case of a left frontal middle cerebral artery (MCA) distribution chronic cerebral infarction.\n\nSagittal T1 MR image shows the chronic MCA infarct as an area of hypointensity in the frontal lobe that is isointense to CSF (arrow). Axial T2 MR image shows the focal chronic MCA ischemia as encephalomalacia surrounded by gliotic hyperintense borders (curved arrows). The adjacent sulci are prominent and there is enlargement of the ipsilateral lateral ventricle (open arrow) related to the volume loss.', 'history': None, 'imagePoolId': 'dca3590f-710e-4f16-b3b7-07de8d137c0a', 'name': 'MCA infarct', 'teachingPoint': None}], 'caseType': 'typical', 'name': 'TYPICAL'}
|
||||
- {'cases': [{'authors': [{'key': '8d5254e9-8dda-478b-8f08-bdee97a32c79', 'value': 'Karen L. Salzman, MD, FACR'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'e39826a6-3eb8-47c8-9dda-3535f6af80f2', 'description': 'Variant CT case of a chronic MCA infarction involving the temporal lobe with calcification.\n\nAxial NECT image shows a focal right temporal lobe infarct as a wedge-shaped area of low density encephalomalacic brain with low density margins (arrow) related to gliotic brain. The associated dystrophic calcification (curved arrow) is very rare. The ipsilateral ventricle is mildly enlarged related to the volume loss (open arrow).', 'history': None, 'imagePoolId': '71dd2ab0-ff54-4572-820c-5bc71e064e0f', 'name': 'Calcified, chronic MCA infarction', 'teachingPoint': None, 'demographics': '81 Years old male'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '67461228-7c92-4977-9c04-d74494d39978', 'description': 'Series of NECT scans (#1-4) shows encephalomalacic changes in both occipital lobes consistent with remote cerebral infarction. What is most interesting (and unusual) about this case is the gyriform calcifications in the cortex (arrows).', 'history': 'Patient had bilateral posterior cerebral artery infarcts one year prior to imaging.', 'imagePoolId': 'b5b26a5b-620e-47be-924d-bee2b65a5942', 'name': 'Calcified bilateral', 'teachingPoint': None, 'demographics': '39 Years old female'}, {'authors': [{'key': '8d5254e9-8dda-478b-8f08-bdee97a32c79', 'value': 'Karen L. Salzman, MD, FACR'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '402e7fe1-cad7-4f15-9319-9f93f2e3d0fa', 'description': 'Variant MR case of a left hemisphere chronic cerebral infarct with involvement of the left posterior (PCA), middle (MCA) and anterior cerebral artery (ACA) distributions.\n\nAxial and sagittal T1 MR images (#1-4) show extensive encephalomalacia in the left temporal, parietal and frontal lobes with surrounding gliotic brain related to chronic cerebral infarcts in the left PCA, MCA, and ACA vascular distributions. There is associated Wallerian degeneration with a decrease in the size of the left cerebral peduncle (arrow). There is relative sparing of the left basal ganglia and thalamus which are supplied by penetrating arteries (lenticulostriate arteries and thalamoperforators). There is involvement of the right ACA as well (open arrow). Axial and coronal T2 MR images (#5-7) show the chronic cerebral infarctions are isointense to CSF with abnormal hyperintensity in the surrounding gliotic brain (curved arrow). The volume loss results in compensatory enlargement of the left lateral ventricle (open arrow).', 'history': 'Patient with a history of a fetal origin posterior cerebral artery arising from the left internal carotid artery who suffered a left internal carotid artery occlusion.', 'imagePoolId': 'c9e705c1-3c99-4b47-b066-c9e498c8fd44', 'name': 'PCA, MCA and ACA vascular territories', 'teachingPoint': None}, {'authors': [{'key': '7cc3ba75-2642-4233-b9f6-0ce69ffe28f3', 'value': 'Sheri L. Harder, MD, FRCPC'}], 'caseVersionId': '311481fe-b9fe-4e60-9a69-94a19059342c', 'description': 'Variant subacute cerebral infarct case related to embolized hyperdense material in the left MCA in an IV drug abuser - ? talc.\n\nAxial NECT images (#1,2) demonstrate markedly hyperdense branching material in the left Sylvian fissure (white arrows) with some surrounding parenchymal hypodensity (black arrows) in the left MCA territory, in keeping with embolized foreign material at the left MCA bifurcation and an associated subacute infarct. Axial NECT (#3) at a higher level demonstrates a wedge-shaped hypodense region (arrow) with foci of increased density (curved arrow), corresponding to infarcted brain and thrombus within more peripheral MCA branches. Note the sulcal effacement. Axial CECT (#4,5) demonstrate the hyperdense filling defect at the MCA bifurcation (white arrows). Axial CECT (#6) demonstrates gyriform enhancement (open arrows) in the left MCA territory, a finding seen in subacute infarcts. Delayed axial NECT images (#7,8) reveal encephalomalacia in the left MCA territory (black arrows), in keeping with a remote infarct. Persistent hyperdensity is noted at the left MCA bifurcation in keeping with the previously noted embolic foreign material (white arrow).', 'history': 'IV drug abuser presents with decreased level of consciousness and endocarditis.', 'imagePoolId': '75b82c8e-8ee6-462f-8208-28e1b7e75c19', 'name': 'Foreign material embolus', 'teachingPoint': None, 'demographics': '23 Years old male'}], 'caseType': 'variant', 'name': 'VARIANT'}
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
*Graphic shows chronic infarct involving the posterior left middle cerebral artery (MCA) territory. Infarct is lined with gliotic white matter (WM). Small lacunar infarctions and atrophy are also depicted.*
|
||||
|
||||
|
||||
*Graphic shows chronic infarct involving the posterior left middle cerebral artery (MCA) territory. Infarct is lined with gliotic white matter (WM). Small lacunar infarctions and atrophy are also depicted.*
|
||||
|
||||
|
||||
*Gross pathology, sectioned through the midventricular level, shows a chronic left MCA infarct with encephalomalacia in the classic MCA vascular distribution <img src='img/arrows/BS.png' alt='black solid arrow'/>. Note the adjacent WM gliosis <img src='img/arrows/BO.png' alt='black open arrow'/> and the mild compensatory enlargement of the left lateral ventricle <img src='img/arrows/BC.png' alt='black curved arrow'/>. (Courtesy R. Hewlett, MD.)*
|
||||
|
||||
|
||||
*Axial NECT 2 days after large territorial infarction in the left MCA territory shows wedge-shaped hypodensity <img src='img/arrows/WS.png' alt='white solid arrow'/> involving cortex, WM, and basal ganglia. Moderate mass effect is present with subfalcine herniation of the lateral ventricles.*
|
||||
|
||||
|
||||
*Follow-up scan 2 months later shows findings of chronic infarct. The mass effect has resolved completely, and there is frank encephalomalacia in the left MCA territory <img src='img/arrows/WS.png' alt='white solid arrow'/>. The left lateral ventricle shows compensatory enlargement <img src='img/arrows/WO.png' alt='white open arrow'/>.*
|
||||
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||||
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||||
*Axial NECT in a patient presenting with acute right hemiparesis shows a large acute infarct <img src='img/arrows/CC.png' alt='cyan curved arrow'/> in the left MCA distribution. Note an area of cystic encephalomalacia <img src='img/arrows/CO.png' alt='cyan open arrow'/> in the right frontal region due to a chronic right MCA infarct.*
|
||||
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||||
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||||
*Axial FLAIR MR in the same patient shows the chronic right frontal infarct following CSF signal <img src='img/arrows/CO.png' alt='cyan open arrow'/> with surrounding gliosis <img src='img/arrows/CS.png' alt='cyan solid arrow'/> and volume loss. In contrast the acute left MCA infarct causes mass effect on the lateral ventricle <img src='img/arrows/CC.png' alt='cyan curved arrow'/> with effacement of the adjacent sulci.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a 75-year-old man shows the remote left MCA infarct <img src='img/arrows/CC.png' alt='cyan curved arrow'/> has mixed signal intensity in the encephalomalacic brain.*
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||||
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||||
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||||
*Axial T2* GRE MR shows residua of hemorrhagic transformation with hemosiderin staining in the caudate nucleus <img src='img/arrows/CO.png' alt='cyan open arrow'/> and parietal cortex <img src='img/arrows/CC.png' alt='cyan curved arrow'/>.*
|
||||
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||||
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||||
*Axial NECT in a 57-year-old woman with history of multiple remote strokes shows 2 wedge-shaped, CSF-like hypodensities <img src='img/arrows/CC.png' alt='cyan curved arrow'/> in the right posterior frontal and parietal lobes. Note the lesions involve both the cortex and subcortical WM.*
|
||||
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||||
|
||||
*Axial FLAIR MR in the same patient shows the CSF-like lesions exhibit complete suppression <img src='img/arrows/CC.png' alt='cyan curved arrow'/>. Adjacent hyperintensity <img src='img/arrows/CO.png' alt='cyan open arrow'/> represents gliotic WM. Classic chronic cortical infarcts in the right MCA distribution are shown.*
|
||||
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||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
*Gross pathology shows encephalomalacia from an old left MCA distribution infarction <img src='img/arrows/WS.png' alt='white solid arrow'/>. (Courtesy of R. Hewlett, MD.)*
|
||||
|
||||
|
||||
*Axial T1 MR in a patient with left hemisphere chronic cerebral infarct shows involvement of the left PCA, MCA, and ACA distributions. Volume loss results in compensatory enlargement of the left lateral ventricle <img src='img/arrows/WS.png' alt='white solid arrow'/>.*
|
||||
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||||
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||||
*Axial T1 MR in the same patient demonstrates wallerian degeneration with a decrease in the size of the left cerebral peduncle <img src='img/arrows/WC.png' alt='white curved arrow'/>.*
|
||||
|
||||
|
||||
*Axial NECT shows a large, chronic left MCA distribution infarct as a low-density encephalomalacic brain with ipsilateral ventricular enlargement.*
|
||||
|
||||
|
||||
*Axial T2 MR shows a small left MCA distribution infarction <img src='img/arrows/BO.png' alt='black open arrow'/>. The infarct is lined with gliotic WM. The left lateral ventricle is slightly dilated.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient demonstrates that gliotic WM is better appreciated with FLAIR weighting <img src='img/arrows/WS.png' alt='white solid arrow'/>, as seen in this image.*
|
||||
|
||||
|
||||
*Axial NECT shows a small chronic infarction involving the right ACA territory within the right superior frontal gyrus <img src='img/arrows/WO.png' alt='white open arrow'/>. Note the surrounding halo of gliosis <img src='img/arrows/WS.png' alt='white solid arrow'/>.*
|
||||
|
||||
|
||||
*Axial NECT shows a chronic-appearing right MCA territory infarction <img src='img/arrows/BS.png' alt='black solid arrow'/>. Note the low-attenuating gliotic margins <img src='img/arrows/WS.png' alt='white solid arrow'/>, distinguishing this from an arachnoid or porencephalic cyst.*
|
||||
|
||||
|
||||
*Axial NECT shows encephalomalacic changes in both occipital lobes, findings consistent with remote cerebral infarction. The gyriform calcifications in the cortex <img src='img/arrows/WS.png' alt='white solid arrow'/> are most interesting (and unusual) in this case.*
|
||||
|
||||
|
||||
*Axial NECT shows classic chronic right MCA infarct <img src='img/arrows/BS.png' alt='black solid arrow'/>. The encephalomalacic brain is low density and the ipsilateral right ventricle is enlarged.*
|
||||
|
||||
|
||||
*Axial T1 MR in the same patient shows the area of encephalomalacic brain <img src='img/arrows/BS.png' alt='black solid arrow'/> is the same signal intensity as CSF in the adjacent ventricle. Gliotic WM <img src='img/arrows/BO.png' alt='black open arrow'/> bordering the infarct is hypointense to normal WM.*
|
||||
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||||
|
||||
*Axial T2 MR in the same patient shows the chronic infarct is isointense with CSF, but the gliotic brain <img src='img/arrows/WO.png' alt='white open arrow'/> adjacent to the stroke is slightly less hyperintense.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient shows the cystic encephalomalacia caused by the stroke suppresses completely while the adjacent gliotic WM <img src='img/arrows/WO.png' alt='white open arrow'/> remains hyperintense.*
|
||||
|
||||
|
||||
*Gross pathology shows encephalomalacia <img src='img/arrows/BO.png' alt='black open arrow'/> from prior infarct in the anterior division of the left MCA. A smaller, more localized cortical infarct <img src='img/arrows/BC.png' alt='black curved arrow'/> is present in the posterior division of the MCA.*
|
||||
|
||||
|
||||
*Sagittal T1 MR in an 80-year-old man with history of remote stroke shows striking encephalomalacia from remote infarct in the MCA territory <img src='img/arrows/WS.png' alt='white solid arrow'/>.*
|
||||
|
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Reference in New Issue
Block a user