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||||
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||||
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|
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||||
---
|
||||
title: "Acute Cerebral Ischemia/Infarction"
|
||||
docid: "a405285f-aaea-43ca-8dc4-6f8120eaabc1"
|
||||
authors:
|
||||
- key: "5cff4116-3654-4b3a-bb75-5ebe0b8c9850"
|
||||
value: "Anne G. Osborn, MD, FACR"
|
||||
- key: "095c34cb-da44-4830-98c9-7e1a24bdda5b"
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value: "Edward P. Quigley, III, MD, PhD"
|
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breadcrumbs:
|
||||
-
|
||||
name: "Brain"
|
||||
slug: "brain"
|
||||
treeNodeId: "6d8829f1-14d7-45af-8675-255189aa526a"
|
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-
|
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name: "Diagnosis"
|
||||
slug: "diagnosis"
|
||||
treeNodeId: "51c00394-446e-4a38-94af-d3b1d14d34e8"
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name: "Pathology-Based Diagnoses"
|
||||
slug: "pathology-based-diagnoses"
|
||||
treeNodeId: "d9d3a8ed-f21b-4831-8c77-591a3500ef77"
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||||
-
|
||||
name: "Stroke"
|
||||
slug: "stroke"
|
||||
treeNodeId: "12307683-f1ff-4823-a7d3-b10b40f9fd82"
|
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|
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name: "Cerebral Ischemia and Infarction"
|
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slug: "cerebral-ischemia-and-infarction"
|
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treeNodeId: "51051846-a223-42f7-b626-2a5a26cf6c44"
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-
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name: "Acute Cerebral Ischemia/Infarction"
|
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slug: "acute-cerebral-ischemiainfarction"
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category: "Brain"
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|
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imageCount: 42
|
||||
lastUpdated: "08/21/20"
|
||||
pageDescription: "Acute Cerebral Ischemia/Infarction"
|
||||
pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Stroke, Cerebral Ischemia and Infarction, Acute Cerebral Ischemia/Infarction"
|
||||
pageTitle: "Acute Cerebral Ischemia/Infarction | STATdx"
|
||||
enhancedTitle: "Acute Cerebral Ischemia/Infarction"
|
||||
type: "DX"
|
||||
references: true
|
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breadcrumbs:
|
||||
- "Brain"
|
||||
- "Diagnosis"
|
||||
- "Pathology-Based Diagnoses"
|
||||
- "Stroke"
|
||||
- "Cerebral Ischemia and Infarction"
|
||||
- "Acute Cerebral Ischemia/Infarction"
|
||||
---
|
||||
# KEY FACTS
|
||||
|
||||
- ## Terminology
|
||||
|
||||
|
||||
- Interrupted blood flow to brain resulting in cerebral ischemia/infarction
|
||||
- Stroke, brain attack = descriptive terms, not diagnosis
|
||||
- ## Imaging
|
||||
|
||||
|
||||
- Major artery (territorial) infarct
|
||||
- Generally wedge-shaped; both gray matter (GM) and white matter (WM) involved
|
||||
- Embolic infarcts
|
||||
- Often focal/small, at GM-WM interface
|
||||
- NECT
|
||||
- Hyperdense vessel = clot (dense MCA sign)
|
||||
- Loss of GM-WM distinction in first 3 hours (50-70%)
|
||||
- Insular ribbon sign: GM-WM interface lost
|
||||
- "Disappearing" basal ganglia sign
|
||||
- Calcified embolus
|
||||
- Do not miss this (high risk of recurrent stroke)
|
||||
- CTA: Excellent for large vessel occlusions (LVOs)
|
||||
- pCT: CBF/CBV "mismatch" estimates penumbra
|
||||
- Beware ghost infarct core!
|
||||
- May exclude patients who would benefit from endovascular treatment
|
||||
- MR
|
||||
- Parenchymal ± intraarterial FLAIR hyperintensity
|
||||
- ↑ intensity on DWI with corresponding ↓ on ADC
|
||||
- ↓ CBF, variable ↓ CBV on MR perfusion
|
||||
- ## Top Differential Diagnoses
|
||||
|
||||
|
||||
- Hyperdense vessel mimics (normal; polycythemia)
|
||||
- Parenchymal hypodensity (many nonvascular causes)
|
||||
- ## Pathology
|
||||
|
||||
|
||||
- Severely ischemic core
|
||||
- CBF < (6-8 cm³)/(100 g/min)
|
||||
- Peripheral penumbra
|
||||
- CBF between (10-20 cm³)/(100 g/min)
|
||||
- ## Clinical Issues
|
||||
|
||||
|
||||
- 2nd most common cause of death worldwide
|
||||
- Most common cause of morbidity in USA
|
||||
- Thrombectomy = treatment of choice for LVOs
|
||||
|
||||
# TERMINOLOGY
|
||||
|
||||
- ## Synonyms
|
||||
|
||||
|
||||
- Stroke and brain attack
|
||||
- Not diagnosis; terms for sudden onset of neurologic deficit
|
||||
- ## Definitions
|
||||
|
||||
|
||||
- Interrupted blood flow to brain resulting in cerebral ischemia/infarction
|
||||
|
||||
# IMAGING
|
||||
|
||||
- ## General Features
|
||||
|
||||
|
||||
- ### Best diagnostic clue
|
||||
|
||||
|
||||
- High signal on DWI + low signal on ADC = reduced diffusivity
|
||||
- ↓ cerebral blood flow (CBF), variable cerebral blood volume (CBV) on CT perfusion (pCT) or MR perfusion (pMR)
|
||||
- ### Location
|
||||
|
||||
|
||||
- Vascular territory or at border zones (watershed)
|
||||
- ### Size
|
||||
|
||||
|
||||
- Dependent on degree of compromise and collateral circulation
|
||||
- ### Morphology
|
||||
|
||||
|
||||
- Large vessel occlusion (LVO)
|
||||
- Conforms to arterial territory [most common = middle cerebral artery (MCA)]
|
||||
- Generally wedge-shaped, involves both gray matter (GM) and white matter (WM)
|
||||
- Embolic infarcts (often focal, at GM-WM interface)
|
||||
- Watershed infarcts (border zone between perforating, cortical arteries)
|
||||
- ## CT Findings
|
||||
|
||||
|
||||
- ### NECT
|
||||
|
||||
|
||||
- Hyperdense vessel (high specificity, low sensitivity)
|
||||
- Represents acute thrombus in cerebral vessel(s)
|
||||
- Hyperdense M1 MCA in 35-50%
|
||||
- Dot sign: Occluded MCA branches in sylvian fissure (16-17%)
|
||||
- Loss of GM-WM distinction in first 3 hours (50-70%)
|
||||
- Obscuration of deep gray nuclei
|
||||
- "Disappearing" basal ganglia
|
||||
- Loss of cortical "ribbon"
|
||||
- Parenchymal hypodensity
|
||||
- **A**lberta **S**troke **P**rogram **E**arly **C**omputed **T**omographic **S**core (ASPECTS)
|
||||
- Numerical calculation (1 point subtracted for each affected area)
|
||||
- Can be automatically generated with artificial intelligence (AI)
|
||||
- Gyral swelling, sulcal effacement appears between 12-24 hours
|
||||
- "Hemorrhagic transformation" in 15-45%
|
||||
- Delayed onset (24-48 hours) most typical
|
||||
- Can be gross (parenchymal) or petechial
|
||||
- Calcified embolus (1-2%)
|
||||
- Round/ovoid hyperdensity in vessel lumen or sulcus
|
||||
- Calcific valvular disease > cervical atrioventricular septal defect (ASVD) as source
|
||||
- High risk for recurrent strokes
|
||||
- ### CECT
|
||||
|
||||
|
||||
- Enhancing cortical vessels = slow flow or collateralization
|
||||
- Absent vessels = occlusion
|
||||
- Cortical/gyral enhancement after 48-72 hours
|
||||
- CTA: Identify LVOs, dissections, stenoses, status of collaterals
|
||||
- pCT
|
||||
- Shows CBF, CBV, TTP, or MTT
|
||||
- AI programs provide rapid, easy-to-read, real-time views of brain perfusion
|
||||
- Select stroke patients with LVOs for thrombectomy
|
||||
- Ischemic core = volume of area with > 70% ↓ in CBF (rCBF < 0.3)
|
||||
- Often overestimates initial infarct core → ghost infarct core (GIC)
|
||||
- GIC = initial core - final infarct > 10 mL
|
||||
- Common in patients imaged in early time window with fast, complete reperfusion (TICI2b)
|
||||
- pCT CBF may exclude patients who would benefit from endovascular treatment!
|
||||
- ## MR Findings
|
||||
|
||||
|
||||
- ### T1WI
|
||||
|
||||
|
||||
- Early cortical swelling and hypointensity, loss of GM-WM borders
|
||||
- ### T2WI
|
||||
|
||||
|
||||
- Cortical swelling, hyperintensity develops by 12-24 hours
|
||||
- May normalize 2-3 weeks post ictus (MR "fogging")
|
||||
- ### FLAIR
|
||||
|
||||
|
||||
- Parenchymal hyperintensity appears while other sequences normal
|
||||
- Intraarterial hyperintensity = sign of major vessel occlusion or slow flow
|
||||
- **Absence** of FLAIR intravascular hyperintensity associated with future lack of recanalization
|
||||
- ### T2* GRE
|
||||
|
||||
|
||||
- Arterial blooming (thrombosed vessel) ± parenchymal hemorrhage
|
||||
- May see susceptibility from calcified embolus
|
||||
- ### DWI
|
||||
|
||||
|
||||
- Hyperintense (cytotoxic edema)
|
||||
- Improves hyperacute stroke detection to 95%
|
||||
- Usually correlates to "infarct core" (final infarct size); some diffusion abnormalities reversible (TIA, migraine)
|
||||
- Restriction typically lasts 7-10 days
|
||||
- Can persist up to 2 months post ictus
|
||||
- Corresponding low signal on ADC maps
|
||||
- May normalize after tissue reperfusion
|
||||
- After 10 days hyper- or isointensity on ADC map (T2 shine-through)
|
||||
- May mimic diffusion restriction on DWI
|
||||
- DTI
|
||||
- DTI with at least 6 directions can calculate DTI trace, ADC maps
|
||||
- More sensitive for small ischemic foci, emboli, distal cortical strokes
|
||||
- Distinguish cytotoxic from vasogenic edema in complicated cases
|
||||
- ### PWI
|
||||
|
||||
|
||||
- Dynamic contrast bolus or arterial spin-labeled techniques
|
||||
- Maximum slope gives rCBF, rCBV
|
||||
- Deconvolution gives absolute values
|
||||
- Bolus-tracking T2* gadolinium perfusion imaging (PWI) with CBV map
|
||||
- ↓ perfusion; 75% larger than DWI abnormality
|
||||
- DWI/PWI "mismatch": Penumbra or "at-risk" tissue
|
||||
- ### T1WI C+
|
||||
|
||||
|
||||
- Variable enhancement patterns evolve over time
|
||||
- Hyperacute: Intravascular enhancement (stasis from slow antegrade or retrograde collateral flow)
|
||||
- Acute: Meningeal enhancement (pial collateral flow appears in 24-48 hours, resolves over 3-4 days)
|
||||
- Subacute: Parenchymal enhancement (appears after 24-48 hours, can persist for weeks/months)
|
||||
- MRA: Major vessel occlusions, stenoses, status of collaterals
|
||||
- MRS: ↑ lactate, ↓ NAA
|
||||
- ## Angiographic Findings
|
||||
|
||||
|
||||
- DSA
|
||||
- Only used if thrombectomy is considered
|
||||
- Vessel occlusion (cut-off, tapered "rat tail," clot with "tram-track") or stenosis
|
||||
- ± slow antegrade flow, assess retrograde collateral flow
|
||||
- "Bare area" of non- or underperfused brain in late arterial/capillary phases
|
||||
- ## Imaging Recommendations
|
||||
|
||||
|
||||
- ### Protocol advice
|
||||
|
||||
|
||||
- Initial NECT (exclude hemorrhage/stroke mimic)
|
||||
- CTA + pCT
|
||||
- ± MR with fast DWI, FLAIR, T2* GRE
|
||||
- ± MRA, PWI
|
||||
- DSA if thrombectomy is option (selected patients up to 24 hours)
|
||||
|
||||
# DIFFERENTIAL DIAGNOSIS
|
||||
|
||||
- ## Hyperdense Vessel Mimics
|
||||
|
||||
|
||||
- Intraarterial blood is always slightly hyperdense to normal brain!
|
||||
- High hematocrit (polycythemia)
|
||||
- Microcalcification in vessel wall
|
||||
- Diffuse cerebral edema makes vessels appear relatively hyperdense
|
||||
- ## Parenchymal Hypodensity (Nonvascular Causes)
|
||||
|
||||
|
||||
- Infiltrating neoplasm (e.g., astrocytoma)
|
||||
- Cerebral contusion
|
||||
- Inflammation (cerebritis, encephalitis)
|
||||
- Evolving encephalomalacia
|
||||
- Dural venous thrombosis with parenchymal venous congestion and edema
|
||||
- Seizure
|
||||
|
||||
# PATHOLOGY
|
||||
|
||||
- ## General Features
|
||||
|
||||
|
||||
- ### Etiology
|
||||
|
||||
|
||||
- Many causes (thrombotic vs. embolic, dissection, vasculitis, hypoperfusion)
|
||||
- Early: Critical disturbance in CBF
|
||||
- Severely ischemic core has CBF < (6-8 cm³)/(100 g/min) [normal ~ (60 cm³)/(100 g/min)]
|
||||
- Oxygen depletion, energy failure, terminal depolarization, ion homeostasis failure
|
||||
- Bulk of final infarct → cytotoxic edema, cell death
|
||||
- Later: Evolution from ischemia to infarction depends on many factors (e.g., hyperglycemia influences "destiny" of ischemic brain tissue)
|
||||
- Ischemic penumbra CBF between (10-20 cm³)/(100 g/min)
|
||||
- Theoretically salvageable tissue
|
||||
- ### Associated abnormalities
|
||||
|
||||
|
||||
- Cardiac disease, prothrombotic states
|
||||
- Additional stroke risk factors: C-reactive protein, homocysteine
|
||||
- ## Gross Pathologic & Surgical Features
|
||||
|
||||
|
||||
- Acute thrombosis of major vessel
|
||||
- Pale, swollen brain; GM-WM boundaries blurred
|
||||
- ## Microscopic Features
|
||||
|
||||
|
||||
- After 4 hours: Eosinophilic neurons with pyknotic nuclei
|
||||
- 15-24 hours: Neutrophils invade, necrotic nuclei look like "eosinophilic ghosts"
|
||||
- 2-3 days: Blood-derived phagocytes
|
||||
- 1 week: Reactive astrocytosis, ↑ capillary density
|
||||
- End result: Fluid-filled cavity lined by astrocytes
|
||||
|
||||
# CLINICAL ISSUES
|
||||
|
||||
- ## Presentation
|
||||
|
||||
|
||||
- ### Most common signs/symptoms
|
||||
|
||||
|
||||
- Focal acute neurologic deficit
|
||||
- Paresis, aphasia, ↓ mental status
|
||||
- ## Demographics
|
||||
|
||||
|
||||
- ### Age
|
||||
|
||||
|
||||
- Any age; most common in older adults
|
||||
- Consider underlying disease (sickle cell, moyamoya, neurofibromatosis type 1, cardiac, drugs) in children, young adults
|
||||
- ### Sex
|
||||
|
||||
|
||||
- No sex predilection
|
||||
- ### Epidemiology
|
||||
|
||||
|
||||
- 2nd most common cause of death worldwide
|
||||
- Most common cause of morbidity in USA
|
||||
- ## Natural History & Prognosis
|
||||
|
||||
|
||||
- Clinical diagnosis inaccurate in 15-20% of strokes
|
||||
- ~ 50% of patients with LVO, thrombectomy achieve functional independence
|
||||
- Prognosis poor if ASPECTS ≤ 5
|
||||
- Malignant MCA infarct (coma, death)
|
||||
- Up to 10% of all stroke patients (↑ risk with large infarct volumes)
|
||||
- ↑ inflammasome activation → proinflammatory cytokines; fatal brain swelling with ↑ ICP
|
||||
- ## Treatment
|
||||
|
||||
|
||||
- "Time is brain"
|
||||
- IV thrombolysis = ~ 10% successful/sufficient recanalization
|
||||
- IV rTPA window < 3 hours if thrombectomy not available
|
||||
- Thrombolysis in cerebral infarction (TICI scale) = reperfusion grade
|
||||
- Grade ≥ 2B is "successful" reperfusion; 2C = near-perfect reperfusion
|
||||
- TICI 3 = best functional outcome
|
||||
- Now procedure of choice with LVO = mechanical thrombectomy
|
||||
- Stent retriever better outcome than aspiration only
|
||||
- ± new devices to ↓ distal embolization
|
||||
- Patient selection most important factor in outcome
|
||||
- AHA/ASA guidelines: Age ≥ 18 years, ASPECTS/NIHSS score ≥ 6
|
||||
- Symptom onset < 6 hours
|
||||
- No parenchymal hematoma on CT
|
||||
- DAWN, DEFUSE 3 trials have broadened window
|
||||
- Some advocate treating "almost anyone" (ASPECTS = 0-5)
|
||||
- Up to 24 hours in some cases
|
||||
- Even failed/incomplete recanalization shows ↓ likelihood for very poor outcome, not generally harmful
|
||||
|
||||
# DIAGNOSTIC CHECKLIST
|
||||
|
||||
- ## Consider
|
||||
|
||||
|
||||
- Rarely, ischemia or seizure may mimic tumor or encephalitis
|
||||
|
||||
0e086d6e-36ea-4341-abf7-2d480bc1842f
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Aoki J et al: Negative-FLAIR vascular hyperintensities serve as a marker of no recanalization during hospitalization in acute stroke. J Clin Neurosci. 72:233-7, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31836384%5Bpmid%5D)
|
||||
1. [Atchaneeyasakul K et al: Impact of MRI selection on triage of endovascular therapy in acute ischemic stroke: the mri in acute management of ischemic stroke (MIAMIS) registry. Interv Neurol. 8(2-6):135-43, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32508895%5Bpmid%5D)
|
||||
1. [Atchaneeyasakul K et al: Thrombectomy outcomes in acute ischemic stroke due to middle cerebral artery M2 occlusion with stent retriever versus aspiration: a multicenter experience. Interv Neurol. 8(2-6):180-6, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32508900%5Bpmid%5D)
|
||||
1. [Broocks G et al: Incomplete or failed thrombectomy in acute stroke patients with ASPECTS 0-5 - how harmful is trying? Eur J Neurol. ePub, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32449311%5Bpmid%5D)
|
||||
1. [Dhand S et al: Acute ischemic stroke: acute management and selection for endovascular therapy. Semin Intervent Radiol. 37(2):109-18, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32419723%5Bpmid%5D)
|
||||
1. [Miao J et al: Predictors of malignant cerebral edema in cerebral artery infarction: a meta-analysis. J Neurol Sci. 409:116607, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31830611%5Bpmid%5D)
|
||||
1. [Patel P et al: Hyperacute management of ischemic strokes: JACC Focus Seminar. J Am Coll Cardiol. 75(15):1844-56, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32299596%5Bpmid%5D)
|
||||
1. [Sakamoto Y et al: Reducing door-to-reperfusion time in acute stroke endovascular therapy using magnetic resonance imaging as a screening modality. J Neurointerv Surg. ePub, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32051322%5Bpmid%5D)
|
||||
1. [Heit JJ et al: Perfusion computed tomography in acute ischemic stroke. Radiol Clin North Am. 57(6):1109-16, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31582038%5Bpmid%5D)
|
||||
1. [Zhang M et al: Characteristics of cerebral perfusion and diffusion associated with crossed cerebellar diaschisis after acute ischemic stroke. Jpn J Radiol. 38(2):126-34, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31720951%5Bpmid%5D)
|
||||
1. [Martins N et al: Ghost infarct core and admission computed tomography perfusion: redefining the role of neuroimaging in acute ischemic stroke. Interv Neurol. 7(6):513-21, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30410531%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
*Coronal graphic illustrates left M1 occlusion. Proximal occlusion affects the entire middle cerebral artery (MCA) territory, including the basal ganglia (perfused by lenticulostriate arteries <img src='img/arrows/BS.png'/>). Acute ischemia is often identified by subtle loss of the gray matter-white matter interfaces with blurring of the basal ganglia and an insular ribbon sign on the initial CT.*
|
||||
|
||||
|
||||
*Coronal graphic illustrates left M1 occlusion. Proximal occlusion affects the entire middle cerebral artery (MCA) territory, including the basal ganglia (perfused by lenticulostriate arteries <img src='img/arrows/BS.png'/>). Acute ischemia is often identified by subtle loss of the gray matter-white matter interfaces with blurring of the basal ganglia and an insular ribbon sign on the initial CT.*
|
||||
|
||||
|
||||
*Axial NECT in a 46-year-old man shows a very "dense" left MCA <img src='img/arrows/WS.png'/> compared to the normal minimally hyperdense right MCA <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*Graphic shows anatomic regions for calculating the ASPECTS score. M1-M2 represent the MCA cortex with each area allotted 1 point. The insular cortex (I), lentiform nuclei (L), caudate head (C), and internal capsule (IC) are scored with 1 point each.*
|
||||
|
||||
|
||||
*More cephalad graphic shows the superior 3 MCA territories. The ASPECTS score is calculated by subtracting 1 point for each affected area from 10 (normal total score).*
|
||||
|
||||
|
||||
*Axial NECT in a 47-year-old woman with sudden onset of right hemiparesis shows hypodensity in the left lateral basal ganglia, insula, and parietal lobe. The total ASPECTS score was 6.*
|
||||
|
||||
|
||||
*MIP of the CTA in the same patient shows an abrupt cut-off <img src='img/arrows/WC.png'/> of the proximal M1 MCA segment.*
|
||||
|
||||
|
||||
*Axial CT perfusion with cerebral blood volume (CBV) shows reduced CBV <img src='img/arrows/WS.png'/> in the left temporal and parietal lobes, as well as the lateral basal ganglia, external capsule, and insula.*
|
||||
|
||||
|
||||
*Axial cerebral blood flow (CBF) map shows a more extensive area of reduced perfusion, suggesting there is a significant penumbra of brain that is ischemic but not infarcted. CBF in the left basal ganglia and thalamus is also reduced, suggesting the proximal M1 occlusion has also compromised the deep gray nuclei.*
|
||||
|
||||
|
||||
*Automated CT perfusion in the same case shows CBF < 30% = 68 mL, volume of brain with Tmax > 6.0 seconds = 108 mL, and mismatch volume (penumbra) of 40 mL.*
|
||||
|
||||
|
||||
*(L) Pretreatment AP view of the left internal carotid artery (ICA) DSA in the same case shows the proximal MCA occlusion <img src='img/arrows/BS.png'/>. (R) Following stent-retriever thrombectomy, the clot has been removed and the M1 MCA <img src='img/arrows/BC.png'/> appears nearly normal. Blood flow to the distal MCA is mostly restored.*
|
||||
|
||||
![Axial T1WI MRs show the 2 vascular watershed zones (WSZs). Blue depicts the cortical (external) WSZs between the major territorial arteries [anterior cerebral artery (ACA), MCA, posterior cerebral artery (PCA)]. The yellow depicts the subcortical (internal or deep) WSZs between perforating arteries and major territorial arteries.](41e4888b-7a0d-4bc7-8435-a08b5c22a03c)
|
||||
*Axial T1WI MRs show the 2 vascular watershed zones (WSZs). Blue depicts the cortical (external) WSZs between the major territorial arteries [anterior cerebral artery (ACA), MCA, posterior cerebral artery (PCA)]. The yellow depicts the subcortical (internal or deep) WSZs between perforating arteries and major territorial arteries.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a 48-year-old woman with TIAs shows white matter hyperintensities aligned front to back just above the level of the lateral ventricles.*
|
||||
|
||||
|
||||
*Axial DWI MR in the same patient shows acute lacunar infarcts in almost a "string of pearls" configuration.*
|
||||
|
||||
|
||||
*Axial ADC confirms the deep white matter lesions exhibit acutely restricted diffusion.*
|
||||
|
||||
|
||||
*2D TOF MRA of the left ICA in the same patient shows a "flow gap" at the junction of the cavernous and supraclinoid segments, indicating a high-grade stenosis.*
|
||||
|
||||
|
||||
*2D TOF MRA of the right ICA in the same patient shows a high-grade stenosis of the right supraclinoid ICA just before the origin of the PCA. The critical stenoses in both ICAs resulted in the deep WSZ infarcts.*
|
||||
|
||||
|
||||
*Axial NECT in a 65-year-old man with TIAs and a history of mitral valve replacement was initially read as normal. However, this image shows a calcified cerebral embolus <img src='img/arrows/WS.png'/> in the right sylvian fissure.*
|
||||
|
||||
|
||||
*More cephalad NECT in the same patient shows a 2nd calcified embolus <img src='img/arrows/WC.png'/>. A 3rd embolus was present in the interhemispheric fissure (not shown). Calcified cerebral emboli carry ~ 50% risk of repeated strokes. Cardiac sources are most common followed by calcified ASVD plaques at carotid bifurcation.*
|
||||
|
||||
|
||||
*Axial NECT for a brain attack patient in the ER with sudden-onset aphasia is normal.*
|
||||
|
||||
|
||||
*Axial CT perfusion in the same patient was obtained immediately following the NECT. The CBV appears grossly normal.*
|
||||
|
||||
|
||||
*Axial CBF map in the same patient shows markedly reduced perfusion in the inferior division of the left MCA <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*TTD in the same patient shows severely reduced TTD, consistent with acute ischemia without infarction. IV TPA was administered and the symptoms resolved.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
*Axial NECT in a 60-year-old woman admitted for rapid stroke evaluation shows hypodensity in the right posterior frontal lobe <img src='img/arrows/WS.png'/>. The right MCA <img src='img/arrows/WO.png'/> appears slightly hyperdense.*
|
||||
|
||||
|
||||
*Axial CTA in the same patient shows an abrupt cut-off of contrast in the right MCA <img src='img/arrows/WS.png'/> just distal to its origin from the ICA.*
|
||||
|
||||
|
||||
*Axial T2* GRE MR in the same patient shows striking blooming <img src='img/arrows/BC.png'/> from a right M1/proximal M2 thrombus.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient shows edematous right posterior frontal gyri <img src='img/arrows/WC.png'/> as well as hyperintensity in the ipsilateral insula <img src='img/arrows/WS.png'/>, caudate head, and putamen <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*Axial DWI MR confirms acute infarction in the territories of the lateral lenticulostriate arteries and superior division of the right MCA.*
|
||||
|
||||
|
||||
*Axial NECT in an 89-year-old man who had several visits to the ER for several falls (to "rule out subdural hematoma") shows a calcified cerebral embolus <img src='img/arrows/WS.png'/> in a right hemisphere sulcus.*
|
||||
|
||||
|
||||
*Sagittal reformatted NECT in the same patient shows the location in the right superior temporal sulcus <img src='img/arrows/WS.png'/>. The patient was subsequently shown to have calcific mitral valve disease. Calcified cerebral emboli carry a high risk of repeated stroke.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows intravascular signal <img src='img/arrows/WS.png'/> beginning near the genu.*
|
||||
|
||||
|
||||
*More cephalad FLAIR MR in the same patient shows gyral hyperintensity <img src='img/arrows/WO.png'/> and intravascular signal in the M2 (insular) MCA segments <img src='img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Axial NECT in a 35-year-old man shows a dense left MCA <img src='img/arrows/WS.png'/>, indicating acute thrombus involving the entire MCA from its origin to its bifurcation.*
|
||||
|
||||
|
||||
*More cephalad NECT shows the basal ganglia are effaced and the gray matter-white matter interfaces in the insula, left posterior frontal lobe, and opercula are poorly defined.*
|
||||
|
||||
|
||||
*The left basal ganglia are edematous and have "disappeared" as they are now nearly the same density as the surrounding white matter. The gray matter-white matter interfaces in the posterior temporal and anterior parietal lobes are effaced.*
|
||||
|
||||
|
||||
*More cephalad NECT shows loss of sulci and gray matter-white matter differentiation in the left parietal lobe. Because of his poor ASPECTS score (2, being generous) he was not considered a good candidate for thrombectomy despite his relatively young age.*
|
||||
|
||||
|
||||
*Axial FLAIR MR scan obtained 3 hours later in the same patient shows hyperintensity in the left basal ganglia, insula, and the entirety of the left cerebral hemisphere supplied by the MCA.*
|
||||
|
||||
|
||||
*Axial DWI MR in the same patient shows restricted diffusion in the complete left MCA territory.*
|
||||
|
||||
|
||||
*Axial NECT at 6 hours in the same patient shows thrombus in the horizontal MCA <img src='img/arrows/WO.png'/> as well as hypodensity in the left frontal and anterior temporal lobes <img src='img/arrows/WS.png'/>. The suprasellar cistern <img src='img/arrows/WC.png'/> is normal and there is as yet no evidence for descending transtentorial herniation.*
|
||||
|
||||
|
||||
*Axial NECT through the basal ganglia and insula shows extensive hypodensity in the entire left MCA territory <img src='img/arrows/WS.png'/>. Mass effect is developing with compression of the left frontal horn <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
*More cephalad NECT in the same patient at 6 hours following ictus shows the wedge-shaped hypodensity involves the complete left frontal and parietal opercula. The massive edema developing in the entire left MCA territory makes this a so-called "malignant" MCA infarct.*
|
||||
|
||||
|
||||
*Twelve hours after admission, the same patient became unresponsive. His left pupil was dilated and he was rushed to the operating room where an emergent craniectomy was performed. Postoperative NECT at 20 hours shows hypodensity throughout the left MCA territory. Note the brain bulging out through the craniectomy defect.*
|
||||
|
||||
|
||||
*More cephalad NECT in the same patient shows the completed total MCA territory infarct.*
|
||||
|
||||
+512
File diff suppressed because one or more lines are too long
@@ -0,0 +1,482 @@
|
||||
---
|
||||
title: "Acute Ischemic Stroke"
|
||||
docid: "69a7a1f7-9c78-4ad1-82dd-9b13f2e717b3"
|
||||
authors:
|
||||
- key: "07a2c087-6202-49e7-870b-7aa162d18f06"
|
||||
value: "Bronwyn E. Hamilton, MD"
|
||||
breadcrumbs:
|
||||
-
|
||||
name: "Vasculature"
|
||||
slug: "vasculature"
|
||||
treeNodeId: "9d3db335-364f-44ec-b2e2-30b03ce93228"
|
||||
-
|
||||
name: "Diagnosis"
|
||||
slug: "diagnosis"
|
||||
treeNodeId: "4a210126-9f87-404e-b419-a73f44d0e94c"
|
||||
-
|
||||
name: "Extracranial Cerebral Arteries"
|
||||
slug: "extracranial-cerebral-arteries"
|
||||
treeNodeId: "593e17de-cd84-4587-8349-872ed33d28c4"
|
||||
-
|
||||
name: "Acute Ischemic Stroke"
|
||||
slug: "acute-ischemic-stroke"
|
||||
treeNodeId: null
|
||||
category: "Vasculature"
|
||||
cmeTopicId: "269a1301-f57a-4247-b62a-de2d927ea3bf"
|
||||
documentVersionId: "90d363cc-bb77-48d7-ae31-85fefda3de0c"
|
||||
imageCount: 32
|
||||
lastUpdated: "04/18/16"
|
||||
pageDescription: "Acute Ischemic Stroke"
|
||||
pageKeywords: "Vasculature, Diagnosis, Extracranial Cerebral Arteries, Acute Ischemic Stroke"
|
||||
pageTitle: "Acute Ischemic Stroke | STATdx"
|
||||
enhancedTitle: "Acute Ischemic Stroke"
|
||||
type: "DX"
|
||||
references: true
|
||||
breadcrumbs:
|
||||
- "Vasculature"
|
||||
- "Diagnosis"
|
||||
- "Extracranial Cerebral Arteries"
|
||||
- "Acute Ischemic Stroke"
|
||||
---
|
||||
# KEY FACTS
|
||||
|
||||
- ## Terminology
|
||||
|
||||
|
||||
- Interrupted blood flow to brain resulting in cerebral ischemia/infarction with variable neurologic deficit
|
||||
- ## Imaging
|
||||
|
||||
|
||||
- Major artery (territorial) infarct
|
||||
- Generally wedge-shaped; both GM & WM involved
|
||||
- Embolic infarcts
|
||||
- Often focal/small, at GM-WM interface
|
||||
- NECT
|
||||
- Hyperdense vessel (high specificity, low sensitivity)
|
||||
- "Dense MCA" sign: Acute thrombus in middle cerebral artery
|
||||
- Loss of GM-WM distinction in 1st 3 hours (50-70%)
|
||||
- "Insular ribbon" sign: Loss of GM-WM differentiation of insular cortex
|
||||
- MR
|
||||
- Best diagnostic clue is high signal on DWI with corresponding low signal on ADC
|
||||
- ↓ CBF and ↓ CBV on perfusion MR (or CT)
|
||||
- ## Top Differential Diagnoses
|
||||
|
||||
|
||||
- Hyperdense vessel mimics
|
||||
- Parenchymal hypodensity (nonvascular causes)
|
||||
- ## Pathology
|
||||
|
||||
|
||||
- Severely ischemic core
|
||||
- CBF < (6-8 mL)/(100 g/min)
|
||||
- Peripheral penumbra
|
||||
- CBF = (10-20 mL)/(100 g/min)
|
||||
- ## Clinical Issues
|
||||
|
||||
|
||||
- 2nd most common cause of death worldwide
|
||||
- Leading cause of morbidity in USA
|
||||
- Treatment
|
||||
- IV thrombolysis (< 3 hours of symptom onset)
|
||||
- IA thrombolysis (selected acute strokes < 6 hours)
|
||||
- Clinical diagnosis inaccurate in 15-20% of strokes
|
||||
|
||||
# TERMINOLOGY
|
||||
|
||||
- ## Synonyms
|
||||
|
||||
|
||||
- Stroke, brain attack, cerebrovascular accident
|
||||
- ## Definitions
|
||||
|
||||
|
||||
- Interrupted blood flow to brain resulting in cerebral ischemia/infarction with variable neurologic deficit
|
||||
|
||||
# IMAGING
|
||||
|
||||
- ## General Features
|
||||
|
||||
|
||||
- ### Best diagnostic clue
|
||||
|
||||
|
||||
- High signal on DWI with corresponding low signal on ADC
|
||||
- Decreased cerebral blood flow (CBF) and cerebral blood volume (CBV) on CT or MR perfusion
|
||||
- ### Location
|
||||
|
||||
|
||||
- 1 or more vascular territories or at border zones (watershed)
|
||||
- ### Size
|
||||
|
||||
|
||||
- Dependent on degree of compromise and collateral circulation
|
||||
- ### Morphology
|
||||
|
||||
|
||||
- Territorial infarct
|
||||
- Conforms to arterial territory
|
||||
- Generally wedge-shaped
|
||||
- Both gray matter (GM) and white matter (WM) are involved
|
||||
- Embolic infarcts (often focal, at GM-WM interface)
|
||||
- ## CT Findings
|
||||
|
||||
|
||||
- ### NECT
|
||||
|
||||
|
||||
- Hyperdense vessel (high specificity, low sensitivity)
|
||||
- Represents acute thrombus in cerebral vessel(s)
|
||||
- Hyperdense M1 segment of middle cerebral artery (MCA) in 35-50%; most common vessel involved
|
||||
- "Dot" sign: Occluded MCA branches in sylvian fissure (16-17%)
|
||||
- Loss of gray-white matter (GM-WM) distinction in 1st 3 hours (50-70%)
|
||||
- Obscuration of deep gray nuclei
|
||||
- Loss of cortical "ribbon"
|
||||
- Parenchymal hypodensity
|
||||
- If > 1/3 MCA territory initially hypodense, then larger lesion usually develops later
|
||||
- Temporary transition to isodensity (up to 54%) at 2-3 weeks post ictus (CT "fogging")
|
||||
- Gyral swelling, sulcal effacement 12-24 hours
|
||||
- "Hemorrhagic transformation" in 15-45%
|
||||
- Delayed onset (24-48 hours) most typical
|
||||
- Can be gross (parenchymal) or petechial
|
||||
- ### CECT
|
||||
|
||||
|
||||
- Enhancing cortical vessels: Slow flow or collateralization acutely
|
||||
- Absent vessels: Occlusion
|
||||
- Perfusion CT (pCT): Assess ischemic core vs. penumbra; identify patients who benefit most from revascularization
|
||||
- pCT calculates CBF, CBV, time to peak (TTP)
|
||||
- Deconvolution can give mean transit time (MTT)
|
||||
- Cortical/gyral enhancement after 48-72 hours
|
||||
- CTA: Identify occlusions, dissections, stenoses, collaterals
|
||||
- ## MR Findings
|
||||
|
||||
|
||||
- ### T1WI
|
||||
|
||||
|
||||
- Early cortical swelling and hypointensity, loss of GM-WM borders
|
||||
- ### T2WI
|
||||
|
||||
|
||||
- Cortical swelling, hyperintensity after 12-24 hours
|
||||
- May normalize 2-3 weeks post ictus (MR "fogging")
|
||||
- ### FLAIR
|
||||
|
||||
|
||||
- Parenchymal hyperintensity appears (6 hours post ictus) while other sequences normal
|
||||
- Intraarterial FLAIR hyperintensity is early sign of major vessel occlusion or slow flow
|
||||
- ### T2* GRE
|
||||
|
||||
|
||||
- Detection of acute blood products
|
||||
- Arterial "blooming" (thrombosed vessel) from clot susceptibility
|
||||
- ### DWI
|
||||
|
||||
|
||||
- Hyperintense restriction from cytotoxic edema
|
||||
- Improves hyperacute stroke detection to 95%
|
||||
- Best correlates with "ischemic core" (final infarct size); some diffusion abnormalities reverse
|
||||
- May have reduced sensitivity in brainstem and medulla during 1st 24 hours
|
||||
- Restriction typically lasts 7-10 days
|
||||
- High signal can persist up to 2 months post ictus
|
||||
- After 10 days, T2 effect may predominate over low ADC: T2 "shine-through"
|
||||
- Corresponding low signal on ADC maps
|
||||
- May normalize after tissue reperfusion
|
||||
- Hyper- or isointensity on ADC map (T2 "shine-through") may mimic diffusion restriction
|
||||
- Distinguish cytotoxic from vasogenic edema in complicated cases
|
||||
- May be helpful to evaluate new deficits after tumor resection
|
||||
- ### PWI
|
||||
|
||||
|
||||
- Dynamic contrast bolus or arterial spin-labeling techniques
|
||||
- Maximum slope gives relative CBF and CBV
|
||||
- Deconvolution gives absolute values
|
||||
- Bolus-tracking T2* gadolinium PWI with CBV map
|
||||
- ↓ perfusion; 75% larger than DWI abnormality
|
||||
- DWI/PWI mismatch may identify penumbra (potentially viable but at-risk tissue)
|
||||
- ### T1WI C+
|
||||
|
||||
|
||||
- Variable enhancement patterns evolve over time
|
||||
- Hyperacute: Intravascular enhancement (stasis from slow antegrade or retrograde collateral flow)
|
||||
- Acute: Meningeal enhancement (pial collateral flow appears in 24-48 hours, resolves over 3-4 days)
|
||||
- Subacute: Parenchymal enhancement (appears after 24-48 hours, can persist for weeks/months)
|
||||
- MRA: Major vessel occlusions, stenoses, status of collaterals
|
||||
- MRS: Elevated lactate, decreased NAA
|
||||
- Conventional MR sequences positive in 70-80%
|
||||
- Restricted diffusion improves accuracy to 95%
|
||||
- Diffusion tensor imaging (DTI)
|
||||
- Multidirectional diffusion-weighted images; at least 6 directions can be used to calculate DTI trace and generate ADC maps
|
||||
- Higher spatial resolution
|
||||
- May be more sensitive for small ischemic foci, emboli, cortical strokes
|
||||
- ## Angiographic Findings
|
||||
|
||||
|
||||
- Conventional: Vessel occlusion (cut off, tapered, "tram track")
|
||||
- Slow antegrade flow and slow retrograde collateral flow
|
||||
- Intraluminal thrombus = filling defect
|
||||
- Neurointerventional: Intraarterial (IA) fibrinolytic therapy for treatment of selected acute nonhemorrhagic stroke within 6-hour window
|
||||
- IA mechanical clot removal with retriever device
|
||||
- ## Imaging Recommendations
|
||||
|
||||
|
||||
- ### Best imaging tool
|
||||
|
||||
|
||||
- MR + DWI; T2* GRE
|
||||
- ### Protocol advice
|
||||
|
||||
|
||||
- NECT as initial study to exclude hemorrhage/mass
|
||||
- CT perfusion and CTA if available
|
||||
- MR using DWI/FLAIR/GRE ± MRA, PWI
|
||||
- DSA with thrombolysis in selected patients
|
||||
|
||||
# DIFFERENTIAL DIAGNOSIS
|
||||
|
||||
- ## Hyperdense Vessel Mimics
|
||||
|
||||
|
||||
- High hematocrit (polycythemia)
|
||||
- Microcalcification in vessel wall
|
||||
- Diffuse cerebral edema makes vessels appear relatively hyperdense
|
||||
- Normal circulating blood always slightly hyperdense to normal brain
|
||||
- ## Parenchymal Hypodensity (Nonvascular Causes)
|
||||
|
||||
|
||||
- Infiltrating neoplasm (e.g., astrocytoma)
|
||||
- Cerebral contusion
|
||||
- Inflammation (cerebritis, encephalitis)
|
||||
- Evolving encephalomalacia
|
||||
- Dural venous thrombosis with parenchymal venous congestion and edema
|
||||
|
||||
# PATHOLOGY
|
||||
|
||||
- ## General Features
|
||||
|
||||
|
||||
- ### Etiology
|
||||
|
||||
|
||||
- Common causes
|
||||
- Thrombotic vs. embolic, dissection, vasculitis, hypoperfusion
|
||||
- Unusual causes
|
||||
- Complicated vasculopathy, including posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome; venous stroke
|
||||
- Early: Critical disturbance in CBF
|
||||
- Severely ischemic core: CBF < (6-8 mL)/(100 g/min)
|
||||
- Normal CBF ~ (60 mL)/(100 g/min)
|
||||
- Oxygen depletion, energy failure, terminal depolarization, ion homeostasis failure
|
||||
- Bulk of final infarct → cytotoxic edema, cell death
|
||||
- Later: Evolution from ischemia to infarction depends on many factors (e.g., hyperglycemia influences "destiny" of ischemic brain tissue)
|
||||
- Ischemic penumbra: CBF = (10-20 mL)/(100 g/min)
|
||||
- Theoretically salvageable tissue
|
||||
- Target of thrombolysis, neuroprotective agents
|
||||
- ### Associated abnormalities
|
||||
|
||||
|
||||
- Cardiac disease, prothrombotic states
|
||||
- Additional stroke risk factors: C-reactive protein, homocysteine
|
||||
- ## Gross Pathologic & Surgical Features
|
||||
|
||||
|
||||
- Acute thrombosis of major vessel
|
||||
- Pale, swollen brain; GM-WM boundaries blurred
|
||||
- ## Microscopic Features
|
||||
|
||||
|
||||
- After 4 hours: Eosinophilic neurons with pyknotic nuclei
|
||||
- 15-24 hours: Neutrophils invade, and necrotic nuclei look like "eosinophilic ghosts"
|
||||
- 2-3 days: Blood-derived phagocytes
|
||||
- 1 week: Reactive astrocytosis, ↑ capillary density
|
||||
- End result: Fluid-filled cavity lined by astrocytes
|
||||
|
||||
# CLINICAL ISSUES
|
||||
|
||||
- ## Presentation
|
||||
|
||||
|
||||
- ### Most common signs/symptoms
|
||||
|
||||
|
||||
- Focal acute neurologic deficit
|
||||
- Paresis, aphasia, decreased mental status
|
||||
- ## Demographics
|
||||
|
||||
|
||||
- ### Age
|
||||
|
||||
|
||||
- Usually older adults
|
||||
- ### Gender
|
||||
|
||||
|
||||
- No gender predilection
|
||||
- ### Epidemiology
|
||||
|
||||
|
||||
- 2nd most common cause of death worldwide
|
||||
- Among leading causes of morbidity in USA
|
||||
- ## Natural History & Prognosis
|
||||
|
||||
|
||||
- Clinical diagnosis inaccurate in 15-20% of strokes
|
||||
- Malignant MCA infarct (coma, death)
|
||||
- Up to 10% of all stroke patients
|
||||
- Fatal brain swelling with increased ICP
|
||||
- ## Treatment
|
||||
|
||||
|
||||
- "Time is brain": IV thrombolytic therapy window < 3 hours
|
||||
- IA window < 6 hours except for vertebrobasilar thrombosis (up to 24 hours because of high morbidity and mortality)
|
||||
- Patient selection most important factor in outcome
|
||||
- Symptom onset < 6 hours
|
||||
- No parenchymal hematoma on CT
|
||||
- < 1/3 MCA territory hypodensity
|
||||
|
||||
# DIAGNOSTIC CHECKLIST
|
||||
|
||||
- ## Consider
|
||||
|
||||
|
||||
- DWI positive for acute stroke only if ADC correlates
|
||||
- Rarely, ischemia may mimic tumor or encephalitis
|
||||
|
||||
ba323bb3-7781-4789-81b2-774e4fcadb49
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Parrilla G et al: Hemorrhage/contrast staining areas after mechanical intra-arterial thrombectomy in acute ischemic stroke: imaging findings and clinical significance. AJNR Am J Neuroradiol. 33(9):1791-6, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22538076%5Bpmid%5D)
|
||||
1. [Wang DJ et al: The value of arterial spin-labeled perfusion imaging in acute ischemic stroke: comparison with dynamic susceptibility contrast-enhanced MRI. Stroke. 43(4):1018-24, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22328551%5Bpmid%5D)
|
||||
1. [Harris AD et al: Diffusion and perfusion MR imaging of acute ischemic stroke. Magn Reson Imaging Clin N Am. 17(2):291-313, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19406360%5Bpmid%5D)
|
||||
1. [Kranz PG et al: Does diffusion-weighted imaging represent the ischemic core? An evidence-based systematic review. AJNR Am J Neuroradiol. 30(6):1206-12, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19357385%5Bpmid%5D)
|
||||
1. [Lee KY et al: Distal hyperintense vessels on FLAIR: an MRI marker for collateral circulation in acute stroke? Neurology. 72(13):1134-9, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19211928%5Bpmid%5D)
|
||||
1. [Sanossian N et al: Angiography reveals that fluid-attenuated inversion recovery vascular hyperintensities are due to slow flow, not thrombus. AJNR Am J Neuroradiol. 30(3):564-8, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19022866%5Bpmid%5D)
|
||||
1. [Soares BP, Chien JD, Wintermark M. MR and CT monitoring of recanalization, reperfusion, and penumbra salvage: everything that recanalizes does not necessarily reperfuse! Stroke. 40(3 Suppl):S24-7, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19064812%5Bpmid%5D)
|
||||
1. [Chen Z et al: Evaluating ischemic stroke with diffusion tensor imaging. Neurol Res. 30(7):720-6, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18513464%5Bpmid%5D)
|
||||
1. [Provenzale JM et al: Optimization of perfusion imaging for acute cerebral ischemia: review of recent clinical trials and recommendations for future studies. AJR Am J Roentgenol. 191(4):1263-70, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18806174%5Bpmid%5D)
|
||||
1. [Lell MM et al: New techniques in CT angiography. Radiographics. 26 Suppl 1:S45-62, 2006](http://www.ncbi.nlm.nih.gov/pubmed/?term=17050518%5Bpmid%5D)
|
||||
1. [Bourekas EC et al: Intraarterial thrombolytic therapy within 3 hours of the onset of stroke. Neurosurgery. 54(1):39-44; discussion 44-6, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14683539%5Bpmid%5D)
|
||||
1. [Diaz J et al: Cerebral ischemia: new risk factors. Cerebrovasc Dis. 17 Suppl 1:43-50, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14694279%5Bpmid%5D)
|
||||
1. [Fiebach JB et al: Stroke magnetic resonance imaging is accurate in hyperacute intracerebral hemorrhage: a multicenter study on the validity of stroke imaging. Stroke. 35(2):502-6, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14739410%5Bpmid%5D)
|
||||
1. [Fiehler J et al: Predictors of apparent diffusion coefficient normalization in stroke patients. Stroke. 35(2):514-9, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14739409%5Bpmid%5D)
|
||||
1. [Gass A et al: Diffusion-weighted MRI for the "small stuff": the details of acute cerebral ischaemia. Lancet Neurol. 3(1):39-45, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14693110%5Bpmid%5D)
|
||||
1. [Kelly PJ et al: Inflammation, homocysteine, and vitamin B6 status after ischemic stroke. Stroke. 35(1):12-5, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14657454%5Bpmid%5D)
|
||||
1. [Kidwell CS et al: Comparison of MRI and CT for detection of acute intracerebral hemorrhage. JAMA. 292(15):1823-30, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15494579%5Bpmid%5D)
|
||||
1. [Mahagne MH et al: Voxel-based mapping of cortical ischemic damage using Tc 99m L,L-ethyl cysteinate dimer SPECT in acute stroke. J Neuroimaging. 14(1):23-32, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14748205%5Bpmid%5D)
|
||||
1. [Nakajima M et al: Relationships between angiographic findings and National Institutes of Health stroke scale score in cases of hyperacute carotid ischemic stroke. AJNR Am J Neuroradiol. 25(2):238-41, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14970023%5Bpmid%5D)
|
||||
1. [Borisch I et al: Preoperative evaluation of carotid artery stenosis: comparison of contrast-enhanced MR angiography and duplex sonography with digital subtraction angiography. AJNR Am J Neuroradiol. 24(6):1117-22, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12812936%5Bpmid%5D)
|
||||
1. [Eastwood JD et al: Quantitative assessment of the time course of infarct signal intensity on diffusion-weighted images. AJNR Am J Neuroradiol. 24(4):680-7, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12695203%5Bpmid%5D)
|
||||
1. [Leary MC et al: Validation of computed tomographic middle cerebral artery "dot"sign: an angiographic correlation study. Stroke. 34(11):2636-40, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=14593125%5Bpmid%5D)
|
||||
1. [Tomandl BF et al: Comprehensive imaging of ischemic stroke with multisection CT. Radiographics. 23(3):565-92, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12740462%5Bpmid%5D)
|
||||
1. [Toyoda K et al: Fluid-attenuated inversion recovery intraarterial signal: an early sign of hyperacute cerebral ischemia. AJNR Am J Neuroradiol. 22(6):1021-9, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11415892%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
*Coronal graphic illustrates a left M1 occlusion. A proximal occlusion affects the entire middle cerebral artery (MCA) territory, including the basal ganglia, which are perfused by lenticulostriate (perforating) arteries <img src='img/arrows/BS.png'/>. Acute ischemia is often identified by subtle loss of the gray-white matter interfaces with blurring of the basal ganglia and an "insular ribbon" sign on the initial CT.*
|
||||
|
||||
|
||||
*Coronal graphic illustrates a left M1 occlusion. A proximal occlusion affects the entire middle cerebral artery (MCA) territory, including the basal ganglia, which are perfused by lenticulostriate (perforating) arteries <img src='img/arrows/BS.png'/>. Acute ischemia is often identified by subtle loss of the gray-white matter interfaces with blurring of the basal ganglia and an "insular ribbon" sign on the initial CT.*
|
||||
|
||||
|
||||
*Axial NECT demonstrates a hyperdense MCA sign representing acute thrombus <img src='img/arrows/WS.png'/> in a patient with acute stroke symptoms.*
|
||||
|
||||
|
||||
*Axial NECT shows subtle loss of the right temporal gray-white matter interfaces <img src='img/arrows/WS.png'/> representing an "insular ribbon" sign.*
|
||||
|
||||
|
||||
*Axial pCT (CBF) shows decreased blood flow <img src='img/arrows/BO.png'/> in the right hemisphere related to hyperacute MCA ischemia. The CBF and CBV color maps cephalad to this slice showed a large MCA wedge-shaped defect. There was a similar perfusion abnormality on the TTP maps (not shown). Lack of a mismatch between CBV and TTP maps suggests that no ischemic penumbra is present.*
|
||||
|
||||
|
||||
*Axial DWI MR shows a large wedge-shaped hyperintensity related to restricted diffusion <img src='img/arrows/WO.png'/> representing acute ischemia in a left MCA distribution. There is sparing of the basal ganglia, consistent with distal M1 occlusion.*
|
||||
|
||||
|
||||
*Axial NECT shows a hypodense wedge-shaped region of acute infarct <img src='img/arrows/WS.png'/> with mild mass effect and sulcal effacement related to a right M1 embolic occlusion due to a calcified thrombus <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*Axial NECT demonstrates bilateral posterior circulation hypodensities <img src='img/arrows/WS.png'/> in a 20-month-old boy presenting with seizures after recent circumcision complicated by hematoma.*
|
||||
|
||||
|
||||
*Axial NECT shows hyperdense thrombus <img src='img/arrows/WS.png'/> in the distal basilar artery of a 66-year-old woman with altered sensorium. Percutaneous thrombolysis is usually considered at later time points, up to 24 hours, because of the high morbidity and mortality associated with basilar thrombosis.*
|
||||
|
||||
|
||||
*Axial DWI MR shows hyperintensity related to restricted diffusion in a patient with vertebrobasilar disease and a posterior inferior cerebellar artery acute infarct. MR is superior to CT in evaluation of a posterior fossa stroke.*
|
||||
|
||||
|
||||
*Coronal CTA MIP reconstruction shows a focal filling defect within the proximal M1 segment <img src='img/arrows/WS.png'/> in a patient with acute MCA ischemia. Intraarterial thrombolysis may be helpful if the patient presents to the emergency department within 6 hours of symptoms onset.*
|
||||
|
||||
|
||||
*Angiography in a 27-year-old man with a history of methamphetamine and tobacco use shows focal tight stenosis within the distal right M1 segment <img src='img/arrows/WS.png'/>. He presented with stuttering symptoms of left-sided weakness and face droop.*
|
||||
|
||||
|
||||
*Sagittal T2WI MR shows multiple watershed ischemic foci in the deep white matter <img src='img/arrows/WS.png'/> in a "string of pearls" configuration.*
|
||||
|
||||
|
||||
*Axial T2* GRE MR shows multifocal hemorrhages <img src='img/arrows/WS.png'/> within an ischemic infarct in a 13-year-old boy with 3 weeks of fatigue, epistaxis, and acute loss of consciousness. He was found to have leukemia complicated by disseminated intravascular coagulation.*
|
||||
|
||||
|
||||
*Axial NECT shows cerebellar infarcts <img src='img/arrows/WS.png'/> in a 34-year-old woman with bilateral vertebral artery dissections. Note effacement of basal cisterns <img src='img/arrows/WO.png'/> and temporal horn dilation <img src='img/arrows/WC.png'/> indicating upward transtentorial herniation.*
|
||||
|
||||
|
||||
*Axial T2WI MR shows bilateral wedge-shaped occipital areas of hyperintensity <img src='img/arrows/WS.png'/> in a 77-year-old woman, which do not allow for a reliable distinction between chronic and acute ischemia.*
|
||||
|
||||
|
||||
*Axial DWI MR in the same patient accurately reflects the acute area of left occipital ischemia <img src='img/arrows/WS.png'/>, while encephalomalacia is apparent in the right occipital lobe <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*Axial NECT shows multifocal hypodensities in the left cerebellum <img src='img/arrows/WS.png'/>, consistent with embolic infarction within the left PICA distribution in this 40-year-old man with longstanding insulin-dependent diabetes and chronic renal failure. He presented with acute severe headache, nausea, and vomiting without localizing neurological finding.*
|
||||
|
||||
|
||||
*Axial CTA shows occlusion of the left vertebral artery <img src='img/arrows/WS.png'/>. Compare with a normal dominant right vertebral artery <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*Axial CTA shows intimal flap <img src='img/arrows/WS.png'/> in a 47-year-old woman with bilateral internal carotid artery dissections.*
|
||||
|
||||
|
||||
*Axial NECT shows hyperdense left deep nuclei <img src='img/arrows/WS.png'/> in a patient post recent IV thrombolytic therapy followed by mechanical thrombectomy for left MCA occlusion. These may reflect contrast staining &/or hemorrhage. Contrast gradually fades over time and does not imply worse prognosis. Matching hypointensity on GRE suggests hemorrhage.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR shows heterogeneous gyriform enhancement in right MCA territory due to breakdown of BBB in subacute infarction. This appearance can mimic glioblastoma. Follow-up imaging may be important in patients without available imaging at the time of ictus to ensure appropriate evolution.*
|
||||
|
||||
|
||||
*Anteroposterior angiography shows left M1 occlusion <img src='img/arrows/BO.png'/> and associated prominent lenticulostriate vessels <img src='img/arrows/BC.png'/>.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
*Axial DWI MR in a patient 2 hours after stroke onset shows restricted diffusion. Correlative ADC hypointensity was also demonstrated within the same geographic area (not shown).*
|
||||
|
||||
|
||||
*Axial CECT shows abrupt right MCA cut-off <img src='img/arrows/WC.png'/> in a patient with hyperacute stroke symptoms. (Courtesy J. Eastwood, MD.)*
|
||||
|
||||
|
||||
*Axial DWI MR shows small emboli infarcts <img src='img/arrows/WS.png'/> in the left hemisphere.*
|
||||
|
||||
|
||||
*Axial CT perfusion map in the same patient reveals significantly prolonged mean transit time within the MCA distribution (red region).*
|
||||
|
||||
|
||||
*Axial DWI MR shows restricted diffusion within the right occipital lobe in a patient with sudden onset of visual symptoms.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows multiple foci of intraarterial high signal <img src='img/arrows/WS.png'/> suggesting slow flow in this patient with left internal carotid artery dissection.*
|
||||
|
||||
|
||||
*Coronal CTA shows slight irregularity within the reconstituted left vertebral artery segment <img src='img/arrows/BS.png'/>, consistent with dissection in this symptomatic patient.*
|
||||
|
||||
|
||||
*Axial single-phase arterial spin-labeling (ASL) perfusion shows hemispheric asymmetry, decreased on the left <img src='img/arrows/WS.png'/>, in a patient with acute left internal carotid artery dissection.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows classic deep white matter watershed ischemic foci <img src='img/arrows/WS.png'/> in a "string of pearls" appearance.*
|
||||
|
||||
|
||||
*Axial DWI MR in a 35-year-old woman post transsphenoidal surgery for Cushing disease shows multifocal infarctions <img src='img/arrows/WS.png'/> as a complication of Enterobacter meningitis.*
|
||||
|
||||
+370
@@ -0,0 +1,370 @@
|
||||
---
|
||||
title: "Carotid Stenosis, Extracranial"
|
||||
docid: "1ebd8530-ebfc-4b36-9cd9-d9723c06f976"
|
||||
authors:
|
||||
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|
||||
value: "Bronwyn E. Hamilton, MD"
|
||||
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|
||||
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|
||||
slug: "vasculature"
|
||||
treeNodeId: "9d3db335-364f-44ec-b2e2-30b03ce93228"
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|
||||
name: "Diagnosis"
|
||||
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|
||||
treeNodeId: "4a210126-9f87-404e-b419-a73f44d0e94c"
|
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|
||||
name: "Extracranial Cerebral Arteries"
|
||||
slug: "extracranial-cerebral-arteries"
|
||||
treeNodeId: "593e17de-cd84-4587-8349-872ed33d28c4"
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name: "Carotid Stenosis, Extracranial"
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|
||||
imageCount: 18
|
||||
lastUpdated: "07/09/21"
|
||||
pageDescription: "Carotid Stenosis, Extracranial"
|
||||
pageKeywords: "Vasculature, Diagnosis, Extracranial Cerebral Arteries, Carotid Stenosis, Extracranial"
|
||||
pageTitle: "Carotid Stenosis, Extracranial | STATdx"
|
||||
enhancedTitle: "Carotid Stenosis, Extracranial"
|
||||
type: "DX"
|
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references: true
|
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breadcrumbs:
|
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- "Vasculature"
|
||||
- "Diagnosis"
|
||||
- "Extracranial Cerebral Arteries"
|
||||
- "Carotid Stenosis, Extracranial"
|
||||
---
|
||||
# KEY FACTS
|
||||
|
||||
- ## Terminology
|
||||
|
||||
|
||||
- Narrowing of cervical internal carotid artery or common carotid artery
|
||||
- ## Imaging
|
||||
|
||||
|
||||
- Extracranial carotid atherosclerotic vascular disease is most common at carotid bulb
|
||||
- Carotid duplex US shows vessel narrowing with turbulent flow, increased peak systolic velocity, and spectral broadening
|
||||
- CTA allows estimation of stenosis severity
|
||||
- MRA flow gap can occur in stenoses > 95%, causing misdiagnosis of occlusion
|
||||
- DSA is gold standard for evaluating severity of stenosis
|
||||
- "String" sign = very high grade stenosis
|
||||
- Slow antegrade "trickle" blood flow
|
||||
- ## Top Differential Diagnoses
|
||||
|
||||
|
||||
- Dissection
|
||||
- Fibromuscular dysplasia
|
||||
- Extrinsic compressive lesion (rare)
|
||||
- ## Pathology
|
||||
|
||||
|
||||
- Risk of stroke increases with stenosis severity, an indirect measure of plaque volume and potential for complicated plaque or embolization
|
||||
- ## Clinical Issues
|
||||
|
||||
|
||||
- NASCET showed that symptomatic patients with stenosis ≥ 70% (associated with stroke risk) benefit from carotid endarterectomy (CEA)
|
||||
- ACAS showed that asymptomatic patients with 60% stenosis benefit from CEA
|
||||
- SAPPHIRE compared CEA to carotid artery stenting (CAS) in high-risk patients with carotid stenosis
|
||||
- Lower complication rate with CAS
|
||||
- No difference in stroke after 3 years
|
||||
|
||||
# TERMINOLOGY
|
||||
|
||||
- ## Synonyms
|
||||
|
||||
|
||||
- Carotid atherosclerotic vascular disease (ASVD)
|
||||
- ## Definitions
|
||||
|
||||
|
||||
- Narrowing of cervical segment of internal carotid artery (ICA) or common carotid artery (CCA)
|
||||
|
||||
# IMAGING
|
||||
|
||||
- ## General Features
|
||||
|
||||
|
||||
- ### Best diagnostic clue
|
||||
|
||||
|
||||
- Carotid duplex US shows vessel narrowing with turbulent flow, increased peak systolic velocity, and spectral broadening
|
||||
- ### Location
|
||||
|
||||
|
||||
- Extracranial carotid ASVD is most common at carotid bulb
|
||||
- ### Size
|
||||
|
||||
|
||||
- Variable severity and length of stenosis; usually < 3 cm
|
||||
- Smooth or irregular narrowing ± ulceration ± intraluminal thrombus
|
||||
- ## CT Findings
|
||||
|
||||
|
||||
- ### NECT
|
||||
|
||||
|
||||
- Calcified ASVD plaque at CCA bifurcation ± ICA
|
||||
- May show thromboembolic or hemodynamic cerebral infarction
|
||||
- Typically ipsilateral anterior circulation
|
||||
- Posterior cerebral artery (PCA) stroke possible via posterior communicating artery or fetal PCA
|
||||
- ### CTA
|
||||
|
||||
|
||||
- Useful as screening tool
|
||||
- CTA allows estimation of stenosis severity
|
||||
- Multiplanar reformatted images in sagittal and coronal planes are helpful
|
||||
- Accuracy is reduced if extensive lesional calcification is present
|
||||
- Maximal carotid wall thickness ≥ 4 mm is predictive of future carotid ischemic stroke
|
||||
- Dental amalgam artifacts may hinder visualization
|
||||
- May show intraluminal thrombus as filling defect within enhanced vessel
|
||||
- Unreliable visualization of plaque ulceration
|
||||
- Patchy/homogeneous low density in wall may be seen with large necrotic/lipid plaque
|
||||
- ## MR Findings
|
||||
|
||||
|
||||
- ### T1WI
|
||||
|
||||
|
||||
- Reduced caliber of ICA flow void ± intraluminal signal due to thrombus or slow flow
|
||||
- Fat-saturated sequence if dissection is suspected as alternate etiology
|
||||
- Intramural crescentic high signal represents methemoglobin in vessel wall (dissection)
|
||||
- ### DWI
|
||||
|
||||
|
||||
- Most sensitive and specific for acute/subacute ischemia or infarction
|
||||
- ### MRA
|
||||
|
||||
|
||||
- Provides multidirectional imaging (vs. conventional DSA)
|
||||
- Time-of-flight (TOF) MRA: Intravoxel dephasing causes signal loss with flow turbulence due to stenosis
|
||||
- Affects 2D > 3D TOF images
|
||||
- Accentuates severity of stenosis
|
||||
- Gadolinium-enhanced MRA is superior to TOF sequences
|
||||
- Flow gap can occur in stenoses > 95%, causing misdiagnosis of occlusion
|
||||
- Brain T2WI, FLAIR, and DWI may show rosary-like lesions in centrum semiovale ipsilateral to stenosis, indicative of watershed ischemia or infarction
|
||||
- ## Ultrasonographic Findings
|
||||
|
||||
|
||||
- ### Grayscale ultrasound
|
||||
|
||||
|
||||
- Calcified plaque causes acoustic shadowing and may limit assessment of vessel lumen
|
||||
- ### Pulsed Doppler
|
||||
|
||||
|
||||
- Duplex US: Flow velocity within stenosis is proportional to severity of stenosis
|
||||
- Flow turbulence within and beyond stenosis
|
||||
- Spectral broadening: Increased range of velocities is seen in moderate to severe stenoses
|
||||
- ## Angiographic Findings
|
||||
|
||||
|
||||
- Conventional
|
||||
- DSA is gold standard for evaluation of carotid stenosis severity
|
||||
- Use of reverse-curve catheters (e.g., Simmons) can avoid inadvertent crossing of carotid bifurcation stenosis with guidewire and dislodgement of plaque
|
||||
- Intraluminal thrombus is seen as filling defect in contrast column
|
||||
- Can evaluate collateral flow to ischemic hemisphere from communicating arteries and leptomeningeal collaterals by studying contralateral ICA and dominant vertebral artery
|
||||
- "String" sign = very high grade stenosis, slow antegrade "trickle" blood flow
|
||||
- Typically seen during late phase of angiogram
|
||||
- May require prolonged DSA acquisitions for visualization
|
||||
- Preocclusive state with high risk of stroke
|
||||
- Important as carotid endarterectomy (CEA) or carotid artery stenting (CAS) may be an option if ICA is still patent
|
||||
- More sensitive and specific than CTA and MRA for subtotal occlusion with string sign
|
||||
- ## Other Modality Findings
|
||||
|
||||
|
||||
- CT/MR perfusion
|
||||
- Can provide assessment of collateral flow to territory normally perfused by stenotic carotid artery
|
||||
- Collateral circulation correlates with risk of hemodynamic ischemia or infarction
|
||||
- Measurement of carotid stenosis severity
|
||||
- North American Symptomatic Carotid Endarterectomy Trial (NASCET) method is most widely accepted
|
||||
- NASCET: Denominator is normal poststenotic ICA diameter
|
||||
- European Carotid Surgery Trial (ECST): Denominator is estimated normal diameter of carotid bulb
|
||||
- ## Imaging Recommendations
|
||||
|
||||
|
||||
- Ultrasound or CTA as screening tool
|
||||
- CTA/MRA for comprehensive cerebrovascular evaluation
|
||||
- DSA if US/CTA/MRA is equivocal or shows "occlusion"
|
||||
|
||||
# DIFFERENTIAL DIAGNOSIS
|
||||
|
||||
- ## Dissection
|
||||
|
||||
|
||||
- Typically spares carotid bulb and ICA origin
|
||||
- Usually no calcification (dystrophic Ca++ is rare)
|
||||
- Intimal flap with differential filling of true and false lumens on DSA
|
||||
- Crescentic intramural high signal (methemoglobin) on T1WI MR
|
||||
- ## Fibromuscular Dysplasia
|
||||
|
||||
|
||||
- Affects medium to large arteries
|
||||
- M:F = 1:3
|
||||
- Age peak: 25-50 years
|
||||
- Classically shows alternating segments of beading and stenoses involving extracranial ICA and external carotid, vertebral, and renal arteries
|
||||
- ## Extrinsic Compressive Lesion (Rare)
|
||||
|
||||
|
||||
- Carotid space neoplasm (e.g., carotid body paraganglioma, glomus jugulare tumor)
|
||||
|
||||
# PATHOLOGY
|
||||
|
||||
- ## General Features
|
||||
|
||||
|
||||
- ### Etiology
|
||||
|
||||
|
||||
- Risk of stroke increases with stenosis severity, an indirect measure of plaque volume and potential for complicated plaque/embolization
|
||||
- Larger plaques are complicated by hemorrhage, necrosis, and disruption of fibrous cap and intima, causing embolization
|
||||
- Plaque composition and surface morphology are also stroke risk factors
|
||||
- Irregular plaque surface: ↑ stroke risk on medical treatment for all degrees of stenosis
|
||||
- Hypoperfusion may cause watershed infarcts &/or centrum semiovale lesions
|
||||
- Significant ICA narrowing is identified in 20-30% of carotid territory stroke patients (vs. 5-10% of general population)
|
||||
- ## Gross Pathologic & Surgical Features
|
||||
|
||||
|
||||
- Fatty streak: Raised lesion due to fatty deposit in intima
|
||||
- Fibrous (fibrolipid) plaque: Cholesterol + fibrous tissue with collagen cap
|
||||
- Complicated plaque: Unstable; may rupture, thrombose, calcify, or hemorrhage
|
||||
- ## Microscopic Features
|
||||
|
||||
|
||||
- ASVD: Fatty streaks, lipid-laden macrophages and smooth muscle cells, fibrous cap, cholesterol deposits, foam cells, plaque rupture ± thrombus
|
||||
|
||||
# CLINICAL ISSUES
|
||||
|
||||
- ## Presentation
|
||||
|
||||
|
||||
- Stroke is 3rd most common cause of death in Western countries
|
||||
- Transient ischemic attack (TIA): Neurological deficit that spontaneously resolves in < 24 hours
|
||||
- 80% resolve in < 1 hour
|
||||
- Precedes 30% of strokes
|
||||
- 50% of subsequent strokes occur < 1 year from TIA
|
||||
- Reversible ischemic neurological deficit: Neurological deficit > 24 hours but < 3 weeks
|
||||
- Amaurosis fugax (transient, monocular embolic blindness)
|
||||
- Asymptomatic carotid bruit: 20% have > 60% ICA stenosis (3x normal population)
|
||||
- ## Natural History & Prognosis
|
||||
|
||||
|
||||
- Progressive
|
||||
- ## Treatment
|
||||
|
||||
|
||||
- Reduction of risk factors, which include hypertension, smoking, diabetic control, and hypercholesterolemia
|
||||
- Medical: Aspirin, statins
|
||||
- NASCET (1991)
|
||||
- Symptomatic stenosis ≥ 70% (associated with significant stroke risk) benefits from CEA
|
||||
- Symptomatic moderate stenosis (50-69%) also benefits from endarterectomy in selected cases
|
||||
- Asymptomatic Carotid Atherosclerosis Study (ACAS, 1995)
|
||||
- Asymptomatic patients with 60% stenosis benefit from CEA
|
||||
- CAS is becoming increasingly utilized and substantiated as viable alternative to CEA
|
||||
- CAS with distal protection device is associated with risk of periprocedural stroke ≤ CEA
|
||||
- Stenting and Angioplasty With Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) 2004 study
|
||||
- Compared CEA with CAS in high-risk patients (comorbidities, age > 80 years, recent surgery, etc.) with symptomatic and asymptomatic carotid stenoses
|
||||
- Lower complication rate with CAS; no difference in stroke incidence after 3 years (7.1% CAS vs. 6.7% CEA)
|
||||
|
||||
# DIAGNOSTIC CHECKLIST
|
||||
|
||||
- ## Consider
|
||||
|
||||
|
||||
- Use of reverse-curve catheters for catheterization of CCA when carotid stenosis is suspected
|
||||
- ## Image Interpretation Pearls
|
||||
|
||||
|
||||
- MRA often exaggerates degree of stenosis
|
||||
- Look for intraluminal filling defect (CAS is contraindicated if intraluminal thrombus is present)
|
||||
- ## MIPS Considerations
|
||||
|
||||
|
||||
- MIPS Measure 195: Radiology: Stenosis Measurement in Carotid Imaging Reports
|
||||
- Last updated 2021
|
||||
- Percentage of final reports for carotid imaging studies (neck MRA, neck CTA, neck duplex ultrasound, carotid angiogram) performed that include **direct or indirect reference to** **measurements of distal internal carotid diameter as denominator for stenosis measurement**
|
||||
|
||||
60075056-b951-47fe-b646-4817b546b29d
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [MIPS Measure 195: Radiology: Stenosis Measurement in Carotid Imaging Reports (to reference if using CQMS). Centers for Medicare and Medicaid Services (CMS). 2021.](https://qpp.cms.gov/docs/QPP_quality_measure_specifications/CQM-Measures/2021_measure_195_MIPSCQM.pdf)
|
||||
1. [MIPS Measure 195: Radiology: Stenosis Measurement in Carotid Imaging Reports (to reference if using Medicare Part B claims). Centers for Medicare and Medicaid Services (CMS). 2021.](https://qpp.cms.gov/docs/QPP_quality_measure_specifications/Claims-Registry-Measures/2021_measure_195_MedicarePartBClaims.pdf)
|
||||
1. [Magge R et al: Clinical risk factors and CT imaging features of carotid atherosclerotic plaques as predictors of new incident carotid ischemic stroke: a retrospective cohort study. AJNR Am J Neuroradiol. 34(2):402-9, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=22859283%5Bpmid%5D)
|
||||
1. [Brott TG et al: 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease: executive summary: Stroke. 42(8):e420-63, 2011. Erratum in: Stroke. 42(8):e541, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=-1%5Bpmid%5D)
|
||||
1. [Halliday A et al: Prevention of disabling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomised controlled trial. Lancet. 363(9420):1491-502, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15135594%5Bpmid%5D)
|
||||
1. [Yadav JS: Carotid stenting in high-risk patients: design and rationale of the SAPPHIRE trial. Cleve Clin J Med. 71 Suppl 1:S45-6, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14964484%5Bpmid%5D)
|
||||
1. [No authors listed: Carotid endarterectomy for patients with asymptomatic internal carotid artery stenosis. National Institute of Neurological Disorders and Stroke. J Neurol Sci. 129(1):76-7, 1995](http://www.ncbi.nlm.nih.gov/pubmed/?term=7751850%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
*Sagittal reformat CTA shows irregularity and focal high-grade stenosis of the proximal internal carotid artery (ICA) <img src='img/arrows/WS.png'/>, typical of atherosclerotic disease. Note areas of calcified plaque <img src='img/arrows/WO.png'/>, which indicate an atherosclerotic etiology.*
|
||||
|
||||
|
||||
*Sagittal reformat CTA shows irregularity and focal high-grade stenosis of the proximal internal carotid artery (ICA) <img src='img/arrows/WS.png'/>, typical of atherosclerotic disease. Note areas of calcified plaque <img src='img/arrows/WO.png'/>, which indicate an atherosclerotic etiology.*
|
||||
|
||||
|
||||
*Lateral DSA confirms similar findings to the CTA (same patient) typical of atherosclerotic high-grade carotid stenosis: Irregular short-segment narrowing <img src='img/arrows/WS.png'/> with more proximal ulceration <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*Sagittal MRA shows a flow gap in the ICA <img src='img/arrows/WS.png'/>. MRA overestimates stenosis and occlusions; therefore, this must be confirmed with another vascular imaging modality to avoid misinterpretation.*
|
||||
|
||||
|
||||
*Color Doppler ultrasound (same patient) shows high flow velocities, anatomical narrowing, and spectral broadening, confirming that not an occlusion but a high-grade and hemodynamically significant stenosis (~ 80-99%) of the ICA bifurcation is present.*
|
||||
|
||||
|
||||
*Sagittal reformat CTA demonstrates a high-grade stenosis of the internal carotid artery distal to its origin <img src='img/arrows/WS.png'/> and irregular narrowing and ulceration more proximally at the carotid bifurcation <img src='img/arrows/WO.png'/>, findings typical for atherosclerotic narrowing.*
|
||||
|
||||
|
||||
*Lateral DSA (same patient) demonstrates similar findings compared with CTA: Ulceration and narrowing at the internal carotid artery origin <img src='img/arrows/WO.png'/> and more distal high-grade stenosis <img src='img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Sagittal CTA shows irregular ulcerated plaque <img src='img/arrows/WS.png'/> at the internal carotid artery origin, typical of atherosclerotic disease. Although a hemodynamically significant stenosis may not be present, this plaque is morphology prone to embolic complications.*
|
||||
|
||||
|
||||
*Oblique 3D reformation of a CTA shows diffuse beading of the distal cervical internal carotid artery <img src='img/arrows/WS.png'/>, typical in appearance for fibromuscular dysplasia. Both internal carotid and renal arteries (not shown) were similarly affected.*
|
||||
|
||||
|
||||
*Coronal MRA appears nearly normal in this patient with distal cervical left ICA dissection. Note the mild smoothly marginated caliber change <img src='img/arrows/WS.png'/> that is easily missed until compared with the contralateral side. The ICAs, unlike the vertebral arteries, normally demonstrate a symmetric size in the neck.*
|
||||
|
||||
|
||||
*Axial T1WI FS MR can be useful to confirm suspected dissection, as in this case (same patient) where crescentic mural hematoma is visible <img src='img/arrows/WS.png'/> around the luminal flow void.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
*Oblique CCA DSA shows a calcified plaque at the carotid bifurcation extending into the ICA with associated stenosis <img src='img/arrows/WS.png'/>. An intraluminal filling defect <img src='img/arrows/WO.png'/> is seen. It represented a thrombus for which the patient was anticoagulated. DSA 5 days later revealed resolution of the thrombus, and carotid artery stenting was undertaken at that time.*
|
||||
|
||||
|
||||
*Carotid duplex spectral waveform in the same patient shows spectral broadening and a peak systolic velocity of 598 cm/s in keeping with a 70-99% stenosis.*
|
||||
|
||||
|
||||
*Oblique CCA DSA shows an ulcerated ASVD plaque at the carotid bifurcation <img src='img/arrows/WS.png'/>. There is an additional plaque distally <img src='img/arrows/BS.png'/> but no significant carotid stenosis.*
|
||||
|
||||
|
||||
*Carotid duplex ultrasound of the proximal ICA shows a moderate stenosis due to ASVD <img src='img/arrows/WS.png'/>. Within the stenotic segment there is flow turbulence as depicted by variations in color and intensity <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*Sagittal gadolinium-enhanced MRA of the carotid bifurcation shows a flow gap at the ICA origin <img src='img/arrows/WS.png'/>. MRA typically overestimates the degree of stenosis.*
|
||||
|
||||
|
||||
*Sagittal CTA in a different patient shows a pinhole stenosis at the ICA origin <img src='img/arrows/WS.png'/>. Note adjacent calcifications within the ASVD plaque <img src='img/arrows/WC.png'/> and artifact from dental amalgam <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*Lateral CCA DSA shows a high-grade stenosis of the ICA <img src='img/arrows/WS.png'/> and indentation of the vessel lumen by plaque <img src='img/arrows/WO.png'/>. Note gracile cervical ICA <img src='img/arrows/BS.png'/> due to proximal flow restriction.*
|
||||
|
||||
|
||||
*Oblique CCA DSA shows a high-grade ASVD stenosis at the carotid bulb <img src='img/arrows/WS.png'/> with associated calcifications <img src='img/arrows/BS.png'/>.*
|
||||
|
||||
+439
@@ -0,0 +1,439 @@
|
||||
---
|
||||
title: "Cerebral Hyperperfusion Syndrome"
|
||||
docid: "e66febb9-d79e-4f04-88b1-205ba8a0822f"
|
||||
authors:
|
||||
- key: "5cff4116-3654-4b3a-bb75-5ebe0b8c9850"
|
||||
value: "Anne G. Osborn, MD, FACR"
|
||||
breadcrumbs:
|
||||
-
|
||||
name: "Brain"
|
||||
slug: "brain"
|
||||
treeNodeId: "6d8829f1-14d7-45af-8675-255189aa526a"
|
||||
-
|
||||
name: "Diagnosis"
|
||||
slug: "diagnosis"
|
||||
treeNodeId: "51c00394-446e-4a38-94af-d3b1d14d34e8"
|
||||
-
|
||||
name: "Pathology-Based Diagnoses"
|
||||
slug: "pathology-based-diagnoses"
|
||||
treeNodeId: "d9d3a8ed-f21b-4831-8c77-591a3500ef77"
|
||||
-
|
||||
name: "Stroke"
|
||||
slug: "stroke"
|
||||
treeNodeId: "12307683-f1ff-4823-a7d3-b10b40f9fd82"
|
||||
-
|
||||
name: "Cerebral Ischemia and Infarction"
|
||||
slug: "cerebral-ischemia-and-infarction"
|
||||
treeNodeId: "51051846-a223-42f7-b626-2a5a26cf6c44"
|
||||
-
|
||||
name: "Cerebral Hyperperfusion Syndrome"
|
||||
slug: "cerebral-hyperperfusion-syndrome"
|
||||
treeNodeId: null
|
||||
category: "Brain"
|
||||
cmeTopicId: "32753552-21d2-4b3a-bb83-721ad78e8c95"
|
||||
documentVersionId: "26eadfe0-1ff5-4d74-8dfb-927c31c6e893"
|
||||
imageCount: 15
|
||||
lastUpdated: "08/05/20"
|
||||
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 increase 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
|
||||
- Acute hypertensive encephalopathy, 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% increase in rCBF compared to preoperative values
|
||||
- Major increase in ipsilateral CBF well above normal metabolic demands
|
||||
- Usually following carotid revascularization procedure
|
||||
- Carotid endarterectomy
|
||||
- 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 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, 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, hyperintensity
|
||||
- ### FLAIR
|
||||
|
||||
|
||||
- Hyperintense cortex
|
||||
- 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
|
||||
- Prolonged MTT
|
||||
- Side-to-side difference of 3 seconds predictive of CHS
|
||||
- ### T1WI C+
|
||||
|
||||
|
||||
- May be normal
|
||||
- May show slightly increased 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 increase in MCA flow velocity
|
||||
|
||||
# DIFFERENTIAL DIAGNOSIS
|
||||
|
||||
- [Acute Cerebral Ischemia-Infarction](/document/acute-cerebral-ischemiainfarction/a405285f-aaea-43ca-8dc4-6f8120eaabc1)
|
||||
- TTP/MTT prolonged (not decreased)
|
||||
- Typically shows restriction on DWI (CHS often negative)
|
||||
- [Status Epilepticus](/document/status-epilepticus/a058b733-4b80-46a1-8097-d68685ecf921)
|
||||
- Metabolic hyperperfusion in affected brain
|
||||
- History of seizure helpful but may not be available
|
||||
- [Acute Hypertensive Encephalopathy, PRES](/document/acute-hypertensive-encephalopathy--/890c1bd4-c108-49a1-8557-c8c701a7f278)
|
||||
- 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
|
||||
- Baroreceptor reflex breakdown
|
||||
- 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
|
||||
- Cerebral hyperperfusion syndrome
|
||||
|
||||
# CLINICAL ISSUES
|
||||
|
||||
- ## Presentation
|
||||
|
||||
|
||||
- ### Most common signs/symptoms
|
||||
|
||||
|
||||
- Symptoms range from mild to severe/life-threatening
|
||||
- Ipsilateral headache, neurologic deficit and seizures
|
||||
- Other signs/symptoms
|
||||
- Variable cognitive impairment
|
||||
- Face, eye pain
|
||||
- Timing
|
||||
- Peaks at 12 h 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% increase in CBF after treatment
|
||||
- Contralateral stenosis, chronic hypertension do not influence risk of CHS after CEA
|
||||
- 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
|
||||
- Decreased 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
|
||||
|
||||
# DIAGNOSTIC CHECKLIST
|
||||
|
||||
- ## Consider
|
||||
|
||||
|
||||
- Post-CEA/carotid artery stenting patient with neurologic deficit
|
||||
- Need to distinguish stroke/transient ischemic attack from CHS
|
||||
|
||||
8b8b5253-2a1e-4d24-9d1b-dc85e0dde35e
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Lin YH et al: Update on cerebral hyperperfusion syndrome. J Neurointerv Surg. ePub, 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. ePub, 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)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
*A 56-year-old man with > 70% stenosis of his proximal left cervical internal carotid artery (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'/>.*
|
||||
|
||||
|
||||
*A 56-year-old man with > 70% stenosis of his proximal left cervical internal carotid artery (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'/>.*
|
||||
|
||||
|
||||
*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'/>, basal ganglia <img src='img/arrows/WC.png'/>. DWI (not shown) was normal. This is a classic example of postcarotid endarterectomy hyperperfusion syndrome.*
|
||||
|
||||
|
||||
*Anteroposterior view of DSA shows abrupt occlusion of the left MCA just distal to its origin <img src='img/arrows/BS.png'/> 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'/>), 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'/>.*
|
||||
|
||||
|
||||
*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'/>.*
|
||||
|
||||
|
||||
*pMR in the same patient shows increased CBF in the right temporal lobe <img src='img/arrows/WO.png'/>, corresponding to the increased intravascular enhancement noted on 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'/> 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'/> and basal ganglia <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*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'/> 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'/> in the same area. This was cerebral hyperperfusion syndrome.*
|
||||
|
||||
@@ -0,0 +1,388 @@
|
||||
---
|
||||
title: "Chiari 1 Malformation"
|
||||
docid: "97837e15-0d39-4c87-8af0-028652b399a6"
|
||||
authors:
|
||||
- key: "2c9d2e67-05db-4d26-b8cb-02e0f7566179"
|
||||
value: "Usha D. Nagaraj, MD"
|
||||
- key: "b2e6dabb-ee1c-42a4-a332-9f0814c1c607"
|
||||
value: "Surjith Vattoth, MD, FRCR"
|
||||
breadcrumbs:
|
||||
-
|
||||
name: "Brain"
|
||||
slug: "brain"
|
||||
treeNodeId: "6d8829f1-14d7-45af-8675-255189aa526a"
|
||||
-
|
||||
name: "Diagnosis"
|
||||
slug: "diagnosis"
|
||||
treeNodeId: "51c00394-446e-4a38-94af-d3b1d14d34e8"
|
||||
-
|
||||
name: "Pathology-Based Diagnoses"
|
||||
slug: "pathology-based-diagnoses"
|
||||
treeNodeId: "d9d3a8ed-f21b-4831-8c77-591a3500ef77"
|
||||
-
|
||||
name: "Congenital Malformations"
|
||||
slug: "congenital-malformations"
|
||||
treeNodeId: "3595c1ab-3f1d-4896-b6bf-21d939d620b7"
|
||||
-
|
||||
name: "Chiari Malformations"
|
||||
slug: "chiari-malformations"
|
||||
treeNodeId: "62d04f46-bd30-4031-ac59-1b1f8ad544ed"
|
||||
-
|
||||
name: "Chiari 1 Malformation"
|
||||
slug: "chiari-1-malformation"
|
||||
treeNodeId: null
|
||||
category: "Brain"
|
||||
documentVersionId: "dd3b117c-bb35-4cb2-b42e-a22fc96536e7"
|
||||
imageCount: 20
|
||||
lastUpdated: "07/31/20"
|
||||
pageDescription: "Chiari 1 Malformation"
|
||||
pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Congenital Malformations, Chiari Malformations, Chiari 1 Malformation"
|
||||
pageTitle: "Chiari 1 Malformation | STATdx"
|
||||
enhancedTitle: "Chiari 1 Malformation"
|
||||
type: "DX"
|
||||
references: true
|
||||
ddx: true
|
||||
breadcrumbs:
|
||||
- "Brain"
|
||||
- "Diagnosis"
|
||||
- "Pathology-Based Diagnoses"
|
||||
- "Congenital Malformations"
|
||||
- "Chiari Malformations"
|
||||
- "Chiari 1 Malformation"
|
||||
---
|
||||
# KEY FACTS
|
||||
|
||||
- ## Terminology
|
||||
|
||||
|
||||
- Chiari 1 malformation (CM1); synonyms: Chiari type 1, Chiari 1 deformity, cerebellar tonsillar ectopia
|
||||
- ## Imaging
|
||||
|
||||
|
||||
- Pointed cerebellar tonsils extending ≥ 5 mm below foramen magnum (basion-opisthion/McRae line) with effacement of CSF spaces
|
||||
- ± retroflexed odontoid, horizontal shortened clivus, basilar invagination, atlanto-occipital assimilation
|
||||
- ± caudal descent of brainstem, brainstem compression, medullary kink
|
||||
- ± syringohydromyelia, scoliosis
|
||||
- ## Top Differential Diagnoses
|
||||
|
||||
|
||||
- Normal low-lying cerebellar tonsils
|
||||
- Chiari 2 malformation
|
||||
- Tonsillar herniation secondary to increased intracranial pressure
|
||||
- Intracranial hypotension
|
||||
- ## Pathology
|
||||
|
||||
|
||||
- Most common cause believed to be small/underdeveloped posterior fossa; no association with open spinal dysraphism
|
||||
- Can be result of premature closure of sutures
|
||||
- Causes include shunted infantile hydrocephalus, bone dysplasias, genetic syndromes
|
||||
- ## Clinical Issues
|
||||
|
||||
|
||||
- Most common presenting symptom: Occipital headache
|
||||
- Up to 30% of patients asymptomatic
|
||||
- Goal of surgery in symptomatic patients: Restore normal CSF flow at foramen magnum
|
||||
- Suboccipital decompression, resection of C1 posterior arch ± duraplasty, cerebellar tonsil cautery
|
||||
- ## Diagnostic Checklist
|
||||
|
||||
|
||||
- Degree of tonsillar descent does not always correlate with symptoms: CM1 frequently picked up incidentally
|
||||
- Look for presence of syrinx → makes surgical intervention more likely
|
||||
|
||||
# TERMINOLOGY
|
||||
|
||||
- ## Synonyms
|
||||
|
||||
|
||||
- Chiari type 1, Chiari 1 deformity
|
||||
- ## Definitions
|
||||
|
||||
|
||||
- Chiari 1 malformation (CM1): Compressed & pointed cerebellar tonsils extending below foramen magnum with effacement of CSF spaces
|
||||
|
||||
# IMAGING
|
||||
|
||||
- ## General Features
|
||||
|
||||
|
||||
- ### Best diagnostic clue
|
||||
|
||||
|
||||
- Pointed cerebellar tonsils (unilateral or bilateral) extending ≥ 5 mm below foramen magnum (basion-opisthion line, a.k.a. McRae line)
|
||||
- Mild variations in measurement reported in literature; measurement on its own may not be definitive of diagnosis
|
||||
- No consensus statement on exact definition
|
||||
- ### Location
|
||||
|
||||
|
||||
- Craniocervical junction (CCJ)
|
||||
- ## Radiographic Findings
|
||||
|
||||
|
||||
- Shortened horizontal clivus, basilar invagination, CCJ segmentation anomalies, scoliosis
|
||||
- ## CT Findings
|
||||
|
||||
|
||||
- Crowding of foramen magnum on axial CT images
|
||||
- Sagittal reconstructed images are very helpful
|
||||
- Partially imaged superior aspect of spinal cord syrinx may be identified
|
||||
- Associated osseous anomalies may include small posterior fossa, short horizontal clivus, retroverted dens, basilar invagination, platybasia, hypoplastic occipital condyles, segmentation anomalies (such as atlantooccipital assimilation), scoliosis
|
||||
- ## MR Findings
|
||||
|
||||
|
||||
- T1WI, T2WI, FLAIR
|
||||
- Pointed (not rounded) cerebellar tonsils extending ≥ 5 mm below foramen magnum
|
||||
- Crowded foramen magnum with small/effaced cisterns ± brainstem compression (kinking)
|
||||
- ± small posterior fossa, elongated 4th ventricle
|
||||
- ± syringohydromyelia/syrinx, scoliosis
|
||||
- Syrinx reported in 30-70% of cases
|
||||
- Patients with syrinx more likely to have scoliotic curve > 20⁰ (~ 70%) than those without syrinx (~ 45%)
|
||||
- Other descriptions usually considered subtypes
|
||||
- Chiari 1.5: Brainstem herniation
|
||||
- Obex located below foramen magnum
|
||||
- Complex Chiari: Medullary kink, retroflexed dens, abnormal clival-cervical angle, atlantooccipital assimilation, basilar invagination, platybasia
|
||||
- MR cine
|
||||
- Restricted CSF flow through foramen magnum ± ↑ brainstem/cerebellar tonsil motion (pistoning)
|
||||
- Clinical utility of this sequence debatable
|
||||
- ## Imaging Recommendations
|
||||
|
||||
|
||||
- ### Best imaging tool
|
||||
|
||||
|
||||
- Multiplanar MR
|
||||
- Axial True FISP/FIESTA MR of CCJ helpful in assessing degree of foramen magnum crowding
|
||||
- Spine imaging to look for spinal cord syrinx
|
||||
- Syrinx makes surgical intervention more likely
|
||||
|
||||
# DIFFERENTIAL DIAGNOSIS
|
||||
|
||||
- ## Normal Variation of Cerebellar Tonsil Position
|
||||
|
||||
|
||||
- Tonsils may normally lie below foramen magnum
|
||||
- May be accentuated by certain head positions
|
||||
- Tonsils retain normal rounded configuration
|
||||
- [Chiari 2 Malformation](/document/chiari-2/008f0235-43ba-47e6-b51c-cfd8526afd68)
|
||||
- Numerous intracranial findings centered around very small posterior fossa with hindbrain herniation in setting of open spinal dysraphism
|
||||
- More severe clinical phenotype than CM1
|
||||
- ## Tonsillar Herniation Secondary to Increased Intracranial Pressure
|
||||
|
||||
|
||||
- Neoplasm, hemorrhage, hydrocephalus, infarct
|
||||
- [Intracranial Hypotension](/document/intracranial-hypotension/b7e1fbcf-a25c-4b70-b825-0d4c51afc99d)
|
||||
- Look for "slumped" brainstem
|
||||
- Sagging midbrain, sunken hindbrain with diffuse dural thickening/enhancement, distended veins/dural sinuses, ± subdural hygromas
|
||||
- ## Chiari 0
|
||||
|
||||
|
||||
- Syringomyelia without cerebellar tonsillar ectopia; syrinx resolves after posterior fossa decompression
|
||||
- Diagnosis of exclusion (many other causes of spinal cord syrinx)
|
||||
|
||||
# PATHOLOGY
|
||||
|
||||
- ## General Features
|
||||
|
||||
|
||||
- ### Etiology
|
||||
|
||||
|
||||
- Primary congenital malformation vs. secondarily acquired morphologic changes
|
||||
- Primary: Posterior fossa underdevelopment theory most common
|
||||
- Underdevelopment of endochondral occipital bone → small posterior fossa vault + downward hindbrain herniation
|
||||
- Not all Chiari 1 patients have small posterior fossa
|
||||
- Secondary: Premature closure of cranial sutures &/or generalized abnormal bone formation
|
||||
- Shunted infantile hydrocephalus
|
||||
- Calvarial thickening of bone dysplasias or thalassemia
|
||||
- Genetic syndromes
|
||||
- Seen in 2-10% of patients with idiopathic intracranial hypertension (a.k.a. pseudotumor cerebri)
|
||||
- ### Genetics
|
||||
|
||||
|
||||
- Small posterior fossa in isolation is heritable
|
||||
- Multiple potential causative genes on chromosome 1 & 22 identified
|
||||
- Syndromic/familial associations (up to 60% of cases)
|
||||
- Craniosynostosis syndromes (ERF-related, FGFR-related: Apert, Crouzon, Pfeiffer)
|
||||
- Osteopathic syndromes (achondroplasia, rickets)
|
||||
- Vertebral anomalies (Klippel-Feil, VACTERL)
|
||||
- Craniofacial anomalies (Pierre-Robin, Goldenhar)
|
||||
- Macrocerebellum (Costello syndrome, Sotos syndrome, macrocephaly-capillary malformation syndrome, Alexander disease)
|
||||
- Increased brain volume (NF1/RAS/MAPK mutations/RASopathies, PTEN-PI3K/AKT mutations/PTENopathies)
|
||||
- Many others: Ehlers-Danlos syndrome, Marfan syndrome, Williams syndrome, Kabuki syndrome
|
||||
- ## Gross Pathologic & Surgical Features
|
||||
|
||||
|
||||
- Herniated cerebellar tonsils become atrophic/gliotic/necrotic
|
||||
- Arachnoid scarring & adhesions at foramen magnum
|
||||
|
||||
# CLINICAL ISSUES
|
||||
|
||||
- ## Presentation
|
||||
|
||||
|
||||
- ### Most common signs/symptoms
|
||||
|
||||
|
||||
- Occipital headache
|
||||
- Exacerbated by cough, Valsalva, neck extension, or physical exertion
|
||||
- Less common: Cerebellar, brainstem, bulbar, cord motor/sensory symptoms
|
||||
- Cerebellar symptoms: Ataxia, dysarthria, oscillopsia, nystagmus
|
||||
- Brainstem and Bulbar symptoms: Vertigo, diplopia, dysphagia, aspiration, apnea, syncope, bradycardia, sudden death (rare)
|
||||
- Spinal cord dysfunction: Motor and sensory losses, hyporeflexia, hyperreflexia, clonus, gait disturbance, neuropathic joint, urinary incontinence, positive Babinski sign, scoliosis
|
||||
- 15-30% of adults with CM1 are asymptomatic, up to 35% of children with 5-10 mm of tonsillar herniation are asymptomatic
|
||||
- Not much difference in clinical symptoms between complex Chiari & typical Chiari 1
|
||||
- ## Demographics
|
||||
|
||||
|
||||
- True prevalence is unknown given how frequently it is picked up incidentally
|
||||
- Epidemiology: 0.5-3.5% of general population
|
||||
- Age: Evenly distributed in adult & pediatric patients
|
||||
- 3% of children & 1% of adults have imaging findings of CM1, though age of clinical presentation unclear
|
||||
- One series reports median age of presentation in children ≈ 8 years
|
||||
- Sex: F > M (as high as 3:1)
|
||||
- ## Natural History & Prognosis
|
||||
|
||||
|
||||
- Natural history not clearly understood
|
||||
- Many patients asymptomatic for prolonged periods
|
||||
- Increasing ectopia + time → ↑ likelihood of symptoms
|
||||
- Children respond better to treatment than adults
|
||||
- Patients selected for nonsurgical management usually have benign course, though spontaneous improvement & worsening have been described
|
||||
- ## Treatment
|
||||
|
||||
|
||||
- Posterior fossa decompression: Suboccipital craniectomy with C1 laminectomy ± duraplasty, arachnoid opening/dissection, cerebellar tonsil cautery/resection
|
||||
- ↓ of syrinx size in majority of patients after decompression
|
||||
- Complex Chiari 1 may also require odontoid resection or craniocervical junction fusion
|
||||
- Scoliosis may improve from decompression alone but often requires bracing or additional surgery
|
||||
- Postoperative complications in approximately 20% of adults and 37% of children
|
||||
- Most common: CSF leak, pseudomeningocele, infection
|
||||
- Increased risk with duraplasty
|
||||
- 1-11% postoperative mortality
|
||||
- Conservative management for asymptomatic or minimally symptomatic children without syrinx
|
||||
|
||||
# DIAGNOSTIC CHECKLIST
|
||||
|
||||
- ## Consider
|
||||
|
||||
|
||||
- Degree of tonsillar descent does not always correlate with symptoms: CM1 frequently picked up incidentally
|
||||
- ## Image Interpretation Pearls
|
||||
|
||||
|
||||
- Description of additional posterior fossa findings helpful for surgical planning
|
||||
- Look for variant occipital venous sinus (at site of future decompression)
|
||||
|
||||
24070612-ef62-48e4-90d7-6bdaad64902a
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Taylor DG et al: Cerebrospinal fluid area and syringogenesis in Chiari malformation type I. J Neurosurg. 1-6, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32084641%5Bpmid%5D)
|
||||
1. [Dangouloff-Ros V et al: Incidental brain MRI findings in children: a systematic review and meta-analysis. AJNR Am J Neuroradiol. 40(11):1818-23, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31624116%5Bpmid%5D)
|
||||
1. [Saletti V et al: Chiari I malformation in defined genetic syndromes in children: are there common pathways? Childs Nerv Syst. 35(10):1727-39, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31363831%5Bpmid%5D)
|
||||
1. [Poretti A et al: Chiari type 1 deformity in children: pathogenetic, clinical, neuroimaging, and management aspects. Neuropediatrics. 47(5):293-307, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=27337547%5Bpmid%5D)
|
||||
1. [Arnautovic A et al: Pediatric and adult Chiari malformation type I surgical series 1965-2013: a review of demographics, operative treatment, and outcomes. J Neurosurg Pediatr. 15(2):161-77, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25479580%5Bpmid%5D)
|
||||
1. [Brockmeyer DL et al: Complex Chiari malformations in children: diagnosis and management. Neurosurg Clin N Am. 26(4):555-60, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=26408065%5Bpmid%5D)
|
||||
1. [Leonard JR et al: Chiari I malformation: adult and pediatric considerations. Neurosurg Clin N Am. 26(4):xiii-xiv, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=26408069%5Bpmid%5D)
|
||||
1. [Rozenfeld M et al: MRI findings after surgery for Chiari malformation type I. AJR Am J Roentgenol. 205(5):1086-93, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=26496557%5Bpmid%5D)
|
||||
1. [Strahle J et al: The association between Chiari malformation Type I, spinal syrinx, and scoliosis. J Neurosurg Pediatr. 15(6):607-11, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=26030330%5Bpmid%5D)
|
||||
1. [Godzik J et al: Relationship of syrinx size and tonsillar descent to spinal deformity in Chiari malformation Type I with associated syringomyelia. J Neurosurg Pediatr. 13(4):368-74, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24527859%5Bpmid%5D)
|
||||
1. [Lee S et al: Surgical outcome of Chiari I malformation in children: clinico-radiological factors and technical aspects. Childs Nerv Syst. 30(4):613-23, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24604349%5Bpmid%5D)
|
||||
1. [Markunas CA et al: Genetic evaluation and application of posterior cranial fossa traits as endophenotypes for Chiari type I malformation. Ann Hum Genet. 78(1):1-12, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24359474%5Bpmid%5D)
|
||||
1. [McVige JW et al: Imaging of Chiari type I malformation and syringohydromyelia. Neurol Clin. 32(1):95-126, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24287386%5Bpmid%5D)
|
||||
1. [Moore HE et al: Magnetic resonance imaging features of complex Chiari malformation variant of Chiari 1 malformation. Pediatr Radiol. 44(11):1403-11, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24898393%5Bpmid%5D)
|
||||
1. Barkovich AJ et al: Pediatric Neuroimaging. 5th ed. Philadelphia: Lippincott Williams & Wilkins. 491-96, 2012
|
||||
1. [Bollo RJ et al: Complex Chiari malformations in children: an analysis of preoperative risk factors for occipitocervical fusion. J Neurosurg Pediatr. 10(2):134-41, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22725652%5Bpmid%5D)
|
||||
1. [Hwang SW et al: Outcomes of Chiari I-associated scoliosis after intervention: a meta-analysis of the pediatric literature. Childs Nerv Syst. 28(8):1213-9, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22526438%5Bpmid%5D)
|
||||
1. [Brockmeyer DL: The complex Chiari: issues and management strategies. Neurol Sci. 32 Suppl 3:S345-7, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21822705%5Bpmid%5D)
|
||||
1. [Strahle J et al: Natural history of Chiari malformation type I following decision for conservative treatment. J Neurosurg Pediatr. 8(2):214-21, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21806365%5Bpmid%5D)
|
||||
1. [Strahle J et al: Chiari malformation Type I and syrinx in children undergoing magnetic resonance imaging. J Neurosurg Pediatr. 8(2):205-13, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21806364%5Bpmid%5D)
|
||||
1. [Tubbs RS et al: Institutional experience with 500 cases of surgically treated pediatric Chiari malformation type I. J Neurosurg Pediatr. 7(3):248-56, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21361762%5Bpmid%5D)
|
||||
1. [Hofkes SK et al: Differentiation between symptomatic Chiari I malformation and asymptomatic tonsilar ectopia by using cerebrospinal fluid flow imaging: initial estimate of imaging accuracy. Radiology. 245(2):532-40, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17890352%5Bpmid%5D)
|
||||
1. [Tubbs RS et al: A critical analysis of the Chiari 1.5 malformation. J Neurosurg. 101(2 Suppl):179-83, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15835105%5Bpmid%5D)
|
||||
1. [Milhorat TH et al: Chiari I malformation redefined: clinical and radiographic findings for 364 symptomatic patients. Neurosurgery. 44(5):1005-17, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=10232534%5Bpmid%5D)
|
||||
|
||||
## Differential diagnosis
|
||||
|
||||
### Cisterna Magna Mass
|
||||
DDX:047add0c-7e4f-40a0-9933-8d6fa00a24f7
|
||||
|
||||
### Congenital Cerebellar Malformation
|
||||
DDX:e0a671d3-a236-4ff9-a232-a9684218d010
|
||||
|
||||
### Foramen Magnum Mass
|
||||
DDX:a79c61b3-b26a-48c8-bcfb-bf8afd3ef25e
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
*Sagittal graphic demonstrates pointed cerebellar tonsils extending below the foramen magnum to the inferior aspect of the C1 posterior arch. The obex <img src='img/arrows/CS.png'/> is inferiorly displaced as well.*
|
||||
|
||||
|
||||
*Sagittal graphic demonstrates pointed cerebellar tonsils extending below the foramen magnum to the inferior aspect of the C1 posterior arch. The obex <img src='img/arrows/CS.png'/> is inferiorly displaced as well.*
|
||||
|
||||
|
||||
*Sagittal T1 MR of an 8-year-old with boy incidentally noted Chiari 1 malformation (CM1) demonstrates pointed, low-lying cerebellar tonsils reaching the level of the posterior C1 arch <img src='img/arrows/CS.png'/> as well as downward displacement of the brainstem with cervicomedullary junction just below C1 posterior arch <img src='img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Coronal T1 MR in the same patient demonstrates the left cerebellar tonsil <img src='img/arrows/CS.png'/> is lower than the right. In CM1, either one or both cerebellar tonsils may be involved.*
|
||||
|
||||
|
||||
*Axial FIESTA MR through the foramen magnum in the same patient demonstrates posterior displacement of the dens <img src='img/arrows/CS.png'/> with associated deformity of the ventral caudally displaced medulla. Partial effacement of the CSF spaces surrounding the cerebellar tonsils denotes moderate foramen magnum crowding.*
|
||||
|
||||
|
||||
*Sagittal T2 MR in a 5 year old with occipital headaches demonstrates pointed, low-lying cerebellar tonsils <img src='img/arrows/WS.png'/> with associated effacement of CSF spaces. Note the short horizontal clivus <img src='img/arrows/CO.png'/>, retroverted dens <img src='img/arrows/BS.png'/>, and segmentation anomaly at the C3-4 levels <img src='img/arrows/CC.png'/>.*
|
||||
|
||||
|
||||
*Coronal T2 MR in the same patient demonstrates pointed, low-lying cerebellar tonsils <img src='img/arrows/WS.png'/> extending below the C1 ring <img src='img/arrows/CS.png'/>, typical of CM1.*
|
||||
|
||||
|
||||
*Sagittal phase contrast cine MR (with hyperintense signal at sites of active CSF or venous flow) in the same patient shows absence of CSF flow at the craniocervical junction <img src='img/arrows/WC.png'/> due to the CM1.*
|
||||
|
||||
|
||||
*Sagittal phase contrast cine MR in a 16-year-old girl with occipital headaches being worked up for CM1 demonstrates normal CSF flow-related signal ventral <img src='img/arrows/CS.png'/> and dorsal <img src='img/arrows/WS.png'/> to the brainstem. No CM1 was identified on conventional sequences.*
|
||||
|
||||
|
||||
*Sagittal bone CT in a patient with hyperreflexia and severe CM1 demonstrates odontoid retroflexion <img src='img/arrows/WO.png'/> and enlargement of the anterior C1 ring <img src='img/arrows/WS.png'/> (which abnormally articulates with the remodeled clivus).*
|
||||
|
||||
|
||||
*Sagittal T2 MR of the cervical spine in the same patient shows the odontoid process retroflexion <img src='img/arrows/WO.png'/> as well as the cerebellar tonsillar ectopia <img src='img/arrows/WS.png'/> and associated syringohydromyelia <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
*A 5-year-old girl with CM1 demonstrates downward displacement of the cerebellar tonsils below the plane of the foramen magnum caudal to the posterior arch of C1 <img src='img/arrows/CS.png'/> with an abnormal pointed morphology.*
|
||||
|
||||
|
||||
*Sagittal T1 MR in the same patient status post suboccipital decompression with suboccipital craniectomy, C1 laminectomy, expansive duraplasty, and cerebellar tonsillar shrinkage is shown. There is no residual cerebellar ectopia, and the inferior cerebellum <img src='img/arrows/CS.png'/> has a normal, rounded morphology.*
|
||||
|
||||
|
||||
*Axial FIESTA MR in the same patient with CM1 status post posterior fossa decompression demonstrates absence of the posterior arch of C1 from C1 laminectomy and expansive duraplasty <img src='img/arrows/CS.png'/>. There is patent CSF surrounding the cervical spinal cord with no evidence of crowding.*
|
||||
|
||||
|
||||
*Sagittal T2 MR depicts marked cerebellar tonsillar ectopia <img src='img/arrows/WS.png'/>. Clivus <img src='img/arrows/CC.png'/> is mildly foreshortened. There is central edema <img src='img/arrows/WO.png'/> in the cervical spinal cord without frank syringohydromyelia, a finding that has been described as presyrinx edema.*
|
||||
|
||||
|
||||
*Sagittal T1 MR in a patient with osteopetrosis shows cerebellar tonsillar ectopia with extension of the elongated cerebellar tonsils <img src='img/arrows/WS.png'/> to the C2/C3 level. The hypointense marrow signal reflects diffuse sclerosis.*
|
||||
|
||||
|
||||
*Axial T2 MR in the same patient reveals characteristic crowding of the foramen magnum with extension of the ectopic cerebellar tonsils <img src='img/arrows/WS.png'/> into the upper cervical spinal canal.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
*Sagittal T2 MR in an asymptomatic Chiari 1 patient demonstrates severe cerebellar tonsillar ectopia <img src='img/arrows/WS.png'/>. The tonsils produce deformation of the upper cervical spinal cord. There is abnormal T2 prolongation <img src='img/arrows/WO.png'/> in the upper spinal cord reflecting edema and potentially a presyrinx state.*
|
||||
|
||||
|
||||
*Sagittal T2 MR from a 10-year-old patient demonstrates pointed cerebellar tonsils extending below the foramen magnum to the lower C1 level <img src='img/arrows/CO.png'/>, typical of CM1. The CSF is largely effaced at the craniocervical junction, and a syrinx <img src='img/arrows/CC.png'/> is partially seen in the cervical spinal cord.*
|
||||
|
||||
|
||||
*Axial true FISP/FIESTA MR through the foramen magnum in the same patient shows crowding and effacement of the CSF spaces by the low cerebellar tonsils <img src='img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
*Sagittal T1 MR of the cervical spine in the same patient further demonstrates the cerebellar tonsillar ectopia <img src='img/arrows/CO.png'/> and large cervicothoracic spinal cord syrinx <img src='img/arrows/CC.png'/>.*
|
||||
|
||||
@@ -0,0 +1,461 @@
|
||||
---
|
||||
title: "Childhood Stroke"
|
||||
docid: "12f14b63-8dd0-4523-afe1-6fda2331e6bf"
|
||||
authors:
|
||||
- key: "47381de4-c9fd-4999-8dd0-1808cd72db6b"
|
||||
value: "Luke L. Linscott, MD"
|
||||
- key: "b2e6dabb-ee1c-42a4-a332-9f0814c1c607"
|
||||
value: "Surjith Vattoth, MD, FRCR"
|
||||
breadcrumbs:
|
||||
-
|
||||
name: "Brain"
|
||||
slug: "brain"
|
||||
treeNodeId: "6d8829f1-14d7-45af-8675-255189aa526a"
|
||||
-
|
||||
name: "Diagnosis"
|
||||
slug: "diagnosis"
|
||||
treeNodeId: "51c00394-446e-4a38-94af-d3b1d14d34e8"
|
||||
-
|
||||
name: "Pathology-Based Diagnoses"
|
||||
slug: "pathology-based-diagnoses"
|
||||
treeNodeId: "d9d3a8ed-f21b-4831-8c77-591a3500ef77"
|
||||
-
|
||||
name: "Stroke"
|
||||
slug: "stroke"
|
||||
treeNodeId: "12307683-f1ff-4823-a7d3-b10b40f9fd82"
|
||||
-
|
||||
name: "Cerebral Ischemia and Infarction"
|
||||
slug: "cerebral-ischemia-and-infarction"
|
||||
treeNodeId: "51051846-a223-42f7-b626-2a5a26cf6c44"
|
||||
-
|
||||
name: "Childhood Stroke"
|
||||
slug: "childhood-stroke"
|
||||
treeNodeId: null
|
||||
category: "Brain"
|
||||
cmeTopicId: "b9fb5260-1c19-4564-8317-85020cff8575"
|
||||
documentVersionId: "b5f22640-3bb2-4c58-8b6f-4193ac9ef6db"
|
||||
imageCount: 31
|
||||
lastUpdated: "08/06/20"
|
||||
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)
|
||||
- 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
|
||||
- ## Pathology
|
||||
|
||||
|
||||
- Major causes: Cardiac disease (~ 25%), moyamoya-type arteriopathy, dissection, vasculitis, hematologic/metabolic
|
||||
- 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
|
||||
- Treatment in pediatric acute stroke usually conservative
|
||||
- Thrombolysis/thrombectomy not well studied in children
|
||||
- Capacity for recovery in children much > 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 chapter specifically addresses arterial ischemia beyond perinatal period
|
||||
|
||||
# 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
|
||||
- Intimal flap in acutely dissected vessel
|
||||
- Major arterial occlusion may prompt thrombolysis or mechanical thrombectomy in appropriate setting
|
||||
- ## 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****
|
||||
- Suggests ↑ 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
|
||||
- Important to identify 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
|
||||
- Consider dedicated vessel wall imaging
|
||||
|
||||
# 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/40004435-b768-4baf-a31e-651f8a174fe2)
|
||||
- Symmetric basal ganglia involvement common
|
||||
- Usually have manifestations beyond CNS
|
||||
- [Posterior Reversible Encephalopathy Syndrome](/document/acute-hypertensive-encephalopathy--/efc6f9c2-dad9-4eb8-bad2-421bfaf1ec57)
|
||||
- Patchy cortical/subcortical edema most common in parietal & occipital lobes, typically in setting of hypertension
|
||||
- Diffusion restriction uncommon
|
||||
- [Neonatal Herpes Encephalitis](/document/herpes-encephalitis-type-1/556f5f76-c20b-44ca-a913-c53b11c93341)
|
||||
- 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/bafa10c7-e65b-4432-9959-b8e5e4af708c)
|
||||
- Associated vasculitis causes ischemia in small perforating arteries
|
||||
- Unilateral or bilateral deep gray nuclei ischemia
|
||||
|
||||
# PATHOLOGY
|
||||
|
||||
- ## General Features
|
||||
|
||||
|
||||
- 6 major causes of arterial stroke in children
|
||||
- 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)
|
||||
- CNS vasculitis
|
||||
- Hematologic/metabolic (e.g., coagulopathy)
|
||||
- Idiopathic (~ 25%)
|
||||
- No underlying cause discovered
|
||||
|
||||
# CLINICAL ISSUES
|
||||
|
||||
- ## Presentation
|
||||
|
||||
|
||||
- ### Most common signs/symptoms
|
||||
|
||||
|
||||
- Depend 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
|
||||
- Mainstay of chronic therapy for fixed vascular lesions & vasculopathies: Aspirin
|
||||
- Transfusion therapy for at-risk children with sickle cell
|
||||
- Mechanical thrombectomy may be considered in certain patient presentations
|
||||
|
||||
# DIAGNOSTIC CHECKLIST
|
||||
|
||||
- ## Image Interpretation Pearls
|
||||
|
||||
|
||||
- Use same imaging signs as adults
|
||||
- Have low threshold for use of CTA
|
||||
|
||||
994b2dbd-754f-4f23-9516-6f515e4a2678
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Felling RJ et al: Predicting recovery and outcome after pediatric stroke: results from the International Pediatric Stroke Study. Ann Neurol. ePub, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32215969%5Bpmid%5D)
|
||||
1. [Ibrahim AY et al: Fractional flow on TOF-MRA as a measure of stroke risk in children with intracranial arterial stenosis. AJNR Am J Neuroradiol. 41(3):535-41, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32115418%5Bpmid%5D)
|
||||
1. [Morotti A et al: Pediatric ischemic stroke. J Neurol. 267(4):1221-2, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32157384%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. [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. [Beslow LA: Stroke Diagnosis in the pediatric emergency department: an ongoing challenge. Stroke. 48(5):1132-3, 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 NECT in a 15-year-old girl with dilated cardiomyopathy shows a large area of low attenuation in the right middle cerebral artery (MCA) territory <img src='img/arrows/CS.png'/>. Note the sulcal effacement & loss of the gray matter-white matter differentiation.*
|
||||
|
||||
|
||||
*Axial NECT in a 15-year-old girl with dilated cardiomyopathy shows a large area of low attenuation in the right middle cerebral artery (MCA) territory <img src='img/arrows/CS.png'/>. Note the sulcal effacement & loss of the 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'/>. Also note the focus of restricted diffusion in the left periventricular region <img src='img/arrows/WO.png'/>. Multiple infarcts in multiple vascular territories should raise suspicion of a proximal embolic source.*
|
||||
|
||||
|
||||
*Axial DWI MR in a 6 year old with imbalance and acute infarct of the left basal ganglia <img src='img/arrows/CS.png'/> 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'/> and distal <img src='img/arrows/CO.png'/> segments of the middle cerebral artery, consistent with vasculitis.*
|
||||
|
||||
|
||||
*Axial TOF 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'/> in the bilateral thalami, consistent with lenticulostriate collaterals of moyamoya.*
|
||||
|
||||
|
||||
*Axial DWI MR in the same 2-year-old girl with moyamoya-type vasculopathy shows diffusion restriction in the right frontoparietal foci of signal abnormality <img src='img/arrows/CS.png'/>, suggesting an acute/subacute infarct. However, there is no diffusion restriction in the left parietal region <img src='img/arrows/WO.png'/>, suggesting this infarct is of an older age.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR in a 1 year old with arteriopathy & 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'/> within the affected cortex but resolution of acute gyral swelling, as evidenced by prominent sulci <img src='img/arrows/CS.png'/>, suggesting the infarct is in the subacute phase.*
|
||||
|
||||
|
||||
*Axial DWI MR in a 16-year-old boy involved in a motor vehicle collision (MVC) shows multiple small foci of diffusion restriction <img src='img/arrows/CS.png'/>, 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 & an intimal flap in the left internal carotid artery (ICA) <img src='img/arrows/WS.png'/>. The right ICA <img src='img/arrows/CS.png'/> is small & showed areas of irregularity on other images (not shown). The findings are consistent with bilateral ICA dissections.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
*Axial T1 C+ MR in a 2-year-old girl shows cortical enhancement <img src='img/arrows/CS.png'/> in the region of a right frontoparietal infarct, suggesting that it is at least a week old.*
|
||||
|
||||
|
||||
*Axial TOF 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'/>. 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, & vertigo during a game shows gyral swelling & hyperintense signal in the medial temporal lobe <img src='img/arrows/WS.png'/>, which is in the vascular territory of the left posterior cerebral artery. Intracranial MRA acquired at the same time showed a small embolus in the left posterior cerebral artery (PCA).*
|
||||
|
||||
|
||||
*Axial CTA of the cervical arteries in the same patient shows a subtle linear filling defect <img src='img/arrows/WS.png'/> consistent with an intimal flap in the left vertebral artery.*
|
||||
|
||||
|
||||
*Axial NECT in a 2 day old with congenital heart disease & seizures shows a well-defined, wedge-shaped region of decreased attenuation <img src='img/arrows/WS.png'/> 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 & 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'/> due to arterial collaterals distal to a proximal occlusion.*
|
||||
|
||||
|
||||
*Note the segment <img src='img/arrows/WO.png'/> 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'/> in distal territories caused by proximal occlusion from a moyamoya-type vasculopathy. Note the white matter infarct on left <img src='img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Axial DWI MR in the same child shows an acute infarct on the right <img src='img/arrows/WS.png'/> with T2 shine-through in an old left-sided stroke <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*Coronal T2 MR shows multiple areas of infarction <img src='img/arrows/WS.png'/> 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 & vasculitis.*
|
||||
|
||||
|
||||
*Axial NECT in a 14-year-old boy with acute right hemiparesis shows a hyperdense MCA sign <img src='img/arrows/WS.png'/>, indicating acute thrombus in a proximal middle cerebral artery branch.*
|
||||
|
||||
|
||||
*Coronal FLAIR MR in the same patient shows edema in the insular cortex & frontal operculum supplied by the affected MCA branch <img src='img/arrows/WS.png'/>. The patient had complete recovery without direct treatment, & no etiology was found.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a 13-year-old girl with seizures after using ephedra shows foci of increased cortical & subcortical white matter signal in the right PCA & left superior cerebellar artery distributions <img src='img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Sagittal oblique volume-rendered MRA in the same child shows multiple foci of arterial narrowing <img src='img/arrows/WS.png'/> & dilation <img src='img/arrows/WO.png'/> due to a primary arteritis of the CNS.*
|
||||
|
||||
|
||||
*Axial CECT shows a subtle linear filling defect <img src='img/arrows/WC.png'/> 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 & abnormal signal <img src='img/arrows/WS.png'/> of the left parietal lobe, typical of a subacute left MCA territory infarct. ~ 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'/> 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'/> 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'/> 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'/> in a 6 month old. MRA revealed left carotid aneurysm. Proximal arterial pathology should always be investigated at presentation.*
|
||||
|
||||
@@ -0,0 +1,481 @@
|
||||
---
|
||||
title: "Childhood Stroke"
|
||||
docid: "ac8a5544-dee5-4712-ad19-7c649e8af035"
|
||||
authors:
|
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- key: "47381de4-c9fd-4999-8dd0-1808cd72db6b"
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||||
value: "Luke L. Linscott, MD"
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name: "Stroke"
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name: "Childhood Stroke"
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slug: "childhood-stroke"
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lastUpdated: "02/14/24"
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pageDescription: "Childhood Stroke"
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pageKeywords: "Pediatrics, Diagnosis, Pediatric Neuroradiology, Brain, Pathology-Based Diagnoses, Stroke, Childhood Stroke"
|
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pageTitle: "Childhood Stroke | STATdx"
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enhancedTitle: "Childhood Stroke"
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type: "DX"
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references: true
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breadcrumbs:
|
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- "Pediatrics"
|
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- "Diagnosis"
|
||||
- "Pediatric Neuroradiology"
|
||||
- "Brain"
|
||||
- "Pathology-Based Diagnoses"
|
||||
- "Stroke"
|
||||
- "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 much > 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
|
||||
|
||||
# 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****
|
||||
- Suggests ↑ 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
|
||||
- Important to identify 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/40004435-b768-4baf-a31e-651f8a174fe2)
|
||||
- Symmetric basal ganglia involvement common
|
||||
- Usually have manifestations beyond CNS
|
||||
- [Posterior Reversible Encephalopathy Syndrome (PRES)](/document/acute-hypertensive-encephalopathy--/efc6f9c2-dad9-4eb8-bad2-421bfaf1ec57)
|
||||
- Patchy cortical/subcortical edema most common in parietal & occipital lobes, typically in setting of hypertension
|
||||
- Diffusion restriction uncommon
|
||||
- [Neonatal Herpes Encephalitis](/document/herpes-encephalitis-type-1/556f5f76-c20b-44ca-a913-c53b11c93341)
|
||||
- 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/bafa10c7-e65b-4432-9959-b8e5e4af708c)
|
||||
- Associated vasculitis causes ischemia in small perforating arteries
|
||||
- Unilateral or bilateral deep gray nuclei ischemia
|
||||
|
||||
# PATHOLOGY
|
||||
|
||||
- ## General Features
|
||||
|
||||
|
||||
- 6 major causes of arterial stroke in children
|
||||
- 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)
|
||||
- Idiopathic (~ 25%)
|
||||
- No underlying cause discovered
|
||||
|
||||
# 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
|
||||
- Dedicated vessel wall MR imaging often helpful to identify underlying etiology
|
||||
|
||||
196ff412-dec6-4912-8197-f6e80f84bc65
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
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. [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. [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. [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'/> 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'/> 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'/> 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'/> 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'/>, suggesting an acute/subacute infarct. However, there is no diffusion restriction in the left parietal region <img src='img/arrows/WO.png'/>, 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'/> 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'/> and distal <img src='img/arrows/CO.png'/> 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'/> and subcortical <img src='img/arrows/CO.png'/> 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'/> and irregularity <img src='img/arrows/CO.png'/>, 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'/>, 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'/>. The right ICA <img src='img/arrows/CS.png'/> 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'/>. 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'/>. Also note the focus of restricted diffusion in the left periventricular region <img src='img/arrows/WO.png'/>. 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'/> within the affected cortex but resolution of acute gyral swelling, as evidenced by prominent sulci <img src='img/arrows/CS.png'/>, 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'/> 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'/>. 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'/>, 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'/> 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'/> 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'/> due to arterial collaterals distal to a proximal occlusion.*
|
||||
|
||||
|
||||
*Note the segment <img src='img/arrows/WO.png'/> 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'/> 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'/>.*
|
||||
|
||||
|
||||
*Axial DWI MR shows an acute infarct on the right <img src='img/arrows/WS.png'/> with T2 shine-through in an old left-sided stroke <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*Coronal T2 MR shows multiple areas of infarction <img src='img/arrows/WS.png'/> 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'/>, 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'/>. 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'/>.*
|
||||
|
||||
|
||||
*Sagittal oblique volume-rendered MRA in the same patient shows multiple foci of arterial narrowing <img src='img/arrows/WS.png'/> and dilation <img src='img/arrows/WO.png'/> due to a primary arteritis of the CNS.*
|
||||
|
||||
|
||||
*Axial CECT shows a subtle linear filling defect <img src='img/arrows/WC.png'/> 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'/> 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'/> 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'/> 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'/> 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'/> in a 6-month-old. MRA revealed left carotid aneurysm. Proximal arterial pathology should always be investigated at presentation.*
|
||||
|
||||
@@ -0,0 +1,415 @@
|
||||
---
|
||||
title: "Childhood Stroke"
|
||||
docid: "dc608435-4c6c-4b53-985a-4630cd24d5ce"
|
||||
authors:
|
||||
- key: "47381de4-c9fd-4999-8dd0-1808cd72db6b"
|
||||
value: "Luke L. Linscott, MD"
|
||||
breadcrumbs:
|
||||
-
|
||||
name: "Pediatrics"
|
||||
slug: "pediatrics"
|
||||
treeNodeId: "a915965c-d436-44cf-ae65-2f22e7246ea4"
|
||||
-
|
||||
name: "Diagnosis"
|
||||
slug: "diagnosis"
|
||||
treeNodeId: "2b5cea64-a083-489e-ac0c-ec14ba059026"
|
||||
-
|
||||
name: "Brain"
|
||||
slug: "brain"
|
||||
treeNodeId: "95caa0da-bc4f-4103-8551-f58d6e415781"
|
||||
-
|
||||
name: "Traumatic and Vascular Lesions"
|
||||
slug: "traumatic-and-vascular-lesions"
|
||||
treeNodeId: "1b07bd39-2fac-4687-8460-9ea81fa3f9c9"
|
||||
-
|
||||
name: "Childhood Stroke"
|
||||
slug: "childhood-stroke"
|
||||
treeNodeId: null
|
||||
category: "Pediatrics"
|
||||
cmeTopicId: "8bec57b6-3f2c-4787-8f1b-04c07c1848c5"
|
||||
documentVersionId: "3b5f228c-631c-4212-a6aa-4fdbe7fd5d76"
|
||||
imageCount: 24
|
||||
lastUpdated: "11/01/21"
|
||||
pageDescription: "Childhood Stroke"
|
||||
pageKeywords: "Pediatrics, Diagnosis, Brain, Traumatic and Vascular Lesions, Childhood Stroke"
|
||||
pageTitle: "Childhood Stroke | STATdx"
|
||||
enhancedTitle: "Childhood Stroke"
|
||||
type: "DX"
|
||||
references: true
|
||||
breadcrumbs:
|
||||
- "Pediatrics"
|
||||
- "Diagnosis"
|
||||
- "Brain"
|
||||
- "Traumatic and Vascular Lesions"
|
||||
- "Childhood Stroke"
|
||||
---
|
||||
# KEY FACTS
|
||||
|
||||
- ## Terminology
|
||||
|
||||
|
||||
- Acute alteration of neurologic function due to loss of vascular integrity
|
||||
- ## Imaging
|
||||
|
||||
|
||||
- NECT: ↓ attenuation of affected gray matter
|
||||
- Insular ribbon sign → loss of distinct insular cortex
|
||||
- Hyperdense middle cerebral artery (MCA) sign → thrombosed MCA
|
||||
- MR: ↓ diffusion within ~ 30 minutes of arterial occlusion
|
||||
- Cytotoxic edema is 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)
|
||||
- MR perfusion imaging can provide valuable information regarding region at risk in setting of acute stroke
|
||||
- Arterial spin labeling can provide useful perfusion information without contrast administration
|
||||
- MR vessel wall imaging is helpful to identify inflammatory arteriopathy
|
||||
- ## Top Differential Diagnoses
|
||||
|
||||
|
||||
- Complex migraine
|
||||
- Seizure-related injury
|
||||
- Acute encephalitis
|
||||
- Mitochondrial encephalopathies
|
||||
- Posterior reversible encephalopathy syndrome
|
||||
- ## Pathology
|
||||
|
||||
|
||||
- Major causes: Cardiac disease (~ 25%), moyamoya-type arteriopathy, dissection, vasculitis, hematologic/metabolic
|
||||
- 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
|
||||
- Treatment in pediatric acute stroke is often conservative
|
||||
- Thrombolysis/thrombectomy not well studied in children
|
||||
- Capacity for recovery in children much better than adults
|
||||
|
||||
# TERMINOLOGY
|
||||
|
||||
- ## Synonyms
|
||||
|
||||
|
||||
- Cerebrovascular accident, cerebral infarct, cerebral ischemia
|
||||
- ## Definitions
|
||||
|
||||
|
||||
- Acute alteration of neurologic function due to loss of vascular integrity
|
||||
|
||||
# IMAGING
|
||||
|
||||
- ## General Features
|
||||
|
||||
|
||||
- ### Best diagnostic clue
|
||||
|
||||
|
||||
- Cytotoxic edema & restricted diffusion (acutely) in affected vascular territory
|
||||
- ### Location
|
||||
|
||||
|
||||
- Proximal & distal middle cerebral artery (MCA) territories are most commonly affected
|
||||
- ### Morphology
|
||||
|
||||
|
||||
- Stroke caused by arterial occlusion typically conforms to 1 arterial territory
|
||||
- ## CT Findings
|
||||
|
||||
|
||||
- ### NECT
|
||||
|
||||
|
||||
- ↓ attenuation of affected gray matter (GM) with loss of normal GM-white matter (WM) differentiation
|
||||
- ↓ in WM attenuation is less pronounced
|
||||
- Often wedge-shaped & localized to 1 arterial territory
|
||||
- Diffuse ischemic injury can lead to reversal sign with GM diffusely ↓ in attenuation relative to WM
|
||||
- Insular ribbon sign → loss of distinct insular cortex
|
||||
- Hyperdense middle cerebral artery (MCA) sign → ↑ density of acutely thrombosed MCA
|
||||
- Hemorrhagic transformation (HT)
|
||||
- Symptomatic HT in 3%; asymptomatic HT in 30%
|
||||
- Asymptomatic HT is usually parenchymal
|
||||
- WM or deep nuclear hemorrhage is 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
|
||||
- Intimal flap in acutely dissected vessel
|
||||
- Major arterial occlusion may prompt thrombolysis or mechanical thrombectomy in appropriate setting
|
||||
- ## MR Findings
|
||||
|
||||
|
||||
- **T1**: Acute: ↓ signal with gyral swelling
|
||||
- Chronic: ± ↑ signal in cortical laminar necrosis
|
||||
- **T1 FS**: Allows identification of mural hematoma (↑ signal) in dissected vessel
|
||||
- **T2**: 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****
|
||||
- Suggests ↑ extraction fraction & possibly recoverable brain
|
||||
- **T1 C+**: Cortical & leptomeningeal enhancement is seen after 5-7 days following acute infarct
|
||||
- Enhancing climbing ivy sign
|
||||
- **MRA**: Can detect arterial occlusion & stenosis in large- & medium-sized cerebral vessels
|
||||
- Important to identify underlying dissection or arteriopathy
|
||||
- **PWI**: Provides valuable information about affected brain
|
||||
- Ischemic penumbra: ↓ perfusion, no DWI change (PWI-DWI mismatch)
|
||||
- May define brain that is salvageable with acute stroke therapy
|
||||
- Arterial spin labeling can provide useful perfusion information without contrast administration
|
||||
- **MRS**: ↑ lactate is hallmark of ischemia/infarct
|
||||
- Not specific
|
||||
- **Vessel wall imaging**: Vessel wall enhancement suggests inflammatory arteriopathy
|
||||
- Vessel wall enhancement patterns improve discrimination of underlying stroke etiology
|
||||
- ## Ultrasonographic Findings
|
||||
|
||||
|
||||
- ### Grayscale ultrasound
|
||||
|
||||
|
||||
- Affected territory is hyperechoic in acute/subacute stage
|
||||
- ### Color Doppler
|
||||
|
||||
|
||||
- Direct Doppler evaluation is 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 is rarely necessary in acute evaluation of childhood stroke
|
||||
- Only 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 is 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
|
||||
|
||||
# DIFFERENTIAL DIAGNOSIS
|
||||
|
||||
- ## Complex Migraine
|
||||
|
||||
|
||||
- ↓ (early) or ↑ (late) perfusion with normal DWI
|
||||
- Engorgement of vessels on SWI
|
||||
- ## 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/40004435-b768-4baf-a31e-651f8a174fe2)
|
||||
- Symmetric basal ganglia involvement is common
|
||||
- Usually have manifestations beyond CNS
|
||||
- [Posterior Reversible Encephalopathy Syndrome](/document/acute-hypertensive-encephalopathy--/efc6f9c2-dad9-4eb8-bad2-421bfaf1ec57)
|
||||
- Patchy cortical/subcortical edema is most common in parietal & occipital lobes, typically in setting of hypertension
|
||||
- Diffusion restriction is uncommon
|
||||
|
||||
# PATHOLOGY
|
||||
|
||||
- ## General Features
|
||||
|
||||
|
||||
- 6 major causes of arterial stroke in children
|
||||
- Cardiac disease (~ 25%)
|
||||
- Congenital heart disease, valvular heart disease, arrhythmias, & cardiomyopathies
|
||||
- Moyamoya-type arteriopathy
|
||||
- Sickle cell disease
|
||||
- Neurofibromatosis type I
|
||||
- Idiopathic
|
||||
- Arterial dissection (e.g., trauma)
|
||||
- CNS vasculitis
|
||||
- Hematologic/metabolic (e.g., coagulopathy)
|
||||
- Idiopathic (~ 25%)
|
||||
- No underlying cause discovered
|
||||
|
||||
# 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)
|
||||
- Speech difficulties, gait abnormality, seizure
|
||||
- Embolic cause: Sudden onset of symptoms
|
||||
- Stenoocclusive cause: Gradual/intermittent (e.g., TIA)
|
||||
- Focal deficit may be masked by lethargy, coma, irritability
|
||||
- Preceding transient events occur in 25%
|
||||
- Children typically present later than adults (> 24 hours)
|
||||
- Poor recognition/understanding of symptoms by child, caregiver, physician
|
||||
- ## Demographics
|
||||
|
||||
|
||||
- ### Age
|
||||
|
||||
|
||||
- Incidence/mortality greatest < 1 year
|
||||
- ### 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 is better than in adults, due to
|
||||
- Better compensatory mechanisms, collateral recruitment, neuronal plasticity
|
||||
- Fewer concomitant risk factors
|
||||
- ## Treatment
|
||||
|
||||
|
||||
- Clinical window of opportunity/benefit is not as well understood in children as compared to adults
|
||||
- Mainstay of chronic therapy for fixed vascular lesions & vasculopathies: Aspirin
|
||||
- Transfusion therapy for at-risk children with sickle cell disease
|
||||
|
||||
# DIAGNOSTIC CHECKLIST
|
||||
|
||||
- ## Image Interpretation Pearls
|
||||
|
||||
|
||||
- Use same imaging signs as adults
|
||||
- Have low threshold for use of CTA
|
||||
|
||||
4fee7a61-bc2c-4ce0-a2d5-84ed346ac7d5
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [van Es ACGM et al: Endovascular treatment for acute ischemic stroke in children: experience from the MR CLEAN Registry. Stroke. 52(3):781-8, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=33617341%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. [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. [Dlamini N et al: Arterial wall imaging in pediatric stroke. Stroke. 49(4):891-98, 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. [Beslow LA: Stroke diagnosis in the pediatric emergency department: an ongoing challenge. Stroke. 48(5):1132-3, 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. [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. [Lopez-Vicente M et al: Diagnosis and management of pediatric arterial ischemic stroke. J Stroke Cerebrovasc Dis. 19(3):175-83, 2010](http://www.ncbi.nlm.nih.gov/pubmed/?term=20434043%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 DWI MR in a 4-day-old term neonate presenting with seizures shows diffusion restriction <img src='img/arrows/CS.png'/> throughout the left middle cerebral artery (MCA) territory, consistent with a perinatal arterial ischemic stroke (PAIS).*
|
||||
|
||||
|
||||
*Axial DWI MR in a 4-day-old term neonate presenting with seizures shows diffusion restriction <img src='img/arrows/CS.png'/> throughout the left middle cerebral artery (MCA) territory, consistent with a perinatal arterial ischemic stroke (PAIS).*
|
||||
|
||||
|
||||
*Axial T2 MR in the same patient 2 years later shows cystic encephalomalacia <img src='img/arrows/CS.png'/> throughout left MCA territory & passive enlargement of the left lateral ventricle <img src='img/arrows/CO.png'/>. Patients with PAIS who do not present near birth with seizures may later present with early hand preference or extremity weakness.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a 2-year-old girl shows multiple areas of cytotoxic edema <img src='img/arrows/CS.png'/> in both cerebral hemispheres in this patient with moyamoya-type vasculopathy.*
|
||||
|
||||
|
||||
*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'/>, suggesting an acute/subacute infarct. However, there is no diffusion restriction in the left parietal region <img src='img/arrows/WO.png'/>, suggesting this infarct is of an older age. Acute stroke should prompt careful arterial evaluation.*
|
||||
|
||||
|
||||
### 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'/>. Note the sulcal effacement & loss of the 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'/>. Also note the focus of restricted diffusion in the left periventricular region <img src='img/arrows/WO.png'/>. Multiple infarcts in multiple vascular territories should raise suspicion of a proximal embolic source.*
|
||||
|
||||
|
||||
*Axial DWI MR in a 16-year-old boy involved in a motor vehicle collision (MVC) shows multiple small foci of diffusion restriction <img src='img/arrows/CS.png'/>, 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 with multiple infarcts shows vessel wall irregularity & an intimal flap in the left internal carotid artery (ICA) <img src='img/arrows/WS.png'/>, consistent with dissection. The right ICA <img src='img/arrows/CS.png'/> is small & showed areas of irregularity on other images (not shown). The findings are consistent with bilateral ICA dissections.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR in a 2-year-old girl shows cortical enhancement <img src='img/arrows/CS.png'/> in the region of a right frontoparietal infarct, suggesting that it is at least a week old.*
|
||||
|
||||
|
||||
*Axial 3D TOF 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'/>. 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, & vertigo during a game shows gyral swelling & hyperintense signal in the medial temporal lobe <img src='img/arrows/WS.png'/>, which is in the vascular territory of the left posterior cerebral artery. Intracranial MRA acquired at the same time showed a small embolus in the left posterior cerebral artery (PCA).*
|
||||
|
||||
|
||||
*Axial CTA of the cervical arteries in the same patient shows a subtle linear filling defect <img src='img/arrows/WS.png'/>, consistent with an intimal flap in the left vertebral artery.*
|
||||
|
||||
|
||||
*Axial NECT in a 2-da-old with congenital heart disease & seizures shows a well-defined, wedge-shaped region of ↓ attenuation <img src='img/arrows/WS.png'/> 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 I & known bilateral carotid terminus occlusions (resulting in a moyamoya-type vasculopathy pattern) shows abnormal sulcal enhancement (the climbing ivy sign) <img src='img/arrows/CS.png'/> due to arterial collaterals distal to a proximal occlusion.*
|
||||
|
||||
|
||||
*Axial NECT shows a segment <img src='img/arrows/WO.png'/> of the left 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 first 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'/> 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'/>.*
|
||||
|
||||
|
||||
*Coronal T2 MR shows multiple areas of infarction <img src='img/arrows/WS.png'/> 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 & vasculitis.*
|
||||
|
||||
|
||||
*Axial NECT in a 14-year-old boy with acute right hemiparesis shows a hyperdense MCA sign <img src='img/arrows/WS.png'/>, indicating acute thrombus in a proximal middle cerebral artery branch.*
|
||||
|
||||
|
||||
*Coronal FLAIR MR in the same patient shows edema in the insular cortex & frontal operculum supplied by the affected MCA branch <img src='img/arrows/WS.png'/>. The patient had complete recovery without direct treatment, & no etiology was found.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a 13-year-old girl with seizures after using ephedra shows foci of ↑ cortical & subcortical white matter signal in the right PCA & left superior cerebellar artery distributions <img src='img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Sagittal oblique volume-rendered MRA in the same child shows multiple foci of arterial narrowing <img src='img/arrows/WS.png'/> & dilation <img src='img/arrows/WO.png'/> due to a primary arteritis of the CNS.*
|
||||
|
||||
|
||||
*Axial CECT shows a subtle linear filling defect <img src='img/arrows/WC.png'/> 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 & abnormal signal <img src='img/arrows/WS.png'/> 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.*
|
||||
|
||||
@@ -200,14 +200,26 @@ breadcrumbs:
|
||||
**Herniation Syndromes, Intracranial**
|
||||
*Sagittal T1 C+ MR shows a cystic mass with an enhancing nodule <img src='img/arrows/WS.png'/>, consistent with hemangioblastoma, pushing the tonsils inferiorly through the foramen magnum <img src='img/arrows/WO.png'/>. Note effaced 4th ventricle <img src='img/arrows/WC.png'/>, enlarged foramen of Monro <img src='img/arrows/CS.png'/>, and enlarged 3rd <img src='img/arrows/CO.png'/> and lateral <img src='img/arrows/CC.png'/> ventricles, consistent with obstructive hydrocephalus.*
|
||||
|
||||
|
||||
**Herniation Syndromes, Intracranial**
|
||||
*Sagittal T1 C+ MR shows a cystic mass with an enhancing nodule <img src='img/arrows/WS.png'/>, consistent with hemangioblastoma, pushing the tonsils inferiorly through the foramen magnum <img src='img/arrows/WO.png'/>. Note effaced 4th ventricle <img src='img/arrows/WC.png'/>, enlarged foramen of Monro <img src='img/arrows/CS.png'/>, and enlarged 3rd <img src='img/arrows/CO.png'/> and lateral <img src='img/arrows/CC.png'/> ventricles, consistent with obstructive hydrocephalus.*
|
||||
|
||||
|
||||
**Herniation Syndromes, Intracranial**
|
||||
*Sagittal T1 C+ MR shows a cystic mass with an enhancing nodule <img src='img/arrows/WS.png'/>, consistent with hemangioblastoma, pushing the tonsils inferiorly through the foramen magnum <img src='img/arrows/WO.png'/>. Note effaced 4th ventricle <img src='img/arrows/WC.png'/>, enlarged foramen of Monro <img src='img/arrows/CS.png'/>, and enlarged 3rd <img src='img/arrows/CO.png'/> and lateral <img src='img/arrows/CC.png'/> ventricles, consistent with obstructive hydrocephalus.*
|
||||
|
||||
|
||||
**Herniation Syndromes, Intracranial**
|
||||
*Sagittal T1 C+ MR shows a cystic mass with an enhancing nodule <img src='img/arrows/WS.png'/>, consistent with hemangioblastoma, pushing the tonsils inferiorly through the foramen magnum <img src='img/arrows/WO.png'/>. Note effaced 4th ventricle <img src='img/arrows/WC.png'/>, enlarged foramen of Monro <img src='img/arrows/CS.png'/>, and enlarged 3rd <img src='img/arrows/CO.png'/> and lateral <img src='img/arrows/CC.png'/> ventricles, consistent with obstructive hydrocephalus.*
|
||||
|
||||
|
||||
**Chiari 1**
|
||||
*Sagittal T2 MR in a patient with occipital headaches shows a significantly pointed configuration of a low-lying cerebellar tonsil <img src='img/arrows/WS.png'/> to the level of the midposterior ring of C2. Notice also the dorsally tilted dens <img src='img/arrows/WO.png'/>, effacement of CSF at the foramen magnum, and associated cervicothoracic syrinx <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Chiari 1**
|
||||
*Sagittal T2 MR in a patient with occipital headaches shows a significantly pointed configuration of a low-lying cerebellar tonsil <img src='img/arrows/WS.png'/> to the level of the midposterior ring of C2. Notice also the dorsally tilted dens <img src='img/arrows/WO.png'/>, effacement of CSF at the foramen magnum, and associated cervicothoracic syrinx <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Chiari 2**
|
||||
*Sagittal T2 MR shows a small posterior fossa with extension of the cerebellar peg <img src='img/arrows/WS.png'/> through the foramen magnum to the level of C6. The cervicomedullary junction and 4th ventricle <img src='img/arrows/WO.png'/> are low-lying and there is mild tectal beaking <img src='img/arrows/WC.png'/> and moderate prominence of the massa intermedia <img src='img/arrows/BS.png'/>.*
|
||||
@@ -267,10 +279,18 @@ breadcrumbs:
|
||||
**Dandy-Walker Continuum**
|
||||
*Sagittal T1WI MR demonstrates a markedly enlarged posterior fossa with cystic dilatation of the 4th ventricle <img src='img/arrows/WO.png'/>, upwardly rotated hypoplastic vermis <img src='img/arrows/WS.png'/>, and low-lying torcular Herophili <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Chiari 1**
|
||||
*Sagittal T2 MR in a patient with occipital headaches shows a significantly pointed configuration of a low-lying cerebellar tonsil <img src='img/arrows/WS.png'/> to the level of the midposterior ring of C2. Notice also the dorsally tilted dens <img src='img/arrows/WO.png'/> and effacement of CSF at the foramen magnum.*
|
||||
|
||||
|
||||
**Chiari 1**
|
||||
*Sagittal T2 MR in a patient with occipital headaches shows a significantly pointed configuration of a low-lying cerebellar tonsil <img src='img/arrows/WS.png'/> to the level of the midposterior ring of C2. Notice also the dorsally tilted dens <img src='img/arrows/WO.png'/> and effacement of CSF at the foramen magnum.*
|
||||
|
||||
|
||||
**Chiari 1**
|
||||
*Sagittal T1WI MR shows inferior extension of the peg-like cerebellar tonsils <img src='img/arrows/WS.png'/> well below the level of the foramen magnum <img src='img/arrows/BO.png'/>, consistent with Chiari 1.*
|
||||
|
||||
|
||||
**Chiari 1**
|
||||
*Sagittal T1WI MR shows inferior extension of the peg-like cerebellar tonsils <img src='img/arrows/WS.png'/> well below the level of the foramen magnum <img src='img/arrows/BO.png'/>, consistent with Chiari 1.*
|
||||
@@ -279,14 +299,30 @@ breadcrumbs:
|
||||
**Herniation Syndromes, Intracranial**
|
||||
*Axial T2WI MR at the level of the foramen magnum demonstrates downward tonsillar herniation <img src='img/arrows/WS.png'/> secondary to mass affect from brain death.*
|
||||
|
||||
|
||||
**Herniation Syndromes, Intracranial**
|
||||
*Axial T2WI MR at the level of the foramen magnum demonstrates downward tonsillar herniation <img src='img/arrows/WS.png'/> secondary to mass affect from brain death.*
|
||||
|
||||
|
||||
**Herniation Syndromes, Intracranial**
|
||||
*Sagittal T1WI MR shows cerebellar tonsillar herniation <img src='img/arrows/WC.png'/> from a large left posterior fossa mass. Note compression of 4th ventricle <img src='img/arrows/WO.png'/>. Supratentorial ventricles are enlarged <img src='img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
**Herniation Syndromes, Intracranial**
|
||||
*Sagittal T1WI MR shows cerebellar tonsillar herniation <img src='img/arrows/WC.png'/> from a large left posterior fossa mass. Note compression of 4th ventricle <img src='img/arrows/WO.png'/>. Supratentorial ventricles are enlarged <img src='img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
**Chiari 1**
|
||||
*Sagittal CINE phase-contrast CSF flow - diastolic shows diminished posterior CSF flow <img src='img/arrows/WS.png'/> compared to anterior CSF flow <img src='img/arrows/BO.png'/> at the site of tonsillar impaction.*
|
||||
|
||||
|
||||
**Chiari 1**
|
||||
*Sagittal CINE phase-contrast CSF flow - diastolic shows diminished posterior CSF flow <img src='img/arrows/WS.png'/> compared to anterior CSF flow <img src='img/arrows/BO.png'/> at the site of tonsillar impaction.*
|
||||
|
||||
|
||||
**Chiari 1**
|
||||
*Sagittal T2WI MR shows a classic case of Chiari 1 with pointed cerebellar tonsils <img src='img/arrows/WO.png'/> protruding through the foramen magnum and effacing the cisterna magna.*
|
||||
|
||||
|
||||
**Chiari 1**
|
||||
*Sagittal T2WI MR shows a classic case of Chiari 1 with pointed cerebellar tonsils <img src='img/arrows/WO.png'/> protruding through the foramen magnum and effacing the cisterna magna.*
|
||||
|
||||
@@ -0,0 +1,342 @@
|
||||
---
|
||||
title: "CPA Mass, Adult"
|
||||
docid: "f3cd22f6-53b9-4392-be23-512d221d2e02"
|
||||
authors:
|
||||
- key: "07a2c087-6202-49e7-870b-7aa162d18f06"
|
||||
value: "Bronwyn E. Hamilton, MD"
|
||||
breadcrumbs:
|
||||
-
|
||||
name: "Head and Neck"
|
||||
slug: "head-and-neck"
|
||||
treeNodeId: "ed24ed8c-5d57-4629-879b-447b82d2973d"
|
||||
-
|
||||
name: "Differential Diagnosis"
|
||||
slug: "differential-diagnosis"
|
||||
treeNodeId: "40d68862-8975-4dde-ac2b-ebc43ab0fb5c"
|
||||
-
|
||||
name: "CPA-IAC and Posterior Fossa"
|
||||
slug: "cpa-iac-and-posterior-fossa"
|
||||
treeNodeId: "c590eedb-4a3b-4158-a04f-ad880564c992"
|
||||
-
|
||||
name: "Anatomically Based Differentials"
|
||||
slug: "anatomically-based-differentials"
|
||||
treeNodeId: "debfb06c-8656-4f5d-92c1-eaa468185d78"
|
||||
-
|
||||
name: "CPA Mass, Adult"
|
||||
slug: "cpa-mass-adult"
|
||||
treeNodeId: null
|
||||
category: "Head and Neck"
|
||||
documentVersionId: "3389aa3f-4eea-4b0c-aab3-7b7265e22a43"
|
||||
imageCount: 25
|
||||
lastUpdated: "01/18/24"
|
||||
pageDescription: "CPA Mass, Adult"
|
||||
pageKeywords: "Head and Neck, Differential Diagnosis, CPA-IAC and Posterior Fossa, Anatomically Based Differentials, CPA Mass, Adult"
|
||||
pageTitle: "CPA Mass, Adult | STATdx"
|
||||
enhancedTitle: "CPA Mass, Adult"
|
||||
type: "DDX"
|
||||
references: true
|
||||
breadcrumbs:
|
||||
- "Head and Neck"
|
||||
- "Differential Diagnosis"
|
||||
- "CPA-IAC and Posterior Fossa"
|
||||
- "Anatomically Based Differentials"
|
||||
- "CPA Mass, Adult"
|
||||
---
|
||||
# ESSENTIAL INFORMATION
|
||||
|
||||
- ## Key Differential Diagnosis Issues
|
||||
|
||||
|
||||
- Idealized imaging protocol in evaluating CPA mass lesions
|
||||
- T1 C+ fat-saturated MR is gold standard
|
||||
- Fat saturation differentiates lipoma from vestibular schwannoma
|
||||
- Add DWI for possible epidermoid cyst
|
||||
- Add GRE for aneurysm wall clot & calcification; also useful for tumor calcifications
|
||||
- T2 thin-section, high-resolution MR gives more surgical data when vestibular schwannoma is diagnosed
|
||||
- CISS or FIESTA most commonly used
|
||||
- Helps define amount of CSF cap in lateral IAC
|
||||
- Assesses relationship of cochlear nerve canal to lesion
|
||||
- If small schwannoma, may define nerve of origin (superior vs. inferior vestibular schwannoma)
|
||||
- Knowledge of relative incidence of lesions key in CPA-IAC lesion assessment
|
||||
- Vestibular schwannoma: ~ **90%** of all CPA-IAC masses
|
||||
- Meningioma, epidermoid cyst, aneurysm, & arachnoid cyst together represent ~ **8%** of all CPA-IAC masses
|
||||
- All other diagnoses in differential list: ~ **2%**
|
||||
- Other factors relevant to imaging CPA masses
|
||||
- 3D facial nerve tractography for CPA masses may aid surgical planning to reduce risk of facial nerve injury
|
||||
- CPA tumors in women independent risk factor for intracranial aneurysms
|
||||
- ## Helpful Clues for Common Diagnoses
|
||||
|
||||
|
||||
- **Vestibular Schwannoma**
|
||||
- Morphology
|
||||
- Ovoid intracanalicular mass (IAC)
|
||||
- Ice cream on cone shape (CPA-IAC)
|
||||
- T1 C+ MR
|
||||
- Enhancing well-defined tumor ± intramural cysts
|
||||
- High-resolution thin 0.6-mm 3D T2 MR alternative screening modality for schwannomas without contrast
|
||||
- SWI
|
||||
- Intratumoral microhemorrhages favor schwannoma, rare in meningioma
|
||||
- ## Helpful Clues for Less Common Diagnoses
|
||||
|
||||
|
||||
- **Meningioma in CPA-IAC**
|
||||
- Morphology
|
||||
- Mushroom-shaped dural-based mass capping IAC asymmetrically
|
||||
- T1 C+ MR
|
||||
- Enhancing mass, ± dural tails, ± CSF-vascular cleft if CPA component is larger
|
||||
- 25% of CPA meningiomas have direct extension or dural tail projecting into IAC
|
||||
- **Epidermoid Cyst in CPA-IAC**
|
||||
- Morphology
|
||||
- Insinuating ± scalloping brainstem margin
|
||||
- MR imaging
|
||||
- T1 C+ MR: Nonenhancing
|
||||
- If known or suspected epidermoid develops enhancing margins, consider rare malignant transformation (squamous cell carcinoma); PET avidity can be helpful to confirm suspicion
|
||||
- DWI: Restricted diffusion (high signal) makes diagnosis
|
||||
- T2 MR: Follows fluid signal intensity
|
||||
- FLAIR: Lack of complete fluid suppression
|
||||
- **Aneurysm****in****CPA-IAC**
|
||||
- Morphology
|
||||
- Ovoid or fusiform; rarely IAC
|
||||
- MR imaging
|
||||
- T1 & T1 C+ MR: Complex signal mass from wall calcification, clot, & flow
|
||||
- MRA (CTA, angiography) sorts out diagnosis
|
||||
- **Arachnoid Cyst****in****CPA**
|
||||
- Morphology
|
||||
- Fills cistern with rounded margins
|
||||
- MR imaging
|
||||
- T1 C+ MR: No enhancement
|
||||
- FLAIR: Lesion attenuates
|
||||
- DWI: No restricted diffusion
|
||||
- **Metastases in CPA-IAC**
|
||||
- Morphology
|
||||
- Irregular invasive margins
|
||||
- MR imaging
|
||||
- T1 C+ MR: Single or multiple enhancing masses in CPA
|
||||
- 4 sites primarily involved: Flocculus, choroid plexus, arachnoid-dura, or pia
|
||||
- ## Helpful Clues for Rare Diagnoses
|
||||
|
||||
|
||||
- **Neurofibromatosis Type****2**
|
||||
- Morphology
|
||||
- Bilateral ovoid IAC or ice cream on cone-shaped CPA-IAC masses
|
||||
- MR imaging
|
||||
- T1 C+ MR: Bilateral enhancing CPA-IAC masses
|
||||
- ± additional schwannomas & meningiomas
|
||||
- **Sarcoidosis****in****CPA-IAC**
|
||||
- Laboratory
|
||||
- CSF lymphocytosis
|
||||
- ↑ blood angiotensin converting enzyme
|
||||
- Morphology
|
||||
- En plaque or nodular dural lesion(s)
|
||||
- MR imaging
|
||||
- T1 C+ MR: Enhancing multifocal dural-based lesions
|
||||
- **Choroid Plexus Papilloma****in****CPA**
|
||||
- Morphology
|
||||
- Dumbbell shape with 4th ventricle & CPA cistern components
|
||||
- Pear-shaped if begins in foramen of Luschka
|
||||
- MR imaging
|
||||
- T1 C+ MR: Avidly enhancing mass in 4th ventricle projecting through foramen of Luschka into CPA
|
||||
- **Lipoma****in****CPA-IAC**
|
||||
- Morphology
|
||||
- Ovoid if IAC only
|
||||
- CPA lesion may be broad-based against lateral pons
|
||||
- Nonenhanced CT
|
||||
- Fat-density lesion of CPA ± IAC ± inner ear
|
||||
- MR imaging
|
||||
- T1 MR: High-signal lesion, suppresses with fat saturation
|
||||
- Caveat: If T1 C+ without fat saturation, lipoma may be mistaken for vestibular schwannoma
|
||||
- **Ependymoma in CPA**
|
||||
- Morphology
|
||||
- Irregular soft tumor squeezes out through 4th ventricle foramen of Luschka into CPA
|
||||
- Tumor margins amorphous
|
||||
- Bone CT
|
||||
- Calcifications in 50% of cases
|
||||
- MR imaging
|
||||
- T1 C+ MR: Heterogeneous enhancement of solid tumor components
|
||||
- Marginal enhancement of tumor cyst wall
|
||||
- **Hypertrophic Pachymeningitis**
|
||||
- Varied causes require tissue diagnosis
|
||||
- IgG4-related disease (↑ plasma or tissue IgG4)
|
||||
- Granulomatosis with polyangiitis: Antineutrophil cytoplasmic antibody (ANCA) (+) associated vasculitis
|
||||
- Idiopathic (a.k.a. intracranial idiopathic inflammatory pseudotumor)
|
||||
- Morphology
|
||||
- En plaque
|
||||
- MR imaging
|
||||
- T1 C+ MR: Thickened enhancing dura
|
||||
- Caveat: May mimic meningioma, sarcoidosis, or metastatic disease
|
||||
- **F****acial Nerve****Schwannoma in CPA-IAC**
|
||||
- Morphology
|
||||
- CPA-IAC mass with labyrinthine tail
|
||||
- Bone CT
|
||||
- Labyrinthine segment of CNVII may be enlarged
|
||||
- MR imaging
|
||||
- T1 C+ MR: Enhancing tubular mass in CPA-IAC & labyrinthine segment of CNVII
|
||||
- Caveat: If labyrinthine segment of CNVII not involved, cannot be differentiated from vestibular schwannoma
|
||||
- **Jugular Foramen Schwannoma**
|
||||
- Morphology
|
||||
- Lobular mass projects superomedially from jugular foramen toward lateral brainstem
|
||||
- MR imaging
|
||||
- T1 C+ MR: Enhancing mass arising from jugular foramen
|
||||
- **IAC Venous Malformation ("Hemangioma")**
|
||||
- Morphology
|
||||
- Poorly marginated IAC mass with punctate calcifications
|
||||
- Bone CT
|
||||
- Punctate calcifications in IAC mass
|
||||
- MR imaging
|
||||
- T1 C+ MR: Enhancing IAC mass with focal low-signal foci (calcifications)
|
||||
- **Neurenteric Cyst**
|
||||
- Morphology
|
||||
- Rounded ovoid mass in prepontine cistern
|
||||
- MR imaging
|
||||
- T1: Intermediate to high signal T1 prepontine mass
|
||||
- Nonenhancing
|
||||
- Caveat: ↑ T1 signal differentiates from epidermoid cyst
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Shimanuki MN et al: Imaging of temporal bone mass lesions: a pictorial review. Diagnostics (Basel). 13(16), 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=37627924%5Bpmid%5D)
|
||||
1. [Shimojima Y et al: Hypertrophic pachymeningitis in ANCA-associated vasculitis: clinical and immunopathological features and insights. Autoimmun Rev. 22(6):103338, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=37062439%5Bpmid%5D)
|
||||
1. [Ota Y et al: Advanced MRI to differentiate schwannomas and metastases in the cerebellopontine angle/internal auditory canal. J Neuroimaging. 32(6):1177-84, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35879866%5Bpmid%5D)
|
||||
1. [Ozaki K et al: Arachnoid cyst alone causes hemifacial spasm: illustrative case. J Neurosurg Case Lessons. 3(15), 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=36303502%5Bpmid%5D)
|
||||
1. [Sakamoto H et al: Radio-pathological characteristics of malignant transformation of an epidermoid cyst in the cerebellopontine angle: a case report. Surg Neurol Int. 13:135, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35509542%5Bpmid%5D)
|
||||
1. [Banerjee P et al: Role of neuroimaging in cases of primary and secondary hemifacial spasm. Indian J Ophthalmol. 69(2):253-6, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=33463567%5Bpmid%5D)
|
||||
1. [Connor SEJ: Imaging of the vestibular schwannoma: diagnosis, monitoring, and treatment planning. Neuroimaging Clin N Am. 31(4):451-71, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=34689927%5Bpmid%5D)
|
||||
1. [Saigal G et al: Utility of Microhemorrhage as a diagnostic tool in distinguishing vestibular schwannomas from other cerebellopontine angle (CPA) Tumors. Indian J Otolaryngol Head Neck Surg. 73(3):321-6, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=34471620%5Bpmid%5D)
|
||||
1. [Totten DJ et al: Cerebellopontine angle and internal auditory canal lipomas: case series and systematic review. Laryngoscope. 131(9):2081-7, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=33567134%5Bpmid%5D)
|
||||
1. [Pamela Ferreira Neto B et al: Noncystic cerebellopontine angle hemangioblastoma: A case of an atypical location. Int J Surg Case Rep. 74:234-7, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32892127%5Bpmid%5D)
|
||||
1. [Melenotte C et al: Clinical presentation, treatment and outcome of IgG4-related pachymeningitis: from a national case registry and literature review. Semin Arthritis Rheum. 49(3):430-7, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31155444%5Bpmid%5D)
|
||||
1. [Zheng SF et al: Cerebellopontine angle tumors are associated with a greater incidence of unruptured intracranial aneurysms. World Neurosurg. 122:e561-8, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31108072%5Bpmid%5D)
|
||||
1. [Dunn IF et al: Congress of neurological surgeons systematic review and evidence-based guidelines on the role of imaging in the diagnosis and management of patients with vestibular schwannomas. Neurosurgery. 82(2):E32-4, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29309686%5Bpmid%5D)
|
||||
1. [Prabhu V et al: Preserved cochlear CISS signal is a predictor for hearing preservation in patients treated for vestibular schwannoma with stereotactic radiosurgery. Otol Neurotol. 39(5):628-31, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29561382%5Bpmid%5D)
|
||||
1. [Mishra A et al: Susceptibility weighted imaging - a problem-solving tool in differentiation of cerebellopontine angle schwannomas and meningiomas. Neuroradiol J. 30(3):253-8, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28627983%5Bpmid%5D)
|
||||
1. [Schulze M et al: Improvement in imaging common temporal bone pathologies at 3 T MRI: small structures benefit from a small field of view. Clin Radiol. 72(3):267.e1-12, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28034444%5Bpmid%5D)
|
||||
1. [Rueckriegel SM et al: Probabilistic fiber-tracking reveals degeneration of the contralateral auditory pathway in patients with vestibular schwannoma. AJNR Am J Neuroradiol. 37(9):1610-6, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=27256855%5Bpmid%5D)
|
||||
1. [Watanabe N et al: Imaging alterations due to squamous metaplasia in intracranial neurenteric cysts: A report of two cases. Neuroradiol J. 29(3):187-92, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=27009777%5Bpmid%5D)
|
||||
1. [Mukherjee P et al: Intracranial lipomas affecting the cerebellopontine angle and internal auditory canal: a case series. Otol Neurotol. 32(4):670-5, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21358448%5Bpmid%5D)
|
||||
1. [Warren FM et al: Imaging characteristics of metastatic lesions to the cerebellopontine angle. Otol Neurotol. 29(6):835-8, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18636029%5Bpmid%5D)
|
||||
1. [Barrera JE et al: Cavernous hemangioma of the internal auditory canal: a case report and review of the literature. Am J Otolaryngol. 25(3):199-203, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15124171%5Bpmid%5D)
|
||||
1. [Nakamura M et al: Meningiomas of the internal auditory canal. Neurosurgery. 55(1):119-27; discussion 127-8, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15214980%5Bpmid%5D)
|
||||
1. [Swartz JD: Lesions of the cerebellopontine angle and internal auditory canal: diagnosis and differential diagnosis. Semin Ultrasound CT MR. 25(4):332-52, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15497614%5Bpmid%5D)
|
||||
1. [Daniels RL et al: Causes of unilateral sensorineural hearing loss screened by high-resolution fast spin echo magnetic resonance imaging: review of 1,070 consecutive cases. Am J Otol. 21(2):173-80, 2000](http://www.ncbi.nlm.nih.gov/pubmed/?term=10733180%5Bpmid%5D)
|
||||
1. [Kohan D et al: Uncommon lesions presenting as tumors of the internal auditory canal and cerebellopontine angle. Am J Otol. 18(3):386-92, 1997](http://www.ncbi.nlm.nih.gov/pubmed/?term=9149836%5Bpmid%5D)
|
||||
1. [Smirniotopoulos JG et al: Cerebellopontine angle masses: radiologic-pathologic correlation. Radiographics. 13(5):1131-47, 1993](http://www.ncbi.nlm.nih.gov/pubmed/?term=8210595%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
**Vestibular Schwannoma**
|
||||
*Axial T1 C+ MR demonstrates a mixed solid and cystic enhancing mass in the right CPA cistern <img src='img/arrows/WS.png'/>. A small amount of tumor extension is visible extending into the IAC <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Vestibular Schwannoma**
|
||||
*Axial T1 C+ MR demonstrates a mixed solid and cystic enhancing mass in the right CPA cistern <img src='img/arrows/WS.png'/>. A small amount of tumor extension is visible extending into the IAC <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Vestibular Schwannoma**
|
||||
*Axial T1 C+ MR demonstrates a mixed solid and cystic enhancing mass in the right CPA cistern <img src='img/arrows/WS.png'/>. A small amount of tumor extension is visible extending into the IAC <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Meningioma in CPA-IAC**
|
||||
*Axial T1 C+ MR demonstrates a homogeneously enhancing meningioma in the right CPA <img src='img/arrows/WS.png'/>. There was no substantial IAC component, and a dural tail was present on additional images (not shown).*
|
||||
|
||||
|
||||
**Epidermoid Cyst in CPA-IAC**
|
||||
*Axial T2 MR shows a heterogeneous right CPA mass with insinuating contours around the brainstem and cerebellum <img src='img/arrows/WS.png'/>, typical of an epidermoid cyst. Corresponding DWI showed bright signal (restricted diffusion), and FLAIR showed lack of fluid suppression (not shown).*
|
||||
|
||||
|
||||
**Aneurysm in CPA-IAC**
|
||||
*Axial T1 C+ MR demonstrates a large enhancing distal vertebral artery aneurysm <img src='img/arrows/WS.png'/> projecting up into the CPA cistern and compressing the area where CNVII and CNVIII exit the brainstem <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
**Arachnoid Cyst in CPA**
|
||||
*Axial T2 FS MR shows a high-signal cystic mass <img src='img/arrows/WS.png'/> in the low CPA cistern. Note the anterior displacement of the proximal vestibulocochlear nerve by the arachnoid cyst <img src='img/arrows/WO.png'/>. The high signal results from the absence of CSF flow-related artifact.*
|
||||
|
||||
|
||||
**Metastases in CPA-IAC**
|
||||
*Axial T1 C+ FS MR reveals an inhomogeneously enhancing metastatic focus arising from the dura along the prepontine cistern. This metastasis reaches the anterior margin of the porus acusticus <img src='img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
**Neurofibromatosis Type 2**
|
||||
*Axial T1 C+ MR shows bilateral enhancing CPA-IAC schwannomas <img src='img/arrows/WS.png'/>. The left-sided schwannoma involves the intratemporal anterior genu of facial nerve <img src='img/arrows/WO.png'/>, indicating it is most likely a facial nerve schwannoma.*
|
||||
|
||||
|
||||
**Sarcoidosis in CPA-IAC**
|
||||
*Axial T1 C+ MR shows a heaped-up, dural-based sarcoid deposit in the right CPA cistern <img src='img/arrows/WS.png'/> that enters the IAC <img src='img/arrows/WC.png'/>. The Meckel cave <img src='img/arrows/WO.png'/> is also affected. This lesion mimics meningioma.*
|
||||
|
||||
|
||||
**Choroid Plexus Papilloma in CPA**
|
||||
*Axial T1 C+ MR reveals a pear-shaped, inhomogeneously enhancing papilloma <img src='img/arrows/WS.png'/> projecting from the lateral recess of the 4th ventricle through the foramen of Luschka into the low CPA cistern <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
**Lipoma in CPA-IAC**
|
||||
*Axial NECT performed for trauma shows large, bilateral, fat-attenuation masses within both CPA cisterns <img src='img/arrows/WS.png'/>, compatible with lipomas. The patient has a longstanding history of deafness. Surgery is not indicated, since hearing does not improve with resection.*
|
||||
|
||||
|
||||
**Ependymoma in CPA**
|
||||
*Axial T1 C+ MR demonstrates an aggressive mixed cystic-solid enhancing ependymoma of the right CPA cistern <img src='img/arrows/WS.png'/>, 4th ventricle <img src='img/arrows/WO.png'/>, and cerebellar hemisphere <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Hypertrophic Pachymeningitis**
|
||||
*Axial T1 C+ MR demonstrates an extensive area of enhancing dural thickening <img src='img/arrows/WS.png'/> along the right low CPA cistern. Pachymeningitis also involves the subjacent jugular foramen <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
**Facial Nerve Schwannoma in CPA-IAC**
|
||||
*Axial T1 C+ MR shows a variant facial nerve schwannoma with a solid enhancing CPA-IAC component <img src='img/arrows/WS.png'/> extending into the geniculate ganglion <img src='img/arrows/WO.png'/>. Note the associated arachnoid cyst <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Jugular Foramen Schwannoma**
|
||||
*Axial T1 C+ FS MR shows a bilobed intensely enhancing mass in the right CPA cistern <img src='img/arrows/WS.png'/> distorting adjacent brain. A large enhancing component within the enlarged right jugular foramen <img src='img/arrows/WC.png'/> indicated the site of origin. No extension into the adjacent IAC (not shown) was seen.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
**Vestibular Schwannoma**
|
||||
*Axial T1 C+ MR shows a heterogeneous enhancing CPA mass filling and expanding the right IAC <img src='img/arrows/WS.png'/>. Note characteristic internal cystic foci <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Vestibular Schwannoma**
|
||||
*Axial T1 C+ MR shows an typical, heterogeneously enhancing right CPA schwannoma <img src='img/arrows/WS.png'/> with a colocated arachnoid cyst <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Epidermoid Cyst in CPA-IAC**
|
||||
*Axial T2 MR shows a hyperintense mass in the right CPA with "insinuating" margins <img src='img/arrows/WS.png'/>, typical of epidermoid cysts. No enhancement was noted on postcontrast imaging and DWI (not shown) showed lesion restriction.*
|
||||
|
||||
|
||||
**IAC Venous Malformation ("Hemangioma")**
|
||||
*Axial T1 C+ MR shows an enhancing IAC mass with multiple punctate low-signal foci <img src='img/arrows/WS.png'/>. CT showed that calcifications were present, supporting the diagnosis of IAC hemangioma.*
|
||||
|
||||
|
||||
**Neurenteric Cyst**
|
||||
*Axial FLAIR MR demonstrates an area of high signal <img src='img/arrows/WS.png'/> in the low CPA cistern that was found to be a neurenteric cyst at surgery.*
|
||||
|
||||
|
||||
**Vestibular Schwannoma**
|
||||
*Axial T1 C+ MR reveals an enhancing mass filling the CPA <img src='img/arrows/WS.png'/> and IAC <img src='img/arrows/WO.png'/>. Note that the cochlear nerve canal is involved <img src='img/arrows/WC.png'/>, making resection with hearing preservation difficult.*
|
||||
|
||||
|
||||
**Meningioma in CPA-IAC**
|
||||
*Axial T1 C+ FS MR reveals an enhancing dural-based mass centered over the IAC but with minimal IAC involvement <img src='img/arrows/WS.png'/>. The shape and the associated dural tail <img src='img/arrows/WO.png'/> make meningioma the diagnosis.*
|
||||
|
||||
|
||||
**Epidermoid Cyst in CPA-IAC**
|
||||
*Axial T1WI MR shows a low-signal mass in the right CPA cistern that insinuates and enlarges the foramen of Luschka <img src='img/arrows/WS.png'/> and scallops the ventral cerebellar hemisphere <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
**Lipoma in CPA-IAC**
|
||||
*Axial T1WI MR shows a variant 3-part lipoma affecting the CPA cistern <img src='img/arrows/WS.png'/>, the high anterior jugular foramen <img src='img/arrows/WO.png'/>, and the vestibule of the inner ear <img src='img/arrows/WC.png'/>. Surgical resection is not performed for such lesions.*
|
||||
|
||||
|
||||
**Jugular Foramen Schwannoma**
|
||||
*Coronal T1 C+ FS MR reveals a schwannoma <img src='img/arrows/WS.png'/> projecting cephalad from the jugular foramen <img src='img/arrows/WO.png'/> into the CPA cistern. Note that the normal IAC <img src='img/arrows/WC.png'/> is at the level of the upper margin of the tumor.*
|
||||
|
||||
|
||||
**Epidermoid Cyst in CPA-IAC**
|
||||
*Axial T1 C+ MR shows a partially cystic prepontine and left CPA mass <img src='img/arrows/WS.png'/> with marginal nodular areas of enhancement due to epidermoid cyst, which in this case was complicated by rare malignant transformation into squamous cell carcinoma. Areas of diffusion restriction were noted in the cystic component; however, soft tissue enhancement along the margins <img src='img/arrows/WO.png'/> are unexpected for epidermoid, and raise concern for malignancy.*
|
||||
|
||||
@@ -0,0 +1,174 @@
|
||||
---
|
||||
title: "CPA Mass, Child"
|
||||
docid: "76d2535b-050d-4826-a344-877e5bae4230"
|
||||
authors:
|
||||
- key: "d19354f3-7ff2-495a-ad3f-064122e45602"
|
||||
value: "Bernadette L. Koch, MD"
|
||||
- key: "e8af6d26-3aad-47c9-9083-5128aab09af2"
|
||||
value: "Susan I. Blaser, MD, FRCPC"
|
||||
breadcrumbs:
|
||||
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|
||||
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|
||||
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|
||||
treeNodeId: "ed24ed8c-5d57-4629-879b-447b82d2973d"
|
||||
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|
||||
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|
||||
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|
||||
treeNodeId: "40d68862-8975-4dde-ac2b-ebc43ab0fb5c"
|
||||
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|
||||
name: "CPA-IAC and Posterior Fossa"
|
||||
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|
||||
treeNodeId: "c590eedb-4a3b-4158-a04f-ad880564c992"
|
||||
-
|
||||
name: "Anatomically Based Differentials"
|
||||
slug: "anatomically-based-differentials"
|
||||
treeNodeId: "debfb06c-8656-4f5d-92c1-eaa468185d78"
|
||||
-
|
||||
name: "CPA Mass, Child"
|
||||
slug: "cpa-mass-child"
|
||||
treeNodeId: null
|
||||
category: "Head and Neck"
|
||||
documentVersionId: "388e4ad1-934e-45b0-8fc0-80caff2df890"
|
||||
imageCount: 11
|
||||
lastUpdated: "03/28/22"
|
||||
pageDescription: "CPA Mass, Child"
|
||||
pageKeywords: "Head and Neck, Differential Diagnosis, CPA-IAC and Posterior Fossa, Anatomically Based Differentials, CPA Mass, Child"
|
||||
pageTitle: "CPA Mass, Child | STATdx"
|
||||
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|
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|
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|
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|
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- "Head and Neck"
|
||||
- "Differential Diagnosis"
|
||||
- "CPA-IAC and Posterior Fossa"
|
||||
- "Anatomically Based Differentials"
|
||||
- "CPA Mass, Child"
|
||||
---
|
||||
# ESSENTIAL INFORMATION
|
||||
|
||||
- ## Helpful Clues for Common Diagnoses
|
||||
|
||||
|
||||
- [Arachnoid Cyst in CPA-IAC](/document/cpa-iac-arachnoid-cyst/f1af2d0f-adfd-49c7-a3b9-8a1c66dce2be)
|
||||
- Sharply demarcated extraaxial cyst with CSF density/signal intensity
|
||||
- Isointense to CSF on all MR sequences, including complete fluid attenuation on FLAIR images
|
||||
- Nonenhancing
|
||||
- No diffusion restriction
|
||||
- ## Helpful Clues for Less Common Diagnoses
|
||||
|
||||
|
||||
- [Vestibular Schwannoma](/document/vestibular-schwannoma/48772166-59dc-4909-bc75-538de7dd9ddf)
|
||||
- Ovoid when within internal auditory canal (IAC)
|
||||
- Ice cream on cone shape when CPA-IAC
|
||||
- Hypointense relative to hyperintense CSF on T2 or CISS images, ± intramural cysts
|
||||
- Enhancing, well-circumscribed tumor
|
||||
- Rare in children, unless neurofibromatosis type 2
|
||||
- Infratentorial Ependymoma
|
||||
- Heterogeneously enhancing 4th ventricular mass with irregular margins
|
||||
- Extends through foramen of Luschka → CPA cistern
|
||||
- Calcification in up to 50%
|
||||
- [Infantile Hemangioma in CPA-IAC](/document/infantile-hemangioma/4c91584c-4788-4d4d-b854-15d22fdff6b7)
|
||||
- Smoothly marginated, intensely enhancing mass in CPA-IAC (proliferating phase)
|
||||
- Proliferating, involuting, and involuted phases
|
||||
- Usually, involutional timing similar to extracranial hemangiomas; therefore, no surgical intervention
|
||||
- Glut-1 marker positive
|
||||
- ± PHACE syndrome
|
||||
- **P**osterior fossa malformations, **h**emangioma, **a**rterial cerebrovascular anomalies, **c**oarctation of aorta and cardiac defects, **e**ye abnormalities
|
||||
- [Epidermoid Cyst in CPA-IAC](/document/cpa-iac-epidermoid-cyst/5e83f596-1ca4-41cb-95aa-469147ca5f8f)
|
||||
- Insinuating mass with irregular or scalloped margins
|
||||
- ± scalloping brainstem margin
|
||||
- Iso- to slightly hyperintense to CSF
|
||||
- Nonenhancing, with restricted diffusion
|
||||
- ## Helpful Clues for Rare Diagnoses
|
||||
|
||||
|
||||
- Atypical Teratoid/Rhabdoid Tumor
|
||||
- CPA tumor with lytic bone destruction in infants
|
||||
- Hypointense compared with CSF on T2, with restricted diffusion, enhancing
|
||||
- [Meningioma in CPA-IAC](/document/cpa-iac-meningitis/c3269e91-15d4-4421-917a-216f4d08a038)
|
||||
- Dural-based globular or en plaque mass
|
||||
- Enhancing mass ± dural tail: 23% of CPA meningiomas have extension/dural tail into IAC
|
||||
- Permeative-sclerotic or hyperostotic bone
|
||||
- [Lipoma in CPA-IAC](/document/lipoma-in-cpa-iac/3dc1a638-a325-4390-844f-97e01961734d)
|
||||
- Ovoid or broad-based against lateral pons
|
||||
- Fat signal intensity/density on MR and CT
|
||||
- May be mistaken for vestibular schwannoma if T1 C+ images are performed without fat saturation
|
||||
- [Metastases in CPA-IAC](/document/cpa-iac-metastases/451451c8-7b49-4ce9-bf22-7c02b4652f23)
|
||||
- Irregular, invasive mass; single or multiple
|
||||
- Primarily involves leptomeninges, flocculus, choroid plexus, or dura
|
||||
- Unilateral or bilateral
|
||||
- [Choroid Plexus Papilloma in CPA](/document/choroid-plexus-papilloma/18e712f5-8553-487d-a939-044336cbf0ad)
|
||||
- Dumbbell-shaped mass in 4th ventricle, extending through foramen of Luschka → CPA cistern
|
||||
- Avid contrast enhancement
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Vernon V et al: Surgical management of cerebellopontine angle epidermoid cysts: an institutional experience of 10 years. Br J Neurosurg. 1-10, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=33410366%5Bpmid%5D)
|
||||
1. [Bartindale M et al: Facial schwannoma management outcomes: a systematic review of the literature. Otolaryngol Head Neck Surg. 163(2):293-301, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32228141%5Bpmid%5D)
|
||||
1. [D'Arco F et al: The link between inner ear malformations and the rest of the body: what we know so far about genetic, imaging and histology. Neuroradiology. 62(5):539-44, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32125475%5Bpmid%5D)
|
||||
1. [Giordano M et al: Surgical management of cerebellopontine angle arachnoid cysts associated with hearing deficit in pediatric patients. J Neurosurg Pediatr. 21(2):119-23, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29171799%5Bpmid%5D)
|
||||
1. [Bonneville F et al: Imaging of cerebellopontine angle lesions: an update. Part 2: intra-axial lesions, skull base lesions that may invade the CPA region, and non-enhancing extra-axial lesions. Eur Radiol. 17(11):2908-20, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17569053%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
**Arachnoid Cyst in CPA-IAC**
|
||||
*Axial T2WI MR in a 3-year-old child demonstrates a moderate-sized right extraaxial CPA cyst <img src='img/arrows/WS.png'/>, isointense to intraventricular fluid, moderately compressing the right cerebellar hemisphere and midbrain.*
|
||||
|
||||
|
||||
**Arachnoid Cyst in CPA-IAC**
|
||||
*Axial T2WI MR in a 3-year-old child demonstrates a moderate-sized right extraaxial CPA cyst <img src='img/arrows/WS.png'/>, isointense to intraventricular fluid, moderately compressing the right cerebellar hemisphere and midbrain.*
|
||||
|
||||
|
||||
**Arachnoid Cyst in CPA-IAC**
|
||||
*Axial T2WI MR in a 3-year-old child demonstrates a moderate-sized right extraaxial CPA cyst <img src='img/arrows/WS.png'/>, isointense to intraventricular fluid, moderately compressing the right cerebellar hemisphere and midbrain.*
|
||||
|
||||
|
||||
**Arachnoid Cyst in CPA-IAC**
|
||||
*Axial FLAIR MR in the same patient demonstrates complete attenuation of signal intensity within the cyst <img src='img/arrows/WS.png'/>, typical of an arachnoid cyst. There was no diffusion restriction on DW images (not shown), unlike an epidermoid cyst, which typically demonstrates diffusion restriction.*
|
||||
|
||||
|
||||
**Vestibular Schwannoma**
|
||||
*Axial T1 C+ MR in a 12-year-old boy shows bilateral enhancing CPA-IAC masses <img src='img/arrows/WS.png'/> and a well-defined, enhancing mass involving the left 6th cranial nerve <img src='img/arrows/WC.png'/>, consistent with multiple schwannomas in a child with NF2.*
|
||||
|
||||
|
||||
**Infratentorial Ependymoma**
|
||||
*Axial T1 C+ MR in a 2-year-old child demonstrates a large, heterogeneously enhancing posterior fossa mass <img src='img/arrows/WS.png'/> filling the 4th ventricle, extending through the foramen of Luschka and into the right CPA cistern <img src='img/arrows/WO.png'/>. Notice extension across the midline toward the left foramen of Luschka <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Infantile Hemangioma in CPA-IAC**
|
||||
*Axial T1 C+ MR in a 1-year-old infant shows a massive facial hemangioma <img src='img/arrows/WS.png'/>, a right CPA-IAC hemangioma <img src='img/arrows/WC.png'/>, and ipsilateral cerebellar hemisphere hypoplasia <img src='img/arrows/WO.png'/>. These findings are consistent with PHACE syndrome.*
|
||||
|
||||
|
||||
**Epidermoid Cyst in CPA-IAC**
|
||||
*Axial T1 C+ MR in a teenager with occipital headaches shows an extraaxial hypointense mass <img src='img/arrows/WS.png'/>, similar in signal intensity to intraventricular CSF, compressing the pons. Differential diagnosis would include arachnoid cyst or dermoid/epidermoid cyst.*
|
||||
|
||||
|
||||
**Epidermoid Cyst in CPA-IAC**
|
||||
*Axial FLAIR MR in the same patient as shows heterogeneous, "dirty" signal intensity within the lesion <img src='img/arrows/WS.png'/> adjacent to the pons, hyperintense relative to CSF. Incomplete suppression on FLAIR sequences is typical of epidermoid cysts.*
|
||||
|
||||
|
||||
**Epidermoid Cyst in CPA-IAC**
|
||||
*Axial DWI MR in the same patient shows hyperintense signal intensity <img src='img/arrows/WS.png'/> relative to intraventricular CSF, which on ADC map proved to be hypointense (not shown), consistent with restricted diffusion typical of epidermoid cysts.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
**Arachnoid Cyst in CPA-IAC**
|
||||
*Axial FIESTA in a teenager with epilepsy shows an incidental left CPA arachnoid cyst <img src='img/arrows/WS.png'/>, isointense to intraventricular CSF, without mass effect on the cisternal segments of the 7th/8th cranial nerves <img src='img/arrows/WO.png'/> and without extension into the IAC.*
|
||||
|
||||
|
||||
**Epidermoid Cyst in CPA-IAC**
|
||||
*Axial T2WI MR in a teenager with occipital headaches demonstrates an oblong, T2-hyperintense epidermoid cyst <img src='img/arrows/WS.png'/>, mildly compressing the left ventral pons.*
|
||||
|
||||
|
||||
**Epidermoid Cyst in CPA-IAC**
|
||||
*Axial ADC map in the same patient shows hypointense signal on ADC map image consistent with <img src='img/arrows/WS.png'/> diffusion restriction within the lesion, typical of epidermoid cyst.*
|
||||
|
||||
@@ -0,0 +1,325 @@
|
||||
---
|
||||
title: "Cystic CPA Mass"
|
||||
docid: "6c60db6d-8093-4df5-8cbb-c6f6570ae167"
|
||||
authors:
|
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pageTitle: "Cystic CPA Mass | STATdx"
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- "Differential Diagnosis"
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- "Generic Imaging Patterns"
|
||||
- "Cystic CPA Mass"
|
||||
---
|
||||
# ESSENTIAL INFORMATION
|
||||
|
||||
- ## Key Differential Diagnosis Issues
|
||||
|
||||
|
||||
- This differential diagnosis is constructed around lesions of cerebellopontine angle (CPA) that may have "cystic" imaging features
|
||||
- Typically cystic lesions: Epidermoid, arachnoid, & neurenteric cysts; neurocysticercosis & large endolymphatic sac anomaly
|
||||
- Many solid CPA tumors may have either intramural cysts, necrosis, or extramural cysts as typical or variant MR imaging manifestation
|
||||
- Schwannoma: Vestibular, facial nerve, trigeminal, or jugular foramen schwannoma with intramural or extramural cysts can all be found in CPA area
|
||||
- Hemangioblastoma: Cerebellar cystic & solid tumor that may project into CPA cistern
|
||||
- Endolymphatic sac tumor: CPA involved if large
|
||||
- Cystic meningioma
|
||||
- Idealized imaging protocol in evaluating cystic CPA masses
|
||||
- T1 C+ fat-saturated MR is gold standard
|
||||
- Contrast helps differentiate solid from cystic components of tumors, such as vestibular or facial nerve schwannoma & hemangioblastoma
|
||||
- DWI for possible epidermoid cyst (restricted diffusion)
|
||||
- T2 thin-section, high-resolution MR
|
||||
- Also sorts out solid and cystic components of lesions
|
||||
- Helps with cranial nerve & vascular anatomy
|
||||
- ## Helpful Clues for Common Diagnoses
|
||||
|
||||
|
||||
- **Epidermoid Cyst**
|
||||
- Key facts
|
||||
- Definition: Congenital rest of epithelial tissue in CPA
|
||||
- Imaging findings
|
||||
- Insinuating or scalloping brainstem margin
|
||||
- T1 MR: Iso- to slightly hyperintense relative to CSF
|
||||
- T1 C+ MR: Typically nonenhancing cyst; may be hard to see
|
||||
- Minimal marginal cyst enhancement in 25%
|
||||
- Soft tissue enhancement present in rare cases of malignant degeneration to squamous cell carcinoma; PET avidity can help confirm suspicion
|
||||
- T2 MR: High-signal, well-circumscribed CPA mass
|
||||
- FLAIR: Lack of complete fluid suppression
|
||||
- DWI: Restricted diffusion (high signal) makes diagnosis
|
||||
- **Arachnoid Cyst**
|
||||
- Key facts
|
||||
- Definition: Congenital lesion resulting from failure of embryonic meninges to merge results in cyst between split arachnoid membrane
|
||||
- Imaging findings
|
||||
- Fills cistern with rounded margins
|
||||
- T1 C+ MR: No enhancement
|
||||
- FLAIR: Lesion attenuates (black like CSF)
|
||||
- DWI: Isointense to CSF (no restriction)
|
||||
- ## Helpful Clues for Less Common Diagnoses
|
||||
|
||||
|
||||
- **Vestibular Schwannoma W****ith Intramural Cyst(s)**
|
||||
- Key facts
|
||||
- Definition: Vestibular schwannoma may have either intramural or extramural cysts associated
|
||||
- Imaging findings
|
||||
- Solid CPA-IAC mass with intramural cysts
|
||||
- Bone CT: Larger lesions flare medial IAC component
|
||||
- T1 C+ MR: Enhancing solid tumor component ± intramural cysts (common) ± extramural cyst (rare)
|
||||
- Microhemorrhages on T2* GRE or SWI favor schwannoma over meningioma
|
||||
- **Hemangioblastoma**
|
||||
- Key facts
|
||||
- Definition: Benign tumor composed of stromal cells in small blood vessels of CNS
|
||||
- Adult with intraaxial posterior fossa mass abutting pia
|
||||
- Associated with von Hippel Lindau (VHL) in 25-40%
|
||||
- Supratentorial hemangioblastomas more likely VHL related
|
||||
- Imaging findings
|
||||
- Cerebellar cystic & solid tumor
|
||||
- T1 C+ MR: 60% of tumors with solid enhancing & cystic components (40% solid only)
|
||||
- **Large Endolymphatic Sac Anomaly (IP-II)**
|
||||
- Key facts
|
||||
- Bilateral congenital sensorineural hearing loss that appears in child with cascading hearing loss pattern
|
||||
- Most common congenital imaging abnormality
|
||||
- Recommendation to avoid contact sports
|
||||
- Imaging findings
|
||||
- Bone CT: Enlarged bony vestibular aqueduct
|
||||
- T2 high-resolution MR: Enlarged endolymphatic sac & duct + mild cochlear malformation (modiolar deficiency, deficient apical septation, & scalar chamber asymmetry)
|
||||
- **Neurocysticercosis**
|
||||
- Key facts
|
||||
- Definition: Intracranial infection caused by pork tapeworm (*Taenia solium*)
|
||||
- Imaging findings
|
||||
- Cysts with "dots" inside
|
||||
- Appearance varies with stage
|
||||
- T1 C+ MR: Cysts with enhancing thin or thick wall
|
||||
- May be associated with hydrocephalus
|
||||
- ## Helpful Clues for Rare Diagnoses
|
||||
|
||||
|
||||
- **Vestibular Schwannoma W****ith Extramural Cyst**
|
||||
- Key facts
|
||||
- Vestibular schwannoma with extramural cyst
|
||||
- Cyst may be "trapped CSF" or actual arachnoid cyst
|
||||
- Neurootologists call extramural cyst "herald cyst"
|
||||
- Imaging findings
|
||||
- CPA-IAC mass with extramural cyst
|
||||
- Bone CT: Large lesions flare IAC medial component
|
||||
- T1 C+ MR: Enhancing solid tumor component ± extramural cyst
|
||||
- Microhemorrhages on T2* GRE or SWI favor schwannoma over meningioma
|
||||
- **Facial Nerve Schwannoma in CPA-IAC W****ith Cyst**
|
||||
- Key facts
|
||||
- Rare CPA-IAC mass with labyrinthine tail involving labyrinthine segment of facial nerve canal
|
||||
- Often presents with hearing loss before facial nerve symptoms
|
||||
- Imaging findings
|
||||
- Bone CT: Labyrinthine segment of facial nerve may be enlarged
|
||||
- T1 C+ MR: Enhancing tubular mass in CPA-IAC & labyrinthine segment of facial nerve; intramural or extramural cyst visible
|
||||
- **Schwannoma, Trigeminal, Skull Base**
|
||||
- Key facts
|
||||
- Most common presentation is ipsilateral facial pain
|
||||
- Imaging findings
|
||||
- CPA cystic enhancing mass with tail extending toward or into Meckel cave is characteristic
|
||||
- Look for denervation of masticator space muscles
|
||||
- **Neurenteric****C****yst**
|
||||
- Key facts
|
||||
- Arises at time of notochordal development during transitory existence of neurenteric canal
|
||||
- Benign endodermal lesion of CNS
|
||||
- Often presents as incidental rounded to ovoid mass in prepontine cistern
|
||||
- Imaging findings
|
||||
- MR shows intermediate- to high-signal T1 prepontine "cystic" mass
|
||||
- **Jugular Foramen Schwannoma W****ith Intramural Cyst**
|
||||
- Key facts
|
||||
- Presents with mixture of 9-12 cranial neuropathy
|
||||
- Imaging findings
|
||||
- Bone CT: Enlarged, sharply marginated jugular foramen
|
||||
- T1 MR: Iso-g to hyperintense compared to CSF
|
||||
- T1 C+ MR: Enhancing mass with intramural cysts arising from jugular foramen
|
||||
- Intramural cysts in 25% of jugular foramen schwannomas
|
||||
- Other MR findings: Mass projects superomedially into CPA cistern, often with brainstem compression
|
||||
- **Cystic Metastasis in CPA**
|
||||
- Key facts
|
||||
- Usually in patients with known primary cancer
|
||||
- Imaging findings
|
||||
- T1 C+ MR: Enhancing mass with cystic component may mimic schwannoma or cystic meningioma
|
||||
- Likely to exhibit rapid growth pattern and more symptoms, such as facial nerve palsy, than benign tumors like schwannoma
|
||||
- **Endolymphatic Sac Tumor**
|
||||
- Key facts
|
||||
- Sporadic or associated with VHL
|
||||
- Bilateral tumors &/or concurrent hemangioblastoma indicates VHL
|
||||
- Imaging findings
|
||||
- Bone CT: Permeative destruction of posterior petrous temporal bone centered at vestibular aqueduct
|
||||
- T1 MR: Hyperintense foci due to internal hemorrhage are characteristic
|
||||
- T1 C+ MR: Partly cystic, heterogenous enhancing mass
|
||||
- DOTATATE scan may show mild uptake due to somatostatin receptor type 2A expression in tumor vasculature not tumor cells
|
||||
- **Meningioma, Cystic**
|
||||
- T1 C+ MR: Rare, heterogeneous, partly cystic enhancing mass
|
||||
- Rare meningioma variant that mimics schwannoma; most are clear cell subtype
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Ali NE et al: Natural history of cystic vestibular schwannomas. Ann Otol Rhinol Laryngol. 132(7):795-9, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=35993287%5Bpmid%5D)
|
||||
1. [Adachi S et al: Unusual imaging characteristics of cystic meningioma in cerebellopontine angle. Neuroradiol J. 35(6):777-9, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35503008%5Bpmid%5D)
|
||||
1. [Geng Y et al: Endolymphatic sac tumour: exploring the role of CT and MRI features in the diagnosis of 22 cases. Clin Radiol. 77(8):e592-8, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35643739%5Bpmid%5D)
|
||||
1. [Talukdar R et al: Endolymphatic sac tumor: single-institution series of seven cases with updated review of literature. Eur Arch Otorhinolaryngol. 279(5):2591-8, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=34410472%5Bpmid%5D)
|
||||
1. [Parlak S et al: 3 Tesla MR imaging of the large endolymphatic duct and sac anomaly with audiological correlation. Eur J Radiol. 145:110064, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=34839211%5Bpmid%5D)
|
||||
1. [Saigal G et al: Utility of microhemorrhage as a diagnostic tool in distinguishing vestibular schwannomas from other cerebellopontine angle (CPA) Tumors. Indian J Otolaryngol Head Neck Surg. 73(3):321-6, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=34471620%5Bpmid%5D)
|
||||
1. [Lou R et al: 68Ga-DOTATATE uptake in an endolymphatic sac tumor: radiologic-pathologic correlation. Clin Nucl Med. 45(7):563-5, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32433163%5Bpmid%5D)
|
||||
1. [Connor SEJ et al: Is CT or MRI the optimal imaging investigation for the diagnosis of large vestibular aqueduct syndrome and large endolymphatic sac anomaly? Eur Arch Otorhinolaryngol. 276(3):693-702, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30635710%5Bpmid%5D)
|
||||
1. [Eliezer M et al: Clinical and radiological characteristics of malignant tumors located to the cerebellopontine angle and/or internal acoustic meatus. Otol Neurotol. 40(9):1237-45, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31469787%5Bpmid%5D)
|
||||
1. [Le H et al: Clinicoradiologic characteristics of endolymphatic sac tumors. Eur Arch Otorhinolaryngol. 276(10):2705-14, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31197530%5Bpmid%5D)
|
||||
1. [Touska P et al: Temporal bone tumors: an imaging update. Neuroimaging Clin N Am. 29(1):145-72, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30466638%5Bpmid%5D)
|
||||
1. [Schnack DT et al: Sporadic endolymphatic sac tumor-a very rare cause of hearing loss, tinnitus, and dizziness. J Int Adv Otol. 13(2):289-91, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28716765%5Bpmid%5D)
|
||||
1. [Agarwal A: Intracranial trigeminal schwannoma. Neuroradiol J. 28(1):36-41, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25924170%5Bpmid%5D)
|
||||
1. [Dispenza F et al: Imaging of vestibular schwannoma with prevalent cystic component: cystic vestibular schwannoma. Otol Neurotol. 30(5):681-2, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=18716565%5Bpmid%5D)
|
||||
1. [Piccirillo E et al: Cystic vestibular schwannoma: classification, management, and facial nerve outcomes. Otol Neurotol. 30(6):826-34, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19704364%5Bpmid%5D)
|
||||
1. [Zhang L et al: Trigeminal schwannomas: a report of 42 cases and review of the relevant surgical approaches. Clin Neurol Neurosurg. 111(3):261-9, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19081670%5Bpmid%5D)
|
||||
1. [Bonneville F et al: Imaging of cerebellopontine angle lesions: an update. Part 1: enhancing extra-axial lesions. Eur Radiol. 17(10):2472-82, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17562049%5Bpmid%5D)
|
||||
1. [Bonneville F et al: Imaging of cerebellopontine angle lesions: an update. Part 2: intra-axial lesions, skull base lesions that may invade the CPA region, and non-enhancing extra-axial lesions. Eur Radiol. 17(11):2908-20, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17569053%5Bpmid%5D)
|
||||
1. [Kiliçkesmez O: Endolymphatic sac tumor in a patient with von Hippel-Lindau disease: MR imaging findings. Diagn Interv Radiol. 12(1):14-6, 2006](http://www.ncbi.nlm.nih.gov/pubmed/?term=16538578%5Bpmid%5D)
|
||||
1. [Patel NP et al: The radiologic diagnosis of endolymphatic sac tumors. Laryngoscope. 116(1):40-6, 2006](http://www.ncbi.nlm.nih.gov/pubmed/?term=16481807%5Bpmid%5D)
|
||||
1. [Preece MT et al: Intracranial neurenteric cysts: imaging and pathology spectrum. AJNR Am J Neuroradiol. 27(6):1211-6, 2006](http://www.ncbi.nlm.nih.gov/pubmed/?term=16775266%5Bpmid%5D)
|
||||
1. [Nelson MD Jr et al: A different approach to cysts of the posterior fossa. Pediatr Radiol. 34(9):720-32, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15316692%5Bpmid%5D)
|
||||
1. [Bonneville F et al: Unusual lesions of the cerebellopontine angle: a segmental approach. Radiographics. 21(2):419-38, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11259705%5Bpmid%5D)
|
||||
1. [Davidson HC et al: MR evaluation of vestibulocochlear anomalies associated with large endolymphatic duct and sac. AJNR Am J Neuroradiol. 20(8):1435-41, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=10512225%5Bpmid%5D)
|
||||
1. [Koeller KK et al: Congenital cystic masses of the neck: radiologic-pathologic correlation. Radiographics. 19(1):121-46; quiz 152-3, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=9925396%5Bpmid%5D)
|
||||
1. [Lau KY et al: MRI demonstration of subarachnoid neurocysticercosis simulating metastatic disease. Neuroradiology. 40(11):724-6, 1998](http://www.ncbi.nlm.nih.gov/pubmed/?term=9860122%5Bpmid%5D)
|
||||
1. [Mukherji SK et al: Papillary endolymphatic sac tumors: CT, MR imaging, and angiographic findings in 20 patients. Radiology. 202(3):801-8, 1997](http://www.ncbi.nlm.nih.gov/pubmed/?term=9051037%5Bpmid%5D)
|
||||
1. [Tong KA et al: Large vestibular aqueduct syndrome: a genetic disease? AJR Am J Roentgenol. 168(4):1097-101, 1997](http://www.ncbi.nlm.nih.gov/pubmed/?term=9124122%5Bpmid%5D)
|
||||
1. [Friedman DP et al: Vascular neoplasms and malformations, ischemia, and hemorrhage affecting the spinal cord: MR imaging findings. AJR Am J Roentgenol. 162(3):685-92, 1994](http://www.ncbi.nlm.nih.gov/pubmed/?term=8109522%5Bpmid%5D)
|
||||
1. [Kollias SS et al: Cystic malformations of the posterior fossa: differential diagnosis clarified through embryologic analysis. Radiographics. 13(6):1211-31, 1993](http://www.ncbi.nlm.nih.gov/pubmed/?term=8031352%5Bpmid%5D)
|
||||
1. [Smirniotopoulos JG et al: Cerebellopontine angle masses: radiologic-pathologic correlation. Radiographics. 13(5):1131-47, 1993](http://www.ncbi.nlm.nih.gov/pubmed/?term=8210595%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
**Epidermoid Cyst**
|
||||
*Axial T1 C+ MR reveals a low signal intensity, nonenhancing epidermoid cyst that insinuates into the foramen of Luschka <img src='img/arrows/WS.png'/> and along the right cerebellar hemisphere <img src='img/arrows/WO.png'/>. DWI MR sequence would show restricted diffusion. FLAIR would show lack of complete fluid suppression.*
|
||||
|
||||
|
||||
**Epidermoid Cyst**
|
||||
*Axial T1 C+ MR reveals a low signal intensity, nonenhancing epidermoid cyst that insinuates into the foramen of Luschka <img src='img/arrows/WS.png'/> and along the right cerebellar hemisphere <img src='img/arrows/WO.png'/>. DWI MR sequence would show restricted diffusion. FLAIR would show lack of complete fluid suppression.*
|
||||
|
||||
|
||||
**Arachnoid Cyst**
|
||||
*Axial T1 C+ FS MR demonstrates a right cerebellopontine angle (CPA) cistern arachnoid cyst <img src='img/arrows/WS.png'/> displacing the proximal facial and vestibulocochlear nerves anteriorly <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
**Vestibular Schwannoma With Intramural Cyst(s)**
|
||||
*Axial T1 C+ MR shows a large enhancing vestibular schwannoma projecting from the internal auditory canal (IAC) <img src='img/arrows/WS.png'/> into the CPA cistern. The tumor has a large intramural cyst <img src='img/arrows/WO.png'/> that compresses the brainstem and cerebellum.*
|
||||
|
||||
|
||||
**Vestibular Schwannoma With Intramural Cyst(s)**
|
||||
*Axial T2 MR shows a heterogeneous CPA mass <img src='img/arrows/WS.png'/> extending into the left internal auditory canal. Note numerous large intramural tumor cysts <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Hemangioblastoma**
|
||||
*Axial T1 C+ FS MR shows a superficial, intracerebellar mixed cystic-solid hemangioblastoma projecting into the left CPA cistern area. The solid nodule <img src='img/arrows/WS.png'/> is avidly enhancing.*
|
||||
|
||||
|
||||
**Large Endolymphatic Sac Anomaly (IP-II)**
|
||||
*Axial T2WI MR shows a large endolymphatic sac <img src='img/arrows/WS.png'/> within the posterior wall of the temporal bone. CT (not shown) would reveal a large bony vestibular aqueduct in this patient with large endolymphatic sac anomaly.*
|
||||
|
||||
|
||||
**Neurocysticercosis**
|
||||
*Axial T1 C+ FS MR demonstrates a cystic mass in the right CPA cistern with a peripherally enhancing wall <img src='img/arrows/WS.png'/>. Adjacent enhancing, thickened meninges <img src='img/arrows/WO.png'/> are also seen.*
|
||||
|
||||
|
||||
**Vestibular Schwannoma With Extramural Cyst**
|
||||
*Axial T2WI MR shows a vestibular schwannoma <img src='img/arrows/WS.png'/> projecting from the IAC into the CPA cistern. An associated (extramural) arachnoid cyst is visible <img src='img/arrows/WO.png'/> compressing the brainstem and 4th ventricle <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Facial Nerve Schwannoma in CPA-IAC With Cyst**
|
||||
*Axial T1 C+ MR reveals an enhancing CPA mass <img src='img/arrows/WS.png'/>, with intramural cysts, which projected into the IAC but did not involve the labyrinthine segment. Note atrophy of the right platysma muscle <img src='img/arrows/BS.png'/> from CNVII denervation.*
|
||||
|
||||
|
||||
**Schwannoma, Trigeminal, Skull Base**
|
||||
*Axial T1 C+ MR demonstrates a large CPA cystic mass "pointing" toward the Meckel cave <img src='img/arrows/WS.png'/>, providing a clue to the origin of this mass. Note chronic denervation changes of volume loss and fatty infiltration in the left suprazygomatic masticator space <img src='img/arrows/WO.png'/> compared to the right <img src='img/arrows/WC.png'/>, partly seen here.*
|
||||
|
||||
|
||||
**Neurenteric Cyst**
|
||||
*Axial T1WI MR shows a small mass anterior to the pontomedullary junction <img src='img/arrows/WS.png'/>. The neurenteric cyst is well delineated, demonstrating nearly isointense signal to brain, and does not enhance significantly.*
|
||||
|
||||
|
||||
**Jugular Foramen Schwannoma With Intramural Cyst**
|
||||
*Axial T2 FS MR reveals a large, sharply marginated lesion expanding the left jugular foramen <img src='img/arrows/WO.png'/>. The high-signal mass projects medially into the low CPA cistern where it compresses the brainstem <img src='img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
**Cystic Metastasis in CPA**
|
||||
*Parasagittal T1 C+ FS MR shows a heterogeneous, cystic enhancing mass <img src='img/arrows/WC.png'/> in the right CPA <img src='img/arrows/WS.png'/>. Adjacent brain edema is noted <img src='img/arrows/WO.png'/>. Although the mass might mimic a cystic schwannoma, the presence of a 2nd enhancing mass and a clinical history of lung cancer helps establish diagnosis of metastasis.*
|
||||
|
||||
|
||||
**Endolymphatic Sac Tumor**
|
||||
*Axial high-resolution T2 MR shows a heterogeneous cystic CPA mass <img src='img/arrows/WS.png'/>. The key to diagnosis is identifying the mass origin from the posterior temporal bone in the expected location of the endolymphatic sac.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
**Vestibular Schwannoma With Extramural Cyst**
|
||||
*Axial T1 C+ MR shows an atypical heterogeneously enhancing left vestibular schwannoma <img src='img/arrows/WC.png'/> with an associated arachnoid cyst <img src='img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
**Jugular Foramen Schwannoma With Intramural Cyst**
|
||||
*Coronal T1 C+ MR shows variant MR case of a jugular foramen schwannoma with intramural cyst <img src='img/arrows/WO.png'/> and very large cisternal component. The jugular foramen connection is seen on the next image.*
|
||||
|
||||
|
||||
**Jugular Foramen Schwannoma With Intramural Cyst**
|
||||
*Coronal T1 C+ MR reveals an enhancing schwannoma in the jugular foramen <img src='img/arrows/WS.png'/>. The tumor projects superomedially to fill the CPA cistern <img src='img/arrows/WO.png'/> and compress the brainstem.*
|
||||
|
||||
|
||||
**Schwannoma, Trigeminal, Skull Base**
|
||||
*Axial T1 C+ MR in a patient presenting with left facial pain demonstrates a peripherally enhancing cystic mass in the left CPA with a vector of spread extending towards Meckel cave <img src='img/arrows/WS.png'/>, that was the clue to its origin.*
|
||||
|
||||
|
||||
**Neurocysticercosis**
|
||||
*Coronal T1 C+ FS MR shows multiple cysts in the right CPA cistern <img src='img/arrows/WS.png'/> causing mass effect on the brainstem. Secondary hydrocephalus is present.*
|
||||
|
||||
|
||||
**Hemangioblastoma**
|
||||
*Axial T2WI MR reveals an intracerebellar high signal hemangioblastoma <img src='img/arrows/WS.png'/> projecting into the CPA cistern area. Contrast is required to define enhancing nodule if present.*
|
||||
|
||||
|
||||
**Jugular Foramen Schwannoma With Intramural Cyst**
|
||||
*Axial T1 C+ MR demonstrates an ovoid enhancing mass in the low CPA cistern <img src='img/arrows/WS.png'/>. Multiple intramural cysts suggest the diagnosis of schwannoma. Extension into the jugular foramen <img src='img/arrows/WO.png'/> is evident.*
|
||||
|
||||
|
||||
**Epidermoid Cyst**
|
||||
*Axial T1 C+ MR shows nodular soft tissue enhancement <img src='img/arrows/WO.png'/> along the margins of a cystic prepontine and left CPA epidermoid cyst <img src='img/arrows/WS.png'/>, due to a rare complication: Malignant degeneration into squamous cell carcinoma.*
|
||||
|
||||
|
||||
**Meningioma, Cystic**
|
||||
*Axial T1 C+ MR shows a partly cystic, partly solid mass in the right CPA <img src='img/arrows/WS.png'/> and posterior Meckel cave <img src='img/arrows/WC.png'/>. Biopsy supported meningioma, which rarely may have cystic morphologies that mimic schwannoma.*
|
||||
|
||||
@@ -123,94 +123,94 @@ breadcrumbs:
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
|
||||
**Trauma**
|
||||
*Coronal NECT shows hyperdense acute hemorrhage in the inferior frontal lobes in a patient with a history of motor vehicle collision. The inferior frontal and anterior temporal lobes are the most common locations for traumatic contusions.*
|
||||
|
||||
|
||||
|
||||
**Trauma**
|
||||
*Coronal NECT shows hyperdense acute hemorrhage in the inferior frontal lobes in a patient with a history of motor vehicle collision. The inferior frontal and anterior temporal lobes are the most common locations for traumatic contusions.*
|
||||
|
||||
|
||||
|
||||
**Stroke**
|
||||
*Axial NECT shows loss of gray-white differentiation of the frontal and temporal operculum as well as the insular cortex consistent with infarct <img src='img/arrows/CS.png'/>. Note the hyperdensity in the sylvian fissure from thrombosed middle cerebral artery (MCA) branches <img src='img/arrows/CC.png'/>.*
|
||||
|
||||
|
||||
|
||||
**Infection**
|
||||
*Sagittal T1 C+ MR shows abnormal enhancement in the suprasellar and prepontine cistern <img src='img/arrows/CS.png'/>, inferior frontal lobe <img src='img/arrows/CO.png'/>, and quadrigeminal plate cistern <img src='img/arrows/CC.png'/>, consistent with tuberculomas. CNS tuberculosis is the most common cause of seizures from infection worldwide.*
|
||||
|
||||
|
||||
|
||||
**Metabolic**
|
||||
*Axial b=1000 DWI MR shows increased signal in the tail of the hippocampi <img src='img/arrows/CS.png'/>, medial thalami <img src='img/arrows/CO.png'/>, insular cortex <img src='img/arrows/CC.png'/>, and cingulate cortex <img src='img/arrows/BS.png'/> in a patient with hyperammonemia from hepatic encephalopathy.*
|
||||
|
||||
|
||||
|
||||
**Neoplasms**
|
||||
*Axial T1 C+ MR shows an irregular ring-enhancing mass in the left medial temporal lobe and occipital lobe. This was a glioblastoma, IDH-wildtype at biopsy.*
|
||||
|
||||
|
||||
|
||||
**Neoplasms**
|
||||
*Axial FLAIR MR shows a large, T2-hyperintense mass in the left frontal lobe extending across the corpus callosum to the right frontal lobe and centrally to involve the basal ganglia. This was a 1p/19q co-deleted oligodendroglioma at biopsy. These tumors are often calcified and located in the frontal lobe.*
|
||||
|
||||
|
||||
|
||||
**Mesial Temporal Sclerosis**
|
||||
*Coronal FLAIR MR shows increased T2 signal and relative volume loss of the right hippocampal formation <img src='img/arrows/CS.png'/>, consistent with mesial temporal sclerosis in this patient with temporal lobe seizures.*
|
||||
|
||||
|
||||
|
||||
**Posterior Reversible Encephalopathy Syndrome**
|
||||
*Axial FLAIR MR shows bilateral T2 hyperintensity in the occipital lobe cortex and subcortical white matter. In this patient with hypertension and renal failure, PRES was diagnosed. The DWI images were negative. Imaging of PRES often completely resolves when hypertension is controlled.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
|
||||
**Oligodendroglioma, IDH-Mutant and 1p/19q-Co-Deleted**
|
||||
*Coronal T1 C+ MR shows central heterogeneous enhancement of a low- intensity tumor involving the cortex of the posterior frontal lobe, consistent with oligodendroglioma.*
|
||||
|
||||
|
||||
|
||||
**Paraneoplastic and Autoimmune Encephalitis**
|
||||
*Axial FLAIR MR shows bilateral hyperintensity of the hippocampi and medial temporal lobes <img src='img/arrows/CS.png'/>. In this patient with a history of lung cancer, this is consistent with autoimmune encephalitis.*
|
||||
|
||||
|
||||
|
||||
**Paraneoplastic and Autoimmune Encephalitis**
|
||||
*Axial FLAIR MR shows bilateral hyperintensity of the insular cortex <img src='img/arrows/CS.png'/> in this patient with ovarian cancer, consistent with autoimmune paraneoplastic encephalitis.*
|
||||
|
||||
|
||||
|
||||
**Pleomorphic Xanthoastrocytoma**
|
||||
*Coronal FLAIR MR shows a cortical hyperintense mass in the posterior frontal lobe with a focal cyst <img src='img/arrows/CS.png'/>. This was a pleomorphic xanthoastrocytoma at surgery.*
|
||||
|
||||
|
||||
|
||||
**Oligodendroglioma, IDH-Mutant and 1p/19q-Co-Deleted**
|
||||
*Sagittal T2 MR shows a well-circumscribed T2-hyperintense mass involving the posterior frontal cortex <img src='img/arrows/CS.png'/>. This is a typical location and appearance for oligodendroglioma. 70-90% of patients with this tumor present with seizures due to its cortical nature.*
|
||||
|
||||
|
||||
|
||||
**Mesial Temporal Sclerosis**
|
||||
*Coronal FLAIR MR shows atrophy and hyperintensity of the left hippocampus <img src='img/arrows/CS.png'/>, consistent with left mesial temporal sclerosis. There is also loss of the normal internal architecture of the left hippocampus and ex vacuo dilatation of the left temporal horn <img src='img/arrows/CO.png'/>.*
|
||||
|
||||
|
||||
|
||||
**Mesial Temporal Sclerosis**
|
||||
*Axial CBF map from arterial spin labeling shows relative hypoperfusion of the left temporal lobe <img src='img/arrows/CS.png'/> compared to the right in this patient with left mesial temporal sclerosis. This is consistent with interictal seizure focus.*
|
||||
|
||||
|
||||
|
||||
**Pleomorphic Xanthoastrocytoma**
|
||||
*Axial T1 C+ MR shows a cyst <img src='img/arrows/CS.png'/> and heterogeneously enhancing nodule <img src='img/arrows/CO.png'/> involving the cortex. There is an incidental developmental venous anomaly <img src='img/arrows/CC.png'/>.*
|
||||
|
||||
|
||||
|
||||
**Infection**
|
||||
*Coronal FLAIR MR shows hyperintensity and swelling of the right hippocampus <img src='img/arrows/CS.png'/> and bilateral parahippocampal gyri <img src='img/arrows/CC.png'/>. In a patient with acute encephalopathy, seizures, and fever, herpes encephalitis must be excluded.*
|
||||
|
||||
|
||||
|
||||
**Infection**
|
||||
*Axial T2 FS MR shows bilateral hippocampal hyperintensity and edema <img src='img/arrows/CS.png'/>. Herpes encephalitis typically involves the medial temporal lobes asymmetrically and the insular cortex. The basal ganglia is usually spared, and there is deceased diffusion of the cortex early in the disease.*
|
||||
|
||||
|
||||
|
||||
**Neoplasms**
|
||||
*Axial NECT shows a heterogeneous mass causing a seizure in the right frontal lobe extending to the basal ganglia with midline shift. There are areas of hyperdensity <img src='img/arrows/CS.png'/> suggesting a high-grade neoplasm. This was a glioblastoma at biopsy.*
|
||||
|
||||
|
||||
|
||||
**Paraneoplastic and Autoimmune Encephalitis**
|
||||
*Axial FLAIR MR in this patient with ovarian cancer shows T2 hyperintensity of the temporal lobes <img src='img/arrows/CS.png'/>, consistent with autoimmune, paraneoplastic, limbic encephalitis. Compared to herpes encephalitis, autoimmune encephalitis is more likely to be bilateral, symmetric without decreased diffusion. The basal ganglia are more commonly involved.*
|
||||
|
||||
|
||||
|
||||
**Posterior Reversible Encephalopathy Syndrome**
|
||||
*Axial FLAIR MR shows bilateral T2 hyperintensity in the parietal lobe cortex and subcortical white matter. In this patient with malignant hypertension, PRES was suspected.*
|
||||
|
||||
|
||||
+17
-13
@@ -119,19 +119,23 @@ breadcrumbs:
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
|
||||
**Dolichoectasia**
|
||||
*Axial CT shows fusiform dilatation and tortuosity of the basilar artery <img src='img/arrows/CS.png'/> in an octogenarian related to dolichoectasia. Fusiform dolichoectasia is a common finding in the vertebrobasilar arteries in older patients.*
|
||||
|
||||
|
||||
|
||||
**Dolichoectasia**
|
||||
*Axial CT shows fusiform dilatation and tortuosity of the basilar artery <img src='img/arrows/CS.png'/> in an octogenarian related to dolichoectasia. Fusiform dolichoectasia is a common finding in the vertebrobasilar arteries in older patients.*
|
||||
|
||||
|
||||
|
||||
**Dolichoectasia**
|
||||
*Axial CT shows fusiform dilatation and tortuosity of the basilar artery <img src='img/arrows/CS.png'/> in an octogenarian related to dolichoectasia. Fusiform dolichoectasia is a common finding in the vertebrobasilar arteries in older patients.*
|
||||
|
||||
|
||||
**Atherosclerotic Fusiform Aneurysm**
|
||||
*Coronal CTA shows fusiform dilatation <img src='img/arrows/CS.png'/> of the right supraclinoid internal carotid artery (ICA). Irregularity from atherosclerotic disease can be seen of the M1 segment of the middle cerebral artery <img src='img/arrows/CO.png'/>. No significant mural thrombus was noted in this fusiform aneurysm.*
|
||||
|
||||
|
||||
|
||||
**Dissecting Aneurysm/Pseudoaneurysm**
|
||||
*Dissecting pseudoaneurysm in the V4 segment of the right vertebral artery seen on 3D TOF MRA <img src='img/arrows/WS.png'/>, T2 <img src='img/arrows/BS.png'/>, and T1 pre- <img src='img/arrows/CS.png'/> and post <img src='img/arrows/CO.png'/> DANTE VWI sequences shows peripheral enhancement, suggestive of instability.*
|
||||
|
||||
@@ -139,7 +143,7 @@ breadcrumbs:
|
||||
**Ehlers-Danlos**
|
||||
*3D MIP MRA of the vertebrobasilar arteries in a teenage female with a history of type 4 Ehlers-Danlos shows fusiform dilatation of the vertebral artery <img src='img/arrows/CS.png'/>. The affected gene is COL3A1, and this specific type of Ehlers-Danlos has a higher risk of aneurysm and vascular rupture.*
|
||||
|
||||
|
||||
|
||||
**Marfan Syndrome**
|
||||
*Axial MIP from CT arteriography shows fusiform dilatation of the left middle cerebral artery bifurcation <img src='img/arrows/CS.png'/> in this child with a history of Marfan syndrome.*
|
||||
|
||||
@@ -147,34 +151,34 @@ breadcrumbs:
|
||||
**Familial Thoracic Aneurysm &/or Dissection**
|
||||
*Coronal MIP reformat from CT arteriography shows bilateral fusiform aneurysms of supraclinoid ICAs <img src='img/arrows/CS.png'/>. This patient also had thoracic aortic aneurysm, which is consistent with familial thoracic aortic aneurysm and dissection and is associated with a mutation of ACTA2. This gene is responsible for a component of vascular smooth muscle.*
|
||||
|
||||
|
||||
|
||||
**HIV Infection**
|
||||
*Axial T2WI MR shows strikingly enlarged middle cerebral arteries <img src='img/arrows/CS.png'/> in this child with congenital HIV/AIDS (an uncommon but well-recognized cause of pediatric fusiform arteriopathy). The stroke-like presentations of HIV infection may relate to vasculopathies, including large-vessel aneurysmal vasculopathy.*
|
||||
|
||||
|
||||
|
||||
**Giant Serpentine Aneurysm**
|
||||
*Axial NECT demonstrates a giant serpentine aneurysm in the basilar artery <img src='img/arrows/WC.png'/> with associated mural thrombus <img src='img/arrows/CC.png'/> seen on sagittal CTA.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
|
||||
**Dolichoectasia**
|
||||
*Sagittal T1WI MR shows an elongated basilar artery with a slow-flow, thickened wall <img src='img/arrows/WS.png'/>. The apex of the tortuous basilar artery indents the hypothalamus, 3rd ventricle <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
|
||||
**Dolichoectasia**
|
||||
*Axial T2WI MR shows an elongated, tortuous basilar artery with a thickened arterial wall <img src='img/arrows/BS.png'/>, typical for atherosclerosis-associated fusiform ectasia.*
|
||||
|
||||
|
||||
|
||||
**Atherosclerotic Fusiform Aneurysm**
|
||||
*Lateral angiography shows a large fusiform middle cerebral artery aneurysm <img src='img/arrows/BS.png'/> that extends into smaller, more distal branches <img src='img/arrows/BO.png'/>. This is an unusual example because of the location (ICA, middle cerebral artery).*
|
||||
|
||||
|
||||
|
||||
**Nonaneurysmal Dissection**
|
||||
*Axial T1WI MR shows an enlarged right vertebral artery with high signal intensity <img src='img/arrows/WS.png'/> as well as an absent flow void of the left vertebral artery <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
|
||||
**Ehlers-Danlos Syndrome**
|
||||
*Anteroposterior oblique view of the left vertebral angiogram shows focal elongations and widening of the basilar artery <img src='img/arrows/BS.png'/> in a 6-year-old child with Ehlers-Danlos type 4.*
|
||||
|
||||
@@ -182,7 +186,7 @@ breadcrumbs:
|
||||
**Giant Serpentine Aneurysm**
|
||||
*Axial MRA submentovertex view shows an unusual nonatherosclerotic giant serpentine fusiform aneurysm. The patent channel <img src='img/arrows/WS.png'/> lies within the clot in the partially thrombosed <img src='img/arrows/WO.png'/> lumen.*
|
||||
|
||||
|
||||
|
||||
**Atypical Saccular Aneurysm**
|
||||
*Lateral angiography in 30-year-old man with a subarachnoid hemorrhage shows an elongated, bizarre-appearing, multilobulated aneurysm <img src='img/arrows/BS.png'/> with long aspect ratio, tit-like projections.*
|
||||
|
||||
|
||||
@@ -0,0 +1,304 @@
|
||||
---
|
||||
title: "Hemifacial Spasm"
|
||||
docid: "1b390143-1212-4447-beb3-ed9e85ef34e4"
|
||||
authors:
|
||||
- key: "eef2f839-5706-47b9-89c3-60d8315b2b3a"
|
||||
value: "Nicholas A. Koontz, MD"
|
||||
breadcrumbs:
|
||||
-
|
||||
name: "Head and Neck"
|
||||
slug: "head-and-neck"
|
||||
treeNodeId: "ed24ed8c-5d57-4629-879b-447b82d2973d"
|
||||
-
|
||||
name: "Differential Diagnosis"
|
||||
slug: "differential-diagnosis"
|
||||
treeNodeId: "40d68862-8975-4dde-ac2b-ebc43ab0fb5c"
|
||||
-
|
||||
name: "CPA-IAC and Posterior Fossa"
|
||||
slug: "cpa-iac-and-posterior-fossa"
|
||||
treeNodeId: "c590eedb-4a3b-4158-a04f-ad880564c992"
|
||||
-
|
||||
name: "Clinically Based Differentials"
|
||||
slug: "clinically-based-differentials"
|
||||
treeNodeId: "55dd15ac-e67d-48dd-8134-f52884dab28b"
|
||||
-
|
||||
name: "Hemifacial Spasm"
|
||||
slug: "hemifacial-spasm"
|
||||
treeNodeId: null
|
||||
category: "Head and Neck"
|
||||
documentVersionId: "959076b8-9c94-4244-89b0-0721f3a2387b"
|
||||
imageCount: 23
|
||||
lastUpdated: "08/15/18"
|
||||
pageDescription: "Hemifacial Spasm"
|
||||
pageKeywords: "Head and Neck, Differential Diagnosis, CPA-IAC and Posterior Fossa, Clinically Based Differentials, Hemifacial Spasm"
|
||||
pageTitle: "Hemifacial Spasm | STATdx"
|
||||
enhancedTitle: "Hemifacial Spasm"
|
||||
type: "DDX"
|
||||
references: true
|
||||
breadcrumbs:
|
||||
- "Head and Neck"
|
||||
- "Differential Diagnosis"
|
||||
- "CPA-IAC and Posterior Fossa"
|
||||
- "Clinically Based Differentials"
|
||||
- "Hemifacial Spasm"
|
||||
---
|
||||
# ESSENTIAL INFORMATION
|
||||
|
||||
- ## Key Differential Diagnosis Issues
|
||||
|
||||
|
||||
- Overall statistics
|
||||
- In > 95% of cases, **arterial vascular loop** is cause of hemifacial spasm (HFS)
|
||||
- All other causes listed account for < 5% of cases
|
||||
- HFS
|
||||
- Definition: Segmental myoclonus of muscles of face innervated by facial nerve
|
||||
- Presentation: Patients 50-80 years old, unilateral
|
||||
- Begins around eye, spreads gradually to other facial muscles
|
||||
- Principal symptom: Rhythmic, involuntary, myoclonic facial muscle contractions
|
||||
- Pathophysiology: Irritation of facial nerve or facial nucleus
|
||||
- Vascular loop syndrome affecting CNVII (aka pimary HFS)
|
||||
- By far most common cause of HFS
|
||||
- Aberrant or ectatic vessels in cistern
|
||||
- Anterior inferior cerebellar artery (AICA) most common offending artery (40-50%)
|
||||
- Other less common causal vessels include posterior inferior cerebellar artery (PICA) (~ 30%), vertebral artery (VA) (~ 20%), or large vein (< 5%)
|
||||
- Multivessel impingement is frequent (~ 40%)
|
||||
- High-resolution MR-MRA routinely identifies compressive aberrant or ectatic arteries
|
||||
- T2 SPACE, CISS, or FIESTA sequences most commonly employed
|
||||
- Critical to recognize that vascular contact of facial nerve is very common (~ 50% of population) with only tiny minority (< 0.01 %) manifesting HFS
|
||||
- **In absence of HFS symptoms, this is incidental finding that should be ignored**
|
||||
- ## Helpful Clues for Common Diagnoses
|
||||
|
||||
|
||||
- **Vascular Loop Syndrome Affecting CNVII**
|
||||
- Negative high-resolution MR exam does not preclude surgery for smaller vascular loop causing HFS
|
||||
- High-resolution MR makes this situation far less common
|
||||
- Imaging findings
|
||||
- MR-MRA: Asymmetric looping artery impinges on CNVII in CPA
|
||||
- Root exit zone and attached segment (where CNVII is adherent to pons) are most sensitive to neurovascular compression
|
||||
- AICA > PICA > VA > venous, though all are possible culprits
|
||||
- ## Helpful Clues for Less Common Diagnoses
|
||||
|
||||
|
||||
- **Epidermoid Cyst in CPA**
|
||||
- Morphology: Assumes shape of cistern it occupies
|
||||
- Insinuating margins, encasing cranial nerves and vessels
|
||||
- Imaging findings
|
||||
- Near CSF signal intensity of epidermoid cyst makes it difficult to see on T1, T2, and FLAIR sequences
|
||||
- DWI shows reduced diffusivity
|
||||
- **Meningioma in CPA**
|
||||
- Morphology: Dural-based sessile mass
|
||||
- Imaging findings
|
||||
- Bone CT: Bony hyperostosis possible
|
||||
- MR: Enhancing mass with dural tail(s)
|
||||
- **Aneurysm in CPA****-IAC**
|
||||
- Morphology: Ovoid or fusiform shape
|
||||
- Imaging findings
|
||||
- MR: Complex lesion signal from wall calcification, clot, and flow
|
||||
- **Facial Nerve Schwannoma in CPA-IAC**
|
||||
- Morphology: CPA-IAC "ice cream on cone" mass and labyrinthine segment tail
|
||||
- Imaging findings
|
||||
- Bone CT: Labyrinthine segment CNVII enlarged
|
||||
- MR: Enhancing tubular mass with tail; may have intramural cysts
|
||||
- **Facial Nerve Schwannoma in T-Bone**
|
||||
- Morphology: Tubular mass within enlarged facial nerve canal may pedunculate into middle ear cavity (tympanic segment CNVII) or mastoid air cells (mastoid segment CNVII)
|
||||
- Imaging findings
|
||||
- Bone CT: Obvious enlargement of CNVII canal; geniculate ganglion most commonly affected
|
||||
- MR: Enhancing mass enlarges bony facial nerve canal
|
||||
- **Facial Nerve Perineural Tumor**
|
||||
- Morphology: Enlargement of intratemporal CNVII connected through stylomastoid foramen (usually from invasive parotid malignancy)
|
||||
- Imaging findings
|
||||
- Mastoid segment most common
|
||||
- CT: Soft tissue replacement of fat at stylomastoid foramen ± enlargement of bony CNVII canal
|
||||
- MR: Enhancing minimally enlarged intratemporal CNVII
|
||||
- **Facial Nerve Venous Malformation ("Hemangioma") in T-Bone**
|
||||
- Lesion of abnormal vascular morphogenesis; thus "hemangioma" is misnomer
|
||||
- Morphology: Amorphous geniculate ganglion area mass
|
||||
- Imaging findings
|
||||
- Bone CT: "Honeycomb" bone matrix (50%)
|
||||
- MR: Avidly enhancing mass with foci of low signal intensity and gradient susceptibility (calcifications)
|
||||
- ## Helpful Clues for Rare Diagnoses
|
||||
|
||||
|
||||
- **A****cute****Cerebral Ischemia-Infarction**
|
||||
- Acute onset of brainstem-related symptoms
|
||||
- Pontine CVA secondary to basilar artery perforator injury
|
||||
- Imaging findings
|
||||
- MR: DWI shows reduced diffusivity in pons
|
||||
- **Multiple Sclerosis**
|
||||
- HFS is rare presentation of multiple sclerosis
|
||||
- Imaging findings
|
||||
- Plaques in vicinity of facial nerve nucleus in floor of 4th ventricle may or may not be seen
|
||||
- MR: T2/FLAIR show ↑ signal intensity of supratentorial white matter plaques
|
||||
- **Arteriovenous Malformation**
|
||||
- More commonly supratentorial
|
||||
- Imaging findings
|
||||
- MR: Large ectatic arterial flow voids
|
||||
- Enhancing nidus on T1 C+ fat-saturated sequence
|
||||
- Large draining veins
|
||||
- **Arachnoid Cyst in CPA**
|
||||
- More common than epidermoid cyst in CPA, but epidermoid cyst in CPA more often associated with HFS
|
||||
- Morphology
|
||||
- Fills cistern with rounded or flat margins
|
||||
- Imaging findings
|
||||
- T1 C+: No enhancement
|
||||
- FLAIR: Follows dark CSF signal intensity
|
||||
- DWI: No reduced diffusivity
|
||||
- **Venous Malformation ("Hemangioma") in IAC**
|
||||
- Lesion of abnormal vascular morphogenesis; thus "hemangioma" is misnomer
|
||||
- Morphology: Distal intracanalicular (IAC) ovoid to round cystic mass
|
||||
- Imaging findings
|
||||
- Bone CT: Lesion with punctate calcifications
|
||||
- MR: Avidly enhancing IAC lesion with foci of low signal intensity and gradient susceptibility (calcifications)
|
||||
- ## Alternative Differential Approaches
|
||||
|
||||
|
||||
- Radiologist generally searches for cause of cranial neuropathy by following cranial nerve from origin to functional endplate
|
||||
- Such anatomic approach permits segmentation of potential causes into anatomic groups
|
||||
- Anatomic delineation of HFS causes
|
||||
- 3 general anatomic sites where facial nerve may be injured causing HFS
|
||||
- Intraaxial (nuclear)
|
||||
- Cisternal (CPA or IAC cistern)
|
||||
- Intratemporal (intratemporal facial nerve canal)
|
||||
- Intraaxial (nuclear)
|
||||
- [Acute cerebral ischemia-infarction](/document/acute-cerebral-ischemiainfarction/a405285f-aaea-43ca-8dc4-6f8120eaabc1)
|
||||
- [Multiple sclerosis](/document/multiple-sclerosis/7892b2a2-f52a-4d7f-9858-a326f2b7ab04)
|
||||
- [Arteriovenous malformation](/document/arteriovenous-malformation/55b35b26-df2e-4baf-8860-8073297cb738)
|
||||
- Cisternal (CPA or IAC cistern)
|
||||
- [Vascular loop syndrome affecting CNVII](/document/hemifacial-spasm/00871c72-c6c8-4913-b993-ebdb3da21947)
|
||||
- [Epidermoid cyst in CPA](/document/cpa-iac-epidermoid-cyst/5e83f596-1ca4-41cb-95aa-469147ca5f8f)
|
||||
- [Meningioma in CPA](/document/cpa-iac-meningioma/88301b77-f1c8-4efc-acf7-405999b42c3d)
|
||||
- [Aneurysm in CPA-IAC](/document/cpa-iac-aneurysm/548f4994-c72a-40b8-a94c-d96fd6c39a21)
|
||||
- [Facial nerve schwannoma in CPA-IAC](/document/cpa-iac-facial-nerve-schwannoma/9db01630-23a4-4f42-ad83-0ec399503495)
|
||||
- [Arachnoid cyst in CPA](/document/cpa-iac-arachnoid-cyst/f1af2d0f-adfd-49c7-a3b9-8a1c66dce2be)
|
||||
- [Venous malformation ("hemangioma") in IAC](/document/iac-venous-malformation/3a3d68e3-a087-4749-b13d-758c9ae8b9eb)
|
||||
- Intratemporal (intratemporal CNVII canal)
|
||||
- [Facial nerve schwannoma in T-bone](/document/temporal-bone-facial-nerve-schwann-/cf2bcc82-4a1b-4989-adeb-f4e82116111b)
|
||||
- Facial nerve perineural tumor
|
||||
- [Facial nerve venous malformation ("hemangioma") in T-bone](/document/temporal-bone-facial-nerve-venous--/dcd6a44e-cbe6-457c-9b03-598a2b874ece)
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Donahue JH et al: Imaging of vascular compression syndromes. Radiol Clin North Am. 55(1):123-138, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=27890181%5Bpmid%5D)
|
||||
1. [Deep NL et al: Magnetic resonance imaging assessment of vascular contact of the facial nerve in the asymptomatic patient. J Neurol Surg B Skull Base. 77(6):503-509, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=27857878%5Bpmid%5D)
|
||||
1. [Haller S et al: Imaging of neurovascular compression syndromes: trigeminal neuralgia, hemifacial spasm, vestibular paroxysmia, and glossopharyngeal neuralgia. AJNR Am J Neuroradiol. 37(8):1384-92, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=26892985%5Bpmid%5D)
|
||||
1. [Öcal R et al: Comparison of brain MRI angiography and brain MRI cisternography in patients with hemifacial spasm. Acta Neurol Belg. 116(4):593-598, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=26908032%5Bpmid%5D)
|
||||
1. [Ray DK et al: Surgical outcome and improvement in quality of life after microvascular decompression for hemifacial spasms: a case series assessment using a validated disease-specific scale. Stereotact Funct Neurosurg. 88(6):383-9, 2010](http://www.ncbi.nlm.nih.gov/pubmed/?term=20948243%5Bpmid%5D)
|
||||
1. [Pyen JS et al: Tic convulsif caused by cerebellopontine angle schwannoma. Yonsei Med J. 2001 Apr;42(2):255-7. Retraction in: Yonsei Med J. 49(6):1060, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=19108035%5Bpmid%5D)
|
||||
1. [Desai K et al: Cerebellopontine angle epidermoid tumor presenting with hemifacial spasms. Neurol India. 51(2):288-9, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=14571040%5Bpmid%5D)
|
||||
1. [Iwai Y et al: Hemifacial spasm due to cerebellopontine angle meningiomas--two case reports. Neurol Med Chir (Tokyo). 41(2):87-9, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11255633%5Bpmid%5D)
|
||||
1. [Takano S et al: Facial spasm and paroxysmal tinnitus associated with an arachnoid cyst of the cerebellopontine angle--case report. Neurol Med Chir (Tokyo). 38(2):100-3, 1998](http://www.ncbi.nlm.nih.gov/pubmed/?term=9557537%5Bpmid%5D)
|
||||
1. [Illingworth RD et al: Hemifacial spasm: a prospective long-term follow up of 83 cases treated by microvascular decompression at two neurosurgical centres in the United Kingdom. J Neurol Neurosurg Psychiatry. 60(1):72-7, 1996](http://www.ncbi.nlm.nih.gov/pubmed/?term=8558156%5Bpmid%5D)
|
||||
1. [Moriuchi S et al: Hemifacial spasm due to compression of the facial nerve by vertebral artery-posterior inferior cerebellar artery aneurysm and elongated vertebral artery--case report. Neurol Med Chir (Tokyo). 36(12):884-7, 1996](http://www.ncbi.nlm.nih.gov/pubmed/?term=9002718%5Bpmid%5D)
|
||||
1. [Nagata S et al: Hemifacial spasm caused by CP angle AVM associated with ruptured aneurysm in the feeding artery--case report. Neurol Med Chir (Tokyo). 31(7):406-9, 1991](http://www.ncbi.nlm.nih.gov/pubmed/?term=1720219%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
**Vascular Loop Syndrome Affecting CNVII**
|
||||
*Axial T2 FS MR in a patient with left hemifacial spasm (HFS) shows neurovascular compression of the left facial nerve <img src='img/arrows/WS.png'/> by an ectatic vertebral artery <img src='img/arrows/WO.png'/>. Note the point of neurovascular impingement <img src='img/arrows/WC.png'/> against the adjacent cerebellar flocculus <img src='img/arrows/BO.png'/>.*
|
||||
|
||||
|
||||
**Vascular Loop Syndrome Affecting CNVII**
|
||||
*Axial T2 FS MR in a patient with left hemifacial spasm (HFS) shows neurovascular compression of the left facial nerve <img src='img/arrows/WS.png'/> by an ectatic vertebral artery <img src='img/arrows/WO.png'/>. Note the point of neurovascular impingement <img src='img/arrows/WC.png'/> against the adjacent cerebellar flocculus <img src='img/arrows/BO.png'/>.*
|
||||
|
||||
|
||||
**Vascular Loop Syndrome Affecting CNVII**
|
||||
*Axial T2 FS MR in a patient with left hemifacial spasm (HFS) shows neurovascular compression of the left facial nerve <img src='img/arrows/WS.png'/> by an ectatic vertebral artery <img src='img/arrows/WO.png'/>. Note the point of neurovascular impingement <img src='img/arrows/WC.png'/> against the adjacent cerebellar flocculus <img src='img/arrows/BO.png'/>.*
|
||||
|
||||
|
||||
**Vascular Loop Syndrome Affecting CNVII**
|
||||
*Coronal T2 MR shows an ectatic vertebral artery <img src='img/arrows/WO.png'/> "lifting" the posterior inferior cerebellar artery into the root exit zone of the facial nerve <img src='img/arrows/WS.png'/>. Note compression of the lateral pons.*
|
||||
|
||||
|
||||
**Epidermoid Cyst in CPA**
|
||||
*Axial DWI MR in a patient with chronic left HFS shows a left CPA mass <img src='img/arrows/WS.png'/> with reduced diffusivity and scalloped, insinuating margins, typical of an epidermoid cyst.*
|
||||
|
||||
|
||||
**Meningioma in CPA**
|
||||
*Axial T1 C+ FS MR in a patient with right HFS shows an avidly enhancing mass with the configuration of "ice cream" (CPA component) <img src='img/arrows/WS.png'/> "on cone" (IAC component) <img src='img/arrows/WO.png'/>. Note enhancing dural tails <img src='img/arrows/WC.png'/>, which help differentiate this histologically-proven CPA-IAC meningioma from a schwannoma.*
|
||||
|
||||
|
||||
**Aneurysm in CPA-IAC**
|
||||
*Axial T2 FS MR shows a giant right vetebral artery aneurysm <img src='img/arrows/WS.png'/> with complex signal intensity. The aneurysm obliterates the pontomedullary junction at the region of the right CNVII root exit zone <img src='img/arrows/WO.png'/>. The same tortuous right vertebral artery <img src='img/arrows/WC.png'/> also effaces the left CNVII root exit zone region.*
|
||||
|
||||
|
||||
**Facial Nerve Schwannoma in CPA-IAC**
|
||||
*Axial SPGR C+ MR of left facial nerve schwannoma <img src='img/arrows/WS.png'/> shows an avidly enhancing CPA-IAC mass with a labyrinthine tail of enhancement <img src='img/arrows/WO.png'/> extending to the geniculate ganglion <img src='img/arrows/WC.png'/>, which differentiates it from a vestibular schwannoma.*
|
||||
|
||||
|
||||
**Facial Nerve Schwannoma in T-Bone**
|
||||
*Axial T1 C+ MR shows an aggressive schwannoma involving the tympanic segment <img src='img/arrows/WS.png'/>, posterior genu <img src='img/arrows/WO.png'/>, and descending mastoid segment of the right facial nerve. Note several nonenhancing intramural cysts <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Facial Nerve Perineural Tumor**
|
||||
*Coronal T1 MR shows invasive parotid space malignancy <img src='img/arrows/WS.png'/> with perineural tumor spread cephalad through the stylomastoid foramen to involve the mastoid segment of the facial nerve <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
**Facial Nerve Venous Malformation ("Hemangioma") in T-Bone**
|
||||
*Axial T1 C+ FS MR shows an enhancing lesion <img src='img/arrows/WS.png'/> within enlarged geniculate fossa. Note the black central dot of low signal intensity <img src='img/arrows/WO.png'/> corresponding with punctate calcification and suggesting the diagnosis of facial nerve venous malformation.*
|
||||
|
||||
|
||||
**Acute Cerebral Ischemia-Infarction**
|
||||
*Axial DWI MR shows an acute left pontine infarction <img src='img/arrows/WS.png'/> with reduced diffusivity. Corresponding hypointensity was present on the ADC map (not shown). Patients with brainstem infarctions may develop hemifacial spasm in the subacute to chronic phase.*
|
||||
|
||||
|
||||
**Multiple Sclerosis**
|
||||
*Axial T2 FS MR in patient with multiple sclerosis shows a subtle demyelinating plaque <img src='img/arrows/WS.png'/> in the left lateral pons near the root exit zone of the facial nerve <img src='img/arrows/WO.png'/>. Demyelinating lesions accounting for HFS are often subtle and may not always be seen.*
|
||||
|
||||
|
||||
**Arteriovenous Malformation**
|
||||
*Axial T2 MR shows a left cerebellopontine cistern arteriovenous malformation nidus <img src='img/arrows/WO.png'/> with a large posterior draining vein <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Arachnoid Cyst in CPA**
|
||||
*Axial T2 FS MR shows a right CPA arachnoid cyst <img src='img/arrows/WS.png'/>, which exerts mild mass effect upon the cisternal segments of the vestibulocochlear and facial nerves <img src='img/arrows/WO.png'/>. The cyst also flattens the lateral cerebellum. This cyst follows CSF signal intensity on all sequences.*
|
||||
|
||||
|
||||
**Venous Malformation ("Hemangioma") in IAC**
|
||||
*Coronal T1 C+ MR of an lAC venous malformation shows a lateral IAC enhancing mass <img src='img/arrows/WS.png'/> with focus of internal low signal intensity from punctate intralesional calcification <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
**Vascular Loop Syndrome Affecting CNVII**
|
||||
*Axial T2 MR shows a markedly asymmetric left vertebral artery <img src='img/arrows/WO.png'/> lifting the posterior inferior cerebellar artery <img src='img/arrows/WS.png'/> into the medial aspect of the CPA cistern in the CNVII root exit zone vicinity.*
|
||||
|
||||
|
||||
**Epidermoid Cyst in CPA**
|
||||
*Axial T2 MR demonstrates a right CPA cistern epidermoid cyst with penetration of the porus acusticus <img src='img/arrows/WS.png'/> and lobulated mass effect on the lateral margin of the brachium pontis <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
**Arachnoid Cyst in CPA**
|
||||
*Axial T2 MR through the CPA cistern reveals a CSF intensity arachnoid cyst on the left <img src='img/arrows/WS.png'/>. The arachnoid cyst flattens the cerebellar hemisphere and bows the facial and vestibulocochlear nerves <img src='img/arrows/BO.png'/> anteromedially.*
|
||||
|
||||
|
||||
**Epidermoid Cyst in CPA**
|
||||
*Axial T2 MR shows a right CPA cistern epidermoid cyst <img src='img/arrows/WS.png'/> scalloping the cerebellar contour and bowing the cisternal facial nerve anteriorly <img src='img/arrows/WO.png'/>. The root exit zone is also affected <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Meningioma in CPA**
|
||||
*Axial T2 MR reveals a dural-based CPA mass with IAC penetration <img src='img/arrows/WO.png'/> with a "CSF-vascular cleft" <img src='img/arrows/WS.png'/> between it and the adjacent brachium pontis-pons. Note the normal root exit zone of the contralateral left CNVII <img src='img/arrows/WC.png'/>.*
|
||||
|
||||
|
||||
**Aneurysm in CPA-IAC**
|
||||
*Axial T1 MR shows complex signal associated with a vertebral artery aneurysm <img src='img/arrows/WS.png'/>. The aneurysm is wedged into the medial CPA cistern in the immediate vicinity of the CNVII root exit zone.*
|
||||
|
||||
|
||||
**Facial Nerve Schwannoma in CPA-IAC**
|
||||
*Axial T1 C+ MR shows a small facial nerve schwannoma of the lateral IAC <img src='img/arrows/WS.png'/>, labyrinthine segment <img src='img/arrows/WO.png'/>, and geniculate ganglion <img src='img/arrows/WC.png'/> portions of the facial nerve.*
|
||||
|
||||
|
||||
**Facial Nerve Schwannoma in T-Bone**
|
||||
*Axial T1 C+ MR demonstrates a mastoid segment facial nerve schwannoma <img src='img/arrows/WS.png'/>. Notice that the enhancing tumor has dehisced the posterior wall of the external auditory canal <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
**Multiple Sclerosis**
|
||||
*Axial T2 MR shows a multiple sclerosis plaque <img src='img/arrows/WS.png'/> situated in the lateral right pons near the root exit zone of the facial nerve. Note a 2nd more subtle plaque in the left cerebellum <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
+29
-136
@@ -32,6 +32,7 @@ breadcrumbs:
|
||||
slug: "hypertrophic-olivary-degeneration"
|
||||
treeNodeId: null
|
||||
category: "Brain"
|
||||
cmeTopicId: "b70885e6-d7ea-4f0f-8b2c-c871245fd05c"
|
||||
documentVersionId: "0c307ba9-ac00-479c-9a0f-4201c66bc1f1"
|
||||
imageCount: 26
|
||||
lastUpdated: "09/30/20"
|
||||
@@ -332,7 +333,7 @@ breadcrumbs:
|
||||
- Avoid misdiagnosis of tumor or multiple sclerosis
|
||||
- Bilateral & symmetrical lesions in ION argue against subacute infarct & vertebral artery dissection
|
||||
|
||||
88b7142c-a73e-4046-a5d4-0c12bddb8133
|
||||
9342df55-d4e7-4743-8a78-b03338f00dc0
|
||||
|
||||
## References
|
||||
|
||||
@@ -368,195 +369,87 @@ breadcrumbs:
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
|
||||
*Axial graphic of the upper medulla shows the medullary pyramids <img src='img/arrows/CC.png'/> on each side of the ventral median fissure. The olives <img src='img/arrows/CO.png'/> lie just posterior to the preolivary sulci <img src='img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
|
||||
*Axial graphic of the upper medulla shows the medullary pyramids <img src='img/arrows/CC.png'/> on each side of the ventral median fissure. The olives <img src='img/arrows/CO.png'/> lie just posterior to the preolivary sulci <img src='img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
*Axial graphic of the upper medulla shows the medullary pyramids <img src='img/arrows/CC.png'/> on each side of the ventral median fissure. The olives <img src='img/arrows/CO.png'/> lie just posterior to the preolivary sulci <img src='img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
|
||||
*Coronal graphic of the midbrain, pons, and medulla is sectioned to depict the Guillain-Mollaret triangle (GMT). The GMT is composed of the ipsilateral inferior olivary nucleus (green), dentate nucleus (blue) of the contralateral cerebellum, and the ipsilateral red nucleus (RN, red).*
|
||||
|
||||
|
||||
*Coronal graphic of the midbrain, pons, and medulla is sectioned to depict the Guillain-Mollaret triangle (GMT). The GMT is composed of the ipsilateral inferior olivary nucleus (green), dentate nucleus (blue) of the contralateral cerebellum, and the ipsilateral red nucleus (RN, red).*
|
||||
|
||||
|
||||
*Coronal graphic of the midbrain, pons, and medulla is sectioned to depict the Guillain-Mollaret triangle (GMT). The GMT is composed of the ipsilateral inferior olivary nucleus (green), dentate nucleus (blue) of the contralateral cerebellum, and the ipsilateral red nucleus (RN, red).*
|
||||
|
||||
|
||||
|
||||
*Axial T2 MR of a 40-year-old woman with brainstem glioma and secondary hypertrophic olivary degeneration (HOD) shows a heterogeneous mass lesion involving midbrain <img src='img/arrows/CO.png'/> invading the RN <img src='img/arrows/CS.png'/> (R > L). RN is a component of GMT.*
|
||||
|
||||
|
||||
*Axial T2 MR of a 40-year-old woman with brainstem glioma and secondary hypertrophic olivary degeneration (HOD) shows a heterogeneous mass lesion involving midbrain <img src='img/arrows/CO.png'/> invading the RN <img src='img/arrows/CS.png'/> (R > L). RN is a component of GMT.*
|
||||
|
||||
|
||||
*Axial T2 MR of a 40-year-old woman with brainstem glioma and secondary hypertrophic olivary degeneration (HOD) shows a heterogeneous mass lesion involving midbrain <img src='img/arrows/CO.png'/> invading the RN <img src='img/arrows/CS.png'/> (R > L). RN is a component of GMT.*
|
||||
|
||||
|
||||
|
||||
*Axial T2 MR at the level of medulla in the same patient shows enlarged right inferior olivary nucleus with hyperintense signal <img src='img/arrows/CC.png'/> indicating HOD. Also note normal-appearing left olivary nucleus <img src='img/arrows/BC.png'/> and preolivary sulcus <img src='img/arrows/BS.png'/>.*
|
||||
|
||||
|
||||
*Axial T2 MR at the level of medulla in the same patient shows enlarged right inferior olivary nucleus with hyperintense signal <img src='img/arrows/CC.png'/> indicating HOD. Also note normal-appearing left olivary nucleus <img src='img/arrows/BC.png'/> and preolivary sulcus <img src='img/arrows/BS.png'/>.*
|
||||
|
||||
|
||||
*Axial T2 MR at the level of medulla in the same patient shows enlarged right inferior olivary nucleus with hyperintense signal <img src='img/arrows/CC.png'/> indicating HOD. Also note normal-appearing left olivary nucleus <img src='img/arrows/BC.png'/> and preolivary sulcus <img src='img/arrows/BS.png'/>.*
|
||||
|
||||
|
||||
|
||||
*Axial FLAIR MR of a 58-year-old woman presenting with palatal myoclonus and a history of treated CNS lymphoma shows volume loss and hyperintense signal in left dentate nucleus (DN) <img src='img/arrows/CO.png'/> due to encephalomalacia (DN is a component of GMT).*
|
||||
|
||||
|
||||
*Axial FLAIR MR of a 58-year-old woman presenting with palatal myoclonus and a history of treated CNS lymphoma shows volume loss and hyperintense signal in left dentate nucleus (DN) <img src='img/arrows/CO.png'/> due to encephalomalacia (DN is a component of GMT).*
|
||||
|
||||
|
||||
*Axial FLAIR MR of a 58-year-old woman presenting with palatal myoclonus and a history of treated CNS lymphoma shows volume loss and hyperintense signal in left dentate nucleus (DN) <img src='img/arrows/CO.png'/> due to encephalomalacia (DN is a component of GMT).*
|
||||
|
||||
|
||||
|
||||
*Axial T2 MR in the same patient at the level of medulla shows mild hypertrophy and increased signal involving bilateral inferior olivary nuclei <img src='img/arrows/CC.png'/> indicating HOD.*
|
||||
|
||||
|
||||
*Axial T2 MR in the same patient at the level of medulla shows mild hypertrophy and increased signal involving bilateral inferior olivary nuclei <img src='img/arrows/CC.png'/> indicating HOD.*
|
||||
|
||||
|
||||
*Axial T2 MR in the same patient at the level of medulla shows mild hypertrophy and increased signal involving bilateral inferior olivary nuclei <img src='img/arrows/CC.png'/> indicating HOD.*
|
||||
|
||||
|
||||
|
||||
*Axial T2 of a 67-year-old man with left para median pontine cavernous malformation (CM) involving central tegmental tract resulting in ipsilateral HOD shows hyperintense popcorn lesion with rim of hemosiderin in left para median pons <img src='img/arrows/CS.png'/> due to CM.*
|
||||
|
||||
|
||||
*Axial T2 of a 67-year-old man with left para median pontine cavernous malformation (CM) involving central tegmental tract resulting in ipsilateral HOD shows hyperintense popcorn lesion with rim of hemosiderin in left para median pons <img src='img/arrows/CS.png'/> due to CM.*
|
||||
|
||||
|
||||
*Axial T2 of a 67-year-old man with left para median pontine cavernous malformation (CM) involving central tegmental tract resulting in ipsilateral HOD shows hyperintense popcorn lesion with rim of hemosiderin in left para median pons <img src='img/arrows/CS.png'/> due to CM.*
|
||||
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient shows enlarged left inferior olivary nucleus with hyperintense signal <img src='img/arrows/CO.png'/> due to HOD.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient shows enlarged left inferior olivary nucleus with hyperintense signal <img src='img/arrows/CO.png'/> due to HOD.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient shows enlarged left inferior olivary nucleus with hyperintense signal <img src='img/arrows/CO.png'/> due to HOD.*
|
||||
|
||||
|
||||
|
||||
*Axial T2 MR at 1 day (top left), 4 months (top right), and 7 months (bottom left) postoperative follow-up show edema in left DN <img src='img/arrows/CS.png'/> and normal right olive <img src='img/arrows/CO.png'/>. Note light enlargement and ↑ signal in right olive <img src='img/arrows/CC.png'/>, progressive enlargement and ↑ signal in olive <img src='img/arrows/WC.png'/>, and lack of enhancement in olive <img src='img/arrows/WO.png'/> on postcontrast T1WI (bottom right).*
|
||||
|
||||
|
||||
*Axial T2 MR at 1 day (top left), 4 months (top right), and 7 months (bottom left) postoperative follow-up show edema in left DN <img src='img/arrows/CS.png'/> and normal right olive <img src='img/arrows/CO.png'/>. Note light enlargement and ↑ signal in right olive <img src='img/arrows/CC.png'/>, progressive enlargement and ↑ signal in olive <img src='img/arrows/WC.png'/>, and lack of enhancement in olive <img src='img/arrows/WO.png'/> on postcontrast T1WI (bottom right).*
|
||||
|
||||
|
||||
*Axial T2 MR at 1 day (top left), 4 months (top right), and 7 months (bottom left) postoperative follow-up show edema in left DN <img src='img/arrows/CS.png'/> and normal right olive <img src='img/arrows/CO.png'/>. Note light enlargement and ↑ signal in right olive <img src='img/arrows/CC.png'/>, progressive enlargement and ↑ signal in olive <img src='img/arrows/WC.png'/>, and lack of enhancement in olive <img src='img/arrows/WO.png'/> on postcontrast T1WI (bottom right).*
|
||||
|
||||
|
||||
*Axial graphic of the midbrain at the level of the hypoglossal nuclei shows the distinct wavy pattern of the olives <img src='img/arrows/CS.png'/> corresponding to the FLAIR hyperintensity in the previous image.*
|
||||
|
||||
|
||||
*Axial graphic of the midbrain at the level of the hypoglossal nuclei shows the distinct wavy pattern of the olives <img src='img/arrows/CS.png'/> corresponding to the FLAIR hyperintensity in the previous image.*
|
||||
|
||||
|
||||
|
||||
*Axial graphic of the midbrain at the level of the hypoglossal nuclei shows the distinct wavy pattern of the olives <img src='img/arrows/CS.png'/> corresponding to the FLAIR hyperintensity in the previous image.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
|
||||
*Axial T2WI MR demonstrates hypertrophy of both inferior olivary nuclei, which are also hyperintense <img src='img/arrows/CS.png'/>, secondary to HOD.*
|
||||
|
||||
|
||||
*Axial T2WI MR demonstrates hypertrophy of both inferior olivary nuclei, which are also hyperintense <img src='img/arrows/CS.png'/>, secondary to HOD.*
|
||||
|
||||
|
||||
*Axial T2WI MR demonstrates hypertrophy of both inferior olivary nuclei, which are also hyperintense <img src='img/arrows/CS.png'/>, secondary to HOD.*
|
||||
|
||||
|
||||
|
||||
*Sagittal FLAIR MR shows abnormally ↑ signal intensity in an anterior medullary area <img src='img/arrows/CS.png'/> that corresponds to the inferior olivary nucleus.*
|
||||
|
||||
|
||||
*Sagittal FLAIR MR shows abnormally ↑ signal intensity in an anterior medullary area <img src='img/arrows/CS.png'/> that corresponds to the inferior olivary nucleus.*
|
||||
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient who suffered midbrain hemorrhage (not shown) depicts bilateral hyperintense and hypertrophied inferior olivary nuclei <img src='img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient who suffered midbrain hemorrhage (not shown) depicts bilateral hyperintense and hypertrophied inferior olivary nuclei <img src='img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
|
||||
*Axial FLAIR MR shows high signal intensity and asymmetric enlargement of right anterior medulla corresponding to the region of hypertrophic degeneration of the right inferior olivary nucleus <img src='img/arrows/CS.png'/> .*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows high signal intensity and asymmetric enlargement of right anterior medulla corresponding to the region of hypertrophic degeneration of the right inferior olivary nucleus <img src='img/arrows/CS.png'/> .*
|
||||
|
||||
|
||||
|
||||
*Axial T2WI MR in the same patient shows a right pontine infarct, the primary lesion that led to right HOD.*
|
||||
|
||||
|
||||
*Axial T2WI MR in the same patient shows a right pontine infarct, the primary lesion that led to right HOD.*
|
||||
|
||||
|
||||
|
||||
*Axial T2WI MR shows bilateral symmetric hypertrophy with ↑ signal intensity confined to inferior olivary nuclei, with loss of pre- and postolivary sulci <img src='img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
*Axial T2WI MR shows bilateral symmetric hypertrophy with ↑ signal intensity confined to inferior olivary nuclei, with loss of pre- and postolivary sulci <img src='img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
|
||||
*Axial T2WI MR in the same patient shows the primary midbrain lesion that caused the occurrence of bilateral HOD.*
|
||||
|
||||
|
||||
*Axial T2WI MR in the same patient shows the primary midbrain lesion that caused the occurrence of bilateral HOD.*
|
||||
|
||||
|
||||
|
||||
*Axial T2WI MR in a patient who developed onset of dysarthria and upper extremity dysmetria 15 months following stereotaxic XRT for midbrain arteriovenous malformation shows mixed hyper-/hypointensity in the residual vascular malformation <img src='img/arrows/CO.png'/>.*
|
||||
|
||||
|
||||
*Axial T2WI MR in a patient who developed onset of dysarthria and upper extremity dysmetria 15 months following stereotaxic XRT for midbrain arteriovenous malformation shows mixed hyper-/hypointensity in the residual vascular malformation <img src='img/arrows/CO.png'/>.*
|
||||
|
||||
|
||||
|
||||
*Axial T2WI MR in the same patient shows bilateral inferior olivary hyperintensity and hypertrophy <img src='img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
*Axial T2WI MR in the same patient shows bilateral inferior olivary hyperintensity and hypertrophy <img src='img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
|
||||
*Axial T2WI MR (CISS) shows the normal shape of the medullary olives <img src='img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
*Axial T2WI MR (CISS) shows the normal shape of the medullary olives <img src='img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
|
||||
*Axial T2WI MR in a patient who developed palatal myoclonus ~ 6 months after resection of a midbrain CM shows hyperintensity and enlargement of both olives <img src='img/arrows/CS.png'/>. This pattern is typical in the subacute stage of HOD, which typically appears between 6 months and 3-4 years after injury to the dentato-rubro-olivary pathway.*
|
||||
|
||||
|
||||
*Axial T2WI MR in a patient who developed palatal myoclonus ~ 6 months after resection of a midbrain CM shows hyperintensity and enlargement of both olives <img src='img/arrows/CS.png'/>. This pattern is typical in the subacute stage of HOD, which typically appears between 6 months and 3-4 years after injury to the dentato-rubro-olivary pathway.*
|
||||
|
||||
|
||||
|
||||
*Axial SWI MR demonstrates hemosiderin staining in the dorsal aspect of the brainstem <img src='img/arrows/CC.png'/> in the midline and to the right due to an old hemorrhage.*
|
||||
|
||||
|
||||
*Axial SWI MR demonstrates hemosiderin staining in the dorsal aspect of the brainstem <img src='img/arrows/CC.png'/> in the midline and to the right due to an old hemorrhage.*
|
||||
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient at the level of the medulla shows mild hypertrophy with hyperintensity in the region of the right inferior olivary nucleus <img src='img/arrows/CS.png'/>. Findings are typical for HOD caused by primary lesions in dentato-rubro-olivary pathway (anatomical GMT).*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient at the level of the medulla shows mild hypertrophy with hyperintensity in the region of the right inferior olivary nucleus <img src='img/arrows/CS.png'/>. Findings are typical for HOD caused by primary lesions in dentato-rubro-olivary pathway (anatomical GMT).*
|
||||
|
||||
|
||||
|
||||
*Axial T2WI MR through the medulla shows that the ipsilateral olive is atrophic and hyperintense <img src='img/arrows/CS.png'/>. This patient also has crossed cerebellar atrophy <img src='img/arrows/CO.png'/> due to interruption of the ponto-cerebellar pathway.*
|
||||
|
||||
|
||||
*Axial T2WI MR through the medulla shows that the ipsilateral olive is atrophic and hyperintense <img src='img/arrows/CS.png'/>. This patient also has crossed cerebellar atrophy <img src='img/arrows/CO.png'/> due to interruption of the ponto-cerebellar pathway.*
|
||||
|
||||
|
||||
|
||||
*Axial T2WI MR in a patient who developed palatal myoclonus several months following midbrain surgery for CM. Imaging obtained 1 year later shows residual CM <img src='img/arrows/CO.png'/>.*
|
||||
|
||||
|
||||
*Axial T2WI MR in a patient who developed palatal myoclonus several months following midbrain surgery for CM. Imaging obtained 1 year later shows residual CM <img src='img/arrows/CO.png'/>.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient delineates the somewhat wavy appearance of the hyperintensity conforming to the configuration of the olives <img src='img/arrows/CS.png'/>. The pyramids <img src='img/arrows/CO.png'/> are spared, helping differentiate HOD from perforating artery infarction.*
|
||||
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient delineates the somewhat wavy appearance of the hyperintensity conforming to the configuration of the olives <img src='img/arrows/CS.png'/>. The pyramids <img src='img/arrows/CO.png'/> are spared, helping differentiate HOD from perforating artery infarction.*
|
||||
|
||||
|
||||
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Some files were not shown because too many files have changed in this diff Show More
Reference in New Issue
Block a user