ISCHEMIC STROKE

Neuroimaging in pediatric stroke

David Goldemund M.D.
Updated on 12/09/2024, published on 09/12/2022
  • pediatric stroke is increasingly being recognized as an important cause of morbidity and mortality
    • over 75% of children suffer long-term neurological deficits 
    • mortality ~ 10% 
    • 19% recurrence within 5 years
  • pediatric stroke has a unique presentation (that may delay correct diagnosis) and etiologies (→ etiology of pediatric stroke)
    • the diagnosis of stroke is often challenging in infants and children because nonspecific localizing signs are frequently overlooked
    • according to one study, only 20% of children were diagnosed with stroke within six hours, and stroke was not suspected in over 62% of children at initial presentation (Rafay, 2009)
  • neuroimaging is an essential component of pediatric stroke management as it helps to:
    • confirm the diagnosis and type of stroke (ischemic x hemorrhagic)
    • exclude stroke mimics (PRES, epilepsy, CNS infection, tumor, etc.)
    • identify stroke etiology (dissection, vasculitis, moyamoya, etc.)
    • facilitate treatment decisions (acute therapy, prevention)
    • provide prognostic informations

Overview of neuroimaging modalities

  • the choice of modality depends on the patient’s age, the clinical scenario, and hospital resources; MRI is preferred

CT + CT angiography

  • NCCT has limited sensitivity for the detection of acute ischemic changes and frequent stroke mimics + requires exposure to ionizing radiation and iodinated contrast dye
  • if possible, magnetic resonance imaging (MRI) is preferred
  • if MRI is contraindicated or unavailable, perform NCCT+CT angiography of the head and neck, with or without CT venography

MRI + MR angiography

  • MRI protocol is optimal for obtaining the definitive diagnosis of both ischemic and hemorrhagic lesions, as well as for identifying underlying arteriopathy, thrombus, or arterial dissection in both neonates and older children
  • many centers have implemented rapid brain MR protocols for stroke to shorten examination time; the rapid protocol (7-minute MRI) typically includes:
    • T1  (to detect hemorrhage)
    • diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) maps   → DWI in acute stroke diagnosis
    • gradient echo (GRE) sequences to detect hemorrhage (0,5 min)
    • head MR angiography  –  occlusion site and extent using 1-minute phase contrast angiography (PCA)
    • neck and chest MRA (to exclude type A dissection and to assess approach route)
    • FLAIR (SAH)
  • additional sequences
    • vessel wall imaging (VWI) – to detect inflammatory processes or dissection
    • perfusion imaging (PWI) – calculated values are not validated in children
      • dynamic bolus passage of gadolinium with rapid T2* weighting (dynamic susceptibility contrast, DSC)
      • dynamic bolus passage of gadolinium with T1 weighting (dynamic contrast enhancement, DCE)
      • arterial spin labeling (ASL) (detection of ischemic region); not extensively validated in pediatric stroke

Digital subtractive angiography

  • can be considered when the cause of the infarction is unclear from non-invasive imaging studies and when there is a high clinical suspicion of a medium to small-sized arteriopathy
  • it has better sensitivity for aneurysms, vasculopathies involving medium-small vessels, or other structural vascular disorders

Perfusion methods (CTP, MRP, SPECT)

  • important methods to assess hemodynamic changes when revascularization procedures are considered (bypass or synangiosis considered in vasculopathies such as moyamoya)
  • strict perfusion parameters are not established in children; physiologic and hemodynamic differences should be expected

Neuroimaging in different stroke subtypes

Ischemic stroke

→ Etiology of pediatric stroke

→ Recanalization therapy in pediatric stroke

  • some disorders are more frequent in pediatric stroke compared to adults:
    • focal cerebral arteriopathy (FCA), also known as transient cerebral arteriopathy (TCA)
    • primary and secondary Moyamoya disease
    • genetic or syndromic arteriopathies (such as PHACE syndrome, ACTA2 angiopathy, Grange syndrome, etc.)
    • vasculitis
    • fibromuscular dysplasia
    • iatrogenic stroke
    • dissection
    • hypercoagulable states (thrombophilia)

Computed tomography (CT)

  • CT is often the first imaging modality performed when MRI is not available or the child is unstable
    • excludes intracranial hemorrhage but is insensitive to hyperacute or small ischemic infarctions
    • infarction has an appearance similar to that of the older child or adult, manifesting as a well-defined, often wedge-shaped region of hypoattenuation in an arterial distribution
  • CTA is used to detect arterial stenosis or occlusion

Magnetic resonance imaging (MRI)

  • modality of choice in pediatric stroke; the appearance of infarct is the same as in adults
  • DWI
    • MRI shows reduced diffusivity within minutes, which appears as a high signal on DWI and low calculated values on ADC maps
    • the high signal on DWI increases continuously in the hyperacute and acute phases, peaking commonly after several days
    • a pediatric modification of the ASPECTS (pedASPECTS) score was developed using DWI (Mackay, 2020)

      • the score includes two regions of the anterior (A1 and A2), 10 areas of the middle (M1, M2, M3, M4, M5, M6, insula, internal capsule, caudate, and lentiform nucleus), and three regions of the posterior cerebral artery territories (P1, P2, and thalamus) in each hemisphere. One point is allocated to each infarct-affected area; the total pedASPECTS ranges from 0 for normal to 30 for maximal severity (15 per hemisphere)
  • DWI-FLAIR mismatch
    • positive DWI with negative findings on FLAIR suggests a stroke onset of < 4.5 hours ago
  • MR perfusion (PWI)
    • dynamic susceptibility contrast (DSC) is most commonly performed
    • DWI/PWI mismatch may help assess penumbra (although validation of cut-offs in children is lacking)
    • arterial spin labeling (ASL) is not an established method in the acute stroke setting
    • perfusion imaging helps identify regions of relative ischemia that are at risk for infarction in moyamoya syndrome
  • MRA and Vessel Wall Imaging (VWI)

    • MRA helps identify the location and extent of stenosis or occlusion
    • if arteriopathy is suspected, VWI (using black-blood, T1-weighted post-contrast imaging) can demonstrate abnormal vessel wall enhancement in the setting of active inflammatory processes, as well as assess for intracranial arterial dissection on pre-contrast T1-weighted imaging
    • some genetic arteriopathies have unique imaging appearances, such as the ACTA2 mutation, which demonstrates dilation of the proximal internal carotid arteries, occlusion or stenosis of the distal internal carotid arteries, straight “broomstick-like” arteries of the circle of Willis, and absence of lenticulostriate collaterals

Hemorrhagic stroke

  • pediatric hemorrhagic stroke (intracerebral hemorrhage, ICH) has different causes compared to adults (where hypertensive bleeding prevails)
    • rupture of vascular malformations or aneurysms
    • hemorrhagic venous infarction (CSVT)
    • coagulopathy
    • infant intraventricular hemorrhage (IVH)
    • genetic arteriopathies associated with hemorrhagic stroke (IVA or JAM3 mutations)
  • imaging should:
    • differentiate hemorrhagic transformation (arterial or venous) from primary hemorrhage
    • detect an underlying mass or vascular malformation as a source of bleeding
  • CT – usually the baseline imaging
    • excellent sensitivity for detecting hemorrhage
    • CTA can detect underlying vascular pathology
  • MRI – preferred in stable patients (T1,2, FLAIR, DWI, SWI/GRE, MRA, and/or MRV)
  • DSA – may be considered if no lesion is identified on initial imaging to assess for small vascular malformations
  • if no malformation is identified on baseline imaging, repeat the neuroimaging after the hematoma has resolved (as small lesions may be compressed)

Intracranial venous thrombosis

→ clinical presentation and etiology of CSVT
→ diagnosis of CSVT

  • venous infarcts caused by cerebral sinus venous thrombosis (CSVT) are relatively common (accounting for ~ 40% of CSVT cases)
  • approximately 70% of these infarcts are hemorrhagic
  • thrombosis should be suspected in any child who has an unexplained hemorrhage or an infarction that does not fit an arterial vascular distribution
  • risk factors include:
    • head and neck infections
    • chronic diseases such as connective tissue disorders
    • coagulation disorders
  • MRI is the imaging modality of choice
    • T1- and T2-weighted images + DWI, GRE/SWI images, and MRV
    • acute (<3 days) thrombus exhibits low signal intensity due to the presence of deoxygenated hemoglobin
    • in subacute thrombosis (>4-5 days), T1-weighted images show the high signal intensity of the clot
    • GRE helps detect cortical vein thrombosis
  • CT venography
    • sensitive and specific for diagnosing dural sinus thrombosis
    • disadvantages:
      • exposure to radiation and contrast media
      • limited diagnostic value for diagnosing cortical vein thrombosis
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Neuroimaging in pediatric stroke
link: https://www.stroke-manual.com/neuroimaging-in-pediatric-stroke/