Pediatric Stroke

Presented by: Dr. Samuel Adugna(PCHR3)

: Dr. Daniel Kebede(MD, PCHR3@HU)
Moderator: Dr. Ayalew Moges(MD,Assisstant professor of PCH,Pediatric
neurologist)
Oct 5th ,2024

05/31/2025 Dx and MX of childhood Stroke 1

Outline
• Introduction
• Classification
• Blood supply and venous drainage of the Brain
• Epidemiology
• Etiology/ Risk factors
• Pathophysiology
• Clinical features
• Approach to diagnosis and Evaluation
• Treatment
• Outcome
• Prevention
• References
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Introduction
• Although more common in older adults, stroke also occurs
in neonates, infants, children, and young adults, resulting
in significant morbidity and mortality.
• Childhood stroke has a mortality of 5% to 10% for
ischemic stroke and ~25% for hemorrhagic stroke and is
among the top 10 causes of death in children, but rates
may be declining.
• Male gender and younger age at time of stroke are
associated with increased risk of death
• It is defined as sudden neurological deficit caused by
focal vascular lesion in the brain.

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• It is a neurologic emergency

• With Frequently delayed recognition due to:

Subtle and nonspecific clinical presentations,

 poor awareness by physicians,

a complicated differential diagnosis, and

 a high frequency (>50%) of negative initial brain CT

scans in true AIS

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Classification
• Stroke is classified into 2 based on time of onset:

• Childhood stroke is an acute onset of neurologic sign

or symptom attributable to focal brain infarction or
hemorrhage occurring between ages of 28 days to 18
years and lasting more than 24 hrs.

• Perinatal stroke – between 28(some use 20) weeks of

gestation to 28 days postnatal.
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• Perinatal stroke is further subdivided into
• Perinatal AIS (PAIS) - depending on whether the
presentation is acute seizures and
encephalopathy in the first few days of life, as
seen in PAIS, or
• Presumed perinatal stroke (PPS) - a chronic
evolving hemiparesis at 4 to 8 months of life as
seen in PPS

05/31/2025 Dx and MX of childhood Stroke 6

Also it is classified into 2 types, based on primary pathophysiology of the
disease
 ISCHEMIC STROKE ( interruption of blood flow to a part of brain)

 HEMORRHAGIC STROKE (rupture of blood vessels with bleeding into the

cerebral parenchyma).
The ischemic variants of stroke further classified as Arterial ischemic
stroke(AIS) and cerebral sinovenous thrombosis(CSVT)
Hemorrhagic stroke encompasses spontaneous intracerebral hemorrhage (ICH),
isolated intraventricular hemorrhage, and nontraumatic subarachnoid
hemorrhage .
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 Arterial (AIS)
Ischemic
Venous
Stroke
(CSVT)
Hemorrhagic

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Distribution of the anterior, middle, and posterior cerebral arteries. A, Lateral, B, medial, C, superior, and D, inferior views.

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Venous drainage of the Brain

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Stroke in pediatrics versus
adults
• Stroke in children relatively rare and frequently results in lack of recognition and delay
in diagnosis .
• Recurrence is low in neonates
• There are fundamental, etiologic & developmental differences in children
compared with adults .
• Multiple causes for stroke in children & many risk factors.
• Hemorrhagic stroke higher mortality than ischemic stroke.
• Stroke due to vascular rupture is as common as due to vascular occlusion (55% ischemic, 45%
hemorrhagic).
• Permanent aphasia is rare in children below 4 yrs, even with involvement of dominant
hemisphere.
• Neurodeficit is mild because collateral blood flow is better than adults.

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Epidemiology
• Stroke is an important cause of acquired brain
injury in newborns, children, and adolescents.
• The ischemic varieties of arterial ischemic stroke
(AIS) and cerebral sinovenous thrombosis (CSVT)
are, together, more common than brain
malignancy (incidence ∼5 in 100,000 children per
year).
• Perinatal ischemic stroke is especially common (1
in 2,500-4,000 live births) and is the leading
cause of hemiparetic cerebral palsy.

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• Arterial Ischemic stroke
• Infants and children – Annual incidence rates of arterial ischemic
stroke in infants and children range from 0.6 to 7.9/100,000 children
per year.
• Young adults – In adults <45 years old, the incidence of ischemic
stroke worldwide ranges from 8 to 100/100,000 people per year .
• In the past 3 decades the incidence of AIS had been increasing and
potential factors include
• availability of more sensitive diagnostic tests, particularly
magnetic resonance imaging (MRI), and
• increased survival in previously lethal pediatric diseases that
predispose to stroke, such as congenital heart disease, SCD, and
childhood malignancies.
• Incidence rates are increased in boys, infants, in black and Asian
populations.
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• Hemorrhagic stroke:
• Average annual incidence rate is 1.4 per 100,000
children for hemorrhagic stroke
• The estimated annual incidence of intracerebral
hemorrhage in developed countries ranges from
1.1 to 5.2 per 100,000 children , while the
estimated annual incidence of subarachnoid
hemorrhage is 0.4 per 100,000 children

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• Cerebral sinovenous thrombosis:
• Brain dysfunction occurring due to thrombotic occlusion of
cerebral veins and/or dural venous sinuses
• The available data suggest that CVT is uncommon.
• The annual incidence ranges from 0.22 to 1.57 per 100,000
• Pediatric CSVT: AIS cases = 1:4
• More common in neonates and females
• it is more common in women than men, with a female to
male ratio of 3:1. The imbalance may be due to the
increased risk of CVT associated with pregnancy and
puerperium and with oral contraceptives use.

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• Perinatal stroke:
• All three types could occur with AIS being the
commonest
• Arterial ischemic stroke, hemorrhagic stroke, and
cerebral venous thrombosis account for 70, 20,
and 10 percent of acute symptomatic perinatal
stroke, respectively
• Incidence 10-fold that of childhood stroke
• 35 per 100,000 or 1 in 2800-3500 live births
• Distribution of risk factors varies from infants and
older children
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Etiology/ risk factors
• For Arterial ischemic stroke includes:
• 1)Arteriopathies: accounts for 50% of causes of arterial ischemic
strokes
• Focal cerebral Arteriopathy
• an acute, stenosing, unilateral intracranial arteriopathy of the distal
internal carotid artery and its proximal branches
• Early, often rapid progression over days to weeks, followed by plateau and
later improvement over months.
• It is a self-limited and monophasic disease

• Its mechanism is thought to be inflammatory

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• Arterial dissections can be intracranial or extracranial,
and can be traumatic or spontaneous.
• Moyamoya disease
• stenosing intracranial arteriopathy affecting the distal internal
carotid artery and its proximal branches
• chronic, slowly progressive disease that is usually bilateral.
• Moyamoya syndrome is the arteriopathy in the setting of
another disorder(like trisomy 21, neurofibromatosis 1, Williams
syndrome, sickle cell disease, congenital dwarfism, and as a sequela of cranial
irradiation)
• occurs mainly in Japanese and other Asian populations and may have a genetic
basis.
• typically presents with recurrent transient ischemic attacks (TIAs) or ischemic
strokes, while intracranial hemorrhage is more common in young adults.
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• Vasculitis: can be primary or secondary
• Primary includes - Takayasu arteritis, Giant cell arteritis, Polyarteritis nodosa, Kawasaki
disease, and Primary angiitis of the central nervous system
• Secondary includes(SLE, Bacterial meningitis, HIV, varicella, syphilis & CNS TB)

• Congenital or genetic arteriopathies:

• neurofibromatosis type 1 (NF-1),
• Williams Beuren syndrome ,
• Alagille syndrome ,
• cerebral autosomal dominant arteriopathy with subcortical infarcts (CADASIL; caused by
NOTCH3 mutations),
• cerebral autosomal recessive arteriopathy with subcortical infarcts (CARASIL; caused by
HTRA1 mutations),
• Aicardi Goutières syndrome, and
• ACTA2- and COL4A1-associated arteriopathies.
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• 2)Cardiac causes: mechanisms of ischemic stroke
associated with congenital heart disease include the
following:
• Paradoxical embolism
• Hyper viscosity (eg, from polycythemia and compensatory
erythrocytosis)
• Increased risk of infective endocarditis and septic embolism
• Dilation of cardiac chambers with intracardiac thrombus formation
• Arrhythmias
• Acquired cardiac lesions, including endocarditis,
cardiomyopathy, and prosthetic valve placement, are also
risk factors for stroke
• Risk of stroke 9-12x in young adults and 19x higher for
children with congenital heart disease
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• 3)Hematologic causes:
• Sickle cell disease- 200x higher rate of stroke
• Prothrombotic disorders - Children:
• Anemia (particularly iron deficiency)
• Antiphospholipid syndrome
• Abnormal activated protein C resistance (usually related to the Factor
V Leiden)
• Protein C and S deficiency
• Antithrombin deficiency
• Prothrombin G20210A
• Elevated lipoprotein(a)
• Elevated homocysteine
• L- asparaginase and OCP pill are also associated with stroke
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• 4) metabolic disorders: includes
• Fabry disease
• Homocystinuria
• Menkes disease
• Deficiency of adenosine deaminase(ADA2)
• MELAS syndrome( mitochondrial encephalomyopathy with lactic
acidosis and stroke-like episodes)
• 5) substance abuse:
• Sympathomimetic drugs, such as cocaine and
methamphetamine
• Other include heroin, other opiates, marijuana, synthetic
cannabinoids ("spice"), and gamma hydroxybutyrate
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• Hemorrhagic stroke:
• Ruptured vascular malformations are the most common cause of intracerebral hemorrhage (ICH)
in children. While, hypertension and amyloid angiopathy are the most frequent causes of ICH
in adults.

• Vascular malformations –accounts for 18 – 90% of childhood

ICH cases
• Hematologic: accounts for 10 – 30% of cases
• ITP(1%), Hemophilia(3-12%) and SCD(>200x higher risk)
• Cancer
• Other
• 1ry hypertension, moya moya disease, drugs of abuse, coagulopathy
2ry to liver dysfunction, porphyria and cryptogenic(9 – 23% of cases)

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• Cerebral sinovenous thrombosis:
• Blood coagulation:
• Prothrombotic conditions(20 – 80%): Factor V Leiden, prothrombin gene
mutation 20210A, protein C deficiency, protein S deficiency, antithrombin III
deficiency, lipoprotein a, antiphospholipid antibodies (lupus anticoagulant,
anticardiolipin antibodies), pregnancy/puerperium
• Dehydration (e.g., gastroenteritis, neonatal failure to thrive)
• Anemia(10 – 20%): Including IDA
• Drugs and toxins (e.g., L -asparaginase, oral contraceptives)
• Acute systemic illness (e.g., sepsis, disseminated intravascular coagulation)
• Chronic systemic illness (e.g., inflammatory bowel disease, systemic lupus
erythematosus, leukemia)
• Nephrotic syndrome
• Inborn errors of metabolism (e.g., homocystinuria)

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• Blood vessel associated:
• Infection/thrombophlebitis(24- 62 %) : Otitis media,
mastoiditis, bacterial meningitis, sinusitis, dental
abscess, pharyngitis Lemierre syndrome, Sepsis,
• Trauma: skull fractures, closed head trauma
• Compression: birth, occipital bone compression in
neonates in supine lying
• Iatrogenic: neurosurgery, jugular lines,
extracorporeal membrane oxygenation Venous
malformations (e.g., dural arteriovenous fistulas)
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• Perinatal stroke:
• Placental disease: like chorioamnionitis, fetal thrombotic vasculopathy,
villitis of unknown etiology, and meconium-associated vascular necrosis
• Even though not proven placental causes of strokeare most common
causes of perinatal stroke
• Maternal and antepartum factors: like primiparity, Hx of infertility(10% ),
maternal smoking during pregnancy and preclampsia
• Intrapartum factors: prolonged second stage of labor, prolonged rupture
of membranes, maternal fever, meconium-stained amniotic fluid, 5
minute APGAR scores less than 7, cord abnormalities (tight nuchal cord),
need for intervention during delivery (instrumental delivery or the need
for emergency cesarean section), and non specific fetal heart rate
abnormalities

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• Prothrombotic factors(<20%): protein C deficiency, elevated
lipoprotein a, factor V Leiden, and prothrombin 20210 mutation
• Cardiac factors(15-20%): complex CHD’s, newborn undergoing ECMO
• Infection: like neonatal sepsis, B/meningitis, maternal fever without
infection, chorioamnionitis
• Genetic factors: COL4A1 gene mutation
• PAIS in the preterm newborn: Twin-to-twin transfusion syndrome ,
abnormal heart rate pattern , and hypoglycemia (less than 2 mmol/L)
were independently associated with PAIS

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Pathophysiology
The pathophysiology of cerebral ischemia consists of
primary & secondary injury.
PRIMARY INJURY – implies the cellular dysfunction
caused directly by ischemic insult.
SECONDARY INJURY - the chain of events &
derangements set into motion by the primary injury
constitute the secondary injury.
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Thrombotic occlusion of a cerebral artery is the
principal mechanism underlying AIS.
Thrombus may develop locally within arteries or
travel there from an embolic source.
Thrombosis is a product of both the coagulation
(fibrin-forming) and the platelet hemostatic
systems .
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The balance of which system predominates varies
with flow rate, shear stresses, endothelial
integrity, concentrations of circulating
anticoagulants, and other factors.
In situations of blood stasis or slow blood flow,
the coagulation system may predominate but the
relative balance depends on the specific disease.
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Exposure of blood to arterial wall inflammation
(e.g., vasculitis) or disruption of the endothelium
with exposure to collagen and tissue factor (e.g.,
dissection) activates both platelets and fibrin
formation.
Maturational changes to coagulation and platelets
across childhood are also likely important.
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Venous thrombo emboli can also reach the
cerebral arteries via paradoxical right-to-left intra
cardiac shunting across a patent foramen ovale,
atrial septal defect, or complex congenital heart
lesions.
 Embolism of infectious material (in
endocarditis),fat, air, and inert surgical matter can
05/31/2025 Dx and MX of childhood Stroke 38
In AIS, severity of cerebral tissue damage is a function of multiple
factors

1 duration and extent of ischemia and timing of

reperfusion
 2 availability of collateral arterial blood supply

 3 volume and functional components of brain

structures affected
 4 maturational status of the brain
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
The prominent in the tissue damage caused by cerebral
ischemia is the presence of a CENTRAL CORE – where
ischemia is most severe with rapid development of tissue
infarction & neuronal cell death.
The area surrounding the central core , which is marginally
perfused is called the ‘penumbra’.
 Penumbra has the capacity to recover when perfusion is
recovered promptly.
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In the penumbra,factors that increase the
discrepancy between metabolic rate and the
delivery of oxygen and glucose may result in
additional tissue injury and cell death.
The primary objective of acute neuroprotective
stroke treatment is to rescue this “at-risk”
penumbral tissue to salvage functional brain.
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Clinical features
• Arterial ischemic stroke:

• Acute onset of focal neurologic deficits in childhood is a stroke unless proven

otherwise.
• Hemiparesis and/or facial weakness

• Dysarthria, dysphasia

• Vertigo, ataxia

• Sensory disturbance and neglect

• Abnormal eye movements

• Seizures: focal onset; notable difference to adult

• Nonfocal: headache, irritability and altered mental state

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• Deficits are usually sudden and maximal at onset;
some have fluctuating course
• Clues for mechanism and etiology
 History of infection
 Head or neck trauma
 Previous TIA
 Head or neck irradiation
 Medication history: OCPs, chemotherapy, illicit drugs
 Family history
 Migraine

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• Hemorrhagic stroke:
Depend on location, cause and rate of bleeding
• Acute hemorrhages: instantaneous or thunderclap
headache, LOC, nuchal rigidity, focal neurologic
deficits and seizures.
• HS can be rapidly fatal.
• In bleeds associated with vascular malformations,
pulsatile tinnitus, cranial bruit, macrocephaly, and
high-output heart failure may be present.

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• Cerebral sinovenous thrombosis:

• Usually nonspecific symptoms and signs with

gradual onset

• Diffuse neurologic signs: headache, lethargy,

nausea and vomiting, raised ICP

• Seizures: less common than AIS

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Altered mentation Dx and MX of childhood Stroke 45
• Perinatal stroke: has 2 distinct presentations
• Acute symptomatic neonatal AIS presents with focal
seizures(48 to 88% presentation), altered mental status
and abnormal tone within 24-28 hr of birth.
• Alternatively, some affected neonates are asymptomatic
at birth and present in later infancy with signs of early
hand preference and congenital hemiparesis.
• The diagnosis of perinatal stroke should be suspected in
any newborn with signs or symptoms of
encephalopathy, seizures, lethargy, hypotonia, feeding
difficulties, apnea, or focal neurologic deficits

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• Arterial ischemic stroke:
• If the strokes affect the middle cerebral artery, the arm and
face are likely to be more affected than the leg.
• If the stroke affect the anterior cerebral artery leg is affected
more than the arm and face with associated incontinence
• The left hemisphere is more commonly involved than the right
in perinatal ischemic stroke
• Sensory deficits may occur if the parietal and occipital lobes
are affected.
• If posterior cerebral artery is affected the it results in a visual
field defect such as a homonymous hemianopia or
quadrantanopia .
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• Diencephalic injury may result in disturbed
temperature control and sleep-wake cycles.
• Infants with parasagittal injury will have hypotonia
and weakness of the proximal extremities. Upper
limbs, especially the shoulder girdle region, are
affected more than lower.
• Cerebral sinovenous thrombosis:
• venous thrombosis was more likely to occur in a
superficial than deep location (80 versus 39 percent).
The superior sagittal and lateral sinuses were affected
most often (62 and 39 percent, respectively).
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• Brain edema and areas of hemorrhagic infarction, especially
involving periventricular white matter, frequently accompany CSVT
• Hemorrhagic stroke:
• Most affected infants present in the first days of life with
encephalopathy, seizures, hypotonia, focal weakness, apnea, or
poor feeding
• Periventricular hemorrhagic infarction (part of the spectrum of
germinal matrix and intraventricular hemorrhage) predominantly
affects preterm infants.
• A clinically silent syndrome occurs in 25 to 50 percent of cases, but
can be detected by routine ultrasonographic screening.

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Case scenario
• A 20-year-old, suddenly lost the ability to speak and move his right
arm .Neurologic examination later in the day showed no progression in
his symptoms. He appeared to understand what he was told, but he could
not answer questions. In attempting to speak, he uttered nonsense
words. A very few words were uttered correctly, such as “hello”. His right
arm was paralyzed, and the right cheek and right side of his mouth
drooped. Forehead movements were normal. Leg strength was normal.
He seemed to recognize sensations everywhere. The results of
coordination tests were normal ,except in the right arm. His gait was
normal. Optic fundi were normal.
 Identify the level, side and type of lesion?
 If it is vascular cause, Which cerebral vessels do you think is affected?
 What is the most prominent motor deficit likely to result from this lesion?
 What term is used to describe this speech disorder?
 Why is forehead movement on the right normal?
05/31/2025 Dx and MX of childhood Stroke 50
 Differential Diagnosis(Stroke mimickers)

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Differential Diagnosis
• Migraine
• Neurologic deficits associated with migraine typically evolve slowly
compared with stroke, with sensory disturbance or weakness
• Seizure
• Very rarely, focal seizures can manifest with only “negative” symptoms
producing only hemiparesis or other acute-onset focal neurologic
deficits.
• A known past history of seizures, and EEG findings may be helpful.
Cont….
• Urgent brain imaging should be considered in new cases of prolonged or
recurrent focal seizure with persisting Todd paresis because stroke in
children is often associated with seizures at onset.
• Infection
• Symptom onset in primary CNS infection is typically more gradual and
less focal with fever as a consistent feature.
• Children with bacterial meningitis are at risk for both venous and arterial
stroke.
Cont….
• Demyelination
• The symptom onset and initial progression are more gradual compared with
stroke onset (i.e., typically hours or days versus minutes).
• Multifocal deficits, or concurrent encephalopathy
• Hypoglycemia
• Acute lowering of blood glucose levels can produce focal deficits mimicking
stroke.
• Alternating Hemiplegia of Childhood
• The hemiplegia persists for minutes to weeks and then resolves spontaneously.
• Choreoathetosis and dystonic movements are commonly observed in the
hemiparetic extremity.
Cont….
• Global Hypoxic-Ischemic Encephalopathy
• Clinical presentations would involve more generalized and bilateral
cerebral dysfunction compared
• Hypertensive Encephalopathy
• Posterior regions are selectively involved, possibly resulting in symptoms
of bilateral cortical visual dysfunction in addition to encephalopathy and
seizures
• Inborn Errors of Metabolism
• a history of developmental regression, posterior (and often bilateral)
lesions not respecting vascular territories on MRI, and elevated serum or
cerebrospinal fluid lactate (on MR spectroscopy).
Cont….
• Vestibulopathy and Ataxia
• Acute-onset vertigo and/or ataxia can be confused with brainstem or
cerebellar stroke.
• Simple bedside tests of vestibular function with otherwise intact brainstem
functions are reassuring.
• Channelopathies
• Include the migraine syndromes mentioned above, as well as a growing list of
episodic ataxias.
• A strong family history raises suspicion, but most require additional
investigation.
 DDX

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Diagnosis

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Neuroimaging CT scan findings
• Less prominent sulci,
• Edema,
• Appropriate and timely neuroimaging is essential • Loss of grey white
• to confirm the diagnosis of AIS, differentiation,
• exclude stroke mimics, and • Hypodense lesion,
• guide initial management decisions • Ventricular effacement,
• CT scan • If massive enough midline
• Exclude ICH shifts
• Has low detection rate for acute brain ischemia (16-56%)
• MRI has revolutionized the diagnosis, management, and study of cerebrovascular
disease and avoids radiation exposure investigation of choice
• DWI: hyper intensity
• ADC: hypo intensity
• MRA and CTA
• Conventional angiography (CA) – gold standard for cerebrovascular imaging.

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60
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61 05/31/2025 Dx and MX of childhood Stroke
 A. T2-weighted MRI

b. Conventional angiogram

Figure 109-4. Large-vessel arterial infarct in the right middle cerebral artery territory
associated with “transient cerebral arteriopathy” of childhood in an 11-year-old female
presenting with hemiparesis. A, T2-weighted magnetic resonance imaging shows right
middle cerebral artery infarct maximally involving the cortex. B, Conventional angiogram
shows irregular stenosis in the proximal right middle cerebral artery. (B, Courtesy of Division
62 05/31/2025 Dx and MX of childhood Stroke
of Neuroradiology, Hospital for Sick Children, Toronto, Ontario, Canada.)
 A. CT scan B. DW MRI
C. MR angiography

63
05/31/2025 Dx and MX of childhood Stroke
Figure 109-5. Postvaricella angiopathy in a 4-year-old male presenting with hemiparesis and speech loss 3 months
after chickenpox. A, Initial magnetic resonance imaging shows a “macrolacune” involving the left basal ganglia. B,
Initial angiogram shows normal lumen diameter with abnormal striae in the stem (arrow) of the left middle cerebral
artery (MCA). C, Follow-up angiogram 8 weeks later shows stenosis in the MCA stem (arrow) at the site of the prior
abnormality. D, Repeat angiogram after another 10 months shows persistence without progression of MCA stem
(arrow)05/31/2025
stenosis. (Courtesy of Derek Armstrong,Dx
Division of Neuroradiology, Hospital for Sick Children, Toronto,
and MX of childhood Stroke 64
Ontario, Canada.)
Figure 109-6. Childhood primary angiitis of the central nervous system An 8-year-old boy presented with sudden
onset of mild right-sided weakness and word-finding difficulty. A, Diffusion-weighted magnetic resonance imaging (MRI)
showed a small acute infarct of the left putamen and disease of the left middle cerebral artery. Twelve hours later, the
boy suddenly became aphasic and completely hemiplegic. B, Repeat MRI showed evolution to include large areas of
the frontal, parietal, and temporal lobes. Conventional angiography shows severe irregularity and alternating areas of
stenosis05/31/2025
of the entire M1 segment. Arteriopathy stabilized over time,
Dx and MX of childhood Strokethough the child was left with moderate 65
to severe
motor and language impairments.
Figure 109-7. Moyamoya disease. An 8-year-old boy presented with acute-onset left hemiplegia after 10 months of
transient alternating hemiplegia related to hyperventilation. A, A large-arterial ischemic stroke of the right frontal lobe
is accompanied by additional large-vessel and watershed lesions bilaterally. The patient has severe motor disability
bilaterally, with cognitive delays, and is nonverbal. B, His 15-year-old sister mentioned having headaches at her
brother’s follow-up visit and was imaged. She has several small ischemic lesions in the periventricular white matter
(arrow), but is an honors student with normal examination findings. Both children have moyamoya. C and D, The girl’s
angiogram (anteroposterior view) shows severe narrowing (C) and occlusion (D) of the distal internal carotid arteries,
with abnormal collateral development (arrows). Both
05/31/2025 Dx andpatients haveStroke
MX of childhood been asymptomatic after bilateral revascularization
66
surgery.
Figure 109-8. Acute cardioembolic arterial ischemic stroke. An 11-year-old girl presented with weeks of fatigue, low-
grade fever, and skin lesions. She suddenly developed left-sided hemiplegia in hospital. A, Computed tomography (CT)
scan at 90 minutes shows hypodensity (arrows) and loss of cortical ribbon in the right frontal lobe. She did not receive
thrombolysis because of suspicion of endocarditis. Diffusion-weighted magnetic resonance imaging (MRI; B) and
magnetic resonance angiography (C) confirm arterial ischemic stroke secondary to occlusion (arrow, C). The patient
subsequently grew streptococcus and required aortic valve replacement. D, Follow-up imaging at 6 months included
gradient ECHO MRI, which demonstrated hypodensity in the area of previous occlusion (arrow). E and F, CT
angiography confirmed a mycotic aneurysm (arrow,
05/31/2025 F),
Dx and MXwhich grew
of childhood over the next month and was clipped surgically
Stroke 67
with success.
Neuroimaging CVST
• Cranial ultrasound
• NCCT: (40-60% sensitive)
Better for deep system CSVT: sinus hyperdensity + thalamic
hypodensity or hemorrhage
• CT venography: highly sensitive and specific
Filling defects, enhancement of sinus wall and increased collateral
venous drainage
• MRI: choice of diagnosis
• MR venography
• Conventional angiography

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Figure 110-3. Iron deficiency anemia and birth control pill related CSVT in a teenager. A 14-year-old girl presented
with increasing headache and new-onset focal seizures. She was being treated with iron supplements for iron
deficiency anemia secondary to menorrhagia as well as an oral contraceptive for cycle regulation. (A) Axial plain head
CT scan showing area of bilateral frontal parenchymal hypodensities. (B) Sagittal CT venogram. (C) Axial diffusion-
weighted imaging showing diffusion restriction of the frontal parenchymal lesions that eventually completely reversed
on follow-up imaging. She was treated with low-molecular-weight heparin for 6 months with full recanalization of the
7005/31/2025
thrombus. (D) Sagittal T1-weighted MRI showingDxan
andocclusive thrombus
MX of childhood Stroke in the anterior half of superior sagittal sinus.
CT, computed tomography. MRI, magnetic resonance imaging.
Neuroimaging HS
• CT scan – highly sensitive and initial choice of imaging for
acute HS (hyperdense)
• MRI – increased accuracy and good sensitivity for even small
amount of acute and chronic hemorrhage
• Acute, subacute and chronic characteristics
• Angiography – CT, MRI or conventional

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Cont……
• Age of hematoma as seen on MRI

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 Treatment

“Time is brain; save the punembra”

• Multiple consensus-based guidelines, generated from

panels of child neurologists, thrombosis experts, and
others experienced in pediatric stroke

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05/31/2025 Dx and MX of childhood Stroke 76
Stabilization
• ABC
• Oxygenation

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Neuroprotection
• Initiate in minutes in suspected stroke cases
Normal Blood glucose control,electrolyte,Temperature
control:
Adequate cerebral perfusion: hypo- or hypertension(50th to
90th centile)?Permissive hypertension
Oxygenation >94%
Seizure control: levetiracetam first choice; phenobarbital
Treat cerebral edema(osmolar therapy, surgery)

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Figure 1. Proposed diagnostic pathway in children with suspected AIS. Adapted from the
Australian Childhood Stroke Advisory Committee‘s Guidelines for the Diagnosis and Acute
Management of Childhood Stroke 2017 and Rivkin MJ, Bernard TJ, Dowling MM, Amlie-Lef
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Treatment for AIS
1.Hyper acute therapy
• Need is assessed by PedNIHSS or scores based on
neuroimaging findings.
• Options: Intravenous thrombolysis or endovascular
thrombectomy
• Indications
• Persistent disabling neurologic deficits (PedNIHSS ≥ 6 at time of intervention
• Radiographically confirmed cerebral large artery occlusion

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Cont…….

• t-PA like alteplase; 0.9mg/kg within 4.5hr of presentation

(Adult recommendation)
• Role of steroids is also under study for the acute and rapid
inflammatory nature of FCA
• Issues in children: developing fibrinolytic system and overall
higher concentration of plasminogen activator inhibitor in
children #dosing; smaller anatomy of child’s vasculature;
differences in etiology #safety

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Cont……
2.Acute treatment
• Antithrombotic (ATT) ,DOC?
• Anticoagulation
 Arterial dissection, cardioembolic source, hypercoagulable state
 UFH, LMWH (Enoxaparin 1 mg/kg/dose SC BID) or oral warfarin
 Choice depends on pharmacokinetics, ease of monitoring (PTT, anti-factor Xa level or INR) and
safety

• Antiplatelet: secondary prevention for non cardioembolic AIS

 Aspirin: 3-5 mg/kg per day,clopidogrel 0.5-1mg/kg/day

• Exceptions: sickle cell disease, intracranial hemorrhage

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 Cont……
• Comparing anticoagulants

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Treatment of CVST
• Anticoagulation – mainstay of treatment
Initial: LMWH or UFH
Followed by warfarin for 3-6 months
• Endovascular treatement and thrombolysis
• Progressive neurologic worsening despite adequate anticoagulation
therapy –

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Cont…..
• Non-antithrombotic therapies
• Increased Intracranial Pressure mang’t
• Antibioitics for septic cause
• Aggressive management of seizure
• Treatment of precipitants
• Regular funduscopic examination

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Cont……
• Reimaging
• If ACT is not initiated at diagnosis, early repeat venous imaging (5 to 7 days) is
indicated to exclude thrombus propagation and/or new venous infarction. –
esp Neonates
 One third of children with CSVT who are not treated with ACT will propagate their
thrombus in the first week after diagnosis and 40% of these will develop additional
parenchymal infarction and worse outcome
• For those on ACT – at 3 months usually to decide on drug discontinuation
(together with underlying RF)
• If there are any signs and symptoms of neurologic deterioration
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Treatment of hemorrhagic
stroke
• Limited guidelines
• Management of acute childhood HS requires emergency
neurosurgical intervention for a large or rapidly expanding
hemorrhage.
• Emergency neurosurgical interventions – large or rapidly
expanding hemorrhage
• Address underlying cause

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Cont…….
• The recurrence risk for those with structural lesions is significant, and
serial imaging may be required.
• Definitive repair or removal of the vascular malformation may require a
combined approach with interventional endovascular methods and
neurosurgery.
• Outcomes from childhood HS are not well studied but likely depend on
lesion size, location, and etiology.
• Compared with AIS, the HS mortality rate is higher, but long-term deficits
are less common.
Treatment of Perinatal
Stroke
• Key management differences:
• Reservation on anticoagulant and antiplatelet use,

• Duration of treatment (eg CSVT 6 wks- 3 mo) and

• Special attention to hemorrhagic diseases of the newborn

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 Outcomes

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Outcomes AIS
• Overall case fatality rate < 5%

• Recurrence risk depends on the underlying cause

(overall ~20%)
Arteriopathies may go up to 65%

• Most children will have variable degrees of long-term

neurologic deficit
Age, seizures, infarct location and size
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Cont…..
Factors predicting poor outcome include-
Cerebral cortex involvement
Large size of infarct
Moyamoya disease

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Outcome CVST
• Neurologic deficits range from mild to severe
 Sensorimotor impairments, developmental delay, cognitive and
behavioral difficulties as well as remote symptomatic seizures and
epilepsy
• Predictors of early deterioration and death: Comorbid neurologic
conditions, ICH, and longer follow-up duration
• Adults: depressed consciousness, thrombosis of the deep venous
system, large hemorrhagic lesions
• Recurrence risk: 20% (cerebral or systemic)
 Majority within the first 6 months
 Less common in <2 years
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Cont…..
• Likely depends on lesion size, site and etiology
• Higher mortality rates (~25%) compared to AIS but the long
term deficits in survivors are less common

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Neurorehabilitation
• Constraint-induced movement therapy (CIMT)

• Non-invasive brain stimulation

• Assistive devices, medications or procedures

• Speech, occupational and psychosocial therapies

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Figure 2. Examples of use of person-icons to illustrate the 7 modified Rankin Scale (mRS) health states.
Panel (A) provides a set of male person icons. Panel (B) provides a set of female person-icons. A running figure represents the highest,
symptomfree functional level (mRS score 0); a walking figure carrying a briefcase represents having symptoms but able to work (mRS
score 1); a figure standing still represents being able to live independently (mRS score 2); a bent figure with a cane represents more
severe impairment causing dependency but not loss of ambulation without assistance on another person (mRS score 3); a figure using a
walker being helped by a caregiver represents loss of ambulation without assistance of another person and/or loss of ability to perform
bodily self-care (mRS score 4); a bedridden figure represents needing continuous care (mRS score 5); and gravestones represent fatal
outcome (mRS score 6). These figures are labeled with health-state terms. In the Appendix are figures labeled with scalar/intensity terms
(Figure IIA and IIB in the Data Supplement) and valence terms (Figure IIIA and IIIB in the Data Supplement).

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Prevention
• Primary: focused on the predisposing medical conditions
• Secondary: individualized choices
 Daily aspirin (3 to 5 mg/kg daily) for a minimum of 2 years
[ACCP guidelines] – low risk of recurrence after 2 years
 Cardioembolic or prothrombotic disorders: LMWH or
warfarin for 3 months [ACCP guidelines]
 PFO closure
Recurrent blood transfusion for SCD

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References
• Kleigman, R. K. (2020). Nelson textbook of pediatrics (J. S. St
Geme, Ed.; 21st ed., Vol. 2). Elsevier
• Kleigman, R. K. (2023). Nelson textbook of pediatrics (J. S. St
Geme, Ed.; 22nd ed., Vol. 2). Elsevier
• Swaiman, K. S. (2023). Swaiman’s pediatric neurology principles
and practice (7th ed.). Elsevier
• Upto date 2023
• Mark Mackay, Adam Kirton, and Gabrielle deVeber(2024).Arterial
ischemic Stroke.In:Kenneth F. Swaiman & Et al(7 ed.).Swaiman’s
pediatric neurology principles and practice.Elsevier Inc., pp1041-62

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References
• Lori Billinghurst and Mahendranath Moharir (2024).Sino Venous
Thrombosis.In:Kenneth F. Swaiman & Et al(7 ed.).Swaiman’s pediatric
neurology principles and practice.Elsevier Inc., pp1063-66 .
• Lauren A. Beslow, Lori Jordan, and Edward Smith(2024) .Vascular
Malformations, Intracerebral Hemorrhage, and Subarachnoid
Hemorrhage in Infants and Children. Swaiman’s pediatric neurology
principles and practice.Elsevier Inc., pp1067-91 .
• Nomazulu Dlamini and Gabrielle A. deVeber (2024). Chapter
664:Pediatric stroke. In: Robert, M. K., & Et al (22ed).Nelson text book of
pediatrics .Philadelphia: W.B Saunders co.,pp3742-54.
https://doi.org/10.5603/pjnns.a2020.0010
References
• Oborska, Z., Urban, P., Wychowaniec, K., Jóźwiak, S., 2018. Paediatric
stroke — a review of current guidelines for diagnosis and treatment.
Neurologia i Neurochirurgia Polska..
 THANK YOU!!

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