Pediatric stroke is rare, but very much skill and equipment is needed for diagnosis and treatment

1. APPROACH TO A CHILD WITH ACUTE
STROKE
Dr. Ashik Majumder
Pediatrics

2. INTRODUCTION
 Incidence of pediatrics stroke is 2-8 per 1,00,000
child per year (excluding the neonatal period)
 Approximately 10% of all childhood strokes
results in fatality
 Results in epilepsy in 70% of survivors
 Perinatal stroke is even more common and is the
leading cause of hemiparetic cerebral palsy
 Recurrence in childhood ischemic strokes are in
the range of 20% and are known to occur even 5
years after the index stroke

3. DEFINITION
 Pediatrics stroke includes ischemic strokes and
hemorrhagic strokes
 Ischemic strokes can be due to arterial ischemia
or venous sinus thrombosis
 Hemorrhagic strokes are due to subarachnoid
hemorrhage and intraparenchymal bleeds

4. ARTERIAL ISCHEMIC STROKE (AIS)
 Ischemic stroke is defined as sudden, focal infarction
of brain tissue on neuroimaging or autopsy
 Childhood AIS is a cerebrovascular event that occurs
between the age of one month and 18 year
 It results in an acute neurological deficit that occurs
due to an infarct in a defined arterial territory &
presents with consistent clinical signs and symptoms
 The acute onset of a focal neurologic deficit in a
child is stroke until proven otherwise

5. RISK FACTORS
•Cerebral
arteriopathy
•Transient/Focal cerebral arteriopathy (Primary CNS/Systemic
vasculitis, fibromuscular dysplasia)
•Arterial dissection
•Moyamoya disease, Moyamoya syndrome
•Cardiac •CHD, endocarditis, valvular disease, arrhythmia,
Congenital/acquired cardiomyopathy, cardiac catheterisation
•Hematological •Sickle cell disease, thrombophilia, Iron deficiency
•Genetic •PHACE syndrome (Posterior fossa anomalies, Hemangioma, Arterial
anomalies, Cardiac anomalies & Eye anomalies)
•NF-1, Fabry’s disease, Homocystinuria
•Infection •Meningitis- viral, bacterial, fungal
•Vericella, Mtb, Neuroborreliosis
•Miscellaneous •Air/fat embolism, Cocaine, L-asparaginase, Lymphoma, Leukemia,
Severe dehydration, Mitochondrial encephalopathies, Lactic acidosis,
Stroke like episodes(MELAS)

6.  Hematological
 Max AIS shows iron deficiency (Nutritional) but
no casual relationship
 In India, this is the most common cause &
treatable cause
 In Western world, Homozygous SCD
 Risk increases with increasing age
 Recurrence risk is 50% after 1st stroke
 2-5 yrs mostly AIS, after that H’ge Stroke
 Prothrombotic disorders VST>AIS

7.  Arteriopathies
 Leading cause of childhood AIS
 TCA
Most common site of focal stenosis is in the
proximal segment of the MCA >distal ICA
>proximal ACA >proximal PCA
 Intracranial vasculitis (infectious/inflammatory)
Ischemic/ hemorrhagic stroke
 Can results in arterial & venous thrombosis with both
parenchymal & SAH
 Bacterial meningitis(10%)
 Tubercular meningitis(40%)
 VZV & HIV

8.  Primary Intracranial Angitis
Small & large vessel involvement
Non infective vasculitis
Slowly progressive or indolent course
Characterised by headache, cognitive decline,
memory issue & seizure
 Four vessel cerebral angiography is gold standard
 Confirmed only by a leptomeningeal biopsy
 Biopsy is prerequisite to initiate steroid and
immunosuppressant therapy

9.  Arterial dissection
 Main reason  trauma
Trauma or genetic predisposition
Rupture of intima
Blood enters the layer of arterial wall
Thrombosis within the false lumen
Stenosis or obliteration
Ischemic infarct in the territory

10.  Arterial circulation dissection is common in pediatric
strokes compared to adults
 Pain is prominent in adults
 Spontaneous dissection can occurs in acute
infections
 Blunt trauma can cause carotid artery dissection in
tonsillar fossa, with popsicle injury, pencils etc.
 Posterior circulation dissections in vertebral arteries
occurs at the level of C1-C2 vertebral bodies

11.  Moyamoya Patterns
 Progressive bilateral stenosis of arteries around the
circle of Willis commonly involving the distal
intracranial internal carotid artery
 If primary in origin, then called as Moyamoya disease
 SCD, NF-1, Down’s syndrome also leads to
secondary Moyamoya, called as Moyamoya
Syndrome

12. CLINICAL PRESENTATION
 Commonly occurs in anterior circulation, involving
MCA in majority
 Hemiparesis
 Aphasia
 Visual disturbance (field defect)
 Altered mental status
 Seizures at the onset of stroke suggest a cortical
involvement
 Aphasia, apraxia and agnosia are other cortical
involvement signs

13.  Progression of stroke symptoms & signs over time
suggests an arteriopathy
 Involvement of posterior circulation, commonly seen
in dissection results in ataxia, vertigo,
diplopia,vomiting

14.  Acute MCA territory infarct
 Contralateral weakness of upper & lower limbs
with/without aphasia & visual field defects
 MCA involvement is commonly at its origin
infarct in the territory of the lenticulostriate territory
involving the basal ganglia and internal capsule
 ACA territory infarct
 Behavioral changes
 Weakness of the legs
 Bladder incontinence

15.  Corpus Callosum Disconnection syndrome
 PCA territory infarct
Clinical signs Visual
symptoms
Sensory signs
Involvement of
medial temporal
lobe
Thalamic
involvement
Hemi/quadrantanopia
Agnosia
Cortical blindness

16.  Most neonatal ischemic strokes are embolic
 Source of embolus is pulmonary vascular beds or
degenerating placental vessels
 75% of single infarct occurs in left hemisphere
s/o embolic origin with mixing of aortic flow &
ductus arteriosus flow causing streamline effects
& directing the emboli to left hemisphere
 Manifestation is subtle, hence are missed
 Definite manifestations are irritability, feeding
difficulty, focal motor seizures (usually right side)
and lethargy

17.  Area of infarct in neonate usually watershed zone
betn MCA or ACA territory & MCA or PCA territory
 Second watershed zone is in the tegmentum region
of the brainstem extending longitudinally from the
superior colliculus to the medulla oblongata close to
the floor of the 4th ventricle
 Prematurity/early life infarcts results in H’ge
transformation while adult watershed infarcts usually
leads to coagulative necrosis in the brain
 Moebius syndrome is a classic example of the
brainstem watershed infarct in neonatal period

18. DIAGNOSIS
 History (birth, developmental, family & past medical
history)
 Examination (dysmorphology, blood pressure,
cyanosis, heart defects & murmur, bruits in the neck
& over skull, neurocutaneous stigmata of NF-1,
PHACES, TS, Fabry’s disease)
 Investigations
 Neuroimaging  MRI with angiography/ venography
CT scan

19.  Although CT imaging can demonstrate mature AIS
and exclude hemorrhage, MRI is required to identify
early and small infarcts
 Diffusion-weighted MRI demonstrates AIS within
minutes of onset and up to 7 days post onset
 MR angiography can confirm vascular occlusion and
suggest possible arteriopathy

21.  Blood tests CBC, LFT, KFT, ESR
 Coagulation profile PT/APTT, Ca++
 ECG with prolonged lead II record mandatory
 2D echo
 Serum iron studies, Vit B12 level & homocysteine
level
 Thrombophilia profile with protein C, S,
antithrombin III, factor V Leiden mutation,
prothrombin gene mutation, MTHFR mutation,
factor VIII level, lupus anticoagulants etc

22. ACUTE MANAGEMENT
 Maintaining adequate perfusion, oxygenation &
normoglycemia
 HTN should not be aggressively lowered
 Reduce cerebral edema & raised ICT
 No guidance for thrombolytic therapy
 Mechanical thrombectomy with clot retrieval
 Antiplatelet drug aspirin (used primarily for
secondary prevention of strokes), Clopidogrel

23.  Anticoagulant drug  warferin (mainly used for
recurrent cardioembolic stroke & stroke due to
dissection)
 LMW heparin in cardiogenic stroke
 Surgical management for large hemispheric strokes
or posterior fossa strokes
 Decompressive craniectomy

24. LONG TERM MANAGEMENT
 Survivor endure longterm neurological impairment in
moderate to severe degree
 Notable concern is with development of new seizures
and epilepsy
 Rehabilitation program
 Baclofen and trihexyphenidyl for spasticity and dystonia
 Botulinium toxin
 Epilepsy in 20% children with stroke
 Stroke and TIA recurrence 7-35%
 5-year recurrence rate is 50%

25.  Secondary prevention of stroke is the most important
aspect
 Use of warferin in cardiogenic stroke & arterial
dissection
 Aspirin is preferred
 Aspirin(1-5mg/kg/day), clopidogrel
 Child with SCD are advised for regular blood
transfusion
 HLA matched bone marrow transplantation
 Surgical options EDAMS or EDASS> STA-MCA
bypass

26. PERINATAL ARTERIAL ISCHEMIC STROKE
 Perinatal stroke is very common, differs from childhood
stroke, and has 2 distinct clinical presentations
 Acute symptomatic neonatal AIS presents with focal
seizures at 24-28 hr of life
 MRI diffusion abnormalities in an arterial territory
confirm recent infarction
 Secondly, infants are asymptomatic at birth and present
in later infancy with signs of early hand preference and
congenital hemiparesis
 Imaging reveals focal encephalomalacia in an arterial
territory, typically large middle cerebral artery lesions

28.  In acute neonatal AIS, seizure control is important,
but antithrombotic agents are rarely required
(exception: cardiac embolism)
 Most are idiopathic causes
 Other causes include congenital heart disease,
thrombotic placentopathy, and other prothrombotic
disorders and meningitis
 Most children having lifelong disability
 Perinatal stroke accounts for most cases of
hemiparetic cerebral palsy

29. VENOUS SINUS TROMBOSIS
 Incidence : 0.67 per 1,00,000 children per year
 Seen as a complication of common childhood illnesses
like ear discharge/infections, meningitis, head injury
 Clinical features:
 Acute onset seizure
 Comatose state
 Stroke like presentation
 Cranial nerve palsies
 Headache
 Raised ICT

30.  Risk factors:
 Local/systemic infections
 Iron deficiency anemia
 Malignancies
 Dehydration
 Nephrotic syndrome
 Inflammatory bowel disease
 Drug ingestions & prothrombotic states such as
inherited thrombophilias

31.  Investigations :
 MRI brain with venography (Confirmes the
diagnosis)
 CT brain with contrast
 Parenchymal ischemia in the parietal lobe &
absence of caudate nucleus in the ischemic zone
independently predicts venous sinus thrombosis
 Treatment:
 LMW heparin / unfractionated heparin f/b long
term anticoagulation with warferin

33. HEMORRHAGIC STROKE
 Nearly half of childhood strokes are hemorrhagic
 Two types:
 Intracerebral or parenchymal hemorrhage
 Subarachnoid hemorrhage

34.  Etiology:
 Vascular malformations- AV malformation (40%)
Aneurysms (10%)
Cavernomas (25%)
 Bleeding diathesis (thrombocytopenia, hemophilia
& coagulopathies)
 Brain tumor
 Minor causes- trauma, illicit drug use, infections,
vasculitis etc.

35.  Clinical features:
 Intraparenchymal bleed
Seizure
Focal deficit
Sign of increased ICT
Altered sensorium
Comatose state
 Subarachnoid hemorrhage
Preceded by sentinel headache(Thunder-clap)
Sudden onset vomiting
Altered sensorium
Focal seizure with/without generalisation

36.  Diagnosis:
 CT brain
 Combined MRI with angiography & venography

37.  Treatment:
 Emergency neurosurgical intervention for large or
rapidly expanding hemorrhage
 Neuroprotection
 Reversal of anticoagulant therapy (vitamin K,
fresh-frozen plasma)
 Definitive repair or removal of the vascular
malformation

38. DIFFERENTIAL DIAGNOSIS

39. CONTD.