PEDIATRIC STROKE

BY
Dr.JANAKI.AN
 STROKE IN CHILDREN
“Despite efforts to raise awareness
regarding stroke in children, this condition
is often overlooked as a cause of
symptoms by health care providers and
family.”
Stroke is as common as brain tumour in
children
It is one of the 10 most commonest
causes of childhood death worldwide
2/3 of affected are left with long term
impairment
 WHO definition of STROKE
• Clinical syndrome characterised by rapidly
developing signs of focal / global disturbance
of function lasting for more than 24 hours /
death with no apparent cause other than of
vascular origin
 TYPES
• Perinatal stroke - 22 weeks of gestation to 1
month of postnatal age
• Childhood / pediatric stroke - 1 month of age
to 18 yrs of age
• Young stroke - in people <40 years of age
 Epidemiology
Hemiplegia & hemiparesis is the most common cause of
cp in children born at term and stroke is its leading
cause.

Stroke in children is often underdiagnosed and diagnostic

delays are also more common
• due to confusing presentations
• distracting signs and symptoms leading on to
erroneous line of investigations
• complex differential diagnosis
 Epidemiology cont.,
 The reported annual incidence worldwide varies between
1.2/100000 children to 2.7/100000
 AIS – 2.4 /1 lakh
 CSVT – 1 – 4 /1 lakh
 HS - .67/1lakh
 Mortality – ais – 5-7%, csvt – 3 – 12%
 ½ of survivors develop persistent neurologic cognitive
psychiatric deficits
 1/3rd develop epilepsy
 In INDIA – stroke is <1% of all pediatric admissions and is 5 –
10 % of stroke in the young
• African American children are at more risk
than caucasian and Asian children
• Boys are at more risk compared to girls
 TYPES

Arterial Ischemic Stroke

Cerebral Venous Sinous

Thrombosis

Hemorrhagic Stroke
 ARTERIAL ISCHEMIC STROKE
• It is the focal brain infarction that results from
occlusion of the cerebral arteries most
commonly MCA .
 Overview of cerebral circulation
• 2 principal systems :
• anterior circulation
• Posterior circulation – vertebro basilar system
• Circle of willis – connecting these two
• Small perforating arteries that supply deeper parts
of brain – lenticulostraite vessels from ant
circulation
• thalamostriate vessels from
posterior circulation
Anterior circulation
Circle of willis
• ACA – anterio medial part of cerebral
hemisphere
• leg foot area
• putamen caudate nucleus
• anterio inferior portion of internal
capsule
• MCA – lateral part of cerebral hemisphere
• brocca, wernicke area
• face arm area of motor and sensory
cortex
• basal ganglia
• anterior and posterior superior portion of
ic

• PCA –posterior cortex

• midbrain
• thalamus
• brainstem
 Vascular patterns of AIS
• Large(peripheral wedge shaped lesions in cerebral
cortex) / small vessel infarct
• Most commonly involves left hemisphere
• Most commonly involve MCA and often occurs in
recognizable patterns
• M1 – prox MCA – entire MCA territory infarcted
• M1 - distal MCA – basal ganglia spared
• M2 – anterior (frontal) trunk(temporoparietal) /
posterior
• Lenticulostraite only – basal ganglia and deep white
matter only
• PCA – large vessel infarct – occipital and mesial
temporal lobes
• small vessel infarcts – thalamus and splenium
• Basilar artery – life threatening infarcts in
brainstem, cerebellum and PCA
• Cervical arteries – arterial dissection (infarction via
artery to artery embolus)
• Diffuse hypoperfusion - b/l infarcts in typical
watershed zones
Mechanism of thromboembolism
• Thrombotic occlusion of a cerebral artery

Thromboembolism

From an embolic
Local thrombus
source

Cardiogenic
Arterial (platelet rich Venous(fibrin rich Artery to artery
thrombus) thrombus) Fat
Infective vegetations
 MECHANISM OF INFARCTION
• Focal brain ischemia
• Regional hypoxia and depletion energy stores
• Ischemic neuronal dysfunction – reversible
initially
• Irreversible infarction sets in
• Hypoxia
• No o2 reserve and very few glucose reserve
• Oxidative to glycolysis
• Acidosis
• Accumulation of extracellular glutamate –
• intracellular calcium

• Cascade of cell death with acute necrosis

within hours and apoptosis over days
• Results in a central core of irreversibly
damaged brain
• A sorrounding partially injured , potentially
viable PENUMBRAL ZONE
• The primary objective of acute
neuroprotective and fibrinolytic stroke
trestment is to rescue this “at-risk”
penumbral tissue to salvage functional brain.
 RIAK FACTORS FOR AIS
• Arteriopathy
• Cardiac
• Prothrombotic
• Hematological
• Medications
• Migraine
• metabolic
 ARTERIOPATHY
• Leading cause of AIS
• Increased risk of both recurrence and poor outcome
• Causes – 1.inflammatory/parainfectious –
• Cpacns
• TCA
• FCA
• Post varicella angiopathy
• 2.infectious- bacterial meningitis and HIV
• 3.Dissection
• 4.moyamoya
 CARDIAC
• Complex CHD
• Cardiac sugeries
• Cardiac catheterisation
• Bacterial endocarditis
• PFO
• Atrial septal aneurysm
• Venous thrombosis – rt to lt shunt
 Prothrombotic
• Factor v leiden mutation
• prothrombin gene 20210A mutation
• Elevated lipoprotein a
• Protein C deficiency
• Anticardiolipin antibody
• Lupus anticoagulant
 • Hematological – SCD
IDA
• Metabolic – oral concentratives
chemotherapy
• Metabolic – iem(fabrys disease)
homocystinuria
 PRESENTATION
• Mode of onset of neurological symptoms -
predicts etiological diagnosis
• Nonabrupt onset – arteriopathic
• Abrupt onset – non arteriopathic
Younger children
• Commonly present with irritability,
lethargy,seizure, altered sensorium
• FND like hemiparesis is mc absent /subtle &eaasily
missed
 • Older children
• Mc present with FND – hemiparesis/plegia
• Seizures – presenting symptom in 22 – 52 %
• Language & speech difficulties
• Ataxia, vertigo,vomitting – post circulation
• Horners syndrome – ICA dissection
• Headache – 30%- before, with/shortly after
onset of symptoms
• Dd – hemiplegic migraine
• Ischemia – sudden onset
• Dissection – extracranial – ipl face neck
• intracranial – half sided
• violant type , precede stroke a few
days to few wks
 HISTORY
• Define the time of onset (last seen well)
• Mode of evolution symptoms
• thrombosis – progressive over a period of time
• embolic – precipitated by exertion, max severity at onset,
with progressive improvement
• hemorrhagic – dramatic in onset with signs of raised ict
• h/o infection esp varicella
• Vaccination in past 12 mnths
• Head &neck trauma
• Chiropractic neck manipulation in preceding weeks
• h/o fall with a sharp object in mouth
• Previous TIA
• Symptoms switching sides (prox emboli/moyamoya/AHC)
• h/o head &neck radiation
• Drug h/o – ocp,ct
• Family h/o thrombophilia –
• stroke or MI,50 yrs of age
• clots in legs dvt
• Prescription of bld thinners
 Physical examination
• Vital sign - ABC
• Cyanosis , clubbing – cardiac cause
• Lyphmadenopathy
• BP on all 4 limbs – vasculitis, raised ict
• Look for carotid and cranial bruit
• e/o pharynx for intraoral trauma
• Marfanoid feautures in homocystinuria
• Rash – varicella, herpes, connective tissue disorders
• Nc markers
• Organomegaly and palpable kidney
• Complete cardiac examination
• Evaluate other vascular beds such as skin and eyes
Neurological examination and localisation

Cerebral cortex ACA

• Sparse involvement • Distal – lower limb
• Seizures involvement
• Cortical sensory loss • Presence of snout
• Language palmomental and grasp
reflex
• Hemineglect
• Cortical sensory loss
MCA PCA
• Face and arm • Diatal- visual defects
• Post brnch – only • Loss of colour
speexch without recognition
hemiplegia • Prox – brainstem and
• Hemianesthesia thalamic syndrome
• hemianopia
BASAL GANGLIA – dystonic postures
INTERNAL CAPSULE
• Dense hemiplegia
• Homonymous hemianopia
• Hemisensory loss
THALAMUS – dense sensory loss and hemipainful state
BRAINSTEM – cortical fn preserved
• Crossed hemiplegia
• Ipl CNpalsy
• Ipl horners syndrome and cerebellar signs
 IMAGING
CT
• Has very less sensitivity
• Initial CT miss AIS in 84%of cases
• It is very useful to rule out HS and hemorrhagic
transformation
• Malignant cerebral edema
• Infarction is seen as focal increasing hypodensity in
an arterial territory
• Intraarterial thrombus –hyperdense artery sign
 MRI
• DWI MRI –
• Sensitive at detecting early brain ischemia
• Gold standard diagnostic inv of choice for
acute AIS
• Acute ischemia – restricted diffusion
normalises over wks – help determine infarct
age
• FLAIR –within several hrs – suppress csf effects
on image
• GRADIENT ECHO & SUSCEPTIBILITY WEIGHTED
IMAGING –detect even small amt of blood ,
predict risk of hemorrhagic transformation
• Perfusion weighted imaging – show regional abn
in perfusion
• Arterial spin labeling MRI – asses perfusion and
correlate with final infarct volume
 MR ANGIOGRAPHY
• Reasonable image of 1st &2nd order arteries
• Suggest the nature and extent of underlying
arteriopthy
• abrupt cut off – emboli
• irregular stenosis – arteriopathy
• TIME OF FLIGHT
• GADOLINIUM contrast MRA
• MRI wall imaging
TCA

•T1 WMRI -
Rt MCA infarct
•Conventional
angiogram –
irregular
stenosis of rt
prox MCA
MOYA MOYA
SYNDROME
Large arterial ischemic
stroke of rt frontal
lobe with large vessel
&watershed lesions
b/l

Severe narrowing and

stenosis of distal ICA
with abn collaterals
 management
• Goals of treatment include
•
immediate
• management
•
rescue viable brain
tissue

Minimise recurrence
 Immediate management
• Maintain airway , breathing and circulation
• Adequate supply of oxygen and metabolites
• proper oxygenation
• normoglycemia
• bp btwn 50th and 90th percentile
• Reduce metabolic demands
• control fever and seizures
• contro;l malignant cerebral edema- adequate sedation,
osmotic therapy,decompressing hemicraniectomy
• Prevent aspiration
 Anticoagulation – various guidelines
• Royal College of Physician
• aspirin 5mg/kg/d- exclude SCD/ICH
• Heparin after excluding dissection and csvt

• AHA
• aspirin in children with suspected cardioembolic cause
unrelated to PFO
• UFH/LMWH as a bridge to warfarin in children with suspected
extracranial dissection severe thrombophilia, multiple emboli
• No anticoagulation in intracranial dissection
• SAH due to dissection
• ACCP American College of Chest Physicians
• Empirically start initially heparin/aspirin until
dissection and embolic cause are excluded
• Neonate – no anticoagulation / aspirin except
in recurrent stroke
• Acute mgt – aspirin 1-5 mg/kg/d
• UFH – 28u/kg/hr in infants
• 20u/kg/hr in older children
• LMWH – enoxaparin – 1mg/kg s.c
bd
• Longterm with either aspirin or warfarin
• SCD – acute – optimal hydration and exchange
transfusion
• 2ndary prevention – monthly blood
transfusion in pts with MCA BF .200m/s by
TCD
• Moyamoya – revascularisation surgeries
 rehabilitation
• Physiotherapy
• CIMT- constraint induced movement therapy
• Transcranial magnetic stimulation
• Spasticity interventions- botulinium toxin
• anklefoot orthoses
• lycra hand spilnts
• Occupational therapy
• Psychological family support
• Treatment of complications – epilepsy- AED
• hyperkinetic movt disorders-anticholinergic and
antidopamine drugs
• headache – acetaminophen , cautious nsaid,
flunarizine
CEREBRAL SINOVENOUS
THROMBOSIS
 CSVT
• Thrombosis in the cerebral venous sytem
• Risk highest in neonates and males
• Involves superficial venous system commonly
– causing b/l parasagittal infarcts especially
with hemorrhagic transformation
• Deep venous thrombosis causes venous
edema & infarction of deep white matter ,
basal ganglia and thalamus – with risk of ivh
Blood coagulation
Risk factors
PROTHROMBOTIC CONDITIONS
-Factor v leiden
-Protein c protein s deficiency
-ELev lipoprotein a
-Antiphospholipid antibody
-Prothrombin20210A mutation

DEHYDRATION

IRON DEFICIENCY ANEMIA

DRUGS AND TOXINS

ACUTE SYSTEMIC ILLNESS

-Sepsis and DIC

CHRONIC SYSTEMIC ILLNESS

-SLE,IBD

IEM

NEPHROTIC SYNDROME
BLOOD VESSEL INFECTION & THROMBOPHLEBITIS
-OM, mastoiditis, bact meningitis,
sinusitis, pharyngitis,
-lemieeres syndrome
-Sepsis

TRAUMA

COMPRESSION
-at birth,
-Occipital bone in supine neonate

IATROGENIC
-neurosurgery
-catheterization

VASCULAR
Dural av fistula
 MECHANISM OF INFARCTION
• Venous sinus thrombosis
• Failure of venous emptying
• Rise in venous pressure
• Parenchymal vasogenic edema without true
infarction,accompanied by focal clinical symptoms
• With further increse in tissue pressure exceeding incoming
arterial perfusion pressure – perm infarction occurs

• This back pressure – resp for hemorrhagic transformation

• Collaterals develop over time- thus very rapid complete
occlusion carries incresded risk of tissue infarction
• Hydrocephalus in csvt
 CLINICAL FEATURES
• Diiffuse neurological signs & seizures(40 to
90%) more common
• Headache
• Lethargy
• Nausea vomitting
• Signs of increased intracranial pressure
including 6th nerve palsy papilledema may be
seen
 NEUROIMAGING
• CT – Plain – inadequate
• Contrast enhanced CTV – highly sensitive &
specific
Thrombus – filling defect in vein/sinus
Empty triangle/ empty delta sign
• MRI - diagnostic modality of choice in pediatric csvt
Lacks radiation
Provides additional details regarding brain
parenchyma (age of infarct) and venous system
Modalities sensitive to
Vasogenic edema – FLAIR
Cytotoxic edema and infarction – DWI
Blood product – GRADIENT ECHO
Gadolinium enhanced MRV
A – CT – B/L frontoparietal
hypodensity
C – CTV – filling defect
within a dilated cortical
vein draining the same
area

D – MRI DWI – restricted

diffusion
edema in FLAIR

Hemorrhage in gradient
echo
 TREATMENT OF CSVT
• CSVT WITHOUT ICH
• Antithrombotic treatment is reccomended in all
guidelines
• RCP – anticoagulation until recanalisation /upto 6
months after thrombosis
• ACCP/AHA – initial UFH/LMWH Until
recanalisation or until 3 to 6 months. IF NO
IMPROVEMENT – thrombectomy / surgical
decompression
• CSVT WITH ICH
• ACCP – no initial anticoagulation – repeat
imaging after 5-7 days , if thrombosis has
progressed – anticoagulation
• AHA – UFH / L;MWH bridging to warfarin upto
3 – 6 months
 OTHER MANAGEMENT
• MANAGEMENT OF RISED ICT
• Malignant ict and ischemic optic neuropathy is a dreaded
complication
• Occurs secondary to thrombosis, narrow venous sinuses, or
communicating hydrocephalus
• Global impaired venous drainage are at increased risk
• regular fundoscopy & serial visual field testing
• Treatment – carbonic anhydrase inhibitors
• Serial lumbar punctures
• Optic nerve sheath fenestration
• Lumboperitoneal shunting
• Septic csvt – antigen specific antibiotics
• Mastoiditis – surgical mastoidectomy
• Removing jugular venous lines
• Altering the chemotherpy
• Replacing depleted anticoagulation factors
• Ensuring full hydration
• Replacing iron stores
• DECOMPRESSIVE HEMICRANIECTOMY
 COMPLICTIONS
• Persistent rised ICT
• Communicating hydrocephalus
• Visual sequelae
• Epilepsy
• Incomplete recanalisation
• Recurrence 13 %
HEMORRHAGIC STROKE
 HEMORRHAGIC STROKE
Occurs when cerebral blood vessels rupture
A neurological emergency – high mortality rate –
aacutely & secondory to high reccurence rate

TYPES SITE
• Abn bld vessels • ICH(75%)
• ( vasc malf)
• SAH(25%)
• Normal bld vessels
• (Bleeding diathesis) • IVH mc in neonates/ or due
to extension from ICH/SAH
ISCHEMIC STROKE HS
• Specific cause less likely • Specific cause more likely
• ---- • Definite treatment often
neurosurgerical intervention
• More mortality
• Less mortality • Better neurological outcome
in survivors
• Poor neurological outcome
in survivors
• ---- • Long term recurrence rate is
quite high
 PATHOPHYSIOLOGY
IPH
• Rupture of arteries
• - larger arteries in congenital aneurysms
• -medium arteries in AVM
• -distal small arteries in mycotic aneurysms
• Intraparenchymal hematoma – disrupt neuronal
structures by – mech means & by compromising
perfusion
• Presence of bld products & damage to BBB- cerebral
edema – neurological deficits, seizures, malignant ICT
 SAH
• Larger prox cerebral arteries within CSF in the
subarachnoid space
• Ruptures and spills blood directly into SAH
• Extend in to brain parenchyma
• RISK OF ISCHEMIC STROKE
• RISK OF HYDROCEPHALUS – communicating /
obstructive
 Clinical features
• Instantaneous severe headache – hallmark of HS - >50%
• But subtle slowly progressive presentations also
common
• Asso with nausea vomitting neck stiffness
• Altered consciousness
• Focal neurological deficit based on site of bleed
• high BP
• Unexplained irritability, behavioural changes , bulging
fontanel may be the presentation in young infants
• Vein of Galen malformation presents with ccf and
macrocephaly
 NEUROIMAGING
• CT brain - high sensitivity 92 – 100% in first 24-48hrs
• CTA – spot sign – contrast enhancement within the
primary ICH – site of active dynamic hemorrhage-
predicts early hematoma &hematoma growth
• MRI – Gradient echo, susceptibiliy weighted – detect
extremely small microbleeds
• CA – gold standard in childhood HS
• Done to define the complete characteristics of vascular
pathology and when interventional procedure is also
planned
AV MALFORMATION
Contrast CT –
enhancement of rt
frontal mass

T1 w MRI – multiple
flow voids

FLOW SENSITIVE
SEQUENCE – shows
flow in abn bld vessels
in AVM
SACCULAR ANEURYSM OF
LT ANT CEREBRAL ARTERY
CT
CT SPIRAL ANGIOGRAPHY
CONVENTIONAL ANGIOGRAPHY
 Risk factors
VASCULAR CONGENITAL
-AVM
-cavernous malformation
-venous angiomas
-Aneurysm - primary, osler weber rendu
synrome
-PHACES
-COL4A1
-FMD

ACQUIRED
-Trauma
-brain tumors
-Arteriopathy – moyamoya, SCD, arterial
dissection , vasculities, post radiation,
-DAVF
-infection- bacterial endocarditis, HIV
Vasculopathy, bacterial meningitis
INTRAVASCULAR / SYSTEMIC COAGULOPATHY
-DIC
-hemophilia
-hematological malignancy

THROMBOCYTOPENIA
-ITP
-TTP
-HUS

HYPERTENSION
IATROGENIC
MEDICATIONS – thrombolytics,
anticoagulants, antiplateletdrugs
 treatment
• NEUROSURGICAL INTERVENTION is required in
60 – 80 %of cases
• Intraventricular drains
• Clipping / coiling of aneurysms
• Removal / emblisation of AVM
• Ventriculoperitoneal shunts
• Revascularsation in moyamoya
 Medical Management Of Underlying
Condition
• Antibiotics for infection
• Replacement of deficient factors
• Reversal of offending drugs
• Immunomodulatory therpy
 Outcome
• Blom et al., - 65 % survival rate, 50% favourable outcome

• Long term morbidity includes

• Hemiparesis – (52%)
• Epilepsy –(17%)
• Visual defects
• Language disorders
• Ataxia
• Hydrocephalus

• Mortality - higher with post fossa hemorrhages

• High recurence rate
picture
 Stroke mimics
DISEASE CLINICAL DISTINCTION FROM IMAGIN G DISTINCTION
STROKE FROM STROKE
MIGRAINE Evolving / marching symptoms , normal
complete resolution, headache,
personel/family h/o migraine
SEIZURE Todds paralysis
INFECTION Fever , encephalopathy, gradual Markers of encephalitis
onset, meningismus diffuse, b/l,
Ineffective treatments
Flow chart
organisation
Perinatal stroke