PRESENTED BY GUIDED BY

PRACHITI KARODE DR NILESH JAIN

DR PRAMILA RAMAWAT
Acute onset of a focal neurologic
deficit in a child is stroke until
proved otherwise.

NELSON
Stroke is defined by the World Health Organization as a
clinical syndrome consisting of rapidly developing
clinical signs of focal (or global in case of coma)
disturbance of cerebral function lasting more than 24
hours or leading to death with no apparent cause other
than a vascular origin.
 Broadly Pediatric stroke includes:
1) Ischemic stroke.
2)Hemorrhagic stroke.

 Ischemic stroke includes :

1 )Arterial ischemic stroke (AIS)
 AIS is the focal brain infarction that results from occlusion of the arteries
supplying brain.
 AIS is a leading cause of acquired brain injury in children.
 The perinatal period carries the highest risk for ischemic stroke.

2)Cerebral Sinovenous thrombosis-

 Thrombotic occlusion of the veins supplying brain causes CSVT.
 It can create increased ICP , cerebral edema & in 50% of cases venous
infarction or hemorrhage (stroke)
 CSVT is m/c in children than in adults & its risk is greatest in neonatal period.
Pediatric stroke can also be subdivided into :
1)Perinatal stroke ( 28wk gestation- 28 days after birth)
 Perinatal AIS- 2 distinct clinical presentations.
Acute symptomatic neonatal AIS presents with focal seizures at 24-28 hr
of life .Focal abnormalities in an arterial territory confirm recent
infarction.
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
.
 Neonatal CSVT
2)Late childhood stroke ( 1month – 18yr of age)
 In AIS, severity of cerebral tissue damage is a
function of multiple factors, including
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, and
5)concurrent disease processes and metabolic
demands of the ischemic brain tissue.
 Initial ischemic neuronal dysfunction evolves to irreversible infarction with
increasing duration and/or degree of ischemia, or increased rates of neuronal
metabolic activity.

 In AIS a central core zone of decreased perfusion results in irreversibly

damaged brain. Surrounding this core is an unstable penumbral zone where
collateral perfusion may sustain neuronal viability.

 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.

 Secondary insults include seizures and alterations in temperature, blood

pressure, and serum glucose.

 The primary objective of acute neuroprotective stroke treatment is to rescue this

“at-risk” penumbral tissue to salvage functional brain.
 RISK FACTORS FOR STROKE

AIS HAEMORRHAGIC
CSVT STROKE

1)Vascular disease
1)Arteriopathy 1)Blood coagulation •AVM
•TCA •Prothrombotic •Cavernous
•cPACNS conditions malformation
•Moya Moya Ds/Syndrome •Dehydration 2)Blood disorders
•Vasculitis •IDA •ITP
2)Cardiac •Acute systemic illness •HUS
•CHD •Nephrotic syndrome •Vit K deficiency
•Iatrogenic •2)Blood vessel •Liver failure
•Arrythmia Infection 3)Trauma
3)Hematologic Trauma SDH
•SCA Venous malformation EdH
•IDA Compression SAH
•Prothrombotic conditions Iatrogenic Iatrogenic
Transient Cerebral Arteriopathy (TCA)
 A common syndrome affecting healthy school-age children.
 Unilateral irregular stenosis of the proximal middle cerebral
artery and neighboring arteries presenting with basal ganglia
infarction.
 Synonyms-Post varicella angiopathy (PVA) , nonprogressive
childhood primary angiitis of the central nervous
system(cPACNS), focal cerebral arteriopathy(FCA) .
 Self-limited
Moya Moya Disease
 Progressive occlusion of the distal internal carotid arteries.
 Blood flow is blocked by the constriction, and also by thrombosis.
 A collateral circulation develops around the blocked vessels to
compensate for the blockage, but the collateral vessels are small,
weak, and prone to bleeding, aneurysm and thrombosis. On
conventional MR angiography, these collateral vessels have the
appearance of a "puff of smoke" (described as (moyamoya) in
Japanese).
 Moya Moya Disease-no underlying correlational conditions.
Usually arterial constriction and collateral circulation are bilateral.
 Moya Moya Syndrome - Moyamoya syndrome is unilateral
arterial constriction and is associated with other conditions
like Neurofibromatosis type 1, Trisomy 21, Alagille
syndrome, Sickle cell anemia, Chromosomal
microdeletions/microduplications, Postirradiation.

 Treatment is usually surgical bypass.


T1-weighted MR image of moyamoya
disease. Flow void in the basal ganglia is
indicated by the arrow.
ICA injection in a conventional cerebral
angiogram in a child with moyamoya disease
revealing stenosis of the supraclinoid ICA
(white arrow ) with formation of an extensive
network of collateral vessels .
 The acute onset of focal neurologic deficits in
childhood is a stroke until proven otherwise.
 Hemiparesis is the most common presentation
of AIS in childhood.
( Middle cerebral artery territory – M/c location of
infarcts in children).
 Other focal deficit include dysarthria, dysphasia,
facial weakness, vertigo, abnormal eye
movements, sensory disturbance, ataxia, and
neglect.
 Anterior Cerebral Artery Lesions
 Paracentral Lobule- Paralysis of c/l Leg and feet and Urinary
Incontinence.
 Reappearance of Primitive Reflex.
 Gait Apraxia

 Middle Cerebral Artery Lesions

 Contralateral Hemiplegia and C/L hemisensory Loss.
 Brocas Aphasia
 Cognitive and Behavioural impairment
 All other features suggestive of Parietal and temporal lesions.
 Posterior Cerebral Artery Lesion
 Basal Ganglia- Contralateral Hemiparesis; coma; Cheyne
stroke respiration; Dilated and fixed Pupil
 Thalamus- Hemisensory loss of C/L side; ocular disturbances.
 Pons- Quadriplegia; deep coma; Decerebrate rigidity;
Pinpoint pupil
 Cerebellum- Occipital headache; vomiting; Dizziness;
vertigo; gait ataxia; dysarthria; dysphagia.
 Paracentral lobule lesions (medial frontal lobe)
Contralateral lower limbs weakness and urinary incontinence.
 Parietal lobe lesions
Unilateral lobe- c/l hemisensory loss; astereognosis;
agraphasthesia
Dominant hemisphere-
Dysphasia,dyslexia,dyscalculia,apraxia,agnosia,Gerstman
syndrome
Non Dominant hemisphere- Neglect of contralateral side,
Spatial Disorientation, Constructional apraxia, Dressing apraxia,
Anosognosia
 Temporal Lobe Lesion-
Unilateral- C/L upper quadrantanopia ; complex hallucinations
Bilateral- Deafness; Apathy; Impaired learning and memory;
amnesia
Dominant Hemisphere - Wernicke’s aphasia , Anomic
aphasia,Dyslexia,Impaired verbal memory, Word agnosia,
word deafness
Non Dominant Hemisphere - Impaired non-verbal memory,
Impaired musical skills,Prosopagnosia.
SITE OF LESION FINDINGS
Cortex Seizures
Cortical sensory loss
Aphasia
Corona radiata Complete hemiplegia, no seizure
Internal capsule Complete hemiplegia,
Often sensory loss
Midbrain Contralateral hemiplegia with ipsilateral 3 & 4th
CN paralysis (weber syndrome)
Pons Contralateral hemiplegia with ipsilateral 6 & 7th
CN paralysis b (millard-gubler syndrome)
Medulla Contralateral hemiplegia with ipsilateral seventh
CN paralysis
2 different clinical presentations in perinatal period
1)Acute symptomatic neonatal AIS-
 Presents with focal seizures at 24-28 hr of life .
 MRI diffusionabnormalities in an arterial territory
2) Asymptomatic at birth
 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.
 Clinical presentation are typically gradual, variable & non
specific compared to AIS.

 Neonates often present with encephalopathy and

seizures.

 Children may present with symptoms mimicking

idiopathic intracranial hypertension including progressive
headache , papilledema , diplopia secondary to 6th nerve
palsy , seizures, lethargy ,confusion.
 Clinical presentation varies according to site,
cause and rate of bleeding.

 Acute bleeding : thunderclap headache, loss of

consciousness, neurological deficits and
seizures.

 Associated with vascular malformations:

pulsatile tinnitus, cranial bruits, high output
heart failure,macrocephaly.
 AIS is a clinical and radiographic diagnosis.
 CT imaging can demonstrate mature AIS
 and exclude hemorrhage.
 MRI is required to identify early and small infarcts.
Diffusion-weighted MRI demonstrates AIS within
minutesof onset and up to 7 days postonset;
 Diffusion-weighted MRI can also demonstrate
wallerian degeneration in the descending
corticospinal tract, which correlates with chronic
hemiparesis.
 MR angiography can confirm vascular occlusion and
suggest possible arteriopathy.
 Conventional angiography (CA) - the gold standard for
cerebrovascular imaging.
 Nonenhanced CT is very insensitive for CSVT, and contrast
CT venography or MR venography is necessary to
demonstrate filling
defects in the cerebral venous system.
 MRI offers superior parenchymal imaging compared to CT.
o ECG, CXR, ECHO
o Carotid doppler study
o Hematological - CBC, platelet count, clotting factor
o Neuroimaging
o Collagen vascular screen: ANA , RF , lupus anticoagulant,
anticardiolipin antibodies
o Coagulation profile: PT, APTT, protein C & S, antithrombin III
o Others: VDRL, HIV, lactate, pyruvate, homocystein,
urinary/serum aminoacids/organic acids
Acute management
 Prevention of Recurrent Stroke
 Rehabilitation
 Maintain Airway, Breathing, Circulation

 Management of raised ICT, BP

 Maintain normoglycemia

 Maintain normal body temperature

 Management of seizures

 Treat the specific cause

There is consensus between the guidelines on the
treatment of
 AIS in sickle cell disease
 Nonhaemorrhagic CSVT
 AIS due to cardiogenic embolism or
dissection
 AIS due to vasculopathy
 CHEST Guideline
Neonatal AIS
General No anticoagulants or ASA

Cardioembolic UFH or LMWH for 3 months

Acute childhood AIS

General UFH or LMWH for 5 to 7 days and until
cardioembolic and dissection excluded

Sickle cell disease Intravenous hydration and exchange

transfusion to HbS < 30%

Alteplase Not recommended

 CHEST guideline

Maintainence therapy in childhood

AIS

General For all children with AIS treat with ASA 2 – 5 mg/kg/day
after anticoagulation therapy has been stopped

Dissection After 5 – 7 days UFH or LMWH , treat with LMWH or

warfarin for 3 – 6 months

Cardiogenic embolism After 5 – 7 days UFH or LMWH, treat with LMWH or

warfarin for 3 – 6 months

Vasculopathy ASA 2 – 5 mg/kg/day after anticoagulation therapy has been

stopped

Sickle cell disease Long term blood transfusion

 Outcome of childhood stroke is better than adult stroke.

 Most survivor suffer from some neurological morbidity.

 Language, motor disability , cognitive ,behavioral & psychosocial

therapy is required.

 Constraint induced movement therapy is an upcoming modality to

improve hand function.
 Risk of recurrent stroke in neonates with AIS is < 5%
however , in older infants and children risk is 10-25%
 In AIS treatment without antithrombotic drugs, recurrence
rates is 50%
 In AIS conditions associated with high recurrence rates :
 unilateral intracranial vasculopathy [postvaricella angiopathy
, TCA]
 prothrombotic states [ protein C deficiency & high conc of
lipoprotein A]

 In CSVT prothrombotic states have a prominent etiological

role.
 Presence of multiple risk factors increases recurrence risk.
DISORDER DISTINCTION FROM STROKE
Migraine Evolving or “marching”
symptoms, short duration,
complete resolution, headache,
personal or family
history of migraine
Seizure Positive symptoms, Todd
paralysis is postseizure
and limited
Infection Fever, encephalopathy, gradual
onset, meningismus
IMAGING DISTINCTION FROM
STROKE
Typically normal
Migrainous infarction is rare
Normal or may identify source of
seizures (e.g.,
malformation, old injury, etc.)
Normal or signs of
encephalitis/cerebritis, which
are typically diffuse and bilateral.
Arterial
ischemic stroke and cerebral
sinovenous
thrombosis can occur in bacterial
meningitis
Demyelination Gradual onset, multifocal symptoms, Multifocal lesions,
encephalopathy characteristic appearance
Accompanying optic neuritis or (e.g.,
transverse myelitis patchy in acute disseminated
encephalomyelitis,
ovoid in multiple sclerosis),
typical locations
(e.g., pericallosal in multiple
sclerosis), less likely
to show restricted diffusion

Hypoglycemia Risk factor (e.g., insulin therapy), Bilateral, symmetrical

related to meals, May see restricted diffusion
additional systemic symptoms

Hypertensive Documented hypertension, bilateral Posterior dominant, bilateral,

encephalopathy visual patchy lesions
(posterior reversible symptoms, encephalopathy involving gray and white
leukoencephalopathy matter, usually no
) restricted diffusion

Inborn errors of Preexisting delays/regression, bilateral,

metabolism multisystem disease, Symmetrical lesions, not
abnormal biochemical profiles within vascular territories.
CASES
A healthy 3 yr old boy had sudden onset of left-sided weakness. Examination also demonstrated left-sided
hemisensory loss and neglect. A to C, Diffusion-weighted MRI shows focal increased signal in the right temporal–
parietal region in the territory of the middle cerebral artery (MCA). D, Apparent diffusion coefficient map confirms
restricted diffusion consistent with infarction (ischemic stroke). E, MR angiogram shows decreased flow in the
corresponding branch of the MCA. F, Follow-up MRI at 3 mo shows atrophy and gliosis in the same region
 Perinatal Arterial Ischemic Stroke
A term newborn developed focal right-sided seizures at 16 hr of life.
Diffusion-weighted MRI on day 2 diagnoses neonatal arterial ischemic stroke by
demonstrating restricted diffusion in the left middle cerebral artery territory.
B, Repeat MRI at 12 mo shows cystic encephalomalacia and scarring in the same
territory, a similar appearance to children diagnosed with presumed perinatal
arterial ischemic stroke later in infancy.
 A 9 yr old girl presented with fever and progressive right-sided headache. She
complained of double vision and had papilledema on examination.
Axial (A) and coronal (B) CT venography demonstrates a large thrombus in the right
transverse sinus that fails to opacify with contrast (full arrows).
Note normal filling in superior sagittal and in smaller left transverse sinuses (empty
arrows,
right) and opacification of the mastoid air cells (hatched arrow, left).
Cause was otitis media/mastoiditis with septic thrombophlebitis of transverse
sinus.
Hemorrhagic stroke. A healthy 1 mo old presented with sudden-onset irritability followed by focal left body
seizures.
Plain CT head demonstrates a large hyperdense lesion in the right parietal region with surrounding edema
consistent with acute hemorrhage (A).
Axial (B) and sagittal (C) contrast CT scans suggest an abnormal cluster of vessels in the center of the hemorrhage
consistent with an AVM. T2-weighted MRI differentiates the acute hemorrhage from surrounding edema (D).
Gradient echo MRI, both acutely (E) and at 3 mo (F), demonstrates the presence of blood product.
 Nelson’s textbook of Pediatrics,20th Edition
 Swaiman’s Pediatric Neurology,6th Edition
 AHA/ASA 2019 guidelines for management
of stroke in neonates and children
Thank you