1. What about Us!: Strokes in Infants, Children and Young Adults
Presentation # 1202
Pritish Bawa1 Deborah L. Reede1 Wendy RK Smoker2
1 SUNY Downstate Medical Center Brooklyn NY
2 University of Iowa Hospitals and Clinics Iowa City IA

2. Disclosure
The authors of this educational exhibit have no disclosures, conflicts of interest or financial relationships with commercial products.

3. Objectives The purpose of this exhibit is to:
Heighten awareness that stroke occurs in infants, children and young adults
Review the demographics, risk factors and etiologies of stroke in various age groups
Learn the imaging findings on various modalities (CT,CTA, MRA, MRV, spectroscopy and transcranial ultrasound)

4. Stroke Definition
WHO defines stroke as “a clinical syndrome of rapidly developing focal or global disturbance of brain function lasting >24 hours or leading to death with no obvious nonvascular cause”
Since this definition is far from ideal for children, researchers use other definitions for pediatric arterial ischemic stroke, such as “any neurological event including seizure associated with an acute infarction shown by MRI”

5. Stroke in Children and Young Adults
Among top 10 causes of death in children
Results in death in 10%, neurologic deficit or seizures in 70% and recurrent stroke in 20%
As common as brain tumors

6. Children and Young Adults
Stroke
Adults
Children and Young Adults
Incidence of Cerebro-vascular events (annual)
Ischemic
/100,000
85%
/100,000
55%
Infants – Higher ischemic stroke
Older children (15-19 years) higher hemorrhagic stroke
Presentation
Etiologies (Common)
Abrupt onset of neurological deficit
Atherosclerotic disease
Carotid stenosis
Atrial Fibrillation
Valvular disease DM
Substance abuse
HBP SAH
Coagulopathies
Anticoagulants
Neonates: seizures, hypotonia, lethargy
Infants: early hand preference (abnormal prior to age of 1 year)
Older infants, children and young adults: abrupt onset of neurological deficit
Hypoxic Ischemic
Congenital cardiac disease, Cardioembolic
Vascular abnormalities FMD, Moyamoya,
Hemoglobinopathies – Sickle cell disease
Prothrombotic states- Protein C/S deficiency, OCPs. Pregnancy, Antiphospholipid syndrome, Nephrotic Syndrome
Infection CNS infection, Myocarditis, Sepsis/septic embolism, HIV, Varicella
Trauma
Cerebral sinovenous thrombosis (CSVT)

7. Epidemiology 5% of all strokes occur in people younger than 45 years
Childhood arterial ischemic stroke (AIS) /100,000 per year
Incidence of neonatal stroke less common approx.1 in 4,000 term live births
Sinovenous thrombosis 0.67/100,000 in children and neonates, over 40% in new born
Hemorrhagic stroke /100,000 children (SAH 0.4/100,000 children)
Peak age for both (ischemic and hemorrhagic – 1st yr. of life)
More common in boys and African American children (not explained by sickle cell disease in this population)

8. Imaging Ischemic Stroke CT vs MR
DWI most sensitive for cytotoxic edema
MRI and MRV preferred for CSVT
MRA especially useful for craniocervical dissection
Disadvantage
- Need cooperative patient or sedation
Sensitive for acute bleeding
Sensitivity decreases with time
Bland infarcts – low density within vascular territory
CSVT – Linear densities in deep and cortical veins
CTA for vascular anatomy, rapid assessment of vascular lesions and arterial dissection
Disadvantage
- AIS usually normal CT in first 12 hrs.
- Radiation and IV contrast for CTA

9. Overview Neonates and Infants Children Young Adults
The etiologies of stroke vary in the pediatric and young adult population. Therefore the following discussion will focus on entities commonly encountered in the various age groups as listed below.
Neonates and Infants
Children
Young Adults
Redo—there are only 40 slides total

10. Classification Ischemic Arterial Ischemic Stroke (AIS)
Cerebral Sinovenous Thrombosis (CSVT)
Hemorrhagic
Intracerebral
Subarachnoid

11. Neonates and Infants (Birth-1yr.)
Stroke is rare in neonates, occur in approx.1 in 4,000 term live births
Clinical signs of are often subtle
Congenital cyanotic heart disease is the most common cause of embolic cerebral infarct in neonates
Common Etiologies
Hypoxia-ischemia
Thrombo-embolism
Infection
Metabolic disease
Trauma
Dr. Ferreti

12. Hypoxic-Ischemic Injury (HII)
Occurs in 1-4 infants per 1,000 live births
Usually related to complicated or difficult delivery
Patterns
- Peripheral
- Basal ganglia–thalamus
Pattern depends on the duration and severity of the
insult

13. Hypoxic-Ischemic Injury Patterns
Depends on the severity and duration of hypoxic or ischemic event .
Mild to moderate
Acute (<10 min) - Usually no significant clinical or imaging sequelae
Prolonged (15–25 min) - shunting maintains blood flow to vital structures (peripheral or watershed pattern of injury)
Imaging
Involves parasagittal, watershed, and borderzone
Seen in cerebral cortex and subcortical white matter with the parieto-occipital and posterior temporal lobes typically more affected than the anterior regions

14. Hypoxic-Ischemic Injury (HII) Patterns
Severe (profound)
Acute (<10 min)
- inadequate shunting
- metabolically active regions are most susceptible
- basal ganglia - thalamus pattern of injury
Prolonged (15–25 min)
- catastrophic
- total brain injury
Imaging
DWI - restricted within the first 24 hrs., compare with ADC
Pseudonormalization at 1 wk
Most useful 1–5 days after an asphyxia event.
T1 - days 3–7 - hyperintensity in posterolateral putamina, ventrolateral thalami, and
corticospinal tracts
Absent posterior limb sign - normal hyperintense focus in posterior limb of internal capsule on T1 may be lost
T2 - 2–3 days - normal hypointense foci seen in posterolateral putamina, posterior limb of internal capsule, and ventrolateral thalamus on T2-weighted images become indistinct or abnormally iso- or hyperintense relative to adjacent white matter

15. Imaging Modality Findings Timing MRS DWI T1 T2 US Increased echo
2-10 days CT
Low attenuation
1-7 days
MRI
DWI
Restricted
1-5 days T1
T1 shortening
2 days - months T2
T2 prolongation
T2 shortening
24 hours
6-7 days - months
MRS
DWI T1 T2
Days of Life
Table demonstrates the sensitivity of conventional imaging modalities for the detection of stroke.
Optimal Time to Perform Each Imaging Technique
Proton MR spectroscopy (MRS) is the most sensitive in 1st 24 hrs. Pseudonormalization at 24 hrs. (black box) due to fall in lactate. DWI is most optimal 1-5 days after injury after which is pseudonormalization.

16. Proton MR Spectroscopy
Increased specificity particularly first 24 hrs. of life
Healthy adult and term neonatal brains do not demonstrate a lactate peak
Pitfalls – Preterm infant (may have elevated lactate and decreased N-acetylaspartate - normal), CSF (normally has lactate, so exclude from voxel), pseudonormalization at 24 hrs.
Secondary rise in lactate levels, known as secondary energy failure, occurs after 24–48 hrs., with lactate level peaking at approximately day 5 after an hypoxic ischemic episode

17. Hypoxic-Ischemic Injury Ultrasound
May have hyperechogenicity in the thalami, globi pallidi, putamina, and periventricular white matter
Typically visible at 2–10 days of life
Decreased restive index (RI) - postulated to be due to impaired cerebral autoregulation
However, RI decreases as gestational age increases and must be correlated with gestational age for accurate results
New born – Transfontanellar US on day 1 of life shows slit like ventricles and slightly increased periventricular and thalamic echogenicity, better appreciated with high frequency transducer.

18. Periventricular Leukomalacia
Neonates and Infants
Periventricular Leukomalacia
Most common result of ischemic brain injury in premature
White matter adjacent to ventricles necrosis and cavitation  shrinkage of cavities with focal enlargement of adjacent ventricle
US: periventricular echoes or cysts
MRI: expansion of posterior portions of ventricles from decreased volume; scalloping of lateral margin of ventricle; atrophy of splenium of corpus callosum; periatrial high T2 white matter signal US
Remove “ultrasound”?
“Premature infant”?
Premie 24 week s/p ex lap for spontaneous intestinal perforation , hypotensive and intubation. Ultrasound shows periventricular cysts on both sides, consistent with periventricular leukomalacia.

19. Long-Term Sequelae Neonates and Infants
Long-term sequelae of the basal ganglia-thalamus pattern of injury include atrophy and chronic mineralization in the thalami, posterior limb of the internal capsule, and basal ganglia
Associated generalized loss of volume in cortical gray matter and subcortical white matter may occur from disruption of normal development of neurons and axonal pathways
Premature infants who suffer moderate hypotension typically sustain injury to the periventricular white matter with sparing of the subcortical white matter and cerebral cortex.
Term infants who suffer from moderate hypotension demonstrate injury to cerebral cortex, particularly watershed areas, which lie between the anterior and middle cerebral arteries, and between the middle and posterior cerebral arteries

20. Periventricular Leukomalacia (PVL)
Neonates and Infants
Periventricular Leukomalacia (PVL)
Periventricular leukomalacia persists in the adult brain, even though the insult occurred in the perinatal period.
Etiology
Hypoxia/ischemia +/- maternal/fetal infection
Differentiating glial cells have high metabolic activity and are vulnerable to hypoxia
Imaging Findings
T2/FLAIR hyperintense signal in the periatrial white matter due to gliosis
Periventricular white matter volume loss
focal ventricular scalloping, dilatation and apparent infolding of the adjacent gyri
Ex-premie child
Ex-premie adult * * * *
8y/o ex-premie with grade III IVH and PVL. T2 MR shows expansion of the posterior portions of lateral ventricles 2nd to decreased posterior white matter volume, and scalloped of contour of occipital horns.
26 y/o with spastic quadriplegia with h/o premature birth, twin B, (26 wk gestation) and neonatal asphyxia. T2 MR shows similar findings of PVL.

21. Illustrations shows the location of watershed areas.
Neonates and Infants
Hypoxia-Ischemia
Full-Term
In term infants, moderate hypotension results in injury to the cerebral cortex particularly in watershed areas, which lie between the anterior and middle cerebral arteries and between the middle and posterior cerebral arteries.
3 y/o with spastic quadriplegia, h/o viral myocarditis at 3 months age. T2 image at 3 yrs. shows increased signal in deep posterior watershed regions. Posterior deep white matter watershed infarct.
Illustrations shows the location of watershed areas.

22. Hypoxia-Ischemia with Large Vessel Occlusion Full- Term
Neonates and Infants
Hypoxia-Ischemia with Large Vessel Occlusion Full- Term
Vascular Occlusion
Left MCA > Right MCA > ACA > PCA. The reason for this distribution is unknown. Hypoxic-ischemic injury complicated by large vessel occlusion in the distribution of the MCA is common.
DWI T2
Full term with neonatal distress delivered by C. Section; cardiac workup negative. Acute Lt.. MCA infarct on Imaging.
DWI at 4 days of age shows restricted diffusion in left MCA territory. T2 image at 4 days of age shows increased signal in left MCA territory.

23. Neonatal Hypoglycemia
Neonates and Infants
Neonatal Hypoglycemia
Glucose is vital to normal brain function
Profound hypoglycemia will result in significant brain damage
Acute signs include jitteriness, seizures, and vomiting
Significant hypoglycemia:
Glucose < mg/dL in premature infants
Glucose < mg/dL in first 24 hrs. in term infants
Glucose < mg/dL after 24 hrs. in term infants
Imaging studies reflect diffuse brain damage:
Most severe in parietal and occipital lobes bilaterally
Acute phase:
- Reduced diffusion with edema of cerebral cortex and underlying white matter
- Lack of gray/white matter distinction
Chronic phase: cortex and white matter show cystic encephalomalacia  atrophy
Glucose in premies

24. Neonatal Hypoglycemia
Neonates and Infants * * T2
DWI
ADC
9 y/o F with spastic quadriplegia, blindness, mental retardation and microcephaly had h/o premature birth & neonatal hypoglycemia. MR shows bilateral occipito-parietal old infarcts with dilatation of the occipital horns. Shunt for hydrocephalus resulted in right subdural collection.
4 day old presented with seizures, found to have hypoglycemia. DWI and ADC maps demonstrate bilateral acute infarcts in the parieto-occipital lobes.

25. Thromboembolic Disease
Neonates and Infants
Thromboembolic Disease
Most focal arterial ischemic infarcts in full-term neonates and infants involve the middle cerebral artery (MCA) distribution. Cyanotic congenital heart disease (CHD) is the most common cause of embolic cerebral infarct in neonates and infants. *
9 m/o with hemiparesis and history of CHD. T2 image demonstrates increased signal in the right posterior MCA territory with dilatation of the occipital horn c/w old right posterior temporal-parietal infarct .

26. Neonates and Infants
Thrombocytosis
Abnormal increase in number of platelets thrombotic state
Can be idiopathic or can be secondary to any of the following:
Infection – (e.g. Meningitis, URI, sepsis
Chronic inflammation and vasculitis (e.g.
inflammatory bowel disease such as
ulcerative colitis)
Tissue damage – (e.g. burns, trauma)
Rebound thrombocytosis (e.g. Iron deficiency anemia)
Postsplenectomy – (e.g. ITP)
Hemolytic anemia – (e.g. Sickle cell)
Renal disorders – (e.g. Nephrotic syndrome)
Malignancy – (e.g., osteosarcoma)
Low birth weight/ preterm infants
Febrile illness with dehydration and thrombocytosis at 6 wks of age with subsequent hemiparesis. T2 at 17 mo. shows increased T2 signal in left ACA/MCA territory and dilated left lateral ventricle c/w old large left ACA/MCA infarct. MRA of Circle of Willis shows decreased flow in left ICA, ACA and MCA.
? Needed ACA, MCA???

27. Protein C/S Deficiency
Neonates and Infants
Protein C/S Deficiency
DWI
MRA
Protein C system
Formed by proteins C and S
Natural anticoagulants that regulate coagulation cascade by inhibiting factors Va. and VIIIa
Deficiency of either protein can be inherited or acquired  hypercoagulable state
Associated with cerebral infarction in children
DWI in a patient with neonatal seizures at 4 days of age shows restricted diffusion in left frontal parietal region c/w acute infarct. MRA of Circle of Willis at 4 days of age shows a paucity of left perisylvian MCA branches.

28. Vein of Galen Malformation
Neonates and Infants
Vein of Galen Malformation
Venous infarcts are diagnosed based on characteristic location and appearance.
Thrombus Site
Infarct Location
Sagittal Sinus
Parasagittal
Straight Sinus / Vein of Galen
Thalamus
Vein of Labbe, Transverse or Sigmoid Sinus
Temporal Lobe
Infarct
Malformation
post embo T1
T1 FS Post
Newborn with a vein of Galen malformation diagnosed on prenatal ultrasound. Sagittal T1 image of a newborn shows a vein of Galen malformation. Post contrast image shows increased signal in right basal ganglia and thalamus after embolization suggesting deep venous infarct.

29. Children (1 yr-14 yrs.) Etiologies: Congenital heart disease
Blood dyscrasias
Metabolic disorders
Vasculopathies
Infection
Trauma
Venous thrombosis
Drug ingestion

30. Carotid Dissection * Imaging Children
Rare and under recognized cause of stroke
7.5% of ischemic strokes in children
Mostly extracranial ICA, typically pharyngeal portion
Recanalization occurs in 60%
Risk of recurrent stroke or TIA is 12%
Imaging
Arteriography – String sign; double lumen sign; short smooth tapered stenosis; and occlusion of parent artery
MR with FS T1 and contrast enhanced MRA are valuable *
15 m/o F with non-accidental trauma. CT shows large hypodense right MCA infarct. No contract is identified in the right internal carotid on axial CTA of the neck . Sagittal image demonstrates short smooth tapered narrowing c/w right carotid dissection.

31. Vertebral Artery Dissection
Children
Vertebral Artery Dissection
rare in childhood
Can occur spontaneously or 2nd to injury (blunt trauma, hyperextension etc...)
Cervical segment of carotid artery > vertebral artery > proximal portions of middle cerebral artery
With a tear in the intima, blood separates the intima from the media forming a hematoma which progressively reduces the arterial lumen and can eventually occlude it T1
Vertebral Angiogram
9 y/o F with stroke-like symptoms.
Selective left vertebral angiogram shows vertebral artery dissection. MR shows high T2 signal in left superior cerebellum indicative of left cerebellar infarct from idiopathic vertebral artery dissection .

32. Stroke in Drowning ChildrenCT
ADC
FLAIR
5 year old boy - Accidental Drowning: Initial CT shows diffuse low attenuation in both cerebral hemispheres with sulcal and ventricular effacement suggesting global hypoxia. Follow up MRI shows restricted diffusion and high FLAIR signal c/w bilateral infarcts in the basal ganglia , midbrain and cortical and subcortical regions.

33. Duchenne Muscular Dystrophy
Children
Duchenne Muscular Dystrophy
No direct causal relationship established
Mostly attributed to cardiomyopathy, cardiac failure and arrhythmias CT
DWI
ADC
14 y/o M with Duchenne Muscular Dystrophy:
NCCT shows dense MCA sign and large hypodense area in left MCA territory, confirmed on DWI and ADC as area of restricted diffusion suggesting acute infarct. Also noted is an old infarct in right basal ganglia.

34. Meningitis Etiology Children Meningitis and encephalitis
are the etiologies of stroke in 10% of
arterial ischemic stroke
Etiology
Vascular inflammation and thrombosis
due to reduced cerebral vascular
perfusion 2nd to systemic hypotension,
increase intracranial pressure and
lowers CSF glucose
Middle ear and paranasal sinus
infections can cause cerebral venous
sinus thrombosis (CVST)
T1 Post Contrast
ADC
DWI
5 y/o F presented with fever, altered mental status and left hemiparesis, diagnosed with meningitis. MR shows extensive meningeal thickening and enhancement, mostly perimesencephalic consistent with meningitis. DWI and ACD demonstrate an acute right thalamocapsular infarct.

35. Cerebral Sinovenous Thrombosis (CSVT)
Children
Cerebral Sinovenous Thrombosis (CSVT)
Defined as the presence of thrombus or flow interruption within cerebral veins or dural venous sinuses
Incidence is 0.67 per 100,000 children per yr. over 40% occur in newborns
Location: superior sagittal, transverse or sigmoid sinuses
Risk factors: dehydration, intracranial infection, hypercoagulable states, anemia, pregnancy and mass lesion compressing the dural sinus
Imaging Findings MR
- MR and MRV are studies of choice
- MR: acute clot appears hypointense (deoxyhemoglobin) on T2; subacute clot appears hyperintense (methemoglobin) on T1 and T2 CT
- NCCT: hyperdense cortical vein, subcortical infarct (commonly hemorrhagic), and brain edema
- CCT: filling defect in dural sinus
Cerebral angiography is still the gold standard especially when CT or MRI are not definitive

36. Venous Thrombosis Children
Incidence of sinovenous thrombosis, as per the Canadian Pediatric Ischemic Stroke Registry, was 0.67 cases per 100,000. Children and neonates were the most commonly affected age group. In neonates, clinical presentation included seizures and diffuse neurologic signs. Clinical presentation in non-neonates typically includes decreased level of consciousness, headache, focal neurological sign and cranial nerve palsies.
Old, chronic or nothing?
FLAIR
T1 Post
Post contrast T1 shows thrombosis in superior sagittal and transverse sinuses in this10 y/o M with headaches. Increase signal is noted in the parasagittal white matter c/w venous infarcts. Illustration demonstrates the location of the intracranial venous structures.

37. Fibromuscular Dysplasia (FMD)
Children
Fibromuscular Dysplasia (FMD)
Common in adult women, rarely in children
20-30% have cerebrovascular involvement
Affects medium and large arteries -- unknown etiology
Overgrowth of smooth muscle and fibrous tissue in the vessel wall
Different appearances: Type I “String of beads” (classic), type II long tubular stenosis, type III confined to portion of arterial wall
Renal artery (60%) > ICA or vertebral arteries (35%) > iliac arteries (3%) > visceral arteries (2%)
Fibromuscular dysplasia is a well-recognized cause of stroke and transient ischemic attacks in adults but a seldom-recognized cause of stroke in children.

38. Fibromuscular Dysplasia
Children T2
MRA Circle of Willis
Neck MRA
3 y/o F with acute right hemiplegia and hypertensive encephalopathy. HTN workup demonstrated renal FMD. Further workup showed intracranial and cervical FMD associated with left frontal and parietal infarcts.
T2 image shows left frontal and parietal encephalomalacia. There is decreased flow in the left ICA, ACA and MCA on an MRA of the Circle of Willis . Neck MRA lateral view demonstrates FMD affecting the mid cervical IAC.

39. Sickle Cell Disease Children - Ischemic in children
25% have CVD by age 45 
-  Ischemic in children 
-  Hemorrhagic in adults  
Most common hematologic risk factor for stroke
High recurrence rate
Narrowing of distal ICA, proximal MCA, and ACA 
Sometimes associated with Moyamoya syndrome with progressive vasculopathy of intracranial ICA with distal collateral vessels
Caused by anemia and hypercoagulable state
Silent infarcts occur in MCA territory and/or border zones 
Occasionally develop sinovenous thrombosis or anterior spinal artery syndrome
FLAIR
MRA
30 y\o M SSD with history of strokes in childhood. MRI shows old infarcts in both ACA territories. MRA shows stenotic ACAs with attenuated branches and prominent lenticulostriate collaterals on the right.

40. Segments of the Circle of Willis
Children
Moyamoya
Described in 1969 by Suzuki and Takaku, means “hazy, like a puff or cloud of smoke.”
Associated with wide range of entities (Sickle cell disease, phakomatoses, Down’s syndrome) or idiopathic 20%
Imaging
Anterior circulation > vertebrobasilar system
MRA: Narrowing of supraclinoid ICA
MRA: Multiple collateral vessels from A1/M1
MRI: “Holes” in basal ganglia on T1 & T2
- Collateral flow in thalamoperforating and lenticulostriate arteries accounts for “puff of smoke” in basal ganglia.
- Dilated and more numerous lenticulostriate arteries
Location of the supraclinoid carotid artery
Segments of the Circle of Willis

41. Moyamoya 2nd to Sickle Cell Disease
Children
Moyamoya 2nd to Sickle Cell Disease
Angiographic ICA staging of steno-occlusive lesions:
Stage I: Narrowing of the carotid bifurcation
Stage II: Dilatation of the ACA and MCA with appearance of ICA moyamoya
Stage III: Partial disappearance of ACA and MCA with intensification of ICA moyamoya
Stage IV: Advanced steno-occlusive stages in ICA with small amount of ICA moyamoya
Stage V: Absence of the ACA and MCA with further reduction of ICA moyamoya
Stage VI: Blood supply only from ECA with almost complete disappearance of ICA moyamoya T1
15 y/o M with h/o SSD and headaches: MRI shows prominent bilateral collateral lenticulostriate vessels. Magnified views shows findings to better advantages. Illustration demonstrates the location of the lenticulostriate arteries.

42. Sickle Cell Disease Children
Sickle cell disease causes progressive cerebral vasculopathy in some patients,
causing overt strokes in 5%-10% and silent strokes in 11%-17% of children.
5 y/o M with multiple previous episodes of TIA and stroke. Neck MRA shows absence of flow in right ICA compared to normal left ICA; MRI brain finding (small area of increase T2 signal in the right centrum semiovale) underestimate right brain vascular pathology. MRA of Circle of Willis shows prominent collateral lenticulostriate vessels. MR findings underestimate left brain vascular pathology.

43. Young Adults (15-30 years old)
Etiologies
Cardiac emboli
Arterial dissection
Recent Pregnancy
Coagulopathy
Vasculitis
Smoking and Drug abuse
Premature atherosclerosis, dyslipidemia and hypertension

44. Drug Abuse Young Adults
Cocaine and amphetamines have the strongest association with stroke
May be most common predisposing condition for stroke in patients <35 y/o
12.1% of patients between y/o with AIS have recent drug use
Mechanism of injury mostly hypertensive surges, vasospasm, enhanced
platelet aggregation, cerebral vasculitis, accelerated atherosclerosis an cardio
embolism
GRE CT T1
DSA
21 y/o F with 10 yr. h/o using molly (molecular pure ecstasy). CT and MR GRE and T1 images shows acute hemorrhage in right frontal lobe and thin right hemispheric subdural hemorrhage. DSA image shows vasoconstriction of the ACA branches.

45. Vasculitis Diagnosis of exclusion Caused by wide range of entities
Young Adults
Diagnosis of exclusion
Caused by wide range of entities
- Collagen vascular disease (systemic)
- CNS infection: Meningitis, encephalitis
- Drugs
- Autoimmune disorder (i.e. primary angiitis of CNS)
Imaging Findings
Angiography:
- Long segments of multiple focal arterial narrowing
- Sensitivity = 70%
CT/MRI – nonspecific findings
- Single or multiple infarcts of various sizes
- Hyperintense white matter lesions on T2
- Leptomeningeal enhancement
MRI advocated as sensitive screening tool with high negative predictive value

46. Primary Angiitis of the CNS
Young Adults
Primary Angiitis of the CNS
Necrotizing Vasculitis with a predilection for the central nervous system (CNS), histologically referred to as granulomatous angiitis of the CNS, of unclear etiology
Nonspecific symptoms include headache, malaise, mental status change, focal neurological deficits and seizure.
Rapidly progressive and frequently fatal
Commonly involves vessels of brain parenchyma and leptomeninges with predilection for small arteries and arterioles
Arteriogram
- Focal or multifocal segmental stenoses of small and medium sized vessels in parenchyma and leptomeninges
- May be abnormal in approximately 85% of cases
- May be negative in 15% of cases – when disease involves precapillary arteriole
14 y/o F with headache and altered mental status. T2 image shows frontal and bilateral parietal cortical and subcortical encephalomalacia.

47. Patent Foramen Ovale (PFO)
Young Adults
Patent Foramen Ovale (PFO)
Remnant of embryological development with clinically important consequences including thromboembolism, stroke and migraine headaches. The proposed mechanisms for stroke include paradoxical embolization, in situ thrombosis within the canal of the PFO, and concomitant hypercoagulable states.
PFO is “the back door to the brain”
Small venous thrombi not filtered by the
pulmonary vasculature enter the
systemic circulation
Can result in infarcts in multiple organs
24y/o M with a PFO presented with multiple pulmonary emboli and right hemiplegia . CT shows a large left MCA territory infarct and a smaller right frontal infarct.

48. Stroke Differential Diagnosis
Complicated migraine typically resolves within 24 hours
  Family history of migraine or hemiplegic migraine
Todd’s paresis (post ictal hemiparesis)
Intracranial neoplasms
Intracranial infections like meningitis, brain abscess, herpes encephalitis
Alternating hemiplegia
Metabolic abnormalities 
- Hypoglycemia
-  MELAS (mitochondrial myopathy, encephalopathy,
lactic acidosis, and stroke) 

49. Strokes in Infants Children and Young Adult Etiologies
Hypoxia-ischemia
- Premature or full term newborn with perinatal distress
- Newborn with hypoglycemia
- Infant with hypoperfusion (e.g. viral myocarditis with hypotension)
Thrombo-embolism
- Cardiac causes (congenital heart disease, vascular dissection, patent foramen ovale, mitral valve prolapse)
- Polycythemia
- Trauma
- Vasculopathy (Sickle cell disease, Moyamoya, FMD, Kawasaki)
Infection (viral or bacterial meningitis)
- Maternal drug abuse
Coagulopathy
- (Protein C/S deficiency, Factor V Leiden, antiphospholipid antibody syndrome)
Vascular malformation (Vein of Galen malformation, AVM)
Metabolic disorders (mitochondrial disorders, hyperhomocysteinemia, lysosomal storage disorders, hyperlipoproteinemia, disorders of cholesterol and triglyceride metabolism)

50. Thank you for viewing our exhibit!
References
Barkovich, A. James, and Charles Raybaud. Pediatric neuroimaging. Lippincott Williams & Wilkins, 2012.
Ciceri, Elisa F., et al. "Paediatric stroke: Review of the literature and possible treatment options, including endovascular approach." Stroke research and treatment 2011 (2011).
Ghei, Sonia K., et al. "MR Imaging of Hypoxic-Ischemic Injury in Term Neonates: Pearls and Pitfalls." RadioGraphics 34.4 (2014):
Esse, Katherine, et al. "Epidemic of illicit drug use, mechanisms of action/addiction and stroke as a health hazard." Brain and behavior 1.1 (2011):
Roach, E. Steve, et al. "Management of stroke in infants and children a scientific statement from a Special Writing Group of the American Heart Association Stroke Council and the Council on Cardiovascular Disease in the Young." Stroke 39.9 (2008):
Seidman, Carly, Fenella Kirkham, and Steven Pavlakis. "Pediatric stroke: current developments." Current opinion in pediatrics 19.6 (2007):
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Zadro, Renata, and Desiree Coen Herak. "Inherited prothrombotic risk factors in children with first ischemic stroke." Biochemia medica 22.3 (2012):
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