what about us!: strokes in infants, children and young adults pritish bawa 1 deborah l. reede 1...
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What about Us!: Strokes in Infants, What about Us!: Strokes in Infants, Children and Young AdultsChildren and Young Adults
Pritish BawaPritish Bawa1 1 Deborah L. ReedeDeborah L. Reede1 1 Wendy RK SmokerWendy RK Smoker22 1 SUNY Downstate Medical Center Brooklyn NY 1 SUNY Downstate Medical Center Brooklyn NY
2 University of Iowa Hospitals and Clinics Iowa City IA2 University of Iowa Hospitals and Clinics Iowa City IA
Presentation # 1202
Disclosure Disclosure
The authors of this educational exhibit have The authors of this educational exhibit have no disclosures, conflicts of interest or no disclosures, conflicts of interest or financialfinancial relationships with commercial products.relationships with commercial products.
Objectives Objectives
The purpose of this exhibit is to:The purpose of this exhibit is to:
Heighten awareness that stroke occurs in infants, Heighten awareness that stroke occurs in infants, children and young adultschildren and young adults
Review the demographics, risk factors and etiologies of Review the demographics, risk factors and etiologies of stroke in various age groupsstroke in various age groups
Learn the imaging findings on various modalities Learn the imaging findings on various modalities (CT,CTA, MRA, MRV, spectroscopy and transcranial (CT,CTA, MRA, MRV, spectroscopy and transcranial ultrasound)ultrasound)
StrokeStroke DefinitionDefinition
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”
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
Stroke Adults Children and Young Adults
Incidence of Cerebro-vascular events (annual) Ischemic
100-300/100,000
85%
2.5 - 13/100,000
55%Infants – Higher ischemic strokeOlder children (15-19 years) higher hemorrhagic stroke
Presentation
Etiologies (Common)
Abrupt onset of neurological deficit
Atherosclerotic diseaseCarotid stenosisAtrial FibrillationValvular diseaseDMSubstance abuseHBP SAHCoagulopathiesAnticoagulants
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 IschemicCongenital cardiac disease, CardioembolicVascular abnormalities FMD, Moyamoya,Hemoglobinopathies – Sickle cell diseaseProthrombotic states- Protein C/S deficiency, OCPs. Pregnancy, Antiphospholipid syndrome, Nephrotic SyndromeInfection CNS infection, Myocarditis, Sepsis/septic embolism, HIV, VaricellaTraumaSubstance abuseCerebral sinovenous thrombosis (CSVT)
Epidemiology 5% of all strokes occur in people younger than 45 years Childhood arterial ischemic stroke (AIS) 0.2-7.9/100,000 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 0.7-5.1/100,000 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)
Imaging Ischemic StrokeCT vs MR
MR DWI most sensitive for cytotoxic DWI most sensitive for cytotoxic
edemaedema MRI and MRV preferred for CSVT MRI and MRV preferred for CSVT MRA especially useful for MRA especially useful for
craniocervical dissectioncraniocervical dissection
Disadvantage - Need cooperative patient or - Need cooperative patient or
sedationsedation
CT Sensitive for acute bleedingSensitive for acute bleeding Sensitivity decreases with timeSensitivity decreases with time Bland infarcts – low density within Bland infarcts – low density within
vascular territoryvascular territory CSVT – Linear densities in deep CSVT – Linear densities in deep
and cortical veinsand cortical veins CTA for vascular anatomy, rapid CTA for vascular anatomy, rapid
assessment of vascular lesions assessment of vascular lesions and arterial dissectionand arterial dissection
Disadvantage - AIS usually normal CT in first 12 - AIS usually normal CT in first 12
hrs.hrs.
- Radiation and IV contrast for CTA- Radiation and IV contrast for CTA
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.
Classification
Ischemic Arterial Ischemic Stroke (AIS) Cerebral Sinovenous Thrombosis (CSVT)
Hemorrhagic Intracerebral Subarachnoid
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
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
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
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
Hypoxic-Ischemic Injury (HII)Patterns
Imaging
Modality Findings Timing
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
Optimal Time to Perform Each Imaging TechniqueProton 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.
Table demonstrates the sensitivity of conventional imaging modalities for the detection of stroke.
MRS
DWI
T1
T2
1 2 3 4 5 6Days of Life
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
Hypoxic-Ischemic InjuryUltrasound
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.
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
Neonates and Infants
USPremie 24 week s/p ex lap for spontaneous intestinal perforation , hypotensive and intubation. Ultrasound shows periventricular cysts on both sides, consistent with periventricular leukomalacia.
Long-Term Sequelae
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
Neonates and Infants
Periventricular Leukomalacia (PVL)
Etiology
Hypoxia/ischemia +/- Hypoxia/ischemia +/- maternal/fetal infectionmaternal/fetal infection
Differentiating glial cells have Differentiating glial cells have high metabolic activity and arehigh metabolic activity and are vulnerable to hypoxiavulnerable to hypoxia
Imaging Findings
T2/FLAIR hyperintense signal T2/FLAIR hyperintense signal
in the periatrial white matter in the periatrial white matter
due to gliosisdue to gliosis Periventricular white matter Periventricular white matter
volume lossvolume loss focal ventricular scalloping,
dilatation and apparent infolding of the adjacent gyri
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.
Ex-premie child Ex-premie adult
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.
Neonates and Infants
Periventricular leukomalacia persists in the adult brain, even though the insult occurred in the perinatal period.
*** *
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.
Hypoxia-Ischemia Full-Term
Neonates and Infants
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.
Illustrations shows the location of watershed areas.
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.
T2
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.
Hypoxia-Ischemia with Large Vessel Occlusion Full- Term
DWI
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 < 20-40 mg/dL in premature infants Glucose < 30-35 mg/dL in first 24 hrs. in term infants Glucose < 40-45 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
Neonates and Infants
Neonatal Hypoglycemia
4 day old presented with seizures, found to have hypoglycemia. DWI and ADC maps demonstrate bilateral acute infarcts in the parieto-occipital lobes.
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.
* *T2
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 .
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.
Thromboembolic DiseaseNeonates and 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.
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
ThrombocytosisNeonates and Infants
Abnormal increase in number of platelets thrombotic state
Protein C/S Deficiency
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
Neonates and Infants
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.
DWI MRA
Thrombus Site Infarct LocationSagittal Sinus ParasagittalStraight Sinus / Vein of Galen ThalamusVein of Labbe, Transverse or Sigmoid Sinus
Temporal Lobe
Vein of Galen MalformationVenous infarcts are diagnosed based on characteristic location and appearance.
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.
InfarctInfarct
MalformationMalformationpost embopost embo
T1T1 FS Post
Neonates and Infants
Children (1 yr-14 yrs.)
Etiologies:• Congenital heart disease• Blood dyscrasias• Metabolic disorders• Vasculopathies• Infection• Trauma• Venous thrombosis• Drug ingestion
Carotid DissectionCarotid Dissection
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.
Children
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
Vertebral Artery Dissection
•..
9 y/o F with stroke-like symptoms.Selective left vertebral angiogram shows 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
Children
Vertebral Angiogram T1
Stroke in DrowningChildren
5 year old boy - Accidental Drowning:5 year old boy - Accidental Drowning:
Initial CT shows diffuse Initial CT shows diffuse low attenuation in both cerebral hemispheres low attenuation in both cerebral hemispheres with with sulcal and ventricular effacement suggesting global hypoxia. Follow up MRI sulcal and ventricular effacement suggesting global hypoxia. Follow up MRI shows shows restricted diffusion and and high FLAIR signal c/w bilateral infarcts in the signal c/w bilateral infarcts in the basal ganglia , midbrain and cortical and subcortical regions.
CT ADCFLAIR
Duchenne Muscular Dystrophy• No direct causal relationship established• Mostly attributed to cardiomyopathy, cardiac failure and arrhythmias
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.
Children
CT DWI ADC
Meningitis
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.
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
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
Children
Venous Thrombosis 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.
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.
T1 Post FLAIR
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.
Children
Fibromuscular Dysplasia
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.
Children
T2 MRA Circle of Willis Neck MRA
Sickle Cell Disease
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
Children
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.
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
Children
Moyamoya 2nd to Sickle Cell Disease
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.
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
Children
Sickle Cell DiseaseSickle cell disease causes progressive cerebral vasculopathy in some patients,
causing overt strokes in 5%-10% and silent strokes in 11%-17% of children.
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.
Young Adults (15-30 years old)
Etiologies
Cardiac emboli Arterial dissection Recent Pregnancy Coagulopathy Vasculitis Smoking and Drug abuse Premature atherosclerosis,
dyslipidemia and hypertension
GRE
Drug AbuseDrug Abuse
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.
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 15-44 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
CT T1 DSA
Young Adults
Vasculitis
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
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
Young Adults
14 y/o F with headache and altered mental status. T2 image shows frontal and bilateral parietal cortical and subcortical encephalomalacia.
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.
Young Adults
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)
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)
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References
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