- Etiology in neonates:
— Polycythemia
— Thrombosis
— Embolization
— Vasospasm (cocaine)
— Vascular anomaly
— Generalized circulatory failure - Etiology outside of neonates:
— Cerebral arteriopathies
— Acute or chronic systemic conditions
— Cardiac disorders with risk factors being cardiac procedures (surgery, catheterization, ECMO, cardiac support devices) and cardiac conditions (congenital heart disease, valvular heart disease, cardiac arrhythmias, right to left shunt, cardiomyopathy)
— Infection
— In the majority of children no underlying disorder is found - Imaging US in neonates:
— Distribution: Unilateral in 90%, middle cerebral artery distribution in 86%, Left : Right is 3:1
— Early: Diffuse hyperechoic geographic distribution, gyral and sulcal preservation, diminished vascular pulsations
— Intermediate: Progressive increase in echogenicity, loss of anatomic definition, peripheral luxury perfusion
— Late: Atrophy, reduced blood flow - Imaging CT: Loss of gray matter white matter differentiation and effacement of sulci
- Imaging MRI: DWI normalizes within a week
- DDX of stroke mimics: Hemiplegic migraine in aura phase and seizures in interictal phase
— DWI – Negative
— SWI – Non-territorial asymmetric increased venous conspicuity
— ASL – Non-territorial asymmetric decreased perfusion - DDX of stroke mimics: Hemiplegic migraine in headache phase and seizures in ictal phase
— DWI – Negative
— SWI – Non-territorial asymmetric decreased venous conspicuity
— ASL – Non-territorial asymmetric increased perfusion - DDX: Hemorrhagic stroke caused by dural venous sinus thrombosis or arteriovenous malformation
- Complications:
- Treatment:
- Clinical: Can present as a seizure
Imaging evaluation of acute ischemic stroke
- Identify infarct
- Vascular distribution(s)
- Infarct size
- Presence of vasculopathy or arterial clot
- Presence of gross hemorrhage (precludes treatment)
- Perfusion mismatch
Cerebral arteriopathy
- Most common cause of childhood ischemic stroke
- Defined as in situ arterial abnormality on vascular imaging, not attributable to cardioembolism or a congenital variant
— Dissection
— Moyamoya disease
— Sickle cell arteriopathy
— Post varicella arteriopathy
— Vasculitis
— Post-irradiation arteriopathy
— Focal cerebral arteriopathy - Clinical and imaging characteristics associated with childhood arteriopathy subtypes can be used to facilitate their diagnosis and classification
— Dissection: Trauma, cervical artery
— Focal cerebral arteriopathy: Lenticulostriate region, small infarct volume, banding, proximal middle cerebral artery
— Moyamoya disease: High risk demographic and clinical characteristics, more than 1 vascular territory involved, supraclinoid internal carotid artery
— Vasculitis: History of infection, altered mental status
Focal cerebral arteriopathy
- Etiology:
— Acquired unilateral intracranial arteriopathy – distal internal carotid artery, proximal middle cerebral artery, proximal anterior cerebral artery
— Little available histopathologic data but an inflammatory etiology is suspectected - Imaging:
— Unifocal and unilateral stenosis of anterior circulation (distal internal carotid artery and proximal branches)
— Banded appearance of the artery – typically M1 segment with vessel wall enhancement
— Small subcortical infarcts in the basal ganglia or internal capsule - DDX:
- Complications:
- Treatment:
- Clinical:
— Most common etiology of acute ischemic stroke in children
— Most common subtype of cerebral arteriopathy
— Previously healthy children with sudden hemiplegia
— Mean age around 6 years (2-14 years)
— May be called transient cerebral arteriopathy but is misnomer that really means monophasic
— Initial worsening at maximum of 6 months followed by complete regression, improvement, or stabilization
— Stroke recurrence rate of up to 25%
— 30% of young children with arterial ischemic stroke have post-varicella angiopathy
Radiology Cases of Acute Ischemic Stroke
Radiology Cases of Neonatal Acute Ischemic Stroke
Radiology Cases of Chronic Sequelae of Neonatal Acute Ischemic Stroke
