Clinical and Imaging Features of Intracranial Arterial Aneurysms in the Pediatric Population
ABSTRACT Intracranial arterial aneurysms (IAAs) are rare in children. Nevertheless, IAAs account for at least 10%-15% of hemorrhagic strokes during the first 2 decades of life. Traditional vascular risk factors, which are common in the adult population, are generally absent in the pediatric population, engendering distinct modes of IAA pathogenesis. Classification of pediatric IAAs according to the pathogenetic mechanism shows eight distinct categories: idiopathic, traumatic, those due to excessive hemodynamic stress, vasculopathic, infectious, noninfectious inflammatory, oncotic, and familial. Pathogenetic mechanism is the best predictor of the clinical course of the disease, response to treatment, and long-term prognosis. The pathogenetic subtypes of pediatric IAA show characteristic and variably overlapping features. In most cases, IAAs manifesting during the first 2 decades of life are idiopathic. IAAs that are idiopathic, traumatic (second most common type), or due to excessive hemodynamic stresses (third most common type) account for more than 80% of IAAs in the pediatric age group. Most of the remaining pediatric IAAs are the result of congenital cerebral aneurysmal arteriopathies or infection. Multiple IAAs are unusual in young children except in those with acquired (secondary to immune deficiency states) or congenital cerebral aneurysmal arteriopathies or infectious IAAs.
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ABSTRACT: Intracranial aneurysms are extremely rare in infants, and to our knowledge only seven infants treated for ruptured spontaneous dissecting aneurysms have been reported. Good outcomes have been achieved with endovascular treatment of infantile aneurysm. We the endovascular treatment of a one-month-old girl for ruptured dissecting aneurysm located in the anterior communicating artery, and the unique radiological changes that were observed during the perioperative and follow-up periods. These changes suggest that blood coagulation and fibrinolytic response play a part in the repair and healing processes of dissecting aneurysms. Careful neuroradiological surveys are needed for pediatric dissecting aneurysms treated endovascularly.Interventional Neuroradiology 12/2014; 20(6):796-803. DOI:10.15274/INR-2014-10093 · 0.73 Impact Factor
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ABSTRACT: BACKGROUND AND PURPOSE: Little is known about calcifications associated with pediatric intracranial arterial aneurysms (IAA). We sought to characterize calcifications associated with pediatric IAA according to aneurysm pathogenetic subtype. MATERIALS AND METHODS: Patients with IAA less than 20 years of age were retrospectively identified. Three fellowship-trained neuroradiologists independently reviewed each patient's CT studies for calcifications of the parent artery or aneurysm. Aneurysmal calcification (ANC) was correlated with characteristics of the patient (age, sex) and aneurysm pathogenetic subtype, size, morphology, rupture status, and location. RESULTS: Thirty-three patients (mean age 10 years) with 43 IAA were analyzed. There were no parent artery calcifications. Nine IAA were calcified. IAA in children with non-hemodynamic risk factors (arteriopathy, trauma, infection, tumor) were more commonly calcified than idiopathic IAA (p = 0.029). More than one third of the pediatric IAAs in this group (arteriopathy, infection trauma, tumor) were calcified. IAA ≥ 10 mm were more likely to be calcified (p = 0.03). IAA that were ruptured at presentation were less likely to be calcified (p = 0.03). ANC was not significantly associated with patient age (≤10 years vs. >10 years), sex, morphology (fusiform vs. saccular) or location (anterior vs. posterior circulation). CONCLUSION: Aneurysmal but not parent artery calcifications are associated with a significant minority of pediatric IAA. Pediatric ANCs are associated with underlying non-hemodynamic vascular risk factors (arteriopathy, infection, trauma, and tumor), size ≥10 mm and non-hemorrhagic presentation.Child s Nervous System 12/2012; 29(4). DOI:10.1007/s00381-012-1985-4 · 1.16 Impact Factor