Corpus callosum atrophy in adolescents with antecedents of moderate perinatal asphyxia

Background: The corpus callosum (CC) is a cerebral structure that reflects cognitive status in several neurological pathologies. Visual inspection of MRI has shown that hypoxic-ischemic encephalopathy (HIE) causes callosal damage. Primary objective: To quantify the CC surface in a sample of patients...

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Detalles Bibliográficos
Autores: Mañeru Zunazarren, Cristina, Junqué i Plaja, Carme, 1955-, Salgado Pineda, Pilar, Serra y Grabulosa, Josep Ma., Bartrés Faz, David, Ramírez Ruiz, Blanca, Bargalló Alabart, Núria, Tallada, Mercé, Botet Mussons, Francisco
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2003
País:España
Institución:Universidad de Barcelona
Repositorio:Dipòsit Digital de la UB
OAI Identifier:oai:diposit.ub.edu:2445/226900
Acceso en línea:https://hdl.handle.net/2445/226900
Access Level:acceso abierto
Palabra clave:Neurologia pediàtrica
Lesions cerebrals
Asfíxia neonatal
Pediatric neurology
Brain damage
Asphyxia neonatorum
Descripción
Sumario:Background: The corpus callosum (CC) is a cerebral structure that reflects cognitive status in several neurological pathologies. Visual inspection of MRI has shown that hypoxic-ischemic encephalopathy (HIE) causes callosal damage. Primary objective: To quantify the CC surface in a sample of patients with antecedents of HIE and a group of matched controls. Research design: Comparisons of CC measures among control subjects, mild HIE patients and moderate HIE patients as well as correlates of CC surface and neuropsychological performance. Methods: Twenty-one adolescent patients with childhood antecedents of HIE were compared to 21 controls. ANALYZE software was used to semi-automatically measure the CC area. Main outcomes and results: Patients with moderate HIE showed corpus callosum reduction. The isthmus and genus were the most affected regions. Corpus callosum size correlated with cognitive function. Conclusions: Corpus callosum quantification provides new evidence of subtle residual deficits in subjects with HIE antecedents without apparent neurological sequelae.