Postnatal cerebellar development in preterms with postconceptional age at term equivalent. A neuropathological study

Autores
Jones, Marta
Año de publicación
2008
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
To evaluate postnatal development, we analyzed 65 cerebella from preterm neonates at term-gestational-age equivalent, separated into 2 groups: Group I (GI), cerebellar weight (cw) up to 14 g; Group II (GII), cw more than 14 g. The control group (CG) consisted of 20 term neonates up to 6 days old. Morphometry showed: diminished size, expressed as a coefficient (GI: 2.2; GII:2.9; CG:3.68) and cw [g] (GI:9.8; GII:17.9; CG:26.71); in the lobes, diminished foliar height [μm] (inferior folia; GI: 3.486; GII:4.764; CG:6.458) and foliation; diminished cortical width [μm] (GI:63.9; GII:74.5; CG:92.27), and a high number of Purkinje cells per segment (GI:33.6; GII:21.4; CG:13.95). These results correlated significantly with each other, with brain weight, and to a lesser degree with body weight. No high correlation with gestational age was found. Brain lesions and different serious and protracted illnesses were more frequent in GI. Histology: necrosis and apoptosis of the immature cerebellar cortex as well as reactive astrocytosis and gliosis of the white matter were observed. These findings related to hypoxia-ischemia, infections, and therapies. In summary, the cases examined in this study evinced cerebellar patterns similar to those of 30-32 (GI) and 33-35 (GII) weeks of gestational age, although these preterm neonates had completed a postconceptional age of 37 to 42 weeks. These findings may be interpreted as having resulted from the action of noxa during the cerebellar lobes' vulnerability window. Direct injury of cerebellar cortex and white matter is a fundamental and poorly recognized cause of impaired cerebellar growth.
Para evaluar el desarrollo postnatal se analizaron 65 cerebelos de recién nacidos pretérmino con edad postconcepcional equivalente al término en dos grupos (Grupo I (GI): peso cerebeloso (pc) hasta 14grs; Grupo II (GII): pc superior a 14grs), y 20 controles (C) (recién nacidos de término hasta 6 días de vida). Se halló: reducción del tamaño (medido con un coeficiente) (GI:2,2; GII:2,9; C:3,68), y pc (en grs) (GI:9,8; GII:17,9; C:26,71); en hemisferios, reducción de altura de folias (en μm) (folias inferiores: GI:3486; GII:4764; C:6458) y su ramificación, del espesor cortical (mo-lecular + granos externa en μm) (GI:63,9; GII:74,5; C:92,27), y elevado número de células de Purkinje por segmento (GI:33,6; GII:21,4; C:13,95). Estos resultados se correlacionaron significativamente entre sí y con el peso corporal y cerebral. No se halló una alta correlación con la edad gestacional. Las lesiones cerebrales, y enfermedades ocurridas durante la hospitalización fueron más frecuentes en el GI. Además se halló necrosis y apoptosis en la corteza cerebelosa inmadura, y astrocitosis reactiva y gliosis en la sustancia blanca, vinculables a hipoxia-isquemia, infecciones y/o tratamientos. En conclusión, los casos analizados presentaron una detención del desarrollo con un patrón similar al de cerebelos de 30-32 (GI) y 33-35 (GII) semanas de EG, a pesar de haber completado una edad postconcepcional equivalente al término. Los hallazgos pueden ser interpretados como resultado de la acción de noxas durante la ventana de vulnerabilidad de los hemisferios cerebelosos. Las lesiones primarias y directas de la corteza cerebelosa y de la sustancia blanca constituyen una causa fundamental y poco jerarquizada de alteración del desarrollo cerebeloso.
Materia
Pediatría
Cerebelo
Encefalopatías
neuropatología
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by/4.0/
Repositorio
CIC Digital (CICBA)
Institución
Comisión de Investigaciones Científicas de la Provincia de Buenos Aires
OAI Identificador
oai:digital.cic.gba.gob.ar:11746/2950

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oai_identifier_str oai:digital.cic.gba.gob.ar:11746/2950
network_acronym_str CICBA
repository_id_str 9441
network_name_str CIC Digital (CICBA)
spelling Postnatal cerebellar development in preterms with postconceptional age at term equivalent. A neuropathological studyJones, MartaPediatríaCerebeloEncefalopatíasneuropatologíaTo evaluate postnatal development, we analyzed 65 cerebella from preterm neonates at term-gestational-age equivalent, separated into 2 groups: Group I (GI), cerebellar weight (cw) up to 14 g; Group II (GII), cw more than 14 g. The control group (CG) consisted of 20 term neonates up to 6 days old. Morphometry showed: diminished size, expressed as a coefficient (GI: 2.2; GII:2.9; CG:3.68) and cw [g] (GI:9.8; GII:17.9; CG:26.71); in the lobes, diminished foliar height [μm] (inferior folia; GI: 3.486; GII:4.764; CG:6.458) and foliation; diminished cortical width [μm] (GI:63.9; GII:74.5; CG:92.27), and a high number of Purkinje cells per segment (GI:33.6; GII:21.4; CG:13.95). These results correlated significantly with each other, with brain weight, and to a lesser degree with body weight. No high correlation with gestational age was found. Brain lesions and different serious and protracted illnesses were more frequent in GI. Histology: necrosis and apoptosis of the immature cerebellar cortex as well as reactive astrocytosis and gliosis of the white matter were observed. These findings related to hypoxia-ischemia, infections, and therapies. In summary, the cases examined in this study evinced cerebellar patterns similar to those of 30-32 (GI) and 33-35 (GII) weeks of gestational age, although these preterm neonates had completed a postconceptional age of 37 to 42 weeks. These findings may be interpreted as having resulted from the action of noxa during the cerebellar lobes' vulnerability window. Direct injury of cerebellar cortex and white matter is a fundamental and poorly recognized cause of impaired cerebellar growth.Para evaluar el desarrollo postnatal se analizaron 65 cerebelos de recién nacidos pretérmino con edad postconcepcional equivalente al término en dos grupos (Grupo I (GI): peso cerebeloso (pc) hasta 14grs; Grupo II (GII): pc superior a 14grs), y 20 controles (C) (recién nacidos de término hasta 6 días de vida). Se halló: reducción del tamaño (medido con un coeficiente) (GI:2,2; GII:2,9; C:3,68), y pc (en grs) (GI:9,8; GII:17,9; C:26,71); en hemisferios, reducción de altura de folias (en μm) (folias inferiores: GI:3486; GII:4764; C:6458) y su ramificación, del espesor cortical (mo-lecular + granos externa en μm) (GI:63,9; GII:74,5; C:92,27), y elevado número de células de Purkinje por segmento (GI:33,6; GII:21,4; C:13,95). Estos resultados se correlacionaron significativamente entre sí y con el peso corporal y cerebral. No se halló una alta correlación con la edad gestacional. Las lesiones cerebrales, y enfermedades ocurridas durante la hospitalización fueron más frecuentes en el GI. Además se halló necrosis y apoptosis en la corteza cerebelosa inmadura, y astrocitosis reactiva y gliosis en la sustancia blanca, vinculables a hipoxia-isquemia, infecciones y/o tratamientos. En conclusión, los casos analizados presentaron una detención del desarrollo con un patrón similar al de cerebelos de 30-32 (GI) y 33-35 (GII) semanas de EG, a pesar de haber completado una edad postconcepcional equivalente al término. Los hallazgos pueden ser interpretados como resultado de la acción de noxas durante la ventana de vulnerabilidad de los hemisferios cerebelosos. Las lesiones primarias y directas de la corteza cerebelosa y de la sustancia blanca constituyen una causa fundamental y poco jerarquizada de alteración del desarrollo cerebeloso.2008-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://digital.cic.gba.gob.ar/handle/11746/2950enginfo:eu-repo/semantics/altIdentifier/issn/1514-5654info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/reponame:CIC Digital (CICBA)instname:Comisión de Investigaciones Científicas de la Provincia de Buenos Airesinstacron:CICBA2025-09-04T09:43:16Zoai:digital.cic.gba.gob.ar:11746/2950Institucionalhttp://digital.cic.gba.gob.arOrganismo científico-tecnológicoNo correspondehttp://digital.cic.gba.gob.ar/oai/snrdmarisa.degiusti@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:94412025-09-04 09:43:17.296CIC Digital (CICBA) - Comisión de Investigaciones Científicas de la Provincia de Buenos Airesfalse
dc.title.none.fl_str_mv Postnatal cerebellar development in preterms with postconceptional age at term equivalent. A neuropathological study
title Postnatal cerebellar development in preterms with postconceptional age at term equivalent. A neuropathological study
spellingShingle Postnatal cerebellar development in preterms with postconceptional age at term equivalent. A neuropathological study
Jones, Marta
Pediatría
Cerebelo
Encefalopatías
neuropatología
title_short Postnatal cerebellar development in preterms with postconceptional age at term equivalent. A neuropathological study
title_full Postnatal cerebellar development in preterms with postconceptional age at term equivalent. A neuropathological study
title_fullStr Postnatal cerebellar development in preterms with postconceptional age at term equivalent. A neuropathological study
title_full_unstemmed Postnatal cerebellar development in preterms with postconceptional age at term equivalent. A neuropathological study
title_sort Postnatal cerebellar development in preterms with postconceptional age at term equivalent. A neuropathological study
dc.creator.none.fl_str_mv Jones, Marta
author Jones, Marta
author_facet Jones, Marta
author_role author
dc.subject.none.fl_str_mv Pediatría
Cerebelo
Encefalopatías
neuropatología
topic Pediatría
Cerebelo
Encefalopatías
neuropatología
dc.description.none.fl_txt_mv To evaluate postnatal development, we analyzed 65 cerebella from preterm neonates at term-gestational-age equivalent, separated into 2 groups: Group I (GI), cerebellar weight (cw) up to 14 g; Group II (GII), cw more than 14 g. The control group (CG) consisted of 20 term neonates up to 6 days old. Morphometry showed: diminished size, expressed as a coefficient (GI: 2.2; GII:2.9; CG:3.68) and cw [g] (GI:9.8; GII:17.9; CG:26.71); in the lobes, diminished foliar height [μm] (inferior folia; GI: 3.486; GII:4.764; CG:6.458) and foliation; diminished cortical width [μm] (GI:63.9; GII:74.5; CG:92.27), and a high number of Purkinje cells per segment (GI:33.6; GII:21.4; CG:13.95). These results correlated significantly with each other, with brain weight, and to a lesser degree with body weight. No high correlation with gestational age was found. Brain lesions and different serious and protracted illnesses were more frequent in GI. Histology: necrosis and apoptosis of the immature cerebellar cortex as well as reactive astrocytosis and gliosis of the white matter were observed. These findings related to hypoxia-ischemia, infections, and therapies. In summary, the cases examined in this study evinced cerebellar patterns similar to those of 30-32 (GI) and 33-35 (GII) weeks of gestational age, although these preterm neonates had completed a postconceptional age of 37 to 42 weeks. These findings may be interpreted as having resulted from the action of noxa during the cerebellar lobes' vulnerability window. Direct injury of cerebellar cortex and white matter is a fundamental and poorly recognized cause of impaired cerebellar growth.
Para evaluar el desarrollo postnatal se analizaron 65 cerebelos de recién nacidos pretérmino con edad postconcepcional equivalente al término en dos grupos (Grupo I (GI): peso cerebeloso (pc) hasta 14grs; Grupo II (GII): pc superior a 14grs), y 20 controles (C) (recién nacidos de término hasta 6 días de vida). Se halló: reducción del tamaño (medido con un coeficiente) (GI:2,2; GII:2,9; C:3,68), y pc (en grs) (GI:9,8; GII:17,9; C:26,71); en hemisferios, reducción de altura de folias (en μm) (folias inferiores: GI:3486; GII:4764; C:6458) y su ramificación, del espesor cortical (mo-lecular + granos externa en μm) (GI:63,9; GII:74,5; C:92,27), y elevado número de células de Purkinje por segmento (GI:33,6; GII:21,4; C:13,95). Estos resultados se correlacionaron significativamente entre sí y con el peso corporal y cerebral. No se halló una alta correlación con la edad gestacional. Las lesiones cerebrales, y enfermedades ocurridas durante la hospitalización fueron más frecuentes en el GI. Además se halló necrosis y apoptosis en la corteza cerebelosa inmadura, y astrocitosis reactiva y gliosis en la sustancia blanca, vinculables a hipoxia-isquemia, infecciones y/o tratamientos. En conclusión, los casos analizados presentaron una detención del desarrollo con un patrón similar al de cerebelos de 30-32 (GI) y 33-35 (GII) semanas de EG, a pesar de haber completado una edad postconcepcional equivalente al término. Los hallazgos pueden ser interpretados como resultado de la acción de noxas durante la ventana de vulnerabilidad de los hemisferios cerebelosos. Las lesiones primarias y directas de la corteza cerebelosa y de la sustancia blanca constituyen una causa fundamental y poco jerarquizada de alteración del desarrollo cerebeloso.
description To evaluate postnatal development, we analyzed 65 cerebella from preterm neonates at term-gestational-age equivalent, separated into 2 groups: Group I (GI), cerebellar weight (cw) up to 14 g; Group II (GII), cw more than 14 g. The control group (CG) consisted of 20 term neonates up to 6 days old. Morphometry showed: diminished size, expressed as a coefficient (GI: 2.2; GII:2.9; CG:3.68) and cw [g] (GI:9.8; GII:17.9; CG:26.71); in the lobes, diminished foliar height [μm] (inferior folia; GI: 3.486; GII:4.764; CG:6.458) and foliation; diminished cortical width [μm] (GI:63.9; GII:74.5; CG:92.27), and a high number of Purkinje cells per segment (GI:33.6; GII:21.4; CG:13.95). These results correlated significantly with each other, with brain weight, and to a lesser degree with body weight. No high correlation with gestational age was found. Brain lesions and different serious and protracted illnesses were more frequent in GI. Histology: necrosis and apoptosis of the immature cerebellar cortex as well as reactive astrocytosis and gliosis of the white matter were observed. These findings related to hypoxia-ischemia, infections, and therapies. In summary, the cases examined in this study evinced cerebellar patterns similar to those of 30-32 (GI) and 33-35 (GII) weeks of gestational age, although these preterm neonates had completed a postconceptional age of 37 to 42 weeks. These findings may be interpreted as having resulted from the action of noxa during the cerebellar lobes' vulnerability window. Direct injury of cerebellar cortex and white matter is a fundamental and poorly recognized cause of impaired cerebellar growth.
publishDate 2008
dc.date.none.fl_str_mv 2008-12
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