title: Cerebellar cortex delayed maturation in sudden infant death syndrome.
abstract: The cerebellum shows afferent and efferent connections with intrinsic bulbar nuclei and plays an important role in respiration and cardiovascular control. Pathological and neurochemical abnormalities of bulbar nuclei including the arcuate nucleus have been postulated in sudden infant death syndrome (SIDS). Most of these abnormalities have been related to impairment in brain development. The cerebellar cortex has a well-documented evolution from fetal life until infancy; thus, it may be a very good model to assess brain maturation in SIDS. The present study was conducted to investigate changes in the cerebellar cortex in 19 SIDS cases compared with 12 age-related controls using morphological, quantitative, and statistical approaches. Five-microns paraffin sections from the midsagittal cerebellar vermis were stained with hematoxylin and eosin (H&E). Immunohistochemical staining was carried out using a polyclonal antiserum to glial fibrillary acidic protein (GFAP). Each case consisted of a 25-microns parallel paraffin section stained with H&E, where the cerebellar external granular layer (EGL) cell density was obtained in one field magnification (x1,000) using an optical dissector procedure on the basis of a stereological method. A statistically significant high EGL cell density, mostly related to the presence of immature bipolar, elongated neuronal cells of the premigratory zone with hyperchromatic, oval or poor differentiated nuclei, was observed in SIDS. In these cases, EGL expressed immunoreactivity for GFAP mainly in the subpial and the postmitotic zone. These findings demonstrate a delayed or slower decline in the number of EGL neurons in SIDS, suggesting either a prolongation of the growth phase related to postnatal cerebellar foliation or a delay in inward migration. These results suggest that in SIDS there is delayed maturation of the cerebellar cortex/EGL, which may support the hypothesized cardiopulmonary control dysfunction, leading to death in a vulnerable period of postnatal development.
authors.affiliation: Neurological Tissue Bank, Hospital Clínico-University of Barcelona, Spain.
authors.forename: F F
authors.initials: FF
authors.lastname: Cruz-Sánchez
authors.forename: J
authors.initials: J
authors.lastname: Lucena
authors.forename: C
authors.initials: C
authors.lastname: Ascaso
authors.forename: E
authors.initials: E
authors.lastname: Tolosa
authors.forename: L
authors.initials: L
authors.lastname: Quintò
authors.forename: M L
authors.initials: ML
authors.lastname: Rossi
mesh_terms: D000328:Adult; D002452:Cell Count; D002525:Cerebellar Cortex / Q000254:growth & development* / Q000378:metabolism / Q000473:pathology*; D002657:Child Development; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D007223:Infant; D007231:Infant, Newborn; D012016:Reference Values; D013398:Sudden Infant Death / Q000473:pathology*; D013997:Time Factors
chemical_list: D005904:Glial Fibrillary Acidic Protein