Format

Send to

Choose Destination
J Neuropathol Exp Neurol. 2014 Apr;73(4):312-23. doi: 10.1097/NEN.0000000000000055.

No changes in cerebellar microvessel length density in sudden infant death syndrome: implications for pathogenetic mechanisms.

Author information

1
From the Department of Neuroanatomy, Ludwig Maximilians-University of Munich, Munich, Germany (JMS, MCK, NA, NC, EH, TH, KS, HGF, SM, CS); and Institute of Forensic Medicine, University of Rostock, Rostock, Germany (AB) and Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York (PRH).

Abstract

Sudden infant death syndrome (SIDS) is the leading cause of mortality in infants younger than 1 year in developed countries, but its primary cause remains unknown. Some studies suggest that there may be hypoxia in the cerebellum in SIDS subjects, but mean total Purkinje cell numbers in SIDS versus controls was recently found not to be different. Probably the best marker for chronic hypoxia in a brain region is the microvessel length per unit volume of tissue, that is, the microvessel length density (MLD). Here, we investigated MLDs using a rigorous design-based stereologic approach in all cell layers and white matter in postmortem cerebella from 9 SIDS cases who died between ages 2 and 10 months and from 14 control children, 9 of which were age- and sex- matched to the SIDS cases. We found no differences either in mean MLDs in the cerebellar layers between the SIDS cases and the controls or between controls with a low likelihood of hypoxia and those with a higher likelihood of hypoxia. Immunohistochemical detection of the astrocytosis marker glial fibrillary acidic protein showed no differences between the SIDS and the matched control cases. These data indicate that there is no association of chronic hypoxia in the cerebellum with SIDS.

PMID:
24607967
DOI:
10.1097/NEN.0000000000000055
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Silverchair Information Systems
Loading ...
Support Center