Catecholamine Neurons Alteration in the Brainstem of Sudden Infant Death Syndrome Victims

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Abstract
Background. Sudden infant death syndrome (SIDS) is a leading cause of postneonatal infant death. The pathogenesis of sudden death is still unknown, but an abnormality in the central nervous regulation of breathing during sleep has been suggested. Objective. The aim of study is to confirm the brainstem disorder of SIDS victims. In order to do this, it is necessary to investigate the alterations of brain neurotransmitter systems thought to be involved in respiratory control. Design. Neuropathologic study performed on the brainstem of SIDS victims. Subject/Methods. The disorders of catecholaminergic systems in 22 SIDS victims were examined on the substantia nigra in the midbrain, locus coeruleus in the pons, vagal nuclei, and area reticularis superficialis ventrolateralis with the immunohistochemical method. Immunoperoxidase staining was performed with the antityrosine hydroxylase (TH) and the glial fibrillary acidic protein antibodies. Immunoreactivity was compared with 13 age-matched control infants. For statistical analysis, the χ2 test and the Student9st test were performed. Results. The main finding was diminished TH immunoreactivity in the vagal nuclei and area reticularis superficialis ventrolateralis of SIDS victims, suggesting that adrenaline and noradrenaline neurons are altered in SIDS. In addition, this decrease in TH was closely correlated with brainstem gliosis. Conclusion. These catecholaminergic changes may be caused by chronic hypoxia or ischemia, and also may underlie alterations in respiratory and cardiovascular control in sleep.