PEDIATRICS Vol. 101 No. 2 February 1998, pp. 285-288
Received Nov 12, 1996; accepted Jul 18, 1997.
,
, and
From the * Department of Mental Retardation and Birth Defect
Research, National Institute of Neuroscience, National Center of
Neurology and Psychiatry, Tokyo, Japan; and the
Tokyo Medical
Examiners office, Division of Pathology, Tokyo, Japan.
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
2 test and the Student's
t 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.
Key words: SIDS, brainstem, immunohistochemistry, tyrosine hydroxylase, brainstem gliosis.
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