Abstract
The aim of this critical review was to establish morphologic or biochemical diagnostic markers or indications for the pathogenesis of SIDS in the CNS and to review current literature dealing with CNS changes, especially in the brain stem. The functional disturbances recently discussed as the cause of SIDS, i.e. primary CNS changes in the sense of retardation of neurons in the brain stem, are presented first. Signs of retardation were obtained by quantification of dendritic spines [1, 2] and determination of phenylethanolamine-N-methyltransferase (PNMT), the adrenalin-synthesizing enzyme [3] and disturbances of endorphin immunoreactivity [4, 5]. Dendritic spine density was higher and PNMT activity weaker in the SIDS cases than in the controls, whereas no definitive findings of an increase or decrease in endorphin system activity were found. Signs of secondary CNS changes were established by quantification of the glial cell population in the brain stem [6–8] and determination of Purkinje cell density [9]; some authors found evidence of a brain stem gliosis, but no further indications of chronic systemic hypoxia or chronic hypoperfusion of the CNS could be established in SIDS victims.
Due to differences in the findings as well as methodologic and interpretative problems, no definitive pathogenetic concept based on the available neuropathology findings can be formulated at present, even though many observations tend to indicate that the brain stem, as the central organ controlling respiration, is probably of prime importance in SIDS. Even the classification of the described phenomena as primary and secondary changes can be and is disputed. No diagnostic criteria for classification of SIDS and control cases could be established, since all obtained criteria are nonspecific and the described criteria are not present in all SIDS cases.
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Frank, R.S., Sobol, S.P. (1990). Recent Neuropathologic Research in Sudden Infant Death Syndrome. In: Maehly, A., Williams, R. (eds) Forensic Science Progress. Forensic Science Progress, vol 4. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-75186-8_4
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DOI: https://doi.org/10.1007/978-3-642-75186-8_4
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