Unravelling the Neuropathology of Sudden Deaths During Infancy; Cell Death, Inflammation, Protein Regulation & Morphology (21454)
Background: In Australia, on average, 130 babies per year, die suddenly and unexpectedly. For the majority, the cause is unknown and classified as Sudden Infant Death Syndrome (SIDS). The leading hypothesis for SIDS is a brainstem dysregulation in the face of hypoxic insult(s) causing failed cardiorespiratory responses succumbing with death, and often during a sleep period.
Aims: To determine whether the neuropathology of babies classified as SIDS differs to non-SIDS, and whether hypoxic related insults could have been contributory factors.
Methods: Formalin fixed and paraffin embedded brain tissue from n=160 infants were stained for various markers including caspase-3, TUNEL, acetylcholine, nicotinic receptors, Iba-1 (microglia), GFAP (astrocytes), BDNF and PACAP. Quantitative microscopic image analysis was undertaken to determine the proportion of cells expressing these markers in a total of 26 brain regions of interest. Levels were compared amongst the diagnostic groups and according to hypoxic related parameters of bedsharing, prone sleeping, cigarette smoke exposure and upper respiratory tract infection.
Results & Conclusion: Differences were evident for many of the markers in several of the brain regions of SIDS compared to non-SIDS, yet none were exclusive to SIDS and many changes were attributed to the presence of the hypoxic insult. Of the brain regions, the dorsal motor nucleus of the vagus is highlighted as a region for further in depth study given its involvement for many of the markers, particularly in relation to the cholinergic system.