Neuropathology provides new insight in the pathogenesis of the sudden infant death syndrome

Interleukin-6 and the serotonergic system of the medulla oblongata in the sudden infant death syndrome

“…The study provides evidence for aberrant interactions in SIDS infants between IL-6 and the arcuate nucleus, a key medullary 5-HT-related region involved in protective responses to hypercapnia, potentially induced by the combined effect of prone position and mild infection. This study is in line with current research that indicates brain mechanisms underlie the pathogenesis of SIDS [20] and underscores the need for continued research in the role of the brainstem, cytokines, infection, and chemosensitivity in SIDS.…”

Encephalopathy and death in infants with abusive head trauma is due to hypoxic-ischemic injury following local brain trauma to vital brainstem centers

“…We chose SIDS victims as controls, since this forms a homogenous population without TBI or any other intracranial pathology by definition [10]. Furthermore, since SIDS is believed to result from defective regulatory mechanisms in cardiorespiratory activity with resulting hypoxic-ischemic injury leading to instant or rapid death [39][40][41], we took the immunohistochemical profile in SIDS victims as a model for very early HIE. Therefore, for this comparative approach, only AHT victims in whom instant or rapid death could be assumed with certainty were studied.…”

Role of routine neuropathological examination for determining cause of death in sudden unexpected deaths in infancy (SUDI)

“…Numerous mechanisms for uSUDI have been suggested including neuropathological changes affecting the brainstem 5. These include abnormalities of serotonergic pathways in the medulla oblongata,6 gliosis and other hypoxia-ischaemia related changes,7 and developmental brain abnormalities including hypoplasia of the arcuate nucleus,5 8 9 persistence of the external granular layer of the cerebellar cortex10 and excessive leptomeningeal neurons, predominantly in the brainstem 11.…”

“…These include abnormalities of serotonergic pathways in the medulla oblongata,6 gliosis and other hypoxia-ischaemia related changes,7 and developmental brain abnormalities including hypoplasia of the arcuate nucleus,5 8 9 persistence of the external granular layer of the cerebellar cortex10 and excessive leptomeningeal neurons, predominantly in the brainstem 11. However, while these data suggest that, in some cases of SIDS/SUDI, morphological and functional differences may contribute to sudden death, their demonstration at postmortem examination is difficult and time-consuming and their presence does not change the use of SIDS/SUDI as the cause of death for certification processes.…”