“…Brain-stem gliosis is commonly reported and is usually interpreted as the result of cerebral hypo-perfusion and chronic hypoxia (Kinney, 2009), as well as a sign of delayed brain maturation (Kelmanson, 1994(Kelmanson, /1995. Other reported morphologic findings in SIDS victims are: persistence of the neuronal dendritic spines in the reticular formation (Quattrochi, McBride, & Yates, 1985) potentially associated with abnormal respiratory control (Oehmichen, 1990), reduced number of the cerebellar cortex neurons (Oehmichen, Wullen, Zilles, & Saternus, 1989), dorsal motor nucleus neurons of the n. vagus (Ansari, Sibbons, Parsons, & Rossi, 2002), delayed brain stem myelination (Oehmichen, 1990), and reduced mean nucleus volume of neocortical neurons (Ansari, Sibbons, & Howard, 2001). There are some reports of a reduced number of alpha-2 adrenergic receptors (Ozawa, Takashima, & Tada, 2003), reduced choline acetyltransferase immunoreactivity (Mallard, Tolcos, Leditschke, Campbell, & Rees, 1999) in the brainstem, and deficiency in catecholaminergic neurons in the diencephalon and basal ganglia (Ozawa et al, 1999).…”