Defective serotonin pathways in the brain stem may increase infants’ vulnerability
Children’s Hospital Boston
October 31, 2006
New autopsy data provide the strongest evidence yet that sudden infant death syndrome (SIDS) is not a “mystery” disease but has a concrete biological basis. In the November 1 issue of JAMA, researchers at Children’s Hospital Boston document abnormalities in the brainstem — a part of the brain that regulates breathing, blood pressure, body heat, and arousal — in babies who died from SIDS. SIDS is the leading cause of death in American infants after the newborn period, affecting 0.67 in 1,000 live-born babies. Although epidemiologic studies have identified risk factors for SIDS, such as putting babies to sleep on their stomachs, and protective factors like pacifier use, there has been little understanding of SIDS’s biologic basis.
Researchers led by neuropathologist Hannah Kinney, MD, and neuroscientist David Paterson, PhD, at Children’s Hospital Boston and Harvard Medical School examined brain autopsy specimens from 31 infants who had died from SIDS and 10 who had died acutely from other causes, provided by the San Diego Chief Medical Examiner’s office. Examining the lowest part of the brainstem, known as the medulla oblongata, they found abnormalities in nerve cells that make and use serotonin, one of over 100 chemicals in the brain that transmit messages from one nerve cell to another.
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| Infants who died from SIDS had significantly more serotonergic neurons in their brainstem than controls, particularly in the raphe nucleus (blue dots). |
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