Sudden Infant Death Syndrome (SIDS) may be linked to the build up of carbon dioxide and existing inner ear damage according to a new study in the journal Neuroscience. Author Dr. Daniel Rubens, an anesthesiologist and researcher at Seattle Children’s Research Institute, says the finding could help researchers understand the sequence of events and risk factors that lead to SIDS deaths.
“This is potentially an important breakthrough in understanding the biological underpinnings of what may be causing SIDS,” Rubens said. “We found that exposure to increasing levels of carbon dioxide and inner ear damage in mice resulted in a lack of movement toward safety and fresh air during sleep. We want to fine tune this discovery and study the connection to carbon dioxide in more detail.”
He cites a 2011 study that he co-authored:
Mice with inner ear injury (n=60) displayed a significantly diminished hypercapnic ventilatory response (HCVR). This contrasted with the normal HCVR seen in control mice that had not undergone tympanic injections (n=30), controls that received tympanic injections with saline (n=5), and controls that had gentamicin administered systemically (n=5). In response to inspired CO(2), the mean respiratory frequency of control mice increased by an average of 50% over their baseline values for both parts of the experiment. In contrast, the ear-damaged experimental group mean values increased by only three breaths per minute (bpm) (2%) in the first experiment and by 28 bpm (11%) in the second experiment. Inner ear damage significantly reduces the respiratory response to CO(2) inhalation. In addition to the established role of the inner ear organ in hearing and balance, this alludes to an unidentified function of the inner ear and its interconnecting neuronal pathways in respiratory regulation.
A 2013 review, The physiological determinants of Sudden Infant Death Syndrome cites the above paper:
although perinatal hearing/vestibular impairment by itself may not be robust predictor of SIDS vulnerability, there is an emerging possibility that hearing/vestibular function may be impaired in SIDS vulnerable infants. However, the precise role of the VN in central chemosensitivity and SIDS remains an open issue.
I am skeptical that the inner ear plays a large role in regulating respiration.