Inner ear lesion and the differential roles of hypoxia and hypercarbia in triggering active movements: Potential implication for the Sudden Infant Death Syndrome.

Infants that succumb to Sudden Infant Death Syndrome (SIDS) have been identified with inner ear dysfunction (IED) at birth and on autopsy. We previously investigated whether IED could play a mechanistic role in SIDS. We discovered that animals with IED displayed significant suppression of movement arousal to a hypoxic-hypercarbic gas mixture under light anesthesia. In the current study we investigated the role of each gas in triggering movements and the response to hypercarbia during natural sleep without anesthesia. Seventeen-day-old CD-1 mice received intra-tympanic gentamicin (IT-Gent) injections to precipitate IED. The movement response to hypercarbia, hypoxia and hypoxia-hypercarbia was compared to controls under light anesthesia. Hypercarbia did not stimulate vigorous movements in any animals under either sleep condition. Hypoxia triggered vigorous movements in controls (p<0.05) and a decreased response in IT-Gent animals under light anesthesia. This contrasted with combined hypoxia-hypercarbia, in which IT-Gent animals displaced significantly suppressed movements compared to controls (p<0.05). Our findings portray that a degree of intact inner ear function is necessary for instigating the movement response. Additionally, hypoxia is the trigger for the movement response while carbon dioxide (CO2) suppresses it. The finding that carbon dioxide did not stimulate movement during natural sleep is an important finding. This contrasts with other studies that have identified hypercarbia as an arousal stimulus with EEG. Further studies are warranted to evaluate the precise role of the inner ear in the movement response and potential association with SIDS. The early detection of IED in SIDS predisposed cases could be invaluable.

Placental transfusion insult in the predisposition for SIDS: a mathematical study.

A difference has been observed between the newborn hearing screening tests of thirty-one SIDS cases versus control infants that survived the first year of life [Rubens DD, Vohr BV, Tucker R, O'Neil CA, Chung W. Newborn oto-acoustic emission hearing screening tests. Preliminary evidence for a marker of susceptibility to SIDS. Early Hum Dev 2008;84(4);225-9]. This study is motivated by the hypothesis that the predisposition for SIDS may be caused by inner ear and brainstem damage from a high venous pressure insult at birth that disrupts an infant's ability to detect rising CO(2) levels following the first month of life. The injury is not immediately lethal due to the persistence of fetal physiological responses during the early postnatal period [Guntheroth WG. Crib death, the Sudden Infant Death Syndrome. Armonk NY: Futura Publishing Co.; 1995. p. 291]. Elastic vessels are assumed in the umbilical vein and newborn venous circulation at the time of a potential high pressure placental transfusion insult and pulse wave propagation is simulated using the nonlinear one-dimensional equations of blood flow in elastic vessels. Peak pressures in the auricular veins increase with the amplitude and length of the umbilical surge, reaching over 60 mm Hg when two consecutive surges separated by 100 ms, of a peak pressure of 100 mm Hg, and a pulse interval of 200 ms are propagated in a network with low peripheral reflections. Our findings support the proposed mechanism for inner ear damage in SIDS and the potential benefit of a newborn hearing screening test in identifying susceptibility and early preventative measures following birth.

Newborn oto-acoustic emission hearing screening tests: preliminary evidence for a marker of susceptibility to SIDS.

OBJECTIVE: To evaluate the newborn transient evoked otoacoustic emission (TEOAE) hearing screening tests of infants later diagnosed with the sudden infant death syndrome (SIDS). STUDY DESIGN: In a case-controlled study, the newborn TEOAE hearing screens of 31 infants who subsequently died of SIDS were retrospectively compared to those of 31 newborn infants that survived the first year of life. SIDS cases were individually matched to surviving controls based on gender, term versus preterm age and NICU versus well baby nursery. RESULTS: The TEOAE screens of SIDS infants demonstrated significantly decreased signal to noise ratios at 2000, 3000, and 4000 Hz (p<0.05) on the right side compared to healthy control infants. CONCLUSION: Newborns at risk for SIDS are currently indistinguishable from other newborns and are only identified following a later fatal event. A unilateral difference in cochlear function is a unique finding that may offer the opportunity to identify infants at risk of SIDS during the early postnatal period with a simple non invasive hearing screen test. The ability to implement preventative measures well in advance of a potential critical incident would be an important breakthrough.

Are lethal audiogenic seizures a missing link to the sudden infant death syndrome?

The pathogenesis of human seizure disorders has largely been derived from rodent models. A number of rodent and chick strains exhibit a genetic predisposition for lethal audiogenic seizures (AGSs) in the first year of life. Consideration is warranted that this disorder may be linked to the sudden infant death syndrome (SIDS). Factors that carry a strong association with SIDS such as hyperthermia and the prone sleeping position would conceivably play a significant role in a human AGS syndrome. Importantly, there is data to support the likelihood that motor seizure activity may be absent in infants with an AGS syndrome. Rodent AGSs may hold important clues to unraveling the mystery of SIDS.