Prolongation of the laryngeal chemoreflex after inhibition of the rostral ventral medulla in piglets: a role in SIDS?

2003 ◽  
Vol 94 (5) ◽  
pp. 1883-1895 ◽  
Author(s):  
Liesbeth van der Velde ◽  
Aidan K. Curran ◽  
James J. Filiano ◽  
Robert A. Darnall ◽  
Donald Bartlett ◽  
...  
Keyword(s):  
Eye Movement ◽  
Sudden Infant Death Syndrome ◽  
Rem Sleep ◽  
Infant Death ◽  
Nrem Sleep ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Rapid Eye Movement ◽  
Ventral Medulla ◽  
Before And After

We tested the hypothesis that inhibition of neurons within the rostral ventral medulla (RVM) would prolong the laryngeal chemoreflex (LCR), a putative stimulus in the sudden infant death syndrome (SIDS). We studied the LCR in 19 piglets, age 3–16 days, by injecting 0.05 ml of saline or water into the larynx during wakefulness, non-rapid eye movement (NREM) sleep, and REM sleep, before and after 1 or 10 mM muscimol dialysis in the RVM. Muscimol prolonged the LCR ( P < 0.05), and the prolongation was greater when the LCR was stimulated with water compared with saline ( P < 0.02). The LCR was longer during NREM sleep than during wakefulness and longest during REM sleep (REM compared with wakefulness). Muscimol had no effect on the likelihood of arousal from sleep after LCR stimulation. We conclude that the RVM provides a tonic facilitatory drive to ventilation that limits the duration of the LCR, and loss of this drive may contribute to the SIDS when combined with stimuli that inhibit respiration.

Muscimol dialysis in the rostral ventral medulla reduced the CO2 response in awake and sleeping piglets

2001 ◽  
Vol 90 (3) ◽  
pp. 971-980 ◽  
Author(s):  
Aidan K. Curran ◽  
Robert A. Darnall ◽  
James J. Filiano ◽  
Aihua Li ◽  
Eugene E. Nattie
Keyword(s):  
Eye Movement ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Arcuate Nucleus ◽  
Sudden Infant Death ◽  
Human Infant ◽  
Sudden Infant ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Ventral Medulla

Some victims of sudden infant death syndrome have arcuate nucleus abnormalities. The arcuate nucleus may be homologous with ventral medullary structures in the cat known to be involved in the control of breathing and the response to systemic hypercapnia. We refer to putative arcuate homologues in the piglet collectively as the rostral ventral medulla (RVM). We inhibited the RVM in awake and sleeping, chronically instrumented piglets by microdialysis of the GABAA receptor agonist muscimol. Muscimol dialysis (10 and 40 mM) had no effect on eupnea but caused a significant reduction in the response to hypercapnia during both wakefulness (34.8 ± 8.7 and 30.7 ± 10.1%, respectively) and sleep (36.7 ± 6.7 and 49.5 ± 8.9%, respectively). The effect of muscimol on the CO2 response was entirely via a reduction in tidal volume and appeared to be greater during non-rapid-eye-movement sleep. We conclude that the piglet RVM contains neurons of importance in the response to systemic CO2 during both wakefulness and non-rapid-eye-movement sleep. We hypothesize that dysfunction of homologous regions in the human infant could lead to impaired ability to respond to hypercapnia, particularly during sleep, which could potentially be involved in the pathogenesis of sudden infant death syndrome.

Sleep Apnea in Infants Who Succumb to The Sudden Infant Death Syndrome

PEDIATRICS ◽  
1991 ◽  
Vol 87 (6) ◽  
pp. 841-846
Author(s):  
Vicki L. Schechtman ◽  
Ronald M. Harper ◽  
Adrian J. Wilson ◽  
David P. Southall
Keyword(s):  
Sleep Apnea ◽  
Eye Movement ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Matched Control ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Quiet Sleep

Previous studies have shown the frequency of respiratory pauses to be altered in groups of infants at risk for the sudden infant death syndrome (SIDS). In this study, we assess the frequency of apneic pauses during quiet sleep and rapid eye movement sleep in control infants and infants who subsequently died of SIDS. Sleep states were identified in 12-hour physiological recordings of SIDS victims and matched control infants, and the number of respiratory pauses from 4 to 30 seconds in duration was computed for quiet sleep and rapid eye movement sleep. SIDS victims 40 to 65 days of age showed significantly fewer apneic pauses than did age-matched control infants across the two sleep states. Fewer short respiratory pauses accounted for most of the reduction in number of apneic events in the SIDS victims during both sleep states. During the first month of life, SIDS victims did not differ significantly from control neonates on this measure. The finding that this respiratory difference exists during the second month of life, just before the period of maximal risk for SIDS, but not earlier, may have implications for the etiology of SIDS deaths.

Sleep State Organization in Normal Infants and Victims of the Sudden Infant Death Syndrome

PEDIATRICS ◽  
1992 ◽  
Vol 89 (5) ◽  
pp. 865-870 ◽  
Author(s):  
Vicki L. Schechtman ◽  
Ronald M. Harper ◽  
Arian J. Wilson ◽  
David P. Southall
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Rem Sleep ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Early Morning ◽  
Sudden Infant ◽  
Sleep State ◽  
Quiet Sleep ◽  
Increased Risk ◽  
State Organization

Infants at increased risk of the sudden infant death syndrome (SIDS) show abnormal patterning of sleep-waking states. It was hypothesized that infants who were to die of SIDS would show abnormalities of sleep state distribution prior to their deaths. Twenty-two 12-hour recordings were obtained from infants who subsequently died of SIDS, and sleep state patterns were compared in these records and 66 records of age-matched control infants. Each 1-minute epoch was classified as quiet sleep, rapid eye movement (REM) sleep, waking, indeterminate state, or artifact-contaminated. Victims of SIDS showed less waking and more sleep than control infants during the early-morning hours. Victims of SIDS younger than 1 month of age showed significantly more epochs classified as REM sleep across the night and significantly fewer epochs contaminated by artifacts relative to control infants. Further analysis indicated that the increased number of REM epochs resulted from fewer artifact-contaminated epochs, suggesting reduced motility during REM sleep in the SIDS victims compared with the control infants. The finding of decreased waking time during the early morning is of particular importance since most SIDS deaths occur during this portion of the day. The findings of altered sleep patterns in SIDS victims suggest that central neural changes are associated with SIDS risk.

REM sleep prevents sudden infant death syndrome

1983 ◽  
Vol 140 (4) ◽  
pp. 289-292 ◽  
Author(s):  
K. Watanabe ◽  
K. Inokuma ◽  
T. Negoro
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Rem Sleep ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Sudden Infant

Apnea and Sleep State in Infants with Nasopharyngitis

PEDIATRICS ◽  
1980 ◽  
Vol 65 (4) ◽  
pp. 713-717
Author(s):  
Jeffrey B. Gould ◽  
Austin F. S. Lee ◽  
Peter Cook ◽  
Suzette Morelock
Keyword(s):  
Sleep Apnea ◽  
Eye Movement ◽  
Infant Death ◽  
Sleep Time ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Rapid Eye Movement ◽  
Upper Respiratory Tract ◽  
Sleep State ◽  
Upper Respiratory

Having a mild upper respiratory tract infection does not change the sleep state proportions or total sleep time of an infant. However, infants with colds exhibit some sleep state specific alterations in sleep apnea. At 40, 44, and 48 weeks postconception, the number of respiratory pauses of 2 to 4.9 seconds and of 5 to 9.9 seconds duration per 100 minutes of state, during rapid eye movement, and indeterminate sleep are decreased in infants with colds. The absence of this phenomenon at 52 weeks suggests that it is modified by maturation. We hypothesize that the reduction in rapid eye movement and indeterminate sleep apnea is a manifestation of an adaptive response in normal infants, but for infants at risk for the sudden infant death syndrome, this response may be overwhelmed, resulting in increased apnea and, in some instances, sudden infant death.

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