Title: To sleep, perchance to enrich learning?
Authors: Catherine M Hill, Alexandra M Hogan, Annette Karmiloff-Smith
Published: BMJ, August 20, 2007
"It is well established that intermittent hypoxia is an important mediator of neurocognitive deficit in children.45–47"
45 Hogan AM, de Haan M, Datta A, et al. Hypoxia: an acute, intermittent and
chronic challenge to cognitive development. Dev Sci 2006;9:335–7.
46 Bass JL, Corwin M, Gozal D, et al. The effect of chronic or intermittent hypoxia on
cognition in childhood: a review of the evidence. Pediatrics
2004;114(3):805–16.
47 Urschitz MS, Wolff J, Sokollik C, et al. Nocturnal arterial oxygen saturation and
academic performance in a community sample of children. Pediatrics
2005;115(2):e204–9.
"As Stickgold and Walker noted in their review of 46 recently published research articles, 83% supported a relationship between sleep and memory.26"
26 Stickgold R, Walker MP. Sleep and memory: the ongoing debate. Sleep
2005;28(10):1225–7.
"A further interesting discovery is the relevance of neocortical
slow oscillations. These at ,1 Hz are of lower frequency than
classical slow waves. Emerging during the transition into slow
wave sleep, these slow oscillations appear to originate in the
prefrontal cortex and recruit the entire neocortex. Their
appearance in sleep correlates with daytime learning tasks.18
Evidence reviewed by Born et al 10 suggests an intriguing
hypothesis, namely that during slow depolarisation, efferents
to the thalamus trigger reciprocal thalamo-cortical spindle
discharges and activation of hippocampal memories prompting
hippocampo-neocortical discharge. Thus the slow oscillations
are thought to encourage a synchronisation of memory
activation enhancing connections between vital memory
structures in the brain."
10 Born J, Rasch B, Gais S. Sleep to remember. Neuroscientist 2006;12(5):410–24.
Huber R, Ghilardi MF, Massimini M, et al. Local sleep and learning. Nature
2004;430(6995):78–81.
"More recent use of functional imaging techniques provides
illuminating evidence of dysfunctional brain activity after sleep
deprivation. Functional MRI in sleep-deprived healthy young
adults using a verbal learning task revealed increased pre-frontal
and parietal activity and decreased hippocampal activity compared
to controls who experienced normal sleep.12 The sleep
deprived adults performed significantly worse in the task. The
researchers suggested that the hippocampus (as the brain’s
memory encoding centre) failed to engage normally in the sleepdeprived
state, leading to compensatory activity in the cortical
areas associated with high working memory and cognitive load.
Literally the brain had to work harder to complete the task. More
recent research has used a similar experimental model in the
context of visual memory.12a Adult volunteers were tested on
recall of images with negative, positive and neutral emotional
valence. Sleep deprivation negatively impacted on the accurate
recall of all images and emotional valence of images reinforced
recall in both sleep refreshed and sleep deprived subjects.
Functional imaging again indicated a hippocampal deficit in
sleep deprived subjects suggesting off-line processing of emotional
memories during sleep. This latter example also highlights
the importance of emotional and situational context for memory
and the inherent complexity of memory research."
12 Drummond SP, Brown GC, Gillin JC, et al. Altered brain response to verbal
learning following sleep deprivation. Nature 2000;403:655–7.
12a Sterpenich V, Albouy G, Boly ML, et al. The role of sleep in the consolidation of
emotional memories in humans: a fMRI study. J Sleep Res 2006;15(Suppl 1):190.
"In slow wave sleep, reduced cholinergic activity suppresses this
direction of information flow but conversely promotes the
reactivation of hippocampally located memory and transfer to
cortical structures, thus promoting memory consolidation.10"
10 Born J, Rasch B, Gais S. Sleep to remember. Neuroscientist 2006;12(5):410–24.
"While many of the studies of sleep and memory have focused
on slow wave and REM sleep, more recent research has
suggested a role for the sleep spindle, characteristic of stage II
sleep, in triggering cellular mechanisms that enhance lasting
structural or functional neural change.19 20 One research group
found that the number of sleep spindles over the frontal cortex
correlated with the retention of verbal memory,21 whereas the
number of sleep spindles over the parietal cortex correlated
with visuospatial memory retention.22 The authors concluded
that the beneficial effects of sleep on learning are differentiated
according to brain region and memory task."
19 Schabus M, Ho¨dlmoser K, Gruber G, et al. Sleep spindle-related activity in the
human EEG and its relation to general cognitive and learning abilities.
Eur J Neurosci 2006;23:1738–46.
20 Sejnowski TJ, Destexhe A. Why do we sleep? Brain Res 2000;886:208–23.
22 Clemens Z, Fabo´ P, Hala´sz P. Twenty-four hours retention of visuo-spatial
memory correlates with the number of parietal sleep spindles. Neurosci Lett
2006;403:52–6.
Monday, March 30, 2009
Thursday, March 26, 2009
Increased motor cortex white matter volume predicts motor impairment in autism
Title: Increased motor cortex white matter volume predicts motor impairment in autism
Authors; Stewart H. Mostofsky, Melanie P. Burgess, and Jennifer C. Gidley Larson
Published: Brain (2007), 130, 2117-2122
Authors; Stewart H. Mostofsky, Melanie P. Burgess, and Jennifer C. Gidley Larson
Published: Brain (2007), 130, 2117-2122
Intermittent hypoxia induces transient delay in newborn mice
Title: Intermittent hypoxia induces transient delay in newborn mice
Authors: E. Drand, F. Lofaso, S. Dauger, G. Vardona, C. Gaultier, and J. Gallego
Published; J Appl Physiol 96: 1216-1222, 2004
First Published November 14, 2003; 10.1152/japplphysiol.00802.2003.
Summary:
"We conclude that IH (Intermitten Hypoxia) rapidly and reversibly depressed breathing and delayed arousal in newborn mice. Both effects may be due to hypoxia-induced release of inhibitory neurotransmitters acting concomitantly on both functions."
"Previous studies showed that infants who had survived a life-threatening event with OSAs had abnormal arousal responses to hypoxemia (14) and that infants who subsequently died from sudden infant death syndrome (SIDS) showed fewer spontaneous arousals from sleep than did controls (17). These results suggest that defective arousal responses may be major mechanisms in sleep-disordered breathing (SIDS and OSA) in infantcy."
"A previous experiment in lambs showed that one of the mechanisms that impair the arousal response to hypoxemia in newborns in intermitten hypoxemia (IH) (15). In these experiments, lambs exposed to IH showed depressed arousal and ventilatory responses to hypoxia during active sleep. Similarly, both ventilatory and arousal responses to hypoxia were blunted in adult dogs with experimentally induced OSA over 3-4 mo (22). Several processes may depress arousability during IH. First, ventilatory efforts (the input from mechanoreceptors) are an important stimulus to arousal from sleep (1, 20, 21) that decreases if ventilation is depressed. Second, depression of the arousal response to IH may be due to hapituation. Experiments in adult humans have shown that the arousal respiratory effort threshold during upper airway occlusion is in increased by prior sleep apnea (2, 38). Habituation to repeated tactile stimuli has also been shown to depress arousability in infants (29)."
"Recent results supporting a genetic basis for OSA (34) and SIDS (33,45) provide a promising avenue for the development of mouse models of sleep-disordered breathing."
"The main results of this study are that, in newborn mice, IH: (1) increased the arousal latency to hypoxia and (2) depressed normoxic ventilation, while preserving the ventilatory response to hypoxia. After 2 h of normoxia, the arousal responses to hypoxia recovered fully and baseline breathing returned to prehypoxic levels."
"Previous studies in 4- to 5-day-old lambs exposed to hypoxia showed that the increase in arousal latency was associated with a decrease in arterial O2 saturation value at which arousal occurred(13)."
"Previous studies in humans indicated that respiratory mechanoreceptor input to arousal centers in the brain make a major contribution to the arousal response to hypoxia (1)."
"The increase in arousal latency noted in our study fit in well with the observation that habituation to external stimuli depresses arousal, whatever the nature of these stimuli (7,23,29)."
"Previous studies showed that cortical activity was profoundly altered in 12-day-old piglets exposed to similar levels of IH(43)."
"Hypoxia activates several neurotransmitters (or neuromodulators) such as glutamate, which stimulates breathing, and GABA, opiates, and adenosine, which inhibit breathing (36, 40, 42). The platelet-derived growth factor in the nucleus tractus solitarius exerts a strong inhibitory effect on breathing during hypoxia (10, 11). Several of these neurotransmitters are also pivotal to habituation to external stimuli and sleep induction. In particular, adenosine is endogenous sleep factor this is thought to directly inhibit wakefulness-promoting neurons, such as cholinergic neurons in the basal forebrain(35). GABA is involved in habituation of motor responses to new environments (8). Steroid modulation of the GABA(A) receptor has been reported to mediate habituation of the evoked midbrain response to repetitive acoustic clicks (5), although this may not occur at early stages of development (25). Taken together, these results suggest that the dealyed arousal and decrease in baseline ventilation may be two consequences, relatively independent of each other, of the accumulation of central inhibitory neurotransmitters."
"Arousal impairments induced by IH are potentially hazardous in infants at risk for SIDS, because full behavioral awakening is necessary to inititate withdrawal responses in case of positional asphyxia or apnea. On the other hand, previous studies showed that infants with OSA terminated central and obstructive apneas without arousals (scored according to EEG, submental EMG, and behavioral criteria) (27). This indicates that behavioral arousal is not a necessary condition for OSA termination and that delayed arousal may be a protective mechanism avoiding sleep disruption."
Authors: E. Drand, F. Lofaso, S. Dauger, G. Vardona, C. Gaultier, and J. Gallego
Published; J Appl Physiol 96: 1216-1222, 2004
First Published November 14, 2003; 10.1152/japplphysiol.00802.2003.
Summary:
"We conclude that IH (Intermitten Hypoxia) rapidly and reversibly depressed breathing and delayed arousal in newborn mice. Both effects may be due to hypoxia-induced release of inhibitory neurotransmitters acting concomitantly on both functions."
"Previous studies showed that infants who had survived a life-threatening event with OSAs had abnormal arousal responses to hypoxemia (14) and that infants who subsequently died from sudden infant death syndrome (SIDS) showed fewer spontaneous arousals from sleep than did controls (17). These results suggest that defective arousal responses may be major mechanisms in sleep-disordered breathing (SIDS and OSA) in infantcy."
"A previous experiment in lambs showed that one of the mechanisms that impair the arousal response to hypoxemia in newborns in intermitten hypoxemia (IH) (15). In these experiments, lambs exposed to IH showed depressed arousal and ventilatory responses to hypoxia during active sleep. Similarly, both ventilatory and arousal responses to hypoxia were blunted in adult dogs with experimentally induced OSA over 3-4 mo (22). Several processes may depress arousability during IH. First, ventilatory efforts (the input from mechanoreceptors) are an important stimulus to arousal from sleep (1, 20, 21) that decreases if ventilation is depressed. Second, depression of the arousal response to IH may be due to hapituation. Experiments in adult humans have shown that the arousal respiratory effort threshold during upper airway occlusion is in increased by prior sleep apnea (2, 38). Habituation to repeated tactile stimuli has also been shown to depress arousability in infants (29)."
"Recent results supporting a genetic basis for OSA (34) and SIDS (33,45) provide a promising avenue for the development of mouse models of sleep-disordered breathing."
"The main results of this study are that, in newborn mice, IH: (1) increased the arousal latency to hypoxia and (2) depressed normoxic ventilation, while preserving the ventilatory response to hypoxia. After 2 h of normoxia, the arousal responses to hypoxia recovered fully and baseline breathing returned to prehypoxic levels."
"Previous studies in 4- to 5-day-old lambs exposed to hypoxia showed that the increase in arousal latency was associated with a decrease in arterial O2 saturation value at which arousal occurred(13)."
"Previous studies in humans indicated that respiratory mechanoreceptor input to arousal centers in the brain make a major contribution to the arousal response to hypoxia (1)."
"The increase in arousal latency noted in our study fit in well with the observation that habituation to external stimuli depresses arousal, whatever the nature of these stimuli (7,23,29)."
"Previous studies showed that cortical activity was profoundly altered in 12-day-old piglets exposed to similar levels of IH(43)."
"Hypoxia activates several neurotransmitters (or neuromodulators) such as glutamate, which stimulates breathing, and GABA, opiates, and adenosine, which inhibit breathing (36, 40, 42). The platelet-derived growth factor in the nucleus tractus solitarius exerts a strong inhibitory effect on breathing during hypoxia (10, 11). Several of these neurotransmitters are also pivotal to habituation to external stimuli and sleep induction. In particular, adenosine is endogenous sleep factor this is thought to directly inhibit wakefulness-promoting neurons, such as cholinergic neurons in the basal forebrain(35). GABA is involved in habituation of motor responses to new environments (8). Steroid modulation of the GABA(A) receptor has been reported to mediate habituation of the evoked midbrain response to repetitive acoustic clicks (5), although this may not occur at early stages of development (25). Taken together, these results suggest that the dealyed arousal and decrease in baseline ventilation may be two consequences, relatively independent of each other, of the accumulation of central inhibitory neurotransmitters."
"Arousal impairments induced by IH are potentially hazardous in infants at risk for SIDS, because full behavioral awakening is necessary to inititate withdrawal responses in case of positional asphyxia or apnea. On the other hand, previous studies showed that infants with OSA terminated central and obstructive apneas without arousals (scored according to EEG, submental EMG, and behavioral criteria) (27). This indicates that behavioral arousal is not a necessary condition for OSA termination and that delayed arousal may be a protective mechanism avoiding sleep disruption."
Wednesday, March 25, 2009
Effect on Sleep Position on Apnea and Bradycardia in High-Risk Infants
Here is a letter in the Medical Journal Nature in full. Interesting stuff about the origins of the SIDS and Sleep Apnea theory connection.
March 2002, Volume 22, Number 2, Pages 163-164
Commentary
Effect on Sleep Position on Apnea and Bradycardia in High-Risk Infants
Joan E Hodgman MD
Keck School of Medicine, USC Medical Center, University of Southern California, Los Angeles County, Los Angeles, CA, USA
Correspondence to: Joan E. Hodgman, MD, Women's and Children's Hospital, 1240 North Mission Road, Los Angeles, CA 90033, USA
Abstract
Journal of Perinatology (2002) 22, 163-164 DOI: 10.1038/sj/jp/7210658
Hershberger and associates1 recently published a careful study in the Journal of Perinatology of apnea and bradycardia during monitoring of infants considered at risk for SIDS in the prone and side-lying positions during sleep. They hypothesized that there would be increased cardiorespiratory events in the infants when prone. Their results did not bear this out as they found no differences. The expectation of differences was apparently based on the belief that apnea and SIDS are related. There have never been any convincing data linking apnea to SIDS.
The sleep apnea theory was proposed by Steinschneider2 in 1972 based on studies of five infants, two of whom died, with no controls. The cause of the deaths was later proven to be infanticide.3 This theory was rapidly embraced by both the medical and the lay public presumably because it offered the possibility of intervention by monitoring. In spite of widespread monitoring of infants in the United States during almost 30 years, monitoring has not decreased the rate of SIDS.4 Cardiorespiratory abnormalities in the pneumogram were reported to identify infants at risk for SIDS and consequently recommended for infants who should benefit from monitoring. These recommendations were never published in a peer-reviewed journal but rather by the SIDS Foundation, a predominantly lay organization of parents of SIDS infants. The abnormalities described are common in normal infants and the use of pneumograms for this purpose is no longer recommended.5
No studies have related the presence of apnea or bradycardia on monitoring with SIDS. Our own studies of infants following an apparent life-threatening event (ALTE) showed no such differences from controls.6 The extensive report by Southall et al.7 of recordings of infants discharged from a neonatal intensive care unit showed no relation between findings on the recordings and subsequent death. The recent publication of results from the Collaborative Home Infant Monitoring Evaluation (CHIME) study by Ramanathan and colleagues8 reported no differences between term infants at risk and controls. Premature infants had increased apnea and bradycardia only until 43 weeks, well before the peak incidence of SIDS.
There are few epidemiologic data to support the sleep apnea theory. Histories of infants dying of SIDS rarely contain reference to apnea.9 Premature infants are at greater risk for both early apnea and SIDS, but these appear related to maturity rather than directly to each other. In our large premature center, the risk of SIDS in infants of birth weigh <1500 g after discharge has been close to 1 per 100, but those who died were almost entirely asymptomatic in the nursery. Infants who suffered an ALTE due to apnea of prematurity have been reported to be at increased risk for SIDS.10,11 However, a number of the reported infants had two or more preceding familial deaths, which is considered to rule out SIDS in favor of infanticide. In fact, the use of previous terms for an ALTE such as near-miss for SIDS and aborted crib death have been abandoned as misleading. The etiology of apnea of infancy is as mysterious as that of SIDS itself. No studies have demonstrated a reduction in SIDS deaths following an ALTE attributable to monitoring.
The authors of the article under discussion did not elaborate on why they did not complete their study by including infants in the supine position. My hypothesis would be that no differences would be found in apnea and bradycardia between prone and supine positions. It is past time to put the sleep apnea theory to rest.
References
1 Hershberger ML, Peeke KL, Levett J, Spear ML. Effect of sleep position on apnea and bradycardia in high-risk infants. J Perinatol 2000; 21: 85-9.
2 Steinschneider A. Prolonged apnea and the sudden infant death syndrome: clinical and laboratory observations. Pediatrics 197; 50: 646-54.
3 Firstman R, Talan J. The Death of Innocents: A True Story of Murder, Medicine, and High Stakes Science New York: NY Bantam, 1997.
4 Davidson Ward SL, Keens TG, Chan LS et al. Sudden infant death syndrome in infants evaluated by apnea programs in California. Pediatrics 1986; 77: 451-5. MEDLINE
5 Consensus statement: National Institutes of Health Consensus Development Conference on Infantile Apnea and Home Monitoring, Sept 29 to Oct 1, 1986. Pediatr 1987; 79: 292-9.
6 Hodgman JE, Hoppenbrouwers T, Geidel S et al. Respiratory behavior in near-miss sudden infant death syndrome. Pediatrics 1982; 69: 785-92. MEDLINE
7 Southall DP, Richards JM, Rhoden KJ et al. Prolonged apnea and cardiac arrhythmias in infants discharged from neonatal intensive care units: failure to predict an increased risk for sudden infant death syndrome. Pediatrics 1982; 70: 844-51. MEDLINE
8 Ramanathan R, Corwin MJ, Hunt CE et al. Cardiorespiratory events recorded on home monitors. Comparison of healthy infants with those at increased risk for SIDS. JAMA 2001; 285: 2199-2207. MEDLINE
9 Hoffman HJ, Damus K, Hillman L, Drongrad E. Risk factors for SIDS: results of the National Institute of Child Health and Human Development SIDS Cooperative Epidemiological Study. Ann NY Acad Sci 1988; 533: 112-30.
10 Oren J, Kelly D, Shannon DC. Identification of a high-risk group for sudden infant death syndrome among infants who were resuscitated for sleep apnea. Pediatrics 1986; 77: 495-9. MEDLINE
11 Schwartz PJ, Southall DP, Valdez-Idapena M. The Sudden death syndrome: cardiac and respiratory mechanisms and interventions. Ann NY Acad Sci 1988; 533: 1-474.
March 2002, Volume 22, Number 2, Pages 163-164
Commentary
Effect on Sleep Position on Apnea and Bradycardia in High-Risk Infants
Joan E Hodgman MD
Keck School of Medicine, USC Medical Center, University of Southern California, Los Angeles County, Los Angeles, CA, USA
Correspondence to: Joan E. Hodgman, MD, Women's and Children's Hospital, 1240 North Mission Road, Los Angeles, CA 90033, USA
Abstract
Journal of Perinatology (2002) 22, 163-164 DOI: 10.1038/sj/jp/7210658
Hershberger and associates1 recently published a careful study in the Journal of Perinatology of apnea and bradycardia during monitoring of infants considered at risk for SIDS in the prone and side-lying positions during sleep. They hypothesized that there would be increased cardiorespiratory events in the infants when prone. Their results did not bear this out as they found no differences. The expectation of differences was apparently based on the belief that apnea and SIDS are related. There have never been any convincing data linking apnea to SIDS.
The sleep apnea theory was proposed by Steinschneider2 in 1972 based on studies of five infants, two of whom died, with no controls. The cause of the deaths was later proven to be infanticide.3 This theory was rapidly embraced by both the medical and the lay public presumably because it offered the possibility of intervention by monitoring. In spite of widespread monitoring of infants in the United States during almost 30 years, monitoring has not decreased the rate of SIDS.4 Cardiorespiratory abnormalities in the pneumogram were reported to identify infants at risk for SIDS and consequently recommended for infants who should benefit from monitoring. These recommendations were never published in a peer-reviewed journal but rather by the SIDS Foundation, a predominantly lay organization of parents of SIDS infants. The abnormalities described are common in normal infants and the use of pneumograms for this purpose is no longer recommended.5
No studies have related the presence of apnea or bradycardia on monitoring with SIDS. Our own studies of infants following an apparent life-threatening event (ALTE) showed no such differences from controls.6 The extensive report by Southall et al.7 of recordings of infants discharged from a neonatal intensive care unit showed no relation between findings on the recordings and subsequent death. The recent publication of results from the Collaborative Home Infant Monitoring Evaluation (CHIME) study by Ramanathan and colleagues8 reported no differences between term infants at risk and controls. Premature infants had increased apnea and bradycardia only until 43 weeks, well before the peak incidence of SIDS.
There are few epidemiologic data to support the sleep apnea theory. Histories of infants dying of SIDS rarely contain reference to apnea.9 Premature infants are at greater risk for both early apnea and SIDS, but these appear related to maturity rather than directly to each other. In our large premature center, the risk of SIDS in infants of birth weigh <1500 g after discharge has been close to 1 per 100, but those who died were almost entirely asymptomatic in the nursery. Infants who suffered an ALTE due to apnea of prematurity have been reported to be at increased risk for SIDS.10,11 However, a number of the reported infants had two or more preceding familial deaths, which is considered to rule out SIDS in favor of infanticide. In fact, the use of previous terms for an ALTE such as near-miss for SIDS and aborted crib death have been abandoned as misleading. The etiology of apnea of infancy is as mysterious as that of SIDS itself. No studies have demonstrated a reduction in SIDS deaths following an ALTE attributable to monitoring.
The authors of the article under discussion did not elaborate on why they did not complete their study by including infants in the supine position. My hypothesis would be that no differences would be found in apnea and bradycardia between prone and supine positions. It is past time to put the sleep apnea theory to rest.
References
1 Hershberger ML, Peeke KL, Levett J, Spear ML. Effect of sleep position on apnea and bradycardia in high-risk infants. J Perinatol 2000; 21: 85-9.
2 Steinschneider A. Prolonged apnea and the sudden infant death syndrome: clinical and laboratory observations. Pediatrics 197; 50: 646-54.
3 Firstman R, Talan J. The Death of Innocents: A True Story of Murder, Medicine, and High Stakes Science New York: NY Bantam, 1997.
4 Davidson Ward SL, Keens TG, Chan LS et al. Sudden infant death syndrome in infants evaluated by apnea programs in California. Pediatrics 1986; 77: 451-5. MEDLINE
5 Consensus statement: National Institutes of Health Consensus Development Conference on Infantile Apnea and Home Monitoring, Sept 29 to Oct 1, 1986. Pediatr 1987; 79: 292-9.
6 Hodgman JE, Hoppenbrouwers T, Geidel S et al. Respiratory behavior in near-miss sudden infant death syndrome. Pediatrics 1982; 69: 785-92. MEDLINE
7 Southall DP, Richards JM, Rhoden KJ et al. Prolonged apnea and cardiac arrhythmias in infants discharged from neonatal intensive care units: failure to predict an increased risk for sudden infant death syndrome. Pediatrics 1982; 70: 844-51. MEDLINE
8 Ramanathan R, Corwin MJ, Hunt CE et al. Cardiorespiratory events recorded on home monitors. Comparison of healthy infants with those at increased risk for SIDS. JAMA 2001; 285: 2199-2207. MEDLINE
9 Hoffman HJ, Damus K, Hillman L, Drongrad E. Risk factors for SIDS: results of the National Institute of Child Health and Human Development SIDS Cooperative Epidemiological Study. Ann NY Acad Sci 1988; 533: 112-30.
10 Oren J, Kelly D, Shannon DC. Identification of a high-risk group for sudden infant death syndrome among infants who were resuscitated for sleep apnea. Pediatrics 1986; 77: 495-9. MEDLINE
11 Schwartz PJ, Southall DP, Valdez-Idapena M. The Sudden death syndrome: cardiac and respiratory mechanisms and interventions. Ann NY Acad Sci 1988; 533: 1-474.
Gastroesophageal Reflux: A Critical Review of Its Role in Preterm Infants
Title: Gastroesophageal Reflux: A Critical Review of Its Role in Preterm Infants
Author: Christian F. Poets, M
Published: Pediatrics Vol. 113 No. 2 February 2004
Summary Information:
The author states: "GER is common in infants, which is related to their large fluid intake (corresponding to 14 L/day in an adult) and supine body position, resulting in the gastroesophageal junction's being constantly "under water." pH monitoring, the standard for reflux detection, is of limited use in preterm infants whose gastric pH is >4 for 90% of the time."
The author states "After the recent withdrawal of cisapride, there is now increasing interest in the use of erythromycin, which binds to neural motilin receptors and stimulates antral contractions and, in lower doses, induces antral migrating motor complexes, which are important for gastric emptying (8)."
The author also calls into question the use of Pro-kinetics.
The author states "Gastroesophageal reflux (GER) is common in preterm infants, occurring on average 3 to 5 tmes per hour (1,2), but to what extent is it a clinical problem? A recent survey of current practice estimated that 19% of preterm infants admitted to U.S. teaching hospitals received cisapride(3). Thus, many neonatologists seem to consider GER indeed a problem, but what is the evidence?"
In Pathogenesis of GER in Infants the author states "Reflux may occur when the lower esophageal sphincter relaxes. In an upright adult, gas will exit the stomach during these transient lower esophageal sphincter relaxations (TLESRs), causing belching. In a subject lying supine, however, the gastroesophageal junction is constantly under water, and liquid instead of gas will enter the esophagus. The quantity of the reflux depends on the fluid volume inside the stomach. The volume of fluid given to an infant (180 mL/kg per day) would correspond to a daily intake of ~14 L/day in an adult. GER, in an otherwise healthy infant may simply serve as a pop-off valve to cope with this high volume (4)."
The author states in the Apnea section "Problems that are frequently cited in conjunction with GER are apnea, failure to thrive, and airway problems such as recurrent aspiration or wheezing (26)."
Evidence from animal studies "show that apnea can be induced by the instillation of small amounts of liquid into the larynx, resulting in stimulation of laryngeal chemoreceptors (28), and the observation that apneas are mor likely to occur after episodes of regurgitation (29)."
The author states "Several issues remain unclear from these studies. First, assuming a causal relationship, is GER cause or effect of the respiratory symptoms, i.e., does it result in airway narrowing via stimulation of airway receptors and/or recurrent aspiration, or do the large intrathoracic pressure swings caused by the upper airway narrowing facilitate GER? Although the respiratory response to GER treatment described above supports the first option, it cannot prove it."
the author concludes "Thus, despite the above data from older infants, there is currently no evidence that GER is a significant contributor to chronic airway problems in preterm infants. Why then treat it?"
Author: Christian F. Poets, M
Published: Pediatrics Vol. 113 No. 2 February 2004
Summary Information:
The author states: "GER is common in infants, which is related to their large fluid intake (corresponding to 14 L/day in an adult) and supine body position, resulting in the gastroesophageal junction's being constantly "under water." pH monitoring, the standard for reflux detection, is of limited use in preterm infants whose gastric pH is >4 for 90% of the time."
The author states "After the recent withdrawal of cisapride, there is now increasing interest in the use of erythromycin, which binds to neural motilin receptors and stimulates antral contractions and, in lower doses, induces antral migrating motor complexes, which are important for gastric emptying (8)."
The author also calls into question the use of Pro-kinetics.
The author states "Gastroesophageal reflux (GER) is common in preterm infants, occurring on average 3 to 5 tmes per hour (1,2), but to what extent is it a clinical problem? A recent survey of current practice estimated that 19% of preterm infants admitted to U.S. teaching hospitals received cisapride(3). Thus, many neonatologists seem to consider GER indeed a problem, but what is the evidence?"
In Pathogenesis of GER in Infants the author states "Reflux may occur when the lower esophageal sphincter relaxes. In an upright adult, gas will exit the stomach during these transient lower esophageal sphincter relaxations (TLESRs), causing belching. In a subject lying supine, however, the gastroesophageal junction is constantly under water, and liquid instead of gas will enter the esophagus. The quantity of the reflux depends on the fluid volume inside the stomach. The volume of fluid given to an infant (180 mL/kg per day) would correspond to a daily intake of ~14 L/day in an adult. GER, in an otherwise healthy infant may simply serve as a pop-off valve to cope with this high volume (4)."
The author states in the Apnea section "Problems that are frequently cited in conjunction with GER are apnea, failure to thrive, and airway problems such as recurrent aspiration or wheezing (26)."
Evidence from animal studies "show that apnea can be induced by the instillation of small amounts of liquid into the larynx, resulting in stimulation of laryngeal chemoreceptors (28), and the observation that apneas are mor likely to occur after episodes of regurgitation (29)."
The author states "Several issues remain unclear from these studies. First, assuming a causal relationship, is GER cause or effect of the respiratory symptoms, i.e., does it result in airway narrowing via stimulation of airway receptors and/or recurrent aspiration, or do the large intrathoracic pressure swings caused by the upper airway narrowing facilitate GER? Although the respiratory response to GER treatment described above supports the first option, it cannot prove it."
the author concludes "Thus, despite the above data from older infants, there is currently no evidence that GER is a significant contributor to chronic airway problems in preterm infants. Why then treat it?"
Tuesday, March 24, 2009
Title: The Effect of Body Position on Sleep Apnea in Children Younger Than 3 Years
Authors: Kevin D. Periera, MD; Jeremy C. Roebuck, MD; Lori Howell, BS
Published: ARCH OTOLARYGOL HEAD NECK SURG/VOL 131. NOV 2005
WWW.ARCHOTO.COM
Summary:
The Objective of this study was "To determine the association between body position and obstructive events during determined by polysomnography (PSG) in very young children (age, <= 3 years) with obstructive sleep apnea syndrome.
All children subsequently underwent adenotonsillectomy.
"The PSGs were analyzed for data on the respiratory disturbance index (RDI), time spent in each body position, number of apneic events in each position, oxygen saturation, and time spent in each stage of sleep."
Results:
"Sixty patients satisfied the criteria for inclusion in the study. The mean supine sleep RDI was 8.5 compared with 4.9 for the mean nonsupine sleep RDI. The mean RDI increased from 5.6 to 8.5 when more than 50% of the time was spent in supine sleep. There was a further increase to 10.5 when supine sleep increased to 75% of the total sleep time. The mean RDI in rapid eye movement sleep was 20.5 compared with 5.3 in non-rapid eye movement sleep. The mean +- SD supine sleep RDI was 18.5 +- 5.1, and the mean nonsupine RDI was 7.2 +- 1.9, which was statistically significant (P=.02)."
"Obstructive Sleep Apnea syndrome is a serious medical problem, affecting 500,000 children per year in the United States. Pediatric OSAS peaks between the ages of 2 and 5 years, with an overall prevalence of 2% (3). The hallmarks of OSAS include episodes or partial or complete upper airway obstruction that occur during sleep, manifested by snoring, retractions, paradoxical chest motion, and poor quality of sleep. The condition is usally accompanied by a nocturnal reduction in oxygen saturation and bypercarbia (3). Symptoms during the day include mouth breathing, behavior problems, hyperactivity, and excessive daytime sleepiness (less than in adults). Nocturnal enuresis and asphyxic encephalopathy have also been reported. When these manifestations result from adenotonsillar hypertrophy, most of them have been shown to be reversed adenotonsillectomy (4)"
"The results of our study indicate that supine sleep does correlate with an increase in RDI as well as with OSAS in pediatric patients younger than 3 years. This finding is in contrast to previous studies that have demonstrated no correlation between sleep position and OSAS in children (2). In 2001, Penzel et al (6) demonstrated the collapsibility of the upper airways in adults who were in the supine position and showed that this outcome depended on sleep position and not sleep stage. However, adult sleep apnea differs from pediatric apnea in several aspects, and the exact mechanism of pediatrics OSAS has not been fully elucidated. A recent study suggested that children younger than 10 years actually breathe better in the supine position than in the lateral or the prone position (2). In that study, the patients had a lower RDI in the supine position compared with other positions. Our study in very young children showed evidence to the contrary. Our observations suggest that toddlers have sleep characteristics that are different from those of older children."
Authors: Kevin D. Periera, MD; Jeremy C. Roebuck, MD; Lori Howell, BS
Published: ARCH OTOLARYGOL HEAD NECK SURG/VOL 131. NOV 2005
WWW.ARCHOTO.COM
Summary:
The Objective of this study was "To determine the association between body position and obstructive events during determined by polysomnography (PSG) in very young children (age, <= 3 years) with obstructive sleep apnea syndrome.
All children subsequently underwent adenotonsillectomy.
"The PSGs were analyzed for data on the respiratory disturbance index (RDI), time spent in each body position, number of apneic events in each position, oxygen saturation, and time spent in each stage of sleep."
Results:
"Sixty patients satisfied the criteria for inclusion in the study. The mean supine sleep RDI was 8.5 compared with 4.9 for the mean nonsupine sleep RDI. The mean RDI increased from 5.6 to 8.5 when more than 50% of the time was spent in supine sleep. There was a further increase to 10.5 when supine sleep increased to 75% of the total sleep time. The mean RDI in rapid eye movement sleep was 20.5 compared with 5.3 in non-rapid eye movement sleep. The mean +- SD supine sleep RDI was 18.5 +- 5.1, and the mean nonsupine RDI was 7.2 +- 1.9, which was statistically significant (P=.02)."
"Obstructive Sleep Apnea syndrome is a serious medical problem, affecting 500,000 children per year in the United States. Pediatric OSAS peaks between the ages of 2 and 5 years, with an overall prevalence of 2% (3). The hallmarks of OSAS include episodes or partial or complete upper airway obstruction that occur during sleep, manifested by snoring, retractions, paradoxical chest motion, and poor quality of sleep. The condition is usally accompanied by a nocturnal reduction in oxygen saturation and bypercarbia (3). Symptoms during the day include mouth breathing, behavior problems, hyperactivity, and excessive daytime sleepiness (less than in adults). Nocturnal enuresis and asphyxic encephalopathy have also been reported. When these manifestations result from adenotonsillar hypertrophy, most of them have been shown to be reversed adenotonsillectomy (4)"
"The results of our study indicate that supine sleep does correlate with an increase in RDI as well as with OSAS in pediatric patients younger than 3 years. This finding is in contrast to previous studies that have demonstrated no correlation between sleep position and OSAS in children (2). In 2001, Penzel et al (6) demonstrated the collapsibility of the upper airways in adults who were in the supine position and showed that this outcome depended on sleep position and not sleep stage. However, adult sleep apnea differs from pediatric apnea in several aspects, and the exact mechanism of pediatrics OSAS has not been fully elucidated. A recent study suggested that children younger than 10 years actually breathe better in the supine position than in the lateral or the prone position (2). In that study, the patients had a lower RDI in the supine position compared with other positions. Our study in very young children showed evidence to the contrary. Our observations suggest that toddlers have sleep characteristics that are different from those of older children."
Magnetic Resonance Imaging of the Upper Airway Structure of Children with Obstructive Sleep Apnea Syndrome
Title: Magnetic Resonance Imaging of the Upper Airway Structure of Children with Obstructive Sleep Apnea Syndrome
Authors: Raanan Arens, Joseph M. McDonough, Andrew T. Costarino, Soroosh Mahboubi, Catherine E. Tayag-Kier, Greg Maislin, Richard J. Schwab, adn Allan I. Pack
Published: Am J Respir Crit Care Med Vol. 164. pp 698-703, 2001
Summary: They state that "We conclude that in children with moderate OSAS, the upper airway is restricted both by the adenoids and the tonsils; however, the soft palate is also larger in this group, adding further restriction."
Subjects with OSAS:"Eighteen children were recruited from the pool of patients evaluated for sleep-disordered breathing at the Children's Hospital of Philadelphia (Philadelphia, PA). After OSAS was confirmed by polysomnography, patients were allowed to undergo MRI of the upper airway under sedation."
Control Subjects:"Eighteen Children with normal growth and development were matched to subjects with OSAS by age, sex, ethnicity, weight, and height. Control subjects were selected from patients who underwent head MRI at the Children's Hospital of Philadelphia for other medical indications."
Authors: Raanan Arens, Joseph M. McDonough, Andrew T. Costarino, Soroosh Mahboubi, Catherine E. Tayag-Kier, Greg Maislin, Richard J. Schwab, adn Allan I. Pack
Published: Am J Respir Crit Care Med Vol. 164. pp 698-703, 2001
Summary: They state that "We conclude that in children with moderate OSAS, the upper airway is restricted both by the adenoids and the tonsils; however, the soft palate is also larger in this group, adding further restriction."
Subjects with OSAS:"Eighteen children were recruited from the pool of patients evaluated for sleep-disordered breathing at the Children's Hospital of Philadelphia (Philadelphia, PA). After OSAS was confirmed by polysomnography, patients were allowed to undergo MRI of the upper airway under sedation."
Control Subjects:"Eighteen Children with normal growth and development were matched to subjects with OSAS by age, sex, ethnicity, weight, and height. Control subjects were selected from patients who underwent head MRI at the Children's Hospital of Philadelphia for other medical indications."
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