Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The polygraphic findings from 11 future victims of sudden infant death syndrome (SIDS) are reported and compared with those of matched pairs of control infants. The recordings had been done to alleviate parental anxiety about sleep apnea. Four infants had siblings who were victims of SIDS. Two infants were studied 3.5 to 9.5 weeks before their deaths because of an unexplained apparent life-threatening event that had occurred during sleep. For each victim of SIDS, two control infants were selected from the 2,000 infants who had been tested in the same hospitals. They were matched for sex, gestational age, postnatal age, and weight at birth with the SIDS victims. Their polygraphic recordings had been performed within similar conditions. Each record was allocated a random code number and was analyzed without knowledge of the patient's identity by two independent scorers. Most sleep and cardiorespiratory variables studied did not differentiate SIDS victims from control infants. Only four variables significantly characterized the future SIDS victims: the maximal duration of central apneas, the number of sighs followed by a central apnea, the presence of obstructive apneas, and the presence of mixed apneas. Central apneas were longer during all sleep states in the SIDS victims compared with their matched controls, but none exceeded 14 seconds. Sighs immediately followed by an apnea were significantly less frequent in the future SIDS group. Obstructive and mixed sleep apneas were seen in eight of 11 SIDS victims and in only three of 22 control infants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Polysomnographic studies of infants who subsequently died of sudden infant death syndrome. 318 51

Pneumograms of 33 fullterm infants (age 1-16 weeks) with idiopathic sleep apnea syndrome (SAS), treated with aminophyllin administered orally, were compared with pneumograms of 12 age-matched infants without aminophyllin treatment. In a one hour oxycardiorespirography (OCRG) all infants had pneumogram abnormalities defined as apneas greater than or equal to 15 s, greater than or equal to 3 apneas lasting 10 s, MA-value (mean duration of all apneas during sleep time) greater than or equal to 7 s/min, and greater than or equal to 3 episodes of periodic breathing. The diagnosis of an SAS, discussed as a possible risk factor of SIDS, was made in general in the presence of clinical symptoms such as apneas, cyanosis during sleep, poorly coordinated sucking, swallowing and respiration, and gastro-esophageal reflux (GER) in combination with an abnormal pneumogram. Of the 33 infants 12 with a history of an SIDS sibling were clinically asymptomatic. We found that after one week of aminophyllin treatment in 88% the pneumograms were normal. The mean plasma concentration of aminophyllin at this time was 8.3 micrograms/ml (range 4-19 micrograms/ml). All abnormalities showed a statistically significant reduction. In the infants without aminophyllin the pneumogram was still abnormal and no abnormality was significantly reduced. After at least 6 weeks we discontinued aminophyllin and one week later we monitored the OCRG. In 83% of the infants we found a normal pneumogram and compared to the initial pneumogram there was again a statistically significant difference.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of aminophylline therapy in mature infants with sleep apnea syndrome]. 321 Nov 67

Recreational diving is a popular sport, although human ability to stay in and under water is severely limited physiologically. An understanding of these limitations enhances safety and enjoyment of sports diving. Breath-hold diving involves head-out water immersion, apnoea and submersion, exercise, cold stress, and pressure exposure. Each of these components, by itself, elicits prominent and specific physiological effects. Combination of these factors produces a unique and interesting physiological response generally known as diving reflex. Humans display weak diving responses, but exhibit no oxygen conservation function. Nevertheless, application of diving-induced physiological changes is now finding its way into clinical practice. Apnoea, face immersion, and head-out water immersion all show promise of clinical application. There are several spin-offs from diving research worth noting. Diuresis, enhancement of cardiac performance, and redistribution of blood flow, all produced by head-out water immersion, have been shown to be clinically useful, besides providing physiological data useful to space travel. Results from investigations on apnoea have been shown to be relevant to the following: treating some forms of cardiac arrhythmias; understanding drowning, sudden infant death syndrome and sleep apnoea; and confirming hyperventilation as the major cause of drowning. In comparison to marine mammals, humans are poor divers because of severe physiological constraints which limit their breath-hold time, diving depth, and ability to conserve body heat. Although under special circumstances humans can achieve unusually long breath-hold time and reach exceptional depth with a single breath, the sustainable working time and depth are only about 1 minute and 5 metres, respectively. Hypothermia inevitably results in divers working in the ocean. Without thermal protection, the intolerable limit of 35 degrees C is reached within 30 minutes in winter (10 degrees C) water and within 60 to 90 minutes in summer. Nevertheless, effective harvest work can be performed by humans in the ocean, and recreational benefits enhanced when these physiological limitations are respected. An unusual circulatory state exists during head-out water immersion in that there is a sustained increase of stroke volume. This results in 30% increase in cardiac output when the subject is resting in thermal neutral water, indicating a substantial overperfusion for the oxygen requirement. Furthermore, animal experiments showed that the elevated blood flow is preferentially channeled to the liver, fat, and the organs in the splanchnic region.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Applied physiology of diving. 327 55

The soft palate is a muscular fold suspended from the posterior border of the bony palate and extending downwards and backwards into the oropharynx. Usually, the soft palate and tongue are in tight apposition, closing the oropharyngeal isthmus; the soft palate can however rise and touch the posterior pharyngeal wall, closing the nasopharynx: thus the soft palate regulates the flow of air through nose and/or mouth. During oronasal breathing (as during exercise, speech or smoking) the impedance of naso and oropharynx respectively is determined by the position of the soft palate. Hence partitioning of the airflow through nose and mouth will depend on the latter. This is true in both adults and babies. Babies are not obligatory nasal breathers (as was previously thought). This applies as well as to near miss for sudden infant death syndrome babies. The soft palate is also involved in the genesis of snoring and the sleep apnea syndrome.
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PMID:[The role of the soft palate in respiration]. 336 31

We have examined in a group of normal infants and in an "at-risk" group with clinical sleep apnea syndrome the duration and frequency distribution of apneas during sleep. In order to improve the estimation of an apnea factor, we introduced a weighting function which is based on the expected frequency distribution of apnea durations of normal infants. We were able to observe a good agreement between clinical rating, based on anamnestic symptoms, and numerical scoring. All infants of the at-risk group were treated with aminophylline, and the respiratory state improved significantly in nearly all cases. Breathing hypoxic gas mixtures tended to depress respiration, especially in the at-risk group, with a pronounced drop of pO2-values. Investigations on the coordination of respiration, sucking, and swallowing during nutritive sucking demonstrated a correspondence between disturbed coordination ability and the sleep apnea syndrome (SAS). This relationship is interpreted to be a result of an immaturity of the autonomic nervous system. In order to evaluate possible hereditary components in conjunction with respiratory disorders and, possibly, SIDS, we studied siblings of SIDS victims, of near-miss infants, and of infants with SAS. Only siblings of SAS and near-miss infants showed clinical signs of respiratory disorders with a rather high prevalence, whereas most of the siblings of SIDS victims were completely lacking conspicuous respiratory symptoms. Our results suggest that not all infants with sleep apnea syndrome are necessarily at increased risk for SIDS.
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PMID:Physiological approaches to respiratory control mechanisms in infants. Assessing the risk for SIDS. 342 35

The observation that the narcotic antagonist naloxone could inhibit analgesia produced by electrical stimulation of the brain indicated the involvement of an endogenous chemical in the relief of pain. Multiple endogenous opioid peptides have been identified that have similar pharmacological properties to known narcotic analgesics. The biosynthesis, release, and degradation of opioid peptides have been studied in order to better understand how the manipulation of endogenous opioid systems can be used to produce or augment analgesia. The results of our studies reveal that various conditions and manipulations, such as electrical brain stimulation, acupuncture, stress, and the administration of opioid analgesics, can cause the release of endogenous opioid peptides and possibly endogenous nonpeptide substances. It has also been discovered that nonopioid peptides, such as cholecystokinin, calcitonin, and angiotensin II, can alter the action of opioid analgesics by antagonizing or potentiating their effects. An understanding of the role of endogenous peptides in endogenous opioid mechanisms is necessary for the development of new ways to treat pain and such other disorders as sleep apnea in children (sudden infant death syndrome), head injury, and opioid addiction that involve the activation or alteration of endogenous opioid systems.
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PMID:The role of endogenous peptides in the action of opioid analgesics. 352 91

Since the value of home apnea monitoring for subsequent siblings (subsibs) of an infant who died of sudden infant death syndrome is uncertain, we describe an evaluation and monitoring program for subsibs. Eighty subsibs were screened in hospital at an average age of 4.6 weeks. The most valuable investigations included history, physical examination, blood gas tests, and four days on an apnea monitor in hospital. Sleep recordings added no decision-making data. Only 23 infants met one of the following criteria for home apnea monitoring: (1) sleep apnea for more than 15 s (either on sleep recording or recognized by apnea alarm), (2) more than 4.5 episodes of apnea per hour of sleep, (3) periodic breathing greater than 24% of sleep time, or (4) severe parental anxiety. Twenty-two infants were monitored until they were aged 6 months and had spent two months apnea free. Twelve had apnea at home. All of the infants survived. Excessive periodic breathing alone did not seem to be a valid reason for home monitoring. Our screening program is simple, acceptable to families, and useful to select a smaller number of subsibs for home apnea monitoring.
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PMID:Screening of subsequent siblings of children who die of sudden infant death syndrome. 359 73

The authors investigated the incidence of sudden infant death syndrome (S.I.D.S.) in families of government employees who benefited of free health care. Out of approximately 400 families with around 2000 children, 29 reported at least one infant death meeting the chosen criteria for S.I.D.S. A total of 41 children, mostly males, died between 1 day and 30 months of age, amongst the 149 children born in these families; most of them died during the first 3 months of life. The mothers were generally house wives, aged 26.2 +/- 1.0 years. Sickle cell trait was found in at least one parent of 21 families. In the other 8 families, 11 out of 38 children died, giving a prevalence rate of 6.9/1000 live births for S.I.D.S. in the healthy population. In the sickle cell trait population, the prevalence rate for S.I.D.S. reached 75.0/1000 live births, the prevalence of sickle cell anemia being about 20% in Niger. When very strict criteria were used for diagnosing S.I.D.S., the prevalence rate was 2.5/1000 and 40/1000 live births in the healthy and the sickle trait populations respectively. This study is the first attempt to determine the place of S.I.D.S. in the infant mortality rate in Sahelian Africa. In families with sickle cell disease, the risk of S.I.D.S. was 11.5 times greater than in healthy families. The role of sleep apnea as a cause of S.I.D.S. is discussed. It may represent a common cause of death in both healthy families at risk and sickle cell trait families.
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PMID:[Sudden infant death and sickle cell anemia in the Sahel region of Africa]. 362 17

Home apnea/bradycardia monitoring is commonly utilized in the management of infants who have had apnea episodes. Little is established, however, regarding appropriate decision-making guidelines and efficacy. The 5-year experience of the Western Massachusetts Apnea Evaluation Program was reviewed to examine patient outcome and to identify prognostic clinical features. Significant recurrent sleep apnea occurred in 7 of 110 infants in the combined awake and asleep group, and in 2 of 45 siblings of babies dying of SIDS. Unclear histories, normal laboratory tests, and uncertain diagnoses made it impossible to identify features that would indicate infants at risk for recurrence of apnea. Our data indicate that home apnea monitoring lacks specificity but is probably effective in reducing morbidity and mortality. It currently appears to be the most optimal means of managing infantile apnea.
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PMID:Infant home apnea monitoring. A five-year assessment. 364 52

Based on results on central chemosensitivity in cats, paired stimuli were applied for therapy to infants with central respiratory insufficiency of various degrees. An unspecific respiratory stimulus, e.g. light for 1 s, was followed by a jet of either O2 or 2% CO2 in O2 for 1.5 s. The unspecific and the chemical stimuli were interspaced by 0.5 s. The combined stimulation was repeated every 10 s. The program was triggered by using threshold values of transcutaneous pO2. In infants with intratrachial tubes or tracheostoma we used the end tidal pCO2 for triggering the stimulation. The method could prevent hypoxemia during sleep in non-ventilated subjects with sleep apnea syndromes or in infants with severe hypoxemia during sleep after being rescued from Sudden Infant Death Syndrome (SIDS). In patients with Ondine's Curse Syndrome (OCS) with its CO2 insensitivity, paired stimuli were used in order to condition the chemical function of the respiratory system. Polysomnograms from 310 clinically healthy infants including healthy siblings of SIDS victims revealed instability of arterial pO2 and low CO2 sensitivity during sleep within the second month and the fourth to ninth month of life, respectively. These data challenge the described method as a potential preventive or therapeutic measure to defeat SIDS and sleep apnea syndromes in conjunction with disturbed chemical regulation of respiration.
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PMID:Transcutaneous monitoring as trigger for therapy of hypoxemia during sleep. 367 92


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