Pneumograms in infants who subsequently died of sudden infant death syndrome

Kelly, Dorothy H.; Golub, Howard; Carley, David W.; Shannon, Daniel C.

doi:10.1016/s0022-3476(86)80380-8

Cited by 122 publications

(47 citation statements)

References 16 publications

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“…This curve included the respiratory bandwidth which accounted for the most discrimination ofa single variable along with respiratory frequency from the current investigation and three variables derived from analysis of the entire 10-h long pneumogram recording from the previous investigation: episodes of bradycardia, chronologie age, and the longest episode of PB. This result improved substantially the previous discriminant function obtained solely from the pneumogram parameters (4) that yielded a 6.5% false-positive identification at the same true-positive rate (4).…”

Section: Resultssupporting

confidence: 71%

“…Recordings on three infants were technically inadequate for analysis by the software program already described (4) because of excessive high frequency noise that affected the entire recording. The remaining 17 infants included seven asymptomatic siblings and 10 infants who had apnea (4). Only two of these 17 served as the basis for our preliminary report of power spectrum abnormalities (2); the other six from that report were excluded because of the coexistence of seizures or gastroesophageal reflux (three babies) or noisy recordings (three babies).…”

Section: Methodsmentioning

confidence: 99%

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Increased Respiratory Frequency and Variability in High Risk Babies Who Die of Sudden Infant Death Syndrome

et al. 1987

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ABSTRACT. We have tested the hypothesis that autonomic instability, reflected in increased variability of heart rate and respiratory frequency, characterized high risk babies who died of sudden infant death syndrome. Using computer-based methods, we compared the power spectra of instantaneous heart rate and respiration on coded tape recordings from seven asymptomatic siblings and 10 babies with symptomatic apnea who died of sudden infant death syndrome to 34 age-and sex-matched controls. We confirmed our previous observation of increased respiratory bandwidth, an index of variability in respiratory frequency (p = 0.009) but failed to confirm our finding of increased low frequency fluctuations in heart rate (p = 0.18). In addition, we found an increase in mean respiratory frequency during quiet breathing (p = 0.001) and a significant relationship between respiratory bandwidth and mean respiratory frequency (r = 0.604,p = 0.0002). These variables along with those from a previous analysis of the same data base yield a discriminant function with 82% sensitivity and 100% specificity. These results confirm previous suggestions that high risk babies who die of sudden infant death syndrome exhibit autonomic instability. (Pediatr Res 22: 158-162,1987) Abbreviations RBW, respiratory band width SIDS, sudden infant death syndrome ROC, receiver operating curve HR, heart rate PB, periodic breathing Hz, Hertz (cycles/s)We have hypothesized that the at-risk state for sudden and unexplained death in infants (SIDS) is characterized by abnormal patterns of fluctuations in heart rate and respiratory activity (1, 2). In our first test of this hypothesis, we compared fluctuations in instantaneous heart rate and respirations using power spectrum analysis and identified two abnormalities that were statistically different in high risk babies who died of SIDS compared to controls (2). SIDS babies exhibited increased fluctuations in heart rate at frequencies of 0.02-0.10 Hz and increased variability of respiratory frequency. However, in a blinded trial of this hypothesis, using recordings obtained prospectively by Gordon et al. (3) on English babies, we were unable to identify SIDS Received June 10,1986; accepted February 26, 1987. Address correspondence to Dan iel G. Shannon, M.D., Pediatric Pulmonary Unit, Massachusetts General Hospital, Boston, MA 02114. babies among control s by either increased low frequency HR fluctuations or increased variability of respiratory frequency. We concluded that the differences between these two studies might be explained by differences in methods or most probably in the populations. In order to test the initial hypothesis, we have repeated the analysis of data from our high risk population using a larger, blinded and coded data set in order to avoid any possibility of bias. The coding was performed by a technician who was unaware of the past history of the subjects and of the results ofa pneumogram analysis of recordings obtained with an independent software program (4). Using the latter program ,...

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Section: Resultssupporting

confidence: 71%

Section: Methodsmentioning

confidence: 99%

Increased Respiratory Frequency and Variability in High Risk Babies Who Die of Sudden Infant Death Syndrome

et al. 1987

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“…For example, increased incidence of periodic breathing and apnea (Steinschneider, 1972;Guilleminault et al, 1979;Kelly et al, 1986), impaired regulation of alveolar ventilation (Shannon and Kelly, 1977), abnormal fluctuations in heart rate and respiratory patterns (Gordon et al, 1984;Schechtman et al, 1988Schechtman et al, , 1990Schechtman et al, , 1992, and abnormal development of vagal nerve fibers (Becker et al, 1993) have all been implicated as factors contributing to the Sudden Infant Death Syndrome. Impaired hypoxic ventilatory responsiveness may also contribute to some forms of congenital chronic hypoventilation syndrome (Marcus et al, 1991;Weese-Mayer et al, 1992;Ogawa et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Mice Lacking Brain-Derived Neurotrophic Factor Exhibit Visceral Sensory Neuron Losses Distinct from Mice Lacking NT4 and Display a Severe Developmental Deficit in Control of Breathing

Erickson

Conover

Borday³

et al. 1996

J. Neurosci.

277

243

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The neurotrophins brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT4) act via the TrkB receptor and support survival of primary somatic and visceral sensory neurons. The major visceral sensory population, the nodose-petrosal ganglion complex (NPG), requires BDNF and NT4 for survival of a full complement of neurons, providing a unique opportunity to compare gene dosage effects between the two TrkB ligands and to explore the possibility that one ligand can compensate for loss of the other. Analysis of newborn transgenic mice lacking BDNF or NT4, or BDNF and NT4, revealed that survival of many NPG afferents is proportional to the number of functional BDNF alleles, whereas only one functional NT4 allele is required to support survival of all NT4-dependent neurons. In addition, subpopulation analysis revealed that BDNF and NT4 can compensate for the loss of the other to support a subset of dopaminergic ganglion cells. Together, these data demonstrate that the pattern of neuronal dependencies on BDNF and NT4 in vivo is far more heterogeneous than predicted from previous studies in culture. Moreover, BDNF knockout animals lack a subset of afferents involved in ventilatory control and exhibit severe respiratory abnormalities characterized by depressed and irregular breathing and reduced chemosensory drive. BDNF is therefore required for expression of normal respiratory behavior in newborn animals.

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“…Nonetheless, our findings should be linked to SIDS as many characteristics of typical SIDS infants seem to point in the direction of a vicious circle that includes the presence of apneas: periodic breathing and apneas, sleep, vomiting, low gestational age, overheating, hypoxia, infection, and release of interleukines. [12][13][14][15][16] These characteristics are separately known to enhance, produce, and prolong apneas, and interfere with normal autoresuscitation after apnea. 9,11,[17][18][19] Early in life, the infant is more susceptible to apnea by laryngeal stimulation 11 and hypoxia during apnea, 20 and probably responds inadequately to mild hypoxia by increased periodic breathing.…”

Section: Discussionmentioning

confidence: 99%

Adverse Effects of Nicotine and Interleukin-1β on Autoresuscitation After Apnea in Piglets: Implications for Sudden Infant Death Syndrome

et al. 2000

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ABSTRACT. Objectives. Maternal cigarette smoking is established as a major dose-dependent risk factor for sudden infant death syndrome (SIDS). Both prenatal and postnatal exposures to constituents of tobacco smoke are associated with SIDS, but no mechanism of death attributable to nicotine has been found. Breastfeeding gives a substantial increase in absorbed nicotine compared with only environmental tobacco smoke when the mother smokes, because the milk:plasma concentration ratio of nicotine is 2.9 in smoking mothers. Furthermore, many SIDS victims have a slight infection and a triggered immune system before their death, thus experiencing a release of cytokines like interleukin-1␤ (IL-1␤) that may depress respiration. Because apneas in infancy are associated with SIDS, we have tested the hypothesis that postnatal exposure to tobacco constituents and infections might adversely affect an infant's ability to cope with an apneic episode. This is performed by investigating the acute effects of nicotine and IL-1␤ on apnea by laryngeal reflex stimulation and on the subsequent autoresuscitation.Design. Thirty 1-week-old piglets (؎1 day) were sedated with azaperone. A tracheal and an arterial catheter were inserted during a short halothane anesthesia. The piglets were allowed a 30-minute stabilization period before baseline values were recorded and they were randomized to 4 pretreatment groups (avoiding siblings in the same group): 1) immediate infusion of 10 pmol IL-1␤ intravenously/kg (IL-1␤ group; n ‫؍‬ 8); 2) slow infusion of 5 g nicotine intravenously/kg 5 minutes later (NIC group; n ‫؍‬ 8); 3) both IL-1␤ and NIC combined (NIC ؉ IL-1␤ group; n ‫؍‬ 6); or 4) placebo by infusion of 1 ml .9% NaCl (CTR group; n ‫؍‬ 8). Fifteen minutes later, apnea was induced by insufflation of .1 ml of acidified saline (pH ‫؍‬ 2) in the subglottic space 5 times with 5-minute intervals, and variables of respiration, heart rate, blood pressure, and blood gasses were recorded.Results. Stimulation of the laryngeal chemoreflex by insufflation of acidified saline in the subglottic space produced apneas, primarily of central origin. This was followed by a decrease in heart rate, a fall in blood pressure, swallowing, occasional coughs, and finally autoresuscitation with gasping followed by rapid increase in heart rate, rise in blood pressure, and (in the CTR group) an increase of respiratory rate. Piglets pretreated with nicotine had more spontaneous apneas, and repeated spontaneous apneas caused an inability to perform a compensatory increase of the respiratory rate after induced apnea. This resulted in a lower SaO 2 than did CTR at 2 minutes after apnea (data shown as median ABBREVIATIONS. SIDS, sudden infant death syndrome; IL-1␤, interleukin-1␤; CRP, C-reactive protein; IL-6, interleukin-6; IL-1␤ group, 10 pmol IL-1␤ intravenously/kg; NIC group, 5 g nicotine intravenously/kg; NIC ϩ IL-1␤ group, both IL-1␤ and NIC combined; CTR group, placebo. M aternal cigarette smoking is established as a major dose-dependent risk factor for sudden infan...

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Pneumograms in infants who subsequently died of sudden infant death syndrome

Cited by 122 publications

References 16 publications

Increased Respiratory Frequency and Variability in High Risk Babies Who Die of Sudden Infant Death Syndrome

Increased Respiratory Frequency and Variability in High Risk Babies Who Die of Sudden Infant Death Syndrome

Mice Lacking Brain-Derived Neurotrophic Factor Exhibit Visceral Sensory Neuron Losses Distinct from Mice Lacking NT4 and Display a Severe Developmental Deficit in Control of Breathing

Adverse Effects of Nicotine and Interleukin-1β on Autoresuscitation After Apnea in Piglets: Implications for Sudden Infant Death Syndrome

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