Discharge pattern of reticular formation unit pairs in waking and REM sleep.
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Biomedical subjects
Publications and source records attributed to R M Harper.
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This study examined fetal heart rate (FHR) variables during maternal sleep in subsequent siblings of infants who died of sudden infant death syndrome (SIDS) and who are thus at increased statistical risk for SIDS, and controls. Four findings differentiated the tracings of subsequent siblings of SIDS infants and controls: 1) FHR variability in subsequent siblings of SIDS infants ranged between 11 and 25 beats/min, compared with 6 to 10 beats/min in controls (P less than .001). 2) Bradycardia was more frequent in subsequent siblings of SIDS infants. 3) FHR accelerations (more than 150 beats/min) followed by heart rates below 120 beats/min were elevated in subsequent siblings of SIDS infants (P less than .01). 4) Strong respiratory arrhythmia was more frequent in subsequent siblings of SIDS infants. These siblings exhibited more reactive FHR patterns. Although these data cannot be interpreted as clinical markers to identify the infant who will die of SIDS, they are compatible with the hypothesis that mild chronic hypoxia is associated with risk for SIDS.
This study was designed to provide normative data on fetal heart rate (FHR), FHR variability, accelerations, and decelerations during maternal sleep in the third trimester of pregnancy and to identify rhythmicity in FHR variability. Twenty-four polygraphic recordings were obtained in 16 pregnant women at 32 and 36 weeks' gestation. FHR parameters were not predictably influenced by maternal sleep states. Cyclic changes in FHR variability with median cycle length of 53 minutes were observed. Accelerations and decelerations occurred an average of 12.2 and 4 times per 100 minutes, respectively. Bradycardia and tachycardia persisting beyond 10 minutes were not seen. FHR variability ranged from marked to decreased within recordings of the same subject; this observation has implications for non-stress testing of the fetus.
Spontaneous activity from simultaneously recorded pairs of neurons in the nucleus parabrachialis medialis(NPBM) was examined in unanesthetized, unrestrained cats during each sleep-waking state. Functional interconnections between pairs of neurons were studied with cross-correlation techniques. A total of 40 neuronal pairs were studied, 38 of which were recorded on separate, but proximal electrodes, and two pairs of which were recorded on the same electrode. Of the 40 pairs of neurons examined, 22 showed short delay (< 4 msec) peaks in the cross correlogram of their spike activity. These correlations tended to be highest in quiet sleep (QS). Increased probability of shared discharge with intermediate delays in the peaks of the cross-correlogram (5-150 msec) was observed in 16 of 40 pairs. The increase in correlation at intermediate delays followed a period of decreased shared activity. Activity at intermediate delay peaks was reduced during rapid eye movement (REM) sleep, and appeared with a shorter delay during that state. Long delay correlation peaks ranging from 0.5 to 6 sec appeared in 23 of 40 neuronal pairs, but only in waking and in REM sleep.
Neuronal activity in the nucleus parabrachialis medialis (NPBM) was examined in unanesthetized, unrestrained cats during each sleep-waking state. Discharge related to the cardiac cycle was assessed by calculating cross-correlation functions between neuronal and cardiac events (using the peak of the EKG 'R' wave as a reference). Of the 60 NPBM neurons examined, the activity of 20 cells showed discharge relationships to the cardiac cycle. Firing of NPBM neurons in phase with the cardiac cycle was observed during each sleep-waking state, but was most apparent during awake (AW) and rapid eye movement (REM) sleep states. State-related changes in the correlation of NPBM neuronal discharge to the cardiac cycle included variations in the extent of rhythmic modulation of activity, and shifts in the phase relationship to the cardiac reference. The predominant phase relationship of NPBM neuronal activity to the cardiac cycle was an increased probability of discharge during a period ranging from 50 msec preceding to 50 msec following the peak of the EKG 'R' wave.
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Respiratory rates and breathing pauses of various durations were examined in 19 normal infants, 12 male and 7 female, during the first 6 months of life. Twelve-hour all-night polygraphic recordings were obtained during the first week of life and at 1, 2, 3, 4 and 6 months. A computer program and visual analysis were used to score sleep state and calculate respiratory rates and apnea densities. In the newborn period there were no gender differences. Males breathed faster and exhibited fewer breathing pauses between 2 and 5 sec from one month of age on. The close correlation between respiratory rate and short breathing pauses suggests that the latter are an integral part of normal respiratory regulation. These findings can be explained by gender-related differences in metabolic rate or maturation of the central nervous system.
The objective of the present study is to compare the emergence of a circadian respiratory pattern in subsequent siblings of SIDS and controls infants to see whether the unique time and age of SIDS is correlated with altered circadian manifestations. During the first three months of life, a pattern in respiratory rates emerged which appeared to be the nightly portion of a circadian rhythm. Subsequent siblings of SIDS exhibited transient accelerated maturation of this circadian pattern. During the first month of life, minima in respiratory rates in quiet sleep occurred during the second and third intervals of the night in subsequent siblings, a pattern not seen until three months of age in control infants.
Subsequent siblings of infants who died of the Sudden Infant Death Syndrome are at a four- to six-times increased risk to die of this syndrome. This study compares the respiratory development during sleep state of this epidemiologic high risk group with that of normal infants during the first six months of life. Subsequent siblings exhibited higher respiratory rates in all states at 3 months of age. Quiet sleep and indeterminate respiratory rates were elevated at 1 week of age compared to control infants. Indeterminate respiratory rates remained higher at 6 months of age. These differences were accompanied by a reduced incidence of total breathing pauses of two to five seconds and six to nine seconds duration in siblings. Study groups could not be differentiated on the basis of either breathing pauses of more than ten seconds of central apnea of six seconds or more. Obstructive and mixed apnea (6 seconds or more) were infrequently observed in these study groups. A high degree of intersubject variability characterized all data on breathing pauses.
Apneic episodes in normal 10-, 20-, and 40-day-old kittens were assessed with polygraphic recordings. End expiratory apneas, usually preceded by somatic activity and/or augmented breaths, with durations less than 10 sec were observed in quiet sleep, active sleep, and transitions between states in all age groups. The highest apnea density was found at state transitions. Heart rate decelerations occurred before, during, and following apneas, but decelerations were not related to apnea duration. Combined central and obstructive components were associated with 9% of apneas in normal kittens.
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The development of variability in heart rate (HR) due to respiration (sinus arrhythmia; SA) has been examined in normal infants from birth through the first 6 months of life. Two aspects of HR variation were examined: the absolute variation at the median respiratory frequency, or extent of sinus arrhythmia (XSA), and the degree to which HR follows respiration regardless of the absolute amount of variation, or coherence of sinus arrhythmia (CSA). Extent of sinus arrhythmia tended to be highest in quiet sleep (QS), lower in active or REM sleep (AS), and lowest in waking (AW), especially after 2 months of age. Extent declined at 1 month of age in QS, but rose over the first 6-month period in all states. During this same period, CSA was also highest in QS, lower in AS, and lowest in AW. Coherence in QS also declined at 1 month and rose between 1 and 6 months; however, no age effects were found in other states. Heart rate was negatively correlated with XSA, but less so with CSA. Sleep state appears to have a significant effect on cardiorespiratory coupling, and this coupling undergoes dramatic changes at 1 month in QS.
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Spontaneous heart rate and variability were examined as a function of age and state from birth to 6 months of age in 10 normal infants and 10 infants at risk for sudden infant death syndrome (SIDS). The risk group showed a higher heart rate at 3 months of age, particularly in the waking state. The risk infants' heart rate also increased more markedly during the first month after birth in both quiet and active sleep. Heart rate in both groups declined after 2 months in every state; however, the risk infants lagged in the 2- to 3-month decline seen with the normal infants. In the awake state, heart rate variability in the risk group did not follow the increase seen with the normals during the 1-week to 2-month age period.
The sequence of developmental changes in sleep pattern organization was derived from 12-hr recordings in 10-, 20 and 40-day-old kittens. Each characteristic of sleep patterning exhibited a distinct maturational sequence. Earlier changes (10-20 days) included quiet sleep (QS) increments and somatic activity decrements; later changes (20-40 days) included emergence of EEG slow waves and spindles, decrements in active sleep (AS), and diminution of QS respiratory variability. Changes in the lengths of state epochs and the types of state transitions spanned the period studied. We suggest that the differential development of the characteristics of sleep patterns reflects differential maturation of distinct nervous system elements.