M. B. Sterman
University of California, Los Angeles
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Featured researches published by M. B. Sterman.
Pediatric Research | 1976
Ronald M. Harper; Toke Hoppenbrouwers; M. B. Sterman; Dennis McGinty; Joan E. Hodgman
Extract: This study examined spontaneous heart rate (HR) and variability as a function of age and sleep state in eight normal full term infants from birth to 6 months of age. Heart rates recorded during sleep were lower and less regular at 1 week (quiet sleep (QS) mean rate = 128, interquartile range = 6.4 beats/min; rapid eye movement (REM) = 134.5, 11.6) than at 1 month (QS = 138.6, 3.4; REM 139.6, 4.2). Rate decreased sharply from 1 to 3 months (QS = 118; REM 123.8) and decreased only slightly thereafter (6-month QS = 113.5; REM 118.9). Variability decreased rapidly in REM from 2 to 4 months (from 11.4 to 9.1) and less quickly from 4 to 6 months (from 9.1 to 8.2), while QS variability decreased at 1 month (from 6.4 to 5.7) and became stable from that point (6.0 at 6 months). Waking heart rate and variability were both relatively low at 1 week (163, 11.2 beats/min) and increased from that age to 1 month (167.4, 14.3). Rate decreased rapidly in waking at 3 months (152 beats/min) and more slowly thereafter (152 beats/min at 4 months, 149 beats/min at 6 months), whereas variability remained elevated until after 3 months, becoming stable at a lower level during later infancy (3 months = 14.8, 6 months 11.7). Lowest values of rate and variability were found in QS and the highest values were found in waking at all ages, except at 1 week. Heart rates during REM closely approximated those in QS, whereas variability values more closely resembled those of waking.Speculation: It would appear that, in the normal infant, there are at least three relatively discrete stages in the ontogenetic sequence of cardiac rate and variability characteristics: a newborn period, early infancy (1–3 months), and later infancy. Since regulation of cardiac activity is greatly modified by sleep and waking behavior, the measurement of heart rate and variability must consider state as a factor in such regulation. Moreover, since states undergo both qualitative and quantitative changes during the first 6 months of age, the nature of cardiac regulation during this period may be a function of state maturation.
Experimental Neurology | 1981
Ronald M. Harper; Leake B; L. Miyahara; J. Mason; Toke Hoppenbrouwers; M. B. Sterman; Joan E. Hodgman
All-night polygraphic recordings of 25 normal infants were carried out to describe the early development of sleep-waking-state sequencing. Each minute of the 12-h recordings was coded into quiet sleep, active sleep, or waking states. These data were then transformed into a binary series and subjected to spectral analysis using the fast Fourier transform for determination of periodicity of each state. Spectral estimates of sleep- and waking-state periodicities displayed a high variance early in life, but by 3 to 4 months of age, there was a principal rhythm approximating 1 cycle/h in the active and quiet sleep states. The average frequency for the quiet and active sleep states increased significantly from 0.87 to 1.07 cycles/h during this 6-month period. These data offer evidence that the establishment of the periodic organization of sleep states requires 4 months to develop in the normal infant.
Electroencephalography and Clinical Neurophysiology | 1982
M. B. Sterman; Dennis McGinty; Ronald M. Harper; Toke Hoppenbrouwers; J. Hodgman
Power spectral density measured from central cortical EEG recordings during sleep was compared in two groups of 20 infants each at intervals between 1 week and 6 months of age. One group consisted of siblings of infants who had previously died of the sudden infant death syndrome, as determined by history and autopsy report (sibling group). The second group was made up of age, sex, and socioeconomically matched infants with no familial history of sudden infant death (control group).
Experimental Neurology | 1975
Toke Hoppenbrouwers; M. B. Sterman
Abstract In the present study the maturation of states of sleep in kittens from birth to 6 weeks of age was evaluated in terms of the developmental emergence of temporal concordance between defining physiological parameters. In addition, periodicity of the earliest alternation of states, the REM-non-REM (rapid eye movement-nonrapid eye movement) or “basic rest activity cycle”, was traced during this same interval. Parameters studied included EEG, eye movements, neck EMG, gross motor activity, and respiration patterns. Kittens were monitored in isolation for periods of 2–6 hr, providing for collection of both longitudinal and cross-sectional data. Statistical and computer analyses were performed on these data. The most outstanding feature of polygraphic data from kittens between birth and 4 weeks of age was the gradual coalescence of initially discordant physiological measures of sleep state. Prior to 3 weeks of age, polygraphic patterns differed significantly from those of the adult cat, indicating that individual rates of maturation existed for each physiological system measured. Sleep state periodicity was weak at this time due to marked pattern fragmentation. Detectable cycles were clearly shorter than those observed in the adult cat. These findings suggest that the developmental assessment of polygraphic pattern concordance might be a more useful index of sleep state maturation than evaluation based upon attempted comparisons with stable adult patterns. They suggest further that sleep state development in the kitten consists of several different stages. The initial maturation of a basic rest activity cycle may begin during gestation, and be disrupted by the transition to extrauterine life. A postnatal period of approximately 3–6 weeks is required for maturation of sensorimotor and respiratory functions in the completion of this stage. It is proposed that from this time to approximately 3 months of age, forebrain maturation and environmental influences progressively mediate a mature sleep-wake cycle which is superimposed upon this more basic level of organization.
Experimental Neurology | 1978
Toke Hoppenbrouwers; Juan Carlos Ugartechea; Diane Combs; Joan E. Hodgman; Ronald M. Harper; M. B. Sterman
Abstract The objective of this study was to identify and quantify fetal and maternal heart rate (FHR, MHR) periodicities and to examine their interrelation as well as the relation of fetal cycles with the maternal REM-NREM sleep cycle. Heart rate periodicities of the same subjects after birth were correlated with the neonatal REM-NREM sleep cycle. Sixteen all-night polygraphic recordings were obtained during the last trimester of pregnancy and the 1st week of life in seven subjects. Abdominal leads were used to obtain continuous fetal heart rates. Maternal and infant sleep states were scored according to standard criteria. Minute-by-minute values for maternal, fetal, and neonatal heart rates were analyzed on a PDP-12 computer and subjected to time series analyses including auto spectral techniques and complex demodulation. Period lengths of less than 1 h, between 1 and 2 h, and even longer were present in the tracings of mother, fetus, and neonate. Predictable interaction between maternal and fetal heart rate periodicities could not be established. None of the fetal rhythms bore a consistent relationship with the maternal REM-NREM sleep cycles. Maternal sleep onset or the first sleep cycle was accompanied by an increase in fetal heart rate lasting between 10 and 20 min in six of the nine recordings. Fetal heart rate cycles between 1 and 2 hr are probably early manifestations of the neonatal REM-NREM sleep cycle. The transient rise in fetal heart rate could be an adaptive response to either the fall in blood pressure or the shift in acid-base balance upon maternal sleep onset to which the fetus habituates within a short time.
Experimental Neurology | 1981
Ronald M. Harper; Leake B; L. Miyahara; Toke Hoppenbrouwers; M. B. Sterman; J. Hodgman
Abstract The development of ultradian periodicity at 1 cycle/h in electroencephalogram (EEG) variables and the coalescence of these variables with other somatic and autonomic parameters at hourly periodicities were examined in 23 normal infants at 1 week and at 1, 2, 3, 4, and 6 months of age in order to assess the organization of physiologic parameters which underlie the composition of sleep states. Each minute of a 12-h all-night sleep recording was assessed for the median heart and respiratory rate and variability, as well as for the integrated amplitude of the electromyogram, eye movement, and EEG activity at 0 to 1.5, 4 to 7, and 12 to 14 Hz. The amount of hourly periodicity was determined with spectral techniques, and coalescence between variables was examined with coherence procedures. The hourly organization of 12- to 14-Hz EEG activity increased with age, and the hourly organization of low-frequency, 1.5-Hz EEG activity became weaker. Relative to slower ultradian rhythms, however, activity in all three EEG bands increased during the 1- to 3-month period and then declined. The establishment of a high degree of coupling between EEG parameters and other physiologic variables required 3 to 4 months of development, a time frame which parallels the development of stable sleep state organization. Certain variables, such as respiration, showed an earlier time course for increased coherence with EEG parameters than did other parameters. These data suggest that the assessment of coupling between physiologic parameters at the hourly ultradian rhythm may provide an objective assessment of neurological development. They also suggest that the classification of sleep states might be aided by examination of the temporal organization of covarying physiologic parameters.
Pediatric Research | 1980
Toke Hoppenbrouwers; Debra K Jensen; Joan E. Hodgman; Ronald M. Harper; M. B. Sterman
Summary: The objective of the present study is to compare the emergence of a circadian respiratory pattern in subsequent siblings of SIDS and control 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.Speculation: Two recent reports suggest a developmental model in which a physiological deficit can bring about a transient acceleration in maturation. Glück et al. (9) demonstrated an accelerated pattern of lung development as measured by the appearance of phosphatidylglycerol in amniotic fluid as much as eight wk early in intrauterine growth-retarded fetuses. Minkowsky (23) presented preliminary data of increased levels of neurotransmitters such as serotonin and precursors in fetal rats with experimentally induced intrauterine malnutrition. It is tempting to speculate that accelerated maturation in electroencephalographic sleep frequencies and respiratory circadian patterns in subsequent siblings of sudden infant death syndrome are manifestations of a compensatory response to an oxygen deficit.
Pediatric Research | 1980
Toke Hoppenbrouwers; Joan E. Hodgman; Kazuko Arakawa; Ronald M. Harper; M. B. Sterman
Summary: The first objective of this study was to quantify computer-identified breathing pauses in excess of two sec duration in relation to sleep states. The second objective was to examine which respiratory variables at one wk and one month of age predicted total apnea at 2 and 3 months of age.Short apnea (2 to 5 sec) were abundant in recordings of normal infants during the first one-half year of life. Apnea between 6 and 9 sec should be considered normal, whereas apnea in excess of 9 sec occurred most frequently in the first wk of life and declined sharply thereafter. Recording duration substantially affected apnea counts. Apnea at later ages could not be reliably predicted from recordings during the first wk of life.Speculation: Short breathing pauses in QS during the age span under investigation are probably inversely related to breathing rate and caused by the same mechanism responsible for the decline in rate. The change in breathing pauses over age in AS can probably be accounted for by two sources of variance, first, the decline in rate and second, rate-independent developmental changes in control of ventilation during AS.
Early Human Development | 1980
Toke Hoppenbrouwers; Joan E. Hodgman; Ronald M. Harper; M. B. Sterman
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.
Electroencephalography and Clinical Neurophysiology | 1983
S.S Bowersox; M. B. Sterman
The present study describes changes in circadian state pattern organization associated with somatosensory deafferentation in the adult cat. Nine animals, implanted for chronic monitoring of standard sleep state variables, were divided into 3 groups for study. Six cats received dorsal column transections at either a high (C1-C3, N = 3) or low (C5-T1, N = 3) cervical level. The remaining three served as intact controls. State evaluations of continuous 24 h polygraphic recordings disclosed a significant facilitation of alert waking and a suppression of slow wave sleep in animals with high cervical lesions; REM sleep was not affected. State pattern percentages for animals with low cervical lesions were comparable to those of intact controls; however, lesioned animals of both experimental groups showed changes in the frequency of occurrence and duration of individual sleep/wake episodes. These findings were interpreted in terms of the enhancement of intrinsic rhythmic discharge patterns over ventrobasal thalamocortical pathways.