- Email: [email protected]
Heart rate response related to body movements in healthy and neurologically damaged infants during sleep
Early Human
Development,
31
12 (1985) 31-37
Elseiier
EHD 00676
Heart rate response related to body movements in healthy and neurologically damaged infants during sleep Matti Erkinjuntti Department
of Paediatrrcs,
and Pentti Kero
Turku University Central Hospital, Department
Cardiorespiratory
Research
Accepted
of Physiolow,
and
Unit, University of Turku, Finland
for publication
3 May 1985
Summary Sixteen infants were studied with the static charge sensitive bed (SCSB) method. This method is newly developed for neonatal recordings and it allows recording of body movements, respiration and of the ballistocardiographic signal. Eight healthy newborn infants and eight infants with clear neurological dysfunction were recorded and the heart rate acceleration-deceleration responses to body movements during sleep were studied. Healthy infants had a constant heart rate response to body movements but infants with neurological symptoms had either too weak or hyperactive reactions. This finding can be explained by abnormal function of the autonomic nervous system in infants with disturbance of the central nervous system. static charge sensitive
bed; sleep; heart rate; body movement;
newborn
infant
Introduction The heart rate is regulated by a multilevel pacemaker hierarchy system inside the heart itself. This pacemaker is under sympathetic and vagal control. Impulses from the cerebral cortex can also influence the pacemaker system [17]. The control system has been studied, for example by estimating changes in heart rate and heart rate variation (HRV) [13,14,21,22]. There is a normal level of long-term and short-term HRV which is related to the maturity, age, the sleep state and activity of the neonate
Address
for correspondence;
Hospital,
Kiinamyllynkatu
0378-3782/85/$03.30
Matti Erkinjuntti, M.D., 4-8, 20520 Turku. Finland
0 1985 Elsevier Science Publishers
Dept.
of Paediatrics.
B.V. (Biomedical
Turku
Division)
University
Central
32
[4,6,7,16,18]. In some pathological conditions of the neonate (respiratory distress syndrome, brain death) the HRV is decreased [12,13,23]. It has also been suggested that there are state-related alterations in cardiac activity and that a maturation of the cardio-pulmonary control system is a contributing factor in infants at high risk of SIDS [8,11,19]. In young healthy male adults during sleep the onset of body movement is almost invariably followed by a sudden and strong heart rate acceleration. Correspondingly, a clear heart rate deceleration occurs at the end of body movement during sleep [l]. This kind of acceleration-deceleration reaction can also be seen in fetuses and newborn infants [9,10,20]. The aim of this study was to quantify the acceleration-deceleration reaction of heart rate related to body movements in healthy newborns and in neurologically damaged infants.
Material and Methods
Neonatal recordings have been made with the static charge sensitive bed method (SCSB-method *). This method is already in clinical use for adults and has been newly developed for neonatal recordings [2,5]. In the SCSB-method the neonate or child lies on a mattress system in an ordinary hospital bed (Fig. 1). Various body movements induce a static charge distribution in the active layers of the mattress. These static charges induce potential differences between two metal plates, located under the mattress system and isolated from each other by a stiff insulating plate. Changes related to body movements, respiration, and the ballistocardiogram (BCG) can be recorded [5]. The recordings consisted of the conventional electrocardiogram (ECG) with three chest electrodes, respiration, the BCG and body movement recordings with the SCSB-method. A four-channel tape recorder was used and paper
Fig. 1. The principle
* SCSB-mattress,
of static charge sensitive
model1 BRI-P.,
Vuolahdentie
bed (SCSB) method.
SF-21620,
Kuusisto,
Finland.
33 TABLE
I
Neurological
pathology
of infants
Cerebral haemorrhage + neurologic Convulsions Severe hypokinesia/hypotonia
TABLE
II (high-risk
infants;
n = 8) 5 1 2
signs
II
Histories Group
in Group
of infants
studied Mean
I
Apgar-score Birth weight (g) Gestational age (wk)
9/9/9.3 3387 39.4
Range
Group
2700-3910 38-40
Apgar-score Birth weight (g) Gestational age (wk)
II
Mean
Range
5.5/6.6/&l 2691 36.8
1360-3590 33-40
Recordings were made from 1 week to 3 months postterm. Group I = healthy Group II = infants with neurologic pathology in neonatal period, n = 8.
newborn
infants.
n = 8;
AS
before
during
Fig. 2. The acceleration-deceleration reaction of HR to minor movements during active sleep in healthy newborn infants (Group I. continuous line) and neurologically damaged infants (Group II. interrupted line). The mean acceleration 7.15% (S.D. f 1.78%. range 5.40%). Note: Only one neurologically damaged infant (No. 2) inside the standard deviation in the HR acceleration reaction. Fig. 3. The acceleration-decelerati6n reaction of HR to major movements during active sleep in healthy newborn infants (Group I, continuous line) and nemologically damaged infants (Group II, interrupted line). Mean acceleration of HR 12.3% (SD+ 1.608, range 4.55%). Note: None of the neurologically damaged infants inside the standard deviation in the HR acceleration reaction.
34
recordings were made subsequently. Recordings were made in a laboratory with constant temperature, light, and other environmental conditions. They were made between two feeds and lasted at least two hours. The scoring of the behavioural sleep state was made during recordings using the scoring system described by Prechtl [15]. Sixteen infants were recorded during the first three months after term. Eight infants (Group I) were free from risk-factors during pregnancy, labour, and the neonatal period, and were found to be healthy on clinical neurological examination at the age of one year. The remaining eight infants (Group II) were high-risk infants with clear pathological neurological symptoms during the neonatal period (see Table I). The infants were not medicated during recordings. The etiology of neurologic damage was asphyxia during labour in five cases, birth trauma in two cases, and unknown in one. Six of these eight infants still had clear signs of motor handicap at the age of one year; further follow-up is ongoing. The history of both groups is shown in Table II. Heart rate responses of these infants were studied during body movements in sleep. All body movements lasting 2-5 set (m = minor movements) or more than 5 set (M = major movement) during the state of active sleep were included in the study. There were 518 episodes of body movements (BM) in Group I and 351 in Group II. The mean heart rate was calculated before a BM and correspondingly the mean HR was calculated right at the end of a BM. During body movement the highest heart rate value was calculated. The mean HR acceleration during body movement and deceleration after body movement were calculated in both Groups in percentages, so that the value of HR before a BM is considered to be zero (See Figs. 2 and 3).
Results In Group I (healthy newborn infants), the acceleration of HR during minor (m) and major (M) movements was very constant and the mean acceleration was 7.15 f 1.78%(S.D.) (range 4.30-9.708) in minor movements and 12.3 fl.60%(S.D.) (range 10.41-14.978) in major movements (Figs. 2, and 3). Heart rate decelerated clearly just after a BM, but it still remained higher than the HR before a BM; the mean HR was 3.30 *2.38%(S.D.) (range 0.46-6.74%) higher at the end of a minor movement and 5.0 +3.19%(S.D.) (range 0.53-8.45%) higher at the end of a major movement compared to the HR value before body movements. During minor movements the HR acceleration response was weaker in six patients in Group II compared to the healthy controls. Only two patients had hyperactive HR response (see Fig. 2). On the other hand the HR acceleration response during major movements in Group II were stronger in six infants than in the Group of healthy controls. Two infants had clearly weaker responses. Only one patient (No, 2) from Group II had normal HR acceleration response during minor movements, the others had pathological responses during minor and major movements.
35
Discussion In spite of different kinds of investigations (clinical examination, computed tomography (CT), ultrasound (US), cerebra1 magnetic resonance (MR) and EEG), there is still a need for methods for studying brain damage and the consequent prognosis of neonates. Especially there is a need for methods which give information about functional physiological aspects of the brain to complete the information obtained by anatomical studies like US and CT. These recordings were made with the static charge sensitive bed (SCSB) method which allows very sensitive long-term recording of various body movements, respiratory amplitude and rate, and the ballistocardiogram (BCG). Our experience of neonatal recordings made with the SCSB-method demonstrates that recording of body movements and respiration works well. However, the infra-acoustic noise due to air-conditioning may disturb BCG recordings in the neonate [5]. In this study healthy infants had clear and constant HR acceleration during body movements and HR deceleration at the end of body movements during the state of active sleep. The HR acceleration response was stronger in major movements than in minor movements (Figs. 2 and 3). The same type of HR response has been described in healthy young male adults [l]. The HR acceleration-deceleration response has been studied in fetuses [9,10,20] and also in neonates [20], but studies to quantify this phenomenon in neonates have not been published, especially not in neurologitally damaged infants. The acceleration-deceleration response of HR during body movements in sleep can mostly be explained by a decrease of vagal tone at the beginning of body movement and by vagal activation at the end of body movement [l]. The activation and inactivation of the sympathetic system may support this acceleration-deceleration response especially during long-lasting body movements. The increase of HR during exercise is also due to impulses from the cerebra1 cortex relayed via the hypothalamus to the cardioinhibitory and vasomotor centers [17]. Group II consisted of infants with clear pathological neurological signs during the neonatal period. These infants had abnormal HR response to body movements during sleep. They had either a very high or abnormally weak HR acceleration-deceleration response to body movements. Only one infant (No, 2) of Group II had normal HR acceleration response to minor movements, but seven patients with pathological neurological signs had pathological HR response to both minor and major movements. Infants in Group II seemed to have biphasic HR response to body movements: during small movements HR acceleration is usually weak and during large movements strong compared to healthy controls. These physiological phenomena can best be explained as due, for one reason or another, to abnormal function of the autonomic nervous system. The biphasic HR acceleration response in neurologically damaged infants is probably due to the poor fine tuning of HR regulation control to stimulation. The same unclear regulatory failure which causes pathologic heart rate variations in infants with brain death [12] could be an explanation for pathological HR acceleration-deceleration response to body movements in neurologically damaged infants. The disturbance of the central nervous system seems to affect the function of the autonomic nervous system.
36
Central nervous system damage has been suggested as one possible component of unexpected deaths in infancy (3). On the other hand, increased tonus of the autonomic nervous system has been found in near-miss SIDS infants [8]. It is an interesting question whether the same kind of pathological HR acceleration response occurs in high-risk SIDS infants as in the infants with central nervous system damage in our study. Our findings of pathological HR response to body movements during sleep in neurologically damaged infants can serve as one of the indicators of normal and abnormal condition in neonates.
References
9
10
11
12 13 14 15 16
Alihanka, J. (1982): Sleep movements and associated autonomic nervous activities in young male adults. Acta Physiol. Stand. Suppl. 511, l-85. Alihanka, J., Vaahtoranta, K. and Saarikivi, I. (1981): A new method of long-term monitoring of the ballistocardiogram, heart rate and respiration. Am. J. Physiol. 240, 384-392. Anderson-Huntington, R.B. and Rosenblith, J.F. (1976): Central nervous system damage as a possible component of unexpected deaths in infancy. Dev. Med. Child. Neural. 18, 480-492. DeHaan, R., Patric, J., Chess, G. and Jaco, N. (1977): Definition of sleep state in the newborn infant by heart rate analysis. Am. J. Obstet. Gynaecol. 127, 753-758. Erkinjuntti, M., Vaahtoranta, K., Alihanka, J. and Kero, P. (1984): Use of SCSB-method for monitoring of respiration, body movements and ballistocardiogram in infants. Early Hum. Dev. 9, 119-126. Van Geijn, H., Jongsma, J., DeHaan, J., Eskes, T. and Prechtl, H.F.R. (1980): Heart rate as an indicator of the behavioral state. Am. J. Obstet. Gynaecol. 136, 1061-1066. Harper, R.M., Hoppenbrouwers, T., Sterman, M.B., McGinty, D.J. and Hodgman, J. (1976): Polygraphic studies of normal infants during the first six months of life. I. Heart rate and variability as a function of state. Pediatr. Res. 10, 945-951. Harper, R.M., Leake, B., Hodgman, J. and Hoppenbrouwers, T. (1982): Developmental patterns of heart rate and heart rate variability during sleep and waking in normal infants and infants at risk for the Sudden Infant Death Syndrome. Sleep 5, 28-38. Junge, H.D. (1979): Behavioral states and state related heart rate and motor activity patterns in the newborn infant and the fetus antepartum-A comparative study. I. Technique, -illustration of recordings, and general results. J. Perinat. Med. 7, 85-107. Junge, H.D. (1980): Behavioral states and state-related heart rate and motor activity patterns in the newborn infant and the fetus antepartum. A comparative study. III. Analysis of sleep state-related motor activity patterns. Eur. J. Obstet. Gynecol. Reprod. Biol. 10, 239-246. Katona, P.G. and Egbert, J.R. (1978): Heart rate and respiratory rate differences between preterm and full-term infants during quiet sleep: possible implications for Sudden Infant Death Syndrome. Pediatrics 6, 91-95. Kero, P., Antila, K., Ylitalo, V. and Valimaki, I. (1978): Decreased heart rate variation in decerebration syndrome: quantitative clinical criterion of brain death? Pediatrics 62, 307-311. Kero, P. (1974): Heart rate variation in infants with the respiratory distress syndrome. Acta Pediatr. Stand. Suppl. 250, l-70. Lindqvist, A., Oja, R., Hellman, 0. and Valimaki, I. (1983): Impact of thermal vasomotor control on the heart rate variability of newborn infants. Early Hum. Dev. 8, 37-47. Prechtl, H.F.R. (1974): The behavioral states of the newborn infant (a review). Brain Res. 76, 185-212. Radvanyi, M. and Morel-Kahn, E. (1976): Sleep and heart rate variations in premature and full-term babies. Neuropadiatrie 7, 302-312.
37 17 Ganong, W.F. (ed.) (1983): Review of Medical Physiology, 11th edn. Lange Medical Publ.. Los Altos. California. 18 Siassi, B.. Hodgman, J.E., Cabal, L. and Hon E.H. (1979): Cardiac and respiratory activtty in relation to gestation and sleep states in newborn infants. Pediatr. Res. 13. 1163-I 166. 19 Steinschneider. A. (1970): Possible cardiopulmonary mechanisms. In: Sudden Infant Death Syndrome, pp. 181-198. Editors: Bergman, A.B., Beckwith. J.B. and Ray, C.G. University of Washington Press, Seattle, W.A. 20 Timor-Tritsch, I.E., Dierker, L.J., Zador, 1.. Hertz, R.H. and Rosen, M.G. (1978): Fetal movements associated with fetal heart rate accelerations and decelerations. Am. J. Obstet. Gynecol. 131, 276-280. 21 Valimaki, I. (1969): Tape recordings of the electrocardiogram in newborn infants. Acta Paediatr. Stand. Suppl. 199, l-80. 22 Valimaki, 1. Tarlo, P. (1971): Heart rate patterns and apnea in newborn infants. Am. J. Obstet. Gynec. 110. 343-349. 23 Valimaki, 1.. Rautaharju, P., Roy, S. and Scott, K. (1974): Heart rate patterns in healthy term and premature infants and in respiratory distress syndrome. Eur. J. Cardiol. 4. 41 I-419.
Development,
31
12 (1985) 31-37
Elseiier
EHD 00676
Heart rate response related to body movements in healthy and neurologically damaged infants during sleep Matti Erkinjuntti Department
of Paediatrrcs,
and Pentti Kero
Turku University Central Hospital, Department
Cardiorespiratory
Research
Accepted
of Physiolow,
and
Unit, University of Turku, Finland
for publication
3 May 1985
Summary Sixteen infants were studied with the static charge sensitive bed (SCSB) method. This method is newly developed for neonatal recordings and it allows recording of body movements, respiration and of the ballistocardiographic signal. Eight healthy newborn infants and eight infants with clear neurological dysfunction were recorded and the heart rate acceleration-deceleration responses to body movements during sleep were studied. Healthy infants had a constant heart rate response to body movements but infants with neurological symptoms had either too weak or hyperactive reactions. This finding can be explained by abnormal function of the autonomic nervous system in infants with disturbance of the central nervous system. static charge sensitive
bed; sleep; heart rate; body movement;
newborn
infant
Introduction The heart rate is regulated by a multilevel pacemaker hierarchy system inside the heart itself. This pacemaker is under sympathetic and vagal control. Impulses from the cerebral cortex can also influence the pacemaker system [17]. The control system has been studied, for example by estimating changes in heart rate and heart rate variation (HRV) [13,14,21,22]. There is a normal level of long-term and short-term HRV which is related to the maturity, age, the sleep state and activity of the neonate
Address
for correspondence;
Hospital,
Kiinamyllynkatu
0378-3782/85/$03.30
Matti Erkinjuntti, M.D., 4-8, 20520 Turku. Finland
0 1985 Elsevier Science Publishers
Dept.
of Paediatrics.
B.V. (Biomedical
Turku
Division)
University
Central
32
[4,6,7,16,18]. In some pathological conditions of the neonate (respiratory distress syndrome, brain death) the HRV is decreased [12,13,23]. It has also been suggested that there are state-related alterations in cardiac activity and that a maturation of the cardio-pulmonary control system is a contributing factor in infants at high risk of SIDS [8,11,19]. In young healthy male adults during sleep the onset of body movement is almost invariably followed by a sudden and strong heart rate acceleration. Correspondingly, a clear heart rate deceleration occurs at the end of body movement during sleep [l]. This kind of acceleration-deceleration reaction can also be seen in fetuses and newborn infants [9,10,20]. The aim of this study was to quantify the acceleration-deceleration reaction of heart rate related to body movements in healthy newborns and in neurologically damaged infants.
Material and Methods
Neonatal recordings have been made with the static charge sensitive bed method (SCSB-method *). This method is already in clinical use for adults and has been newly developed for neonatal recordings [2,5]. In the SCSB-method the neonate or child lies on a mattress system in an ordinary hospital bed (Fig. 1). Various body movements induce a static charge distribution in the active layers of the mattress. These static charges induce potential differences between two metal plates, located under the mattress system and isolated from each other by a stiff insulating plate. Changes related to body movements, respiration, and the ballistocardiogram (BCG) can be recorded [5]. The recordings consisted of the conventional electrocardiogram (ECG) with three chest electrodes, respiration, the BCG and body movement recordings with the SCSB-method. A four-channel tape recorder was used and paper
Fig. 1. The principle
* SCSB-mattress,
of static charge sensitive
model1 BRI-P.,
Vuolahdentie
bed (SCSB) method.
SF-21620,
Kuusisto,
Finland.
33 TABLE
I
Neurological
pathology
of infants
Cerebral haemorrhage + neurologic Convulsions Severe hypokinesia/hypotonia
TABLE
II (high-risk
infants;
n = 8) 5 1 2
signs
II
Histories Group
in Group
of infants
studied Mean
I
Apgar-score Birth weight (g) Gestational age (wk)
9/9/9.3 3387 39.4
Range
Group
2700-3910 38-40
Apgar-score Birth weight (g) Gestational age (wk)
II
Mean
Range
5.5/6.6/&l 2691 36.8
1360-3590 33-40
Recordings were made from 1 week to 3 months postterm. Group I = healthy Group II = infants with neurologic pathology in neonatal period, n = 8.
newborn
infants.
n = 8;
AS
before
during
Fig. 2. The acceleration-deceleration reaction of HR to minor movements during active sleep in healthy newborn infants (Group I. continuous line) and neurologically damaged infants (Group II. interrupted line). The mean acceleration 7.15% (S.D. f 1.78%. range 5.40%). Note: Only one neurologically damaged infant (No. 2) inside the standard deviation in the HR acceleration reaction. Fig. 3. The acceleration-decelerati6n reaction of HR to major movements during active sleep in healthy newborn infants (Group I, continuous line) and nemologically damaged infants (Group II, interrupted line). Mean acceleration of HR 12.3% (SD+ 1.608, range 4.55%). Note: None of the neurologically damaged infants inside the standard deviation in the HR acceleration reaction.
34
recordings were made subsequently. Recordings were made in a laboratory with constant temperature, light, and other environmental conditions. They were made between two feeds and lasted at least two hours. The scoring of the behavioural sleep state was made during recordings using the scoring system described by Prechtl [15]. Sixteen infants were recorded during the first three months after term. Eight infants (Group I) were free from risk-factors during pregnancy, labour, and the neonatal period, and were found to be healthy on clinical neurological examination at the age of one year. The remaining eight infants (Group II) were high-risk infants with clear pathological neurological symptoms during the neonatal period (see Table I). The infants were not medicated during recordings. The etiology of neurologic damage was asphyxia during labour in five cases, birth trauma in two cases, and unknown in one. Six of these eight infants still had clear signs of motor handicap at the age of one year; further follow-up is ongoing. The history of both groups is shown in Table II. Heart rate responses of these infants were studied during body movements in sleep. All body movements lasting 2-5 set (m = minor movements) or more than 5 set (M = major movement) during the state of active sleep were included in the study. There were 518 episodes of body movements (BM) in Group I and 351 in Group II. The mean heart rate was calculated before a BM and correspondingly the mean HR was calculated right at the end of a BM. During body movement the highest heart rate value was calculated. The mean HR acceleration during body movement and deceleration after body movement were calculated in both Groups in percentages, so that the value of HR before a BM is considered to be zero (See Figs. 2 and 3).
Results In Group I (healthy newborn infants), the acceleration of HR during minor (m) and major (M) movements was very constant and the mean acceleration was 7.15 f 1.78%(S.D.) (range 4.30-9.708) in minor movements and 12.3 fl.60%(S.D.) (range 10.41-14.978) in major movements (Figs. 2, and 3). Heart rate decelerated clearly just after a BM, but it still remained higher than the HR before a BM; the mean HR was 3.30 *2.38%(S.D.) (range 0.46-6.74%) higher at the end of a minor movement and 5.0 +3.19%(S.D.) (range 0.53-8.45%) higher at the end of a major movement compared to the HR value before body movements. During minor movements the HR acceleration response was weaker in six patients in Group II compared to the healthy controls. Only two patients had hyperactive HR response (see Fig. 2). On the other hand the HR acceleration response during major movements in Group II were stronger in six infants than in the Group of healthy controls. Two infants had clearly weaker responses. Only one patient (No, 2) from Group II had normal HR acceleration response during minor movements, the others had pathological responses during minor and major movements.
35
Discussion In spite of different kinds of investigations (clinical examination, computed tomography (CT), ultrasound (US), cerebra1 magnetic resonance (MR) and EEG), there is still a need for methods for studying brain damage and the consequent prognosis of neonates. Especially there is a need for methods which give information about functional physiological aspects of the brain to complete the information obtained by anatomical studies like US and CT. These recordings were made with the static charge sensitive bed (SCSB) method which allows very sensitive long-term recording of various body movements, respiratory amplitude and rate, and the ballistocardiogram (BCG). Our experience of neonatal recordings made with the SCSB-method demonstrates that recording of body movements and respiration works well. However, the infra-acoustic noise due to air-conditioning may disturb BCG recordings in the neonate [5]. In this study healthy infants had clear and constant HR acceleration during body movements and HR deceleration at the end of body movements during the state of active sleep. The HR acceleration response was stronger in major movements than in minor movements (Figs. 2 and 3). The same type of HR response has been described in healthy young male adults [l]. The HR acceleration-deceleration response has been studied in fetuses [9,10,20] and also in neonates [20], but studies to quantify this phenomenon in neonates have not been published, especially not in neurologitally damaged infants. The acceleration-deceleration response of HR during body movements in sleep can mostly be explained by a decrease of vagal tone at the beginning of body movement and by vagal activation at the end of body movement [l]. The activation and inactivation of the sympathetic system may support this acceleration-deceleration response especially during long-lasting body movements. The increase of HR during exercise is also due to impulses from the cerebra1 cortex relayed via the hypothalamus to the cardioinhibitory and vasomotor centers [17]. Group II consisted of infants with clear pathological neurological signs during the neonatal period. These infants had abnormal HR response to body movements during sleep. They had either a very high or abnormally weak HR acceleration-deceleration response to body movements. Only one infant (No, 2) of Group II had normal HR acceleration response to minor movements, but seven patients with pathological neurological signs had pathological HR response to both minor and major movements. Infants in Group II seemed to have biphasic HR response to body movements: during small movements HR acceleration is usually weak and during large movements strong compared to healthy controls. These physiological phenomena can best be explained as due, for one reason or another, to abnormal function of the autonomic nervous system. The biphasic HR acceleration response in neurologically damaged infants is probably due to the poor fine tuning of HR regulation control to stimulation. The same unclear regulatory failure which causes pathologic heart rate variations in infants with brain death [12] could be an explanation for pathological HR acceleration-deceleration response to body movements in neurologically damaged infants. The disturbance of the central nervous system seems to affect the function of the autonomic nervous system.
36
Central nervous system damage has been suggested as one possible component of unexpected deaths in infancy (3). On the other hand, increased tonus of the autonomic nervous system has been found in near-miss SIDS infants [8]. It is an interesting question whether the same kind of pathological HR acceleration response occurs in high-risk SIDS infants as in the infants with central nervous system damage in our study. Our findings of pathological HR response to body movements during sleep in neurologically damaged infants can serve as one of the indicators of normal and abnormal condition in neonates.
References
9
10
11
12 13 14 15 16
Alihanka, J. (1982): Sleep movements and associated autonomic nervous activities in young male adults. Acta Physiol. Stand. Suppl. 511, l-85. Alihanka, J., Vaahtoranta, K. and Saarikivi, I. (1981): A new method of long-term monitoring of the ballistocardiogram, heart rate and respiration. Am. J. Physiol. 240, 384-392. Anderson-Huntington, R.B. and Rosenblith, J.F. (1976): Central nervous system damage as a possible component of unexpected deaths in infancy. Dev. Med. Child. Neural. 18, 480-492. DeHaan, R., Patric, J., Chess, G. and Jaco, N. (1977): Definition of sleep state in the newborn infant by heart rate analysis. Am. J. Obstet. Gynaecol. 127, 753-758. Erkinjuntti, M., Vaahtoranta, K., Alihanka, J. and Kero, P. (1984): Use of SCSB-method for monitoring of respiration, body movements and ballistocardiogram in infants. Early Hum. Dev. 9, 119-126. Van Geijn, H., Jongsma, J., DeHaan, J., Eskes, T. and Prechtl, H.F.R. (1980): Heart rate as an indicator of the behavioral state. Am. J. Obstet. Gynaecol. 136, 1061-1066. Harper, R.M., Hoppenbrouwers, T., Sterman, M.B., McGinty, D.J. and Hodgman, J. (1976): Polygraphic studies of normal infants during the first six months of life. I. Heart rate and variability as a function of state. Pediatr. Res. 10, 945-951. Harper, R.M., Leake, B., Hodgman, J. and Hoppenbrouwers, T. (1982): Developmental patterns of heart rate and heart rate variability during sleep and waking in normal infants and infants at risk for the Sudden Infant Death Syndrome. Sleep 5, 28-38. Junge, H.D. (1979): Behavioral states and state related heart rate and motor activity patterns in the newborn infant and the fetus antepartum-A comparative study. I. Technique, -illustration of recordings, and general results. J. Perinat. Med. 7, 85-107. Junge, H.D. (1980): Behavioral states and state-related heart rate and motor activity patterns in the newborn infant and the fetus antepartum. A comparative study. III. Analysis of sleep state-related motor activity patterns. Eur. J. Obstet. Gynecol. Reprod. Biol. 10, 239-246. Katona, P.G. and Egbert, J.R. (1978): Heart rate and respiratory rate differences between preterm and full-term infants during quiet sleep: possible implications for Sudden Infant Death Syndrome. Pediatrics 6, 91-95. Kero, P., Antila, K., Ylitalo, V. and Valimaki, I. (1978): Decreased heart rate variation in decerebration syndrome: quantitative clinical criterion of brain death? Pediatrics 62, 307-311. Kero, P. (1974): Heart rate variation in infants with the respiratory distress syndrome. Acta Pediatr. Stand. Suppl. 250, l-70. Lindqvist, A., Oja, R., Hellman, 0. and Valimaki, I. (1983): Impact of thermal vasomotor control on the heart rate variability of newborn infants. Early Hum. Dev. 8, 37-47. Prechtl, H.F.R. (1974): The behavioral states of the newborn infant (a review). Brain Res. 76, 185-212. Radvanyi, M. and Morel-Kahn, E. (1976): Sleep and heart rate variations in premature and full-term babies. Neuropadiatrie 7, 302-312.
37 17 Ganong, W.F. (ed.) (1983): Review of Medical Physiology, 11th edn. Lange Medical Publ.. Los Altos. California. 18 Siassi, B.. Hodgman, J.E., Cabal, L. and Hon E.H. (1979): Cardiac and respiratory activtty in relation to gestation and sleep states in newborn infants. Pediatr. Res. 13. 1163-I 166. 19 Steinschneider. A. (1970): Possible cardiopulmonary mechanisms. In: Sudden Infant Death Syndrome, pp. 181-198. Editors: Bergman, A.B., Beckwith. J.B. and Ray, C.G. University of Washington Press, Seattle, W.A. 20 Timor-Tritsch, I.E., Dierker, L.J., Zador, 1.. Hertz, R.H. and Rosen, M.G. (1978): Fetal movements associated with fetal heart rate accelerations and decelerations. Am. J. Obstet. Gynecol. 131, 276-280. 21 Valimaki, I. (1969): Tape recordings of the electrocardiogram in newborn infants. Acta Paediatr. Stand. Suppl. 199, l-80. 22 Valimaki, 1. Tarlo, P. (1971): Heart rate patterns and apnea in newborn infants. Am. J. Obstet. Gynec. 110. 343-349. 23 Valimaki, 1.. Rautaharju, P., Roy, S. and Scott, K. (1974): Heart rate patterns in healthy term and premature infants and in respiratory distress syndrome. Eur. J. Cardiol. 4. 41 I-419.