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PRENATAL DEPRESSION EFFECTS ON NEONATES. Brenda L. Lundy. Manchester College. Nancy Aaron Jones. Florida Atlantic University, North Palm Beach.
PRENATAL DEPRESSION EFFECTS ON NEONATES Brenda L. Lundy Manchester College

Nancy Aaron Jones Florida Atlantic University, North Palm Beach

Tiffany Field Graciela Nearing Marisabel Davalos Touch Research Institute University of Miami School of Medicine

Paul A. Pietro Jackson Memorial Hospital

Saul Schanberg Cynthia Kuhn Duke University Medical School

Sixty-three pregnant women (36 with depression symptoms) were recruited during their last trimester of pregnancy. The depressed mothers had higher cortisol and norepinephrine levels and lower dopamine levels. Their infants subsequently had higher cortisol and norepinephrine levels and lower dopamine levels at the neonatal stage. The neonates of depressed mothers also showed inferior performance on the orientation, reflex, excitability, and withdrawal clusters of the Brazelton Neonatal Behavioral Assessment. Stepwise regression analysesrevealed that the depressed mothers' prenatal norepinephrine and dopamine levels significantly predicted the newborns' norepinephrine and dopamine levels and their Brazelton scores, highlighting an early biochemical influence on neonatal outcome.

prenataldepression biochemicalcorrelates maternaldepression

• Brenda L. Lundy, Department of Psychology, Manchester College, North Manchester, IN 46962; e-maih [email protected]. INFANT BEHAVIOR & DEVELOPMENT22 (1), 1999, pp. 119-I 29 Copyright © 1999 ElsevierScience Inc.

ISSN 0163-6383 All rights of reproduction in any form reserved.

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INFANT BEHAVIOR & DEVELOPMENT

Maternal depression research has focused primarily on postpartum depression effects on mother-infant interactions (Cohn, Campbell, Matias, & Hopkins, 1990; Field, Healy, Goldstein, & Guthertz, 1990). The negative effects on the infants have typically been assumed to derive from the early interactions with their depressed mothers. However, more recent data suggest that infants of depressed mothers have "depression-like" behavior from birth including an inferior performance on the Brazelton Assessment Scale (Abrams, Field, Scafidi, & Prodromidis, 1995; Lundy, Field, & Pickens, 1996). Newborns of depressed mothers have shown inferior orienting and motor tone, greater irritability, lower activity levels, and less robustness on the Brazelton (Abrams et al., 1995). These findings were replicated in a study that also noted higher levels of excitability and less expressive behavior in the newborns of depressed mothers (Lundy et al., 1996). Other "depression-like" characteristics in infants include behavioral, physiological and biochemical markers similar to those found in depressed mothers (Field, 1995; Jones et al., 1998; Jones, Field, Fox, Lundy, & Davalos, 1997). Infants of depressed mothers show flat affect, relative right frontal EEG activation, and elevated levels of norepinephrine and cortisol (Field, 1995; Jones et al., 1998; Jones, Field, Fox, Lundy et al., 1997). Relative right frontal EEG activation has been noted as a potential marker of chronic depression (Henriques & Davidson, 1991). An asymmetry in cortical activation refers to the degree to which a specific hemisphere is differentially activated in comparison to the homologous region on the opposite side. Resting EEG asymmetry has been shown to be related to depressive symptoms in adults (Tomarken & Davidson, 1989) and in infants of depressed mothers (Dawson et al., 1992; Field, Fox, Pickens, & Nawrocki, 1995; Jones, Field, Fox, Lundy et al., 1997). The differences in EEG asymmetry scores in the right frontal region are reportedly due to reduced left hemisphere activation and associated with a deficit in approach-related

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behaviors (Henriques & Davidson, 1991; Sobotka, Davidson, & Senulis, 1992). Elevated levels of norepinephrine and cortisol have been noted in depressed mothers and in infants with "depression-like" symptoms (Field, 1995; Jones et al., 1998; Jones, Field, Fox, Lundy et al., 1997). In depression research, the focus has primarily been on the neurotransmitters affected by stress (norepinephrine and epinephrine) and on stress hormones (cortisol). With increased levels of stress, and sympathetic activation, there is an increase in the secretion of cortisol. A hypersecretion of cortisol is commonly noted in profoundly depressed individuals (Ktiovet, 1984). Just as the hypothalamic-pituitary-adrenal cortical system has been implicated in depression, the noradrenergic system has also been implicated. Because these "depression-like" characteristics are present prior to infants' experience interacting with the mother, Field (1995) has proposed a prenatal environmental effects model in which infants of depressed mothers may be born "depressed." Very little is known about the genetic or prenatal transmission of depression and the specific mechanisms that may be involved. However, higher rates of obstetric complications, poorer neurobehavioral functioning (Campbell & Cohn, 1991; Sameroff, Seifer, & Zax, 1982) as well as greater fussiness and less consolability have been reported in newborns of mothers who were depressed during their pregnancy (Whiffen & Gottlieb, 1989; Zuckerman, Als, Bauchner, Parker, & Cabral, 1990). Although, most of the prenatal depression research has been based on observational and behavioral data, a biological mechanism has been outlined in research with primates that may account for poor neonatal outcome (Istvan, 1986; Myers, 1977). According to this mechanism, the release of epinephrine and norepinephrine as a result of maternal anxiety, causes a reduction of uterine arterial blood flow. This reduction of blood flow has been found to result in hypoxia, fetal bradycardia and hypotension and a decrease in the oxygen con-

PrenatalDepression Effects tent of the blood in the fetal femoral artery of rhesus monkeys (Myers, 1975, 1977). Maternal stress in primates has been linked to low birth weights, an increase in spontaneous abortions and impaired placental development (Istvan, 1986; Myers, 1975). Transmission of the mother's catecholamine and cortisol across the placental barrier is also possible, although the human data on this mechanism are limited. The applicability of primate data in understanding the effects human neonatal outcome needs to be interpreted with caution. However, it is possible the elevated levels of epinephrine and norepinephrine may have both a direct and indirect effect on human neonatal outcome. Elevated norepinephrine and cortisol levels have been noted in depressed mothers during pregnancy (Field, 1995). The sympathetically aroused (elevated norepinephrine and cortisol levels) states of newborns of depressed mothers may result from prenatal exposure to their depressed mothers' elevated norepinephrine and cortisol levels. Elevated catecholamine and cortisol levels may cross the placental barrier, having a direct effect on the neonates' behavior. It is also possible that elevated levels of the catecholamines associated with stress (norepinephrine and epinephrine) may reduce uterine blood flow, and contribute indirectly, to inferior neuromotor or behavioral development in infants of depressed mothers. A reduction in neuromotor activity would be associated with decreased levels of the dopamine neurotransmitter. Dopamine has been shown to have an interaction effect with norepinephrine (Weiss, Demetrikpoulos, West, & Bonsall, 1996). Weiss et al. (1996) have developed an animal model (in the rat) linking the noradrenergic February 19, 1999 and dopaminergic symptoms in depression. Weiss et al. (1996) suggest that basic research implicates dopamine much more so than norepinephrine in depression-related behavioral responses including motor activity. In their animal model of stress-induced behavioral depression they have traced depressive symptomatology to abnormal activity (hyperresponsivity) of the locus coeruleus neurons which

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then release galanin from the locus coeruleus access terminals, in turn inhibiting (hyperpolarizing) dopamine neurons in the ventral tegmentum to mediate depression-related behavioral changes. Weiss et al. (1996) demonstrated that elevated levels of norepinephrine have a dampening effect on dopamine production and that interaction leads to depressive symptoms, most especially psychomotor retardation and anhedonia. The purpose of the present research was to determine whether prenatal depression, catecholamine (norepinephrine, epinephrine and dopamine), and cortisol levels contribute to neonatal neuromotor performance as measured by the Brazelton Assessment and neonatal catecholamine and cortisol levels. It was expected that newborns of prenatally depressed mothers would have elevated urinary catecholamines (norepinephrine and epinephrine) and cortisol, decreased levels of dopamine, and demonstrate inferior performance on the Brazelton Assessment compared to newborns of prenatally nondepressed mothers.

METHOD

Participants The women were recruited near the middle to end of the third trimester (i.e., 27-35 weeks, M = 32.3, SD = 2.5) from a university hospital prenatal clinic. The women were assigned to a depressed or non-depressed group based on their scores on the Centerfor Epidemiological Studies Depression Scale (CES-D) (Radloff, 1977). Pregnant women with elevated scores (~- 16) were recruited for the depressed symptom group, while women scoring in the normal range (-: 12) were recruited for the nondepressed group. Women who scored zero to two on the CES-D (N = 5) were not included in the study because low scoring mothers in previous studies showed more depression symptoms including lower activity levels, less expressivity and less frequent vocalizing than high scoring mothers, and thus were thought to

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be denying their symptoms or showing a "faking good" syndrome (Field et al., 1992; LyonsRuth, Zoll, Connell, & Grunebaum, 1986). The women's medical charts were also reviewed in order to screen out those who had engaged in recreational drug use during their pregnancy based on routine drug screens. The final sample included 63 pregnant women (36 with elevated depression symptoms) of low socioeconomic status (M= 4.2, SD = 0.8 on the Hollingshead, 1975). The women averaged 19.4 years (SD = 1.9) and 11.3 (SD = 3.4) years education. Seventy-one percent were single and their ethnicity was distributed: 41% African Americans, 46% White, Hispanic and 13% White, Non-Hispanic. The infants were full term (M = 39.3 weeks GA at birth, SD = 1.7), healthy (M = 9.2 on 10-minute APGAR, SD = .5) and were tested within 7 days after birth (M = 2.8 days, SD = 1.0). Fifty-three percent of the depressed group were female infants and 63% of the non-depressed group were female infants. The two groups did not differ on demographic variables.

Procedure The mothers were given the Center for Epidemiological Studies-Depression Scale (CESD) (Radloff, 1977), the Diagnostic Interview Schedule (DIS), (Robins, Helzer, Croughan, & Ratcliff, 1981), the Fetal Attachment Scale (Burkett, 1990), the Maternal Stress Interview (Field et al., 1988) and the Spielberger StateTrait Anxiety Inventory (STAI) (Spielberger, Gorsuch, & Lushene, 1970). Urine samples were obtained from the mothers during the prenatal visit and from them and their newborns within 24 hours after delivery. The CESD was also given shortly after birth, and the medical records were examined to complete the Obstetric Complications Scale (OCS) and the Postnatal Complications Scale (PNS) (Littman & Parmelee, 1978). The Brazelton Neonatal Behavior Assessment Scale (Brazelton, 1984) was also conducted within one week after birth.

Measures The Center for Epldemiological Studies Depression Scale (CES-D; Radloff, 1977). The CES-D is a 20 item self-report scale designed to measure depression symptoms in the general population. The items include depressed mood, feelings of guilt, worthlessness, helplessness and hopelessness, loss of energy and sleep and appetite disturbances (Radloff & Teri, 1986). Respondents rate the frequency (over the past week) of 20 symptoms ranging from "rarely or none of the time" to "most or all of the time." A total score that ranges from 0 to 60 is calculated by summing all items. Reliability and validity have been acceptable across a variety of demographic characteristics including age, education, geographic area, and racial, ethnic, and language groups (Radloff & Teri, 1986). The CES-D was given to the mother at the time of recruitment and again within 24 hours following delivery. Women receiving elevated scores on the CES-D (~- 16) were given the Diagnostic Interview Schedule to determine whether they could be diagnosed as having major depression or dysthymia. The Diagnostic Interview Schedule (DIS) (Robins et al., 1981) is a standardized diagnostic interview that addresses specific symptoms as well as their chronology, duration and associated impairments. Reliability and validity of the DIS have been found to be as good or better than other structured diagnostic interviews. The Maternal-Fetal Attachment Scale (Burkett, 1990) was used to determine the mother's feelings about her pregnancy and her fetus. The scale consists of 32 items summarized by 3 subscales, maternal feelings, fetal attachment and social support. Answers are based on a 5 point (0-4) Likert scale. For each subscale, the number of points for each answer is added and then averaged based on the number of items answered within the subscale. Maternal Stress Interview (Field et al., 1988) was given to evaluate 5 areas of stress: socioeconomic, crowding, child-rearing, early childhood experiences, and social support. The

Prenatal Depression Effects

number of optimal answers are totaled and the five subscales are summed to achieve a total SCOre.

State Trait Anxiety Inventory (Spielberger et al., 1970) was used to assess levels of maternal trait anxiety. This 20-question 4-point Likert scale forms a summed score from 20 to 80 for the trait subscale. Higher scores indicate greater anxiety.

Urine Samples Urine samples were collected from a subsample of 43 mothers (25 depressed, 18 nondepressed) during their pregnancy and within 24 hours following delivery. Urine samples were also collected from 35 newborns of these mothers (20 depressed, 15 non-depressed) within 24 hours after their birth. For the prenatal visit, urine samples were collected from participants during the morning hours. Prior to sampling, participants had been seated in the clinic waiting room for approximately one hour, during which time they were completing all of the behavioral measures. All participants appeared relaxed prior to the sampling. Specific instructions had not been given to either group (depressed or nondepressed) regarding food intake or exercise for the day of their appointment, although the groups did not appear to differ on these variables. For the neonatal samples, first morning urines were collected from the mothers and their infants. Urine samples were collected from the infant in the neonatal nursery before being brought to the mother's hospital room for feeding. When the infant had urinated, the bag was removed and the single urine sample was stored for later analysis. Mothers were also asked to provide a single urine sample prior to any food intake. Although all samples were collected within 24 hours following delivery, no attempt was made to standardize the number of hours post-delivery samples were collected. However, there were no systematic differences in terms of the timing of sampling between the two groups (depressed and nondepressed). First morning samples were collected for both

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groups. Samples were frozen and sent to Duke University to be analyzed, without information regarding the group from which each sample had been collected. Samples were analyzed for norepinephrine, epinephrine, dopamine, and cortisol levels. Since these were single sample urine assays, the values were corrected using creatinine values for each subject. Norepinephfine, epinephrine and cortisol levels were assessed because of their previously reported positive association with stress and depression (Field, 1995) and dopamine because of a recent animal model implicating a negative association between dopamine levels and depression (Weiss et al., 1996).

Obstetric and Postnatal Complications Obstetric complications were quantified using the Obstetric Complications Scale (OCS) (Littman & Parmelee, 1978). This scale consists of 41 items obtained from medical charts and rated as optimal or nonoptimal. The summary score provides an index of the optimal conditions present during pregnancy. Postnatal complications were quantified using the Postnatal Complications Scale (PNS) (Littman & Parmelee, 1978). The PNS consists of 10 items rated as optimal or nonoptimal. A summary score provides an index of the number of complications during the perinatal period. In addition, infant birthweight, gestational age and APGAR scores were recorded from the medical charts. The Brazelton Neonatal Behavior Assessment Scale (Brazelton, 1984) was administered within one week after birth. The Brazelton assessments were performed by researchers who were trained to .90 reliability and were blind to the group classification of the mothers and infants. This neurobehavioral examination consists of 28 items, each scored on a ninepoint scale, and 20 elicited reflexes, each scored on a three-point scale. The infant's performance was summarized according to the traditional Lester, Als, and Brazelton (1982) clusters, and Lester and Tronick's (1992) depression, excitability and withdrawal factors.

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TABLE 1

Self-Report Measures

Depresse@ CES-D Prenatal Postnatal DIS Diagnosis Major Depression Dysthymia Both Disorders

Neither Disorder Trait Anxiety Prenatal Postnatal Maternal Fetal Attachment Scale Fetal Attachment Maternal Feelings Social Support Maternal Stress Interview

Nondepressedb

M

SD

M

23.65 18.13

7.68 11.34

7.51 *** 7.74***

3.29 6.81

45.03

7.60

32.81 ***

38.40

10.95

30.88"*

7.75 10.01

2.66 2.90 2.51 11.83

0.56 0.61 0.82 3.47

2.96* 3.27** 3.01 ** 13.48*

0.54 0.47 0.58 3.05

SD

14% 4% 14%

68%

Values representmeanscores, an = 36. bn = 27. *p < .05. **p < .01. ***p < .001.

RESULTS M A N O V A s followed by ANOVAs were performed separately for the demographic data, prenatal self-report measures, neonatal birth measures, biochemical data and Brazelton clusters using prenatal CES-D scores as the grouping factor. Stepwise regression analyses were then conducted using the prenatal depression, anxiety and biochemical measures as predictor variables to determine the amount of variance they predicted on those infant biochemical and Brazelton scale variables that differentiated the groups.

Multivariate Analyses of Variance Mothers" Self-Report Measures A significant Group by Time (pretest versus posttest) M A N O V A effect, F(1,62) = 7.70,p < .01, suggested that mothers with depressed symptoms: (1) had higher prenatal CES-D scores as expected, F(1,62) = 17.80, p < .001; (2) higher prenatal and postnatal trait anxiety scores, F(1,62) = 7.80, p < .001; (3) lower

Maternal Fetal Attachment Scale scores, F(1,62) = 9.83, p < .01; and (4) an inferior total score on the Maternal Stress Interview, F(1,62) = 5.02, p < .05 (Table 1).

Biochemical Data A M A N O V A on the biochemical data yielded a significant Group effect, suggesting that the depressed mothers had elevated prenatal cortisol, F(1,42) = 4.16, p < .05 and norepinephrine levels, F(1,42) = 5.23, p < .05 and significantly reduced dopamine levels, F(1,42) = 7.88, p < .01. The infants of depressed mothers also had elevated cortisol, F(1,34) = 13.41, p < .01, and norepinephrine levels, F(1,34) = 9.54, p < .01, and reduced dopamine levels, F(1,34) = 4.90, p < .05 (Table 2).

Birth Measures No significant Group differences were obtained on the neonatal birth measures. The means for the neonatal birth measures were as follows: (1) infant birthweight, M = 3277.2 grams, SD = 486.3; (2) 5-minute A P G A R

Prenatal Depression Effects

125 TABLE 2 Biochemical Values

Depressed Cortisol I Mother-Pre Mother Post Baby NorepinephrineI Mother-Pre Mother-Post Baby Epinephrine1 Mother-Pre Mother-Post Baby Dopamine I Mother-Pre Mother-Post Baby

Nondepressed

M

5D

n

M

SD

n

400.05 306.34 562.07

251.36 249.55 179.64

25 25 20

269.17* 302.06 348.20**

121.40 281.43 158.45

18 18 15

49.79 37.70 55.84

25.54 26.92 21.08

25 25 20

33.62* 29.91 34.62**

18.41 14.21 18.71

18 18 15

6.78 8.04 9.27

3.16 5.35 7.64

25 25 20

6.26 9.64 8.22

2.76 9.67 4.57

18 18 15

236.91 212.86 435.51

113.82 149.92 171.05

25 25 20

323.34** 245.29 587.62*

77.18 114.47 235.98

18 18 15

Valuesrepresentmeanscores. *p < .05. **p < .01. ***p < .001. 1 Unitsare nanogramsper milligram(ng/mg),correctedusingcreatinine.

tion effect, F(6,56) : 5.67, p < .001. Subsequent A N O V A s demonstrated that infants of mothers with prenatal depression had (1) lower orientation scores, F(1,62) = 24.31, p < .001; (2) more abnormal reflexes, F(1,62) = 11.66, p < .001; and (3) less optimal scores on the Lester and Tronick excitability, F(1,62) = 7.00, p < .01) and withdrawal factors, F(1,62) = 8.90, p < .005 (Table 3).

score, M = 8.9, SD = .8; (3) Ponderal Index, M = 2.5, SD = .1; (4) obstetric complications scale, M = 110.2, SD = 20.3; and (5) postnatal complications scale, M = 124.5, SD = 27.2.

Brazelton S c a l e Scores A M A N O V A on the Brazelton Scale data revealed a significant Group X Item interac-

TABLE 3 Brazelton and Lester & Tronick Cluster Scores for Infants Nondepressed b

Depressea~ Brazelton Clusters Habituation Orientation Motor Bahavior Range of State Regulation of State Autonomic Stability Abnormal Reflexes Lester & Tronick Factors Depression Excitability Withdrawal Valuesrepresentmeanscores. an = 36. bn = 27.

*p < .OS.**p < ,01. ***p < .001.

M

SD

M

SD

6.1 4.5 4.8 4.2 5.8 7.1 1.9

0.9 0.7 0.8 0.6 1.1 0.5 1.2

6.3 5.4*** 4.9 3.8 6.0 7.3 0.9***

0.8 0.6 0.7 0.9 1.4 0.8 0.8

2.4 1.0 1.4

1.2 0.8 0.8

2.1 0.5**

1.6 0.6 0.7

0.8**

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Stepwise Regression

Stepwise regression analyses were conducted to determine how much variance on the newborn biochemical and Brazelton scores could be explained by the prenatal self-report and biochemical measures. The prenatal variables entered into the analyses as predictor variables included: prenatal CES-D, prenatal trait anxiety and the prenatal cortisol, norepinephrine, epinephrine, and dopamine levels. Those outcome variables that differentiated the groups were used including the neonates' cortisol, norepinephrine, epinephrine, and dopamine levels and performance on the Brazelton orientation, reflex, depression, excitability, and withdrawal factors. The results showed that for the depressed group, mothers' prenatal depression symptom scores and norepinephrine significantly predicted newborn orientation scores. In addition, mothers' prenatal cortisol predicted abnormal newborn reflexes. In addition, the mothers' depressed symptom scores predicted the Lester and Tronick's depression, excitability, and withdrawal scores for the newborn (Table 4). Infant's norepinephrine was predicted by the mother's prenatal trait anxiety and the mothers' prenatal norepinephrine; the infant's epinephrine and cortisol were predicted by

maternal depression and the infant's dopamine was predicted by maternal prenatal dopamine levels (Table 4).

DISCUSSION

Earlier research on infants of depressed mothers has suggested a prenatal environmental effect because of the "depression-like" characteristics found in the newborns shortly after birth (Abrams et al., 1995; Field, 1995; Jones et al., 1998; Jones, Field, Fox, Lundy et al., 1997; Lundy et al., 1996). The "depressionlike" behaviors include inferior performance on the Brazelton Assessment (Abrams et al., 1995; Lundy et al., 1996), and other behavioral, physiological and biochemical markers that are similar to those found in depressed mothers (Field, 1995; Jones, Fox, Davalos et al., 1997; Jones, Field, Fox, Lundy et al., 1997). The present findings suggest that newborns are affected prenatally by their mothers' depression. The depressed mothers' prenatal cortisol and catecholamine levels predicted the newborns' cortisol and catecholamine levels as well as their performance on the Brazelton. Elevated maternal depression symptoms and prenatal norepinephrine levels predicted the

TABLE 4 Stepwise Regression for the Depressed Group using Maternal Prenatal Predictor Variables and Newborn Outcome Variables

Step Maternal

Neonatal

#

Predictor Variables

Outcome Variables

1 2 1 1 1 2 1 2 1 1 2 1 1

CES-D Norepinephrine Cortisol CES-D CES-D Dopamine CES-D Dopamine CES-D Trait Anxiety Norepinephrine CES-D Dopamine

Orientation Abnormal Reflexes Depression Excitability Withdrawal Cortisol Norepinephrine Epinephrine Dopamine

Multiple

F-to-enter

R

R2

.64 .79 .43 .54 .43 .82 .69 .80 .5~9 .57 .66 .62 .49

.41 .63 .1B .29 .19 .51 .47 .51 .35 .33 .44 .38 .14

4.20 6.50 5.11 16.95 8.45 9.64 9.22 9.71 14.60 12.82 9.77 7.99 8.50

Prenatal Depression Effects

neonates' inferior orientation scores and high levels of prenatal cortisol predicted abnormal reflexes. Further, low levels of maternal prenatal dopamine predicted inferior excitability and withdrawal scores. These data support the association between elevated norepinephrine, low dopamine and depressed behaviors noted in the animal model reported by Weiss and his colleagues (1996). In the Weiss et al., model, the noradrenergic system interacts with the dopaminergic system to produce depression symptoms. Depressed mothers in the present study had elevated cortisol and norepinephrine and low levels of dopamine during the last trimester of pregnancy. This profile was mirrored by their newborns' high cortisol and norepinephrine levels and low dopamine levels. Exposure to the depressed mothers' elevated catecholamine and cortisol levels may have had both a direct and indirect affect on the neonates neurobehavioral development, contributing to their inferior performance on the Brazelton Assessment. The mothers' elevated levels of catecholamines, may have crossed the placenta directly affecting the fetus's hormone levels, and/or may have reduced uterine blood flow indirectly affecting neurobehavioral development. The sympathetically aroused state of a newborn and their less optimal neurobehavioral performance is worrisome given that they are already at risk for being less interactive because of their parenting by depressed mothers. As in a bidirectional process, an already sympathetically aroused infant may further depress the mother and make it difficult for her to establish a satisfying relationship with the infant. The sympathetically aroused state of the newborn may then be compounded later by inadequate stimulation and arousal modulation from their depressed mothers. Whether the depressed mothers have a withdrawn (understimulating) or intrusive (over-stimulating) interaction style, their stimulation is inadequate (Field, 1995). Animal data suggest that inadequate stimulation could continue to contribute to the infants' neurotransmitter (elevated norepinephrine) and neuroendocrine

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(elevated cortisol) imbalance (Kraemer, Ebert, Lake, & McKinney, 1984). In turn, the infants may a develop withdrawn behavior (fiat affect and low activity level) or hyperactive behavior (irritable affect and high activity level) as stimulus barriers to block the inappropriate stimulation from their mothers, hence avoiding further sympathetic arousal. The negative characteristics of a depressed newborn, including the elevated catecholamines, and relative fight frontal EEG activation, as reported in previous studies (Field, 1995; Jones et al., 1998; Jones, Field, Fox, Lundy et al., 1997) may contribute to the excessive externalizing and internalizing behaviors noted at the preschool stage and the disproportionate incidence of depression, conduct disorder and aggression reported in older children of depressed mothers (Field, 1995). The present findings indicate that research on the effects of maternal depression and intervention techniques need to begin during the prenatal period. More research is also needed on intervention techniques such as massage therapies that can reduce norepinephrine and increase dopamine levels such that the mother has a more normal hormonal profile during pregnancy and the infant has less risk of having depression-like characteristics from birth (Field, 1995; Field et al., 1996).

Acknowledgments:

The authors would like to thank the mothers and neonates who participated in this study and to acknowledge Cynthia Bemer for her assistance with data collection. This research was supported by an NIMH Research Scientist Award (#MH00331) and an NIMH Research Grant (#MH46586) to Tiffany Field.

REFERENCES

Abrams, S. M., Field, T., Scafidi, F., & Prodromidis, M. (1995). Maternal "depression" effects on infants' Brazelton Scale performance. Infant Mental Health Journal, 16, 231-235. Brazelton, T. B. (1984). Neonatal Behavior Assessment Scale. Philadelphia: Lippincott.

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Burkett, L. (1990). The Maternal-Fetal Attachment

Scale. Campbell, S. B., & Cohn, J. F. (1991). Prevalence and correlates of postpartum depression in firsttime mothers. Journal of Abnormal Psychology, 100, 594--599. Cohn, J. F., Campbell, S. A., Matias, R., & Hopkins, J. (1990). Face-to-face interactions of postpartum depressed and nondepressed mother-infant pairs at 2 months. Developmental Psychology, 26, 15-23. Dawson, G., Klinger, L., Pansgiotides, H., Hill, D., Spieker, S., & Frey, K. (1992). Infants of mothers with depressive symptoms: Electroencephalographic and behavioral findings related to attachment status. Development and Psychopathology, 4, 67-80. Field, T. (1995). Infants of depressed mothers. Infant Behavior and Development, 18, 1-13. Field, T., Fox, N. A., Pickens, J., & Nawrocki, T. (1995). Right frontal EEG activation in 3- to 6month-old infants of depressed mothers. Devel-

opmental Psychology, 31,358-363. Field, T., Grizzle, N., Scafidi, F., Abrams, S., Richardson, S., Kuhn, C., & Schanberg, S. (1996). Massage therapy for infants of depressed mothers. Infant Behavior and Development, 19, 107112. Field, T., Healy, B., Goldstein, S., & Guthertz, M. (1990). Behavior state matching in motherinfant interactions of nondepressed versus depressed mother-infant dyads. Developmental Psychology, 26, 7-14. Field, T., Healy, B., Goldstein, S., Perry, F., Bendell, D., Schanberg, S., Zimmerman, B., & Kuhn, C. (1988). Infants of depressed mothers show "depressed" behavior even with nondepressed adults. Child Development, 59, 15691579. Field, T., Morrow, C., Healy, B., Foster, T., Adelstein, D., & Goldstein, S. (1992). Mothers with zero Beck Depression scores act more "depressed" with their infants. Development and Psychopathology, 3, 253-262. Henriques, J. B., & Davidson, R. J. (1991). Left frontal hypoactivation in depression. Journal of Abnormal Psychology, 100, 535-545. Hollingshead, A. B. (1975). Thefour-factor index of social position. Unpublished manuscript, Yale University. Istvan, J. (1986). Stress, anxiety, and birth outcomes: A critical review of the evidence. Psychological Bulletin, 100, 331-348.

Vol. 22, No. 1, 1999

Jones, N. A., Field, T., Fox, N. A., Davalos, M., Lundy, B., & Hart, S. (1998). Newborns of depressed mothers are physiologically less developed. Infant Behavior and Development,

21,537-541. Jones, N. A., Field, T., Fox, N. A., Davalos, M., Malphurs, J., Carraway, K., Schanberg, S., Kuhn, C. (1997). Infants of Intrusive and withdrawn mothers. Infant Behavior and Development, 20, 175-186. Jones, N. A., Field, T., Fox, N. A., Lundy, B., & Davalos, M. (1997). EEG activation in onemonth-old infants of depressed mothers. Development and Psychopathology, 9, 491-505. Kraemer, G. W., Ebert, M. H., Lake, C. R., & McKinney, W. T. (1984). Cerebrospinal fluid changes associated with pharmacological alteration of the despair response to social separation in rhesus monkeys. Psychiatry Research, 11, 303-315. Ktiovet, J. (1984). Decrease of binding activity of transcortine in major depression. Encephale, 10, 215-216. Lester, B., Als, H., & Brazelton, T.B. (1982). Regional obstetric anesthesia and newborn behavior; A reanalysis toward synergistic effects. Child Development, 53, 687-692. Lester, B., & Tronick, E. (1992). Neurodevelopmental Battery. Unpublished scale. Littman, D., & Parmelee, A. (1978). Medical correlates of infant development. Pediatrics, 61,470482. Lundy, B., Field, T., & Pickens, J. (1996). Infants of mothers with depressive symptoms are less expressive. Infant Behavior and Development,19, 419--424. Lyons-Ruth, K., Zoll, D., Connell, D., & Grnnebaum, H. U. (1986). The depressed mother and her one-year-old infant: Environment, interaction, attachment and infant development. In E. Tronick & T. Field (Eds.),

Maternal depression and infant disturbance (pp.61-82). New York: Jossey-Bass. Myers, R. E. (1975). Maternal psychological stress and fetal asphyxia: A study in the monkey.

American Journal of Obstetrics and Gynecology, 122, 47-59. Myers, R. E. (1977). Production of fetal asphyxia by maternal psychological stress. Pavlovian Journal of Biological Sciences, 12, 51-62. Radloff, L. S. (1977). The CES-D Scale: A selfreport depression scale for research in the gen-

Prenatal Depression Effects eral population. Journal of Applied Psychologi-

cal Measures, 1,385--401. Radloff, L. S., & Teri, L. (1986). Use of the Center for Epidemiological Studies Depression Scale with older infants. Clinical Gerontologist, 5, 119-135. Robins, L., Helzer, J., Croughan, J., & Ratcliff, K. (1981). National Institute of Mental Health Diagnostic Interview Schedule. Archives of General Psychiatry, 38, 381-390. Sameroff, A. J., Seifer, R., & Zax, M. (1982). Early development of children at risk for emotional disorder. With commentary by Norman Garmezy Monographs of the Society for Research in Child Development, 47 (Serial No. 199). Sobotka, S. S., Davidson, R. J., & Senulis, J. A. (1992). Anterior brain electrical asymmetries in response to reward and punishment. Electroen-

129

Tomarken, A. J., • Davidson, R. J. (1989). Laterality and emotion: An electrophysiological approach. In F. Boiler & J. Grafman (Eds.), Handbook of neuropsychology : Vol. 3. (pp. 419441). Elsevier Science Publishers. Weiss, J. M., Demetrikopoulos, M. K., West, C. H. K., & BonsaU, R. W. (1996). Hypothesis linking the noradrenergic and dopaminergic systems in depression. Depression, 3, 225-245. Whiffen, V. E., & Gottlieb, I. M. (1989). Infants of postpartum depressed mothers: Temperament and cognitive status. Journal of Abnormal Psychology, 98, 274-279. Zuckerman, B., Als, H., Bauchner, H., Parker, S., & Cabral, H. (1990). Maternal depressive symptoms during pregnancy, and newborn irritability.

Developmental and Behavioral Pediatrics, 11, 190-194.

cephalography and Clinical Neurophysiology, 83, 236-247. Spielberger, C., Gorsuch, R. L., & Lushene, R. E. (1970). The State-Trait Anxiety Inventory. Consuiting Psychologists Press, Palo Alto: CA.

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