Expressed Emotion Toward Children With Behavioral Inhibition: Associations With Maternal Anxiety Disorder

Expressed Emotion Toward Children With Behavioral Inhibition: Associations With Maternal Anxiety Disorder DINA R. HIRSHfELD, PH.D.. JOSEPH BIEDERMAN, M.D., LESLIE BRODY, PH.D., STEPHEN V. FARAONE, 1'11.0., AND JERROLD E ROSENBAUM, M.D.

ABSTRACT ObJective: To examine the role of maternal psychopathology in influencing "expressed emotion" (EE) directed toward children with behavioral inhibition (BI) or psychiatric disorders. Method: Maternal EE was assessed via Five-MinuteSpeech-Sample in two samples of children previously evaluated for child and maternal lifetime prevalence of DSM-I/I disorders and assessed via laboratory observations for BI. The authors previously reported that maternal EE was associated with Bl and with the number of child behavior and mood disorders in these samples. The at-risk sample (N =

30) consisted of mothers with panic disorder and psychiatric controls and their 4- through 10-year-old children. The

Kagan sample (N

=

41) consisted of children selected at age 21 months as BI or uninhibited and followed through age

11. Results: Interaction effects were found: In mothers with anxiety disorders, but not those without, maternal criticism (a component of EE) was significantly associated with child 81, independently of the child's number of disorders. Similarly, in mothers with anxiety disorders only, maternal criticism was significantly associated with a high number of child disorders. Conclusions: The relationships between mothers who have anxiety disorders and their children who have BI or psychiatric disorders may be marked by criticism or dissatisfaction. If confirmed, these findings offer opportunities for appropriate interventions. J. Am. Acad. Child Ado/esc. Psychiatry, 1997, 36(7):910-917. Key Words: behavioral inhibition, anxiety disorder, expressed emotion.

The familial nature of anxiety disorders has been documented by many authors (Crowe et aI., 1983; Moran and Andrews, 1985). In particular, several studies have reported associations between anxiety disorders in parents and their young off:~pring (Last et aI., 1987; Turtler et aI., 1987). Our group has idel1£ined "behavioral inhibition to the unfamiliar" as a temperamel1£al risk factor for anxiety disorders in childhood (Biederman et al., 1990, 1993; Rosenbaum et aI., 1988). "Behavioral inhibition" (BI) represents a tendency to exhibit physi-

Child and Adolescent Psychiatry.

ological arousal and behavioral restraint in novel situations (Kagan et al., 1988). Inhibited children are fearful and shy as toddlers, quiet and withdrawn with unfamiliar people during the preschool years, and reticent with peers in middle childhood. BI has been found to be associated with increased rates of parental anxiety disorder and higher rates of anxiety disorders in the children themselves (Biederman et aI., 1990; Rosenbaum et aI., 1991). Stability of BI through early childhood (Hirshfeld et aI., 1992) and parenralloading for multiple anxiety disorders (Rosenbaum et al.. 1992) appear to increase the risk that an inhibited child will develop anxiety disorders. While there is evidence that BI (Robinson et al., 1992) and anxiety disorders (Torgersen, 1983) have genetic bases. we would expect their expression to be affecred by environmental factors as well. Little is known, however, about aspects of the parent-child relationship that might mediate the inhibited child's heightened risk for anxiety disorders. A first step toward examining aspects of the parent-child relationship that might mediate the rrans-

910

I. AM. A 1:,\ 11. C1IILIl AIlOLFSC. PSYCHIATRY..\6:7. JULY JIJln

Acrrptrd Seplember 19. 19')6. Drs. Hirshjatl. Biederman, lind ROJenlhlllJII ,Irr Il';'f, ,hf 1~\:y(;'itll1)' ,)'frl'i(f, M,/SS"chusrlls (,r1lmt! Haspilill. /{"/"I'IIrd '>tNlh,t! SdJl)(}I. BOSI01I; I)" Brody iJ wilh Ihe Deptlrll/lflll o/I'5yd)()lo,'{Y. Bmw1I {/1IiI'eniIY (Ur. Brody); ,11J(11)': filrtlOIlt' is

with fhr C(}lIlmollwl'tll,!J

RrH'tlreJ, <:1'1I1t'1". ~f'IJJ'ld,/t;jftlJ

Aft'lll,tI

He"llh Lrmer. B05Iml. The 'It/tlJ()''' gmlejitlly II(k1lo/(OIN{~e I'm/i-J.<"rj'TII/lle Ktlg'/II ,,(tf,,·1 Jep'/rtlllellt ojP5Jchology. HtI/"I'tlrd Ullit''I"5iry. Jill' hi, ,."1It1I,,mlli"lI illthi, .f/url)'. rhi,tlrtid,. is baud on ,hi' first 1l1l1!Jor j tlOl"!onl! diHfrftlfilJ1J. ('OlTfSpollrlma 1(1 Dr. Hinhfi-Irl. M(,H Rr5etln-b lIllil. 51! Sltllli/;ml Slre,·I. 41h Floor. R05lnll. MA OJ I f.1. O!lOO!O''''' JI)I)7 by Ihe Am",;can AcadmlY of

EXPRESSED EMOTION AND MATERNAL ANXIETY

mission of anxiety symptoms from parent to child is to study whether parent-child relationships differ in families of anxious parents. For example, we might ask whether parents with anxiety disorders are more protective or critical than parents without anxiety disorders. We might also seek to determine whether such parental attitudes are influenced primarily by child characteristics, parental characteristics, or other family factors. One way to answer these questions is to examine "expressed emotion" (EE) in parents with anxiety disorders. EE is a measure of an attitude of criticism and/or emotional overinvolvement (EOI) that a parent holds toward a child. It is measured by coding critical remarks and evidence of overinvolved or self-sacrificing behavior expressed by the parent during the course of an open-ended interview or brief speech sample about the child. EE has traditionally been studied as a family environment factor that adversely affects the course of psychiatric disorders in adult patients (Brown et aI., 1972; Hooley et al., 1986; MikJowirz et aI., 1988). High EE in parents has also been found to be associated with poorer course or relapse in childhood depression (Asarnow et al., 1993). Moreover, high EE expressed by parents was found to be cross-sectionally associated with several measures of poor child adjustment (Seifer et al., 1992; Vostanis and Nicholls, 1992) and with disruptive behavior disorders, anxiety disorders, and other major childhood disorders (Asarnow et aI., 1994; Hibbs et aI., 1991; Schwartz et aI., 1990; Stubbe et al., 1993). We previously reported on the association between maternal EE and child BI and psychiatric disorders in a sample of children of parents with panic disorder and other psychiatric controls (Hirshfeld et aI., 1997). We found that child BI was associated with maternal criticism independently of its association with child psychopathology. We also found that the number of behavior and mood disorders in these high-risk children was associated with maternal criticism independently of the association with BI. To fully understand these findings, however, it is necessary to examine associations with maternal psychopathology as well. In this way we can determine to what degree maternal criticism is related to child characteristics, maternal characteristics, or interactions between the two. Three previous studies have investigated the influence of parental psychopathology on EE. Stubbe and colleagues (1993) screened mothers for depressive and

neurotic symptoms using self-report instruments and found that while EOI was related to neuroticism, the association between EOI and childhood anxiety disorders was independent of maternal neuroticism. Hibbs and colleagues (1993) assessed parents with the Schedule for Affective Disorders and Schizophrenia for School-Age Children-Lifetime version and found associations between paternal psychopathology in general ("any disorder") and paternal EE and between maternal affective disorder and maternal EE. Maternal EE was associated both with child and maternal psychopathology, while paternal EE was associated only with paternal psychopathology. Goodman and colleagues (1994) used a modified measure of EE and found that maternal depression was associated with critical and overinvolved comments. No study to date has specifically examined the relation between parental anxiety disorders and EE directed toward children. To address these issues, we therefore examined associations between maternal psychopathology and EE toward the children in our two previously studied samples of children at risk for anxiety disorders. In addition, we examined whether maternal EE toward a particular child reflects the general family environment or rather the particular quality of the mother-child dyad in question. We reasoned that if maternal EE were related to child and maternal but not general family characteristics, it might be considered unique to this dyad. Therefore, the following research questions were examined: (1) whether maternal psychopathology would be associated with high maternal EE; (2) whether maternal psychopathology and child characteristics (BI and psychiatric disorders) would interact to predict high EE; and (3) whether other family environment variables (intactness, size, socioeconomic status [SESJ, conflict, expressiveness, or cohesiveness) would be associated with high EE. On the basis of the available literature, we hypothesized that maternal psychopathology would be associated with high EE and that EE would be more strongly associated with child and maternal characteristics than with aspects of the family as a whole.

J. AM. ACAD. CHIl.D ADOLESC. PSYCHIATRY, 36:7, JUl.Y 1997

911

METHOD Srudy procedures are presented in detail in earlier reports (Hirshfeld et aI.• 1997), Briefly, maternal EE was assessed in a follow-up study of two preexisting samples of children at risk for amriety disorders and comparison children.

HIRSHFELD ET AI..

Samples

Procedures

The at-risk sample consisted of non patient children of adult outpatients at the Massachuserrs General Hospital treated for panic disorder/agoraphobia, major depression, or orher psychiatric disorders and non patient siblings of children in treatmenr for anenrion deficit disorder (Rosenbaum et al.. 1988). Of the original 56 index children, 77% panicipated in the follow-up srudy at ages 4 through 10 (Biederman et aI., 1993). The Kagan et al. longitudinal cohon was composed of children originally recruited at age 21 monrhs for a study of the stabiliry of BI (Garcia-Coli et aI., 1984). Epidemiologically derived groups of roddlers with extreme BI or uninhibition had been idenrified on the basis of laborarory observations across a variety of unfamiliar settings. The children had been followed up at ages 4, 5.5, and 7.5 years (Kagan et aI., 1988). At the last of these visits, they had been evaluated for DSM-lli diagnoses (Biederman et al.. 1990). and all available parents had been assessed for anxiery and mood disorders (Rosenbaum et aI., 199\). In addition, ro ensure blindness of assessmenr, a comparison group had been included consisting of children whose behavior had not been extreme enough when observed at 21 monrhs ro be included in the inhibited or uninhibited samples. Thirry-three index children (80% of the baseline sample) and II comparison children panicipated in the follow-up srudy at ages II ro 12 years.

In the follow-up srudy. mothers were reinrerviewed about the index child. assessed for EE, and given several interview and self-repon measures, as described below. At this time, the at-risk children were 4 through 10 years old and the Kagan children were II through 12 years old. Measures ofPsychopathology. Children's lifetime diagnoses were assessed via structured clinical interviews with mothers (Biederman et aI., 1993). The NIMH Diagnostic Interview for Children and Adolescents-Parent version (Herjanic and Reich, 1982) was used ro assess behavioral, affective, eating, elimination, and substance abuse disorders. and anxiery disorders were assessed using the anxiery module from the Schedule for Affective Disorders and Schizophrenia for School-Age Children-Epidemiologic version (Orvaschel, 1985). Interviews were administered by trained, supervised research assistanrs with high interrater reliabiliry for diagnostic categories (overall l( = .88) (Biederman et aI .• 1993). Numbers of mood, behavior, and anxiery disorders were summed ro derive the variable "number of disorders." Expressed Emotion. EE was assessed via the Five-Minute-SpeechSample (Magana et aI., 1986). Each mother was asked to describe her child and her relationship with him or her and was audiotaped as she spoke without inrerruption for 5 minutes. All tapes were coded blindly ro diagnostic and demographic variables but not to age of child by the first author, who was trained in the procedure and cenified as a reliable rater by Goldstein's laborarory at UCLA, where the measure was developed. Age of child was considered imponant in judging evidence of overprotective behavior in the parent. Twenry of the tapes were also rated by an expen rater at UCLA. Since the two categories of EE---eriticism and EOI-represenr empirically and theoretically distinct constructs, they were analyzed separately. Because very few « 10%) of the cases were rated as highcriticism, the borderline-criticism cases were included with the highcriticism cases in all analyses. For EOI, the pure high category was used since it was rated with much higher reliabiliry than high/borderline EOI. Inrerrater agreemenr rates (percent agreement/total and l( values) for the categories used were good to excellenr: criticism (high/borderline versus low): 85%, l( = .69; EOI (high versus borderline/low): 100%, l( = 1.0. Family Environmmt Scale. Family conflict. cohesion. and expressiveness were measured via the Family Environmenr Scale completed by the morhers. This widely used self-report instrumenr demonstrates high inrernal and test-retest reliabiliry (Moos and Moos, 1974).

Measures of Behavioral Inhibition All assessmenrs of BI were done in the Harvard Infant Study laborarory by Kagan and colleagues. Children in the at-risk sample had been assessed at age 2 through 7 years (2 ro 3 years before measuremenr of EE). Assessments had been made using established age-specific prorocols developed and used previously in Kagan's studies of BI cited above. Children in each age group were classified dichoromouslyas inhibited or nor inhibited, on the basis of their scores on variables previously demonstrated ro be the most sensitive indices of inhibition and to differentiate the inhibited and uninhibited groups (Rosenbaum et al.. 1988). While the inhibited children in this sample were extreme in inhibition, those who were nor inhibited were of average sociabiliry and boldness. In the Kagan sample, the children's original classifications as inhibited or uninhibited at 21 monrhs were used (Garcia-Coli et al.. 1984). In contrast ro the children in the atrisk sample, the uninhibited children in the Kagan sample were extremely bold and sociable in unfamiliar siruations.

Data-Analytic Approach

In both samples. lifetime diagnoses in morhers had been assessed via the National Instirute of Menral Health (NIMH) Diagnostic Interview Schedule (DIS) (Robins et aI., 1981). Retrospeerively worded questions from the Diagnostic Inrerview for Children and Adolescenrs (Herjanic and Reich, 1982) had been used ro assess childhood anxiery diagnoses (Rosenbaum et al.. 199\). In the at-risk sample, lifetime diagnoses in parents had been assessed at the time of initial sample recruitment. In the Kagan sample. parents had been interviewed with the anxiety and affective disorders modules of the NIMH DIS just after the children's 7.5-year assessmcnr. Therefore, the maternal disorders used in this analysis are lifetime diagnoses assessed 2 ro 4 years earlier than the assessmenr of EE and nor concurrenr diagnoses. Specific diagnoses and general categories (any anxiery disorder, any mood disorder) were used in analyses.

As described previously (Hirshfeld et aI., 1997), data from both samples were combined in a manner that checked for possible differences between samples. First, univariate associations between demographic variables (child's age, gender. and birth order, sibship size, family intactness. SES. and mother's age) and EE variables (high/borderline versus low criticism and high versus low/borderline EOI) were tested in the samples combined, using 2 x 2 Xl or Fisher's Exact Tests (categorical variables) or t tests (continuous variables). Univariate associations between EE variables and childhood BI, childhood diagnostic categories (behavior, mood, and anxiery disorders), numbers of child diagnoses (total number of diagnoses and number of behavior. mood, and anxiery disorders, respectively), and maternal diagnostic categories (anxiery and mood disorders) were also examined. Next, to control for associated variables, logistic regression analyses were conducted (Hosmer and Lemeshow. 1989). For each asso-

912

J. AM. ACAD. CIIILD ADOLESC. PSYCHIATRY. 36:7. JULY 1997

Measures of DSM-III Diagnoses in Parents

EXPRESSED EMOTION AND MATERNAL ANXIETY

ciation tested, the EE category (e.g., criticism) was used as the dependent variable, and the diagnostic category being tested (e.g., maternal anxiety disorder) was used as the predictor. In the first step, all demographic and diagnostic variables found to be significantly associated with the EE category in the univariate tests, as well as the variable "sample," were entered as a block. In the second step, the predictor was entered. In the third step, the interaction of predictor and sample was entered. If the interaction term (predictor X sample) was not significant (i.e., if the association between predictor and outcome variable was consistent across samples), findings were reported for both samples combined. If the interaction term was significant at a trend level or lower (p < .I) (i.e., if the association between predictor and outcome variable differed between samples), the association was reanalyzed separately by sample, using X2 analyses or logistic regression as appropriate. Only analyses in which the predictor significantly added to the variance accounted for by the covariates (as indexed by a significant improvement term) were considered significant. Therefore, analyses identified variables uniquely associated with high EE. To test interactions between maternal anxiety disorder and child variables (either number of diagnoses or BI), an interaction term (consisting of the product of the maternal and child variables) was added to the equation as a predictor. In these analyses, all demographic and diagnostic variables found to be significantly associated with the EE category in the univariate tests (including the child and maternal variables in question) were entered as a block in the first step. In the second step, the interaction term (maternal variable X child variable) was entered. If the interaction term was significant, the relation between EE and the child variables was examined separately for different levels of the maternal variable. Since inclusion of the variable "sample" and the interaction term "sample' predictor" would have meant including too many variables in the equation, the latter comparisons were repeated separately by sample to determine whether associations were consistent across samples. The EE categories were used as outcome or dependent variables in these analyses because they were collected last. The intention was not to make any assumptions about causal directions, but rather to examine correlational associations among three sets of variables (maternal diagnosis, child characteristics, and EE). The strengths of association measured would have been mathematically equivalent regardless of which was used as the dependent variable. (The issue of causality is addressed further in the "Discussion. ")

TABLE 1 Rates of Maternal Diagnoses in the Two Samples At-Risk Sample (%) (N= 29) Any major psychopathology" Any anxiety disorder b Panic disorder Agoraphobia Social phobia Simple phobia Two or more anxiety disorders b Any mood disorder Major depressive disorder Dysthymic disorder

Kagan Sample (%) (N= 41)

63.3" 48.3' 44.8'" 17.2 17.2 24.1

24.4 22.0 4.9 4.9 9.8 7.3

31.0'" 41.4

2.4 24.4

41.4 3.4

22.0 2.4

"Includes panic disorder and major depressive disorder. blncludes any adult or childhood anxiety disorder. 'p < .05; "p < .01; '''p < .001 by 2 X 2 X2 analysis.

Logistic regression analysis revealed that lifetime prevalence of anxiety disorder ("any anxiety disorder")

in the mother was positively associated with criticism. This diagnostic category included any of the following: panic disorder, agoraphobia, social phobia, phobic disorder, obsessive-compulsive disorder, or, in childhood, avoidant, overanxious, or separation anxiety disorder. The rate of "any anxiety disorder" was higher in mothers with high/borderline versus low criticism (17/26 versus 17/44, or 65.4% versus 38.6%, respectively, X2 = 4.68, df = 1, P < .05). This association remained significant when controlled for child demographic and diagnostic variables (child age and gender and number of mood and behavior disorders) (improvement with maternal anxiety disorder added: X2 = 4.41, P < .05; odds ratio = 4.27, P < .05). This association was also significant when the analysis was limited to mothers who had anxiety disorder only, without comorbid depression, when compared with mothers who had neither a mood nor an anxiety disorder. No significant unique associations were found between maternal EE and any specific anxiety diagnoses, nor any other general categories of anxiety disorders (e.g., multiple anxiety disorders, any adulthood anxiety disorder, any childhood anxiety disorder). Although the association between maternal criticism and maternal anxiety disorder was reduced to trend significance if child BI was controlled for along with the other child diagnostic and demographic variables, the direction of the findings remained the same (n decreased to 59; improvement with maternal anxiety dis-

]. AM. ACAD. CHILD ADOLESC. PSYCHIATRY, .36:7. JULY 1997

913

RESULTS

Demographic and Diagnostic Characteristics of Samples

As reported previously (Hirshfeld et aI., 1997), children in the at-risk sample were younger, of later birth order, and more likely to be male than children in the Kagan sample. Families in the at-risk sample were of lower SES. Mothers in the clinically derived at-risk sample had much higher rates of psychopathology, accounted for primarily by anxiety disorders (Table 1). Associations Between Maternal Criticism and Maternal Anxiety Disorder

HIRSHFELD ET AL.

TABLE 2 Rates of Maternal Criticism in Dyads Varying on Maternal Anxiety Disorder and Child Behavioral Inhibition Rate of High Criticism Child Inhibited (N = 33)

Child Not Inhibited (N = 26)

Maternal Anxiety Disorder

Rate

%

Rate

%

Present (N = 31) Absent (N = 28)

13/20 3/13

6S" 23

2/11 4/IS

18 27

NOt(: NS

=

Improvement in Predicting Criticism When Inhibition Is Added

Xl = 7.22" NS

Odds Ratio

43.3" NS

not significant.

"p < .OS; "p < .01.

order added: X2 = 2.67, P = .1; odds ratio = 3.53, not significant [NS)). It is interesting that maternal anxiety disorder was significantly related to criticism when child age and gender and BI were controlled for but number of child mood and behavior disorders were excluded from the equation (N = 59; improvement with maternal anxiety disorder added: X2 = 4.95, P < .05; odds ratio = 4.71, P < .05). To examine whether maternal anxiety disorder interacted with child characteristics in predicting criticism, statistical interaction effects were explored. Interaction Between Maternal Anxiety Disorder and Child Behavioral Inhibition

Maternal anxiety disorder interacted with child BI in the combined samples to predict rate of maternal criticism. The interaction term "any anxiety disorder in the mother" (present or absent) X "child BI" (present or absent) was significantly associated with criticism when controlled for child demographic (age and gender) and diagnostic (number of mood and behavior disorders) covariates of criticism (improvement with interaction term added: X2 = 8.68, P < .01). In mothers with anxiety disorders, maternal criticism was highly related to child BI (rates of criticism in inhibited versus noninhib-

ited children: 13/20 or 65.0% versus 2/11 or 18.2%, X2 = 6.23, P < .05) (Table 2). The association remained significant even after age and sex of child and number of child disorders were controlled (improvement with BI added: X2 = 7.22, P < .01; odds ratio = 43.3, P < .05). In nonanxious mothers, however, maternal criticism was unrelated to child BI (rates of criticism in inhibited versus noninhibited children: 3/13 or 23.1 % versus 4/15 or 26.7%, X2 = .05, NS). Interaction Between Maternal Anxiety Disorder and Number of Child Disorders

Maternal anxiety disorder also interacted with number of child disorders in the combined samples to predict maternal criticism. This interaction was at trend significance when controlled for child demographic variables (age and gender) associated with criticism (improvement with interaction term added: X2 = 2.93, P < .1; odds ratio = 2.35, P = .1). In children of mothers with anxiety disorders, the mean number of child disorders was significantly higher if the mothers expressed high criticism (t = -2.76,p = .01) (Table 3). This association remained significant even after age and sex of child and BI were controlled. In contrast, in children of nonanxious mothers, number of diagnoses did not

TABLE 3 Rates of Disorders in Children of Mothers With and Without Anxiety Disorders and High Criticism No. of Diagnoses in Child High Criticism (N = 26) Maternal Anxiety Disorder Present (N = 34) Absent (N = 36) NOt(: NS

Low Criticism (N = 44)

Mean

SD

Mean

SD

2.9 1.6

1.9 I.S

1.4 1.1

1.3 1.1

Improvement in Predicting Criticism With No. of Diagnoses Added

y! = 6.08" NS

Odds Ratio

2.76t NS

= not significant.

tp < .I;"p < .OS.

914

J. AM. ACAD. CHILD ADOLESC. PSYCHIATRY. 36:7. JULY 1997

EXPRESSED EMOTION AND MATERNAL ANXIETY

differ between children of mothers rated high and low on criticism (t = -0.94, NS).

As hypothesized, significant associations between EE and maternal psychopathology were found in these samples of inhibited and noninhibited children. Lifetime history of maternal anxiety disorder was associated with higher criticism toward the child, and in one sample, maternal affective disorder was associated with EOI. It is interesting that maternal anxiety disorder interacted with number of child diagnoses as well as with child BI to predict maternal criticism. Thus, mothers with anxiety disorders who had children with higher numbers of disorders were significantly more likely to express criticism than mothers with anxiety disorders whose children did not have high numbers of disorders or than mothers who did not have anxiety disorders. This association held even when other variables associated with criticism, including child BI, were controlled. In similar fashion, mothers with anxiety disorders expressed significantly more criticism toward inhibited children than noninhibited children, even when all

other variables associated with criticism were controlled. This tendency was not true of nonanxious mothers. Nthough preliminary, these findings suggest that relationships in parent-ehild dyads in which the child is at risk for anxiety disorders are marked by parental criticism or dissatisfaction. Since we measured EE only at a single point, we cannot draw conclusions about causal directions of effects. However, the finding that maternal criticism was predicted by measures of child BI and mother's lifetime anxiety disorders collected several years earlier raises the possibility that maternal criticism may be an outcome of these two factors. That is, child BI may elicit criticism in mothers prone to respond in this manner (i.e., mothers with a history of anxiety disorders). Nternatively, maternal criticism may be an interactively associated variable that both maintains and is maintained by these other factors. Thus, it is possible that the presence of anxiety in a mother and difficult or challenging behavior in the child (such as BI or disruptive behavior) may contribute to a strained mother-child relationship, heightened stress for both, and possibly the exacerbation of symptoms for both. It should be underscored, however, that the maternal criticism found in the present study was not severe and was characterized more by dissatisfaction ("borderline-high criticism") than by clear hostility. As such it may compare in some respects with the "low care" dimension (low acceptance or warmth) described by Parker and others in the family backgrounds of phobic and depressed adults (Parker, 1983). The association between maternal anxiety disorders and maternal criticism merits further discussion. Anxious mothers, with and without comorbid affective disorders, were more likely than others to voice criticism ofchildren who were challenging (i.e., who exhibited BI or psychological disorders). The association was with lifetime history of anxiety disorders in the mothers, including childhood disorders, and this history had been assessed 2 to 4 years prior to assessment of criticism. Mothers from the at-risk sample, who had more severe clinical diagnoses, were typically in ongoing psychopharmacological treatment. Therefore, it is likely that the association between maternal anxiety disorder and criticism is based on long-standing (traitlike) anxiety in the mother, rather than the result of acute symptomatology. While the reason for the association between predisposition for anxiety disorder and expression of criticism

J. AM. ACAn. CHII.\l AIHll.F.SL PSYCHIATRY ..\6:7. JlIl.Y 1')<)7

915

Association Between Maternal EOI and Maternal Mood Disorder

1n the Kagan sample only, the rate of "any mood disorder" was higher in mothers with high EOI than in those with low/borderline EOI (3/4 or 75.0% versus 7/37 or 18.9%, p < .05 by Fisher's Exact Test; odds ratio = 12.9, P < .05). When this analysis was limited to mothers with mood disorder only (without comorbid anxiety disorder) compared with mothers without mood or anxiety disorders, the rate of "mood disorder only" remained higher at a trend in mothers with high versus low EOI (2/3 or 66.7% versus 2/22 or 9.1 %, P = .056 by Fisher's Exact Test). Associations Between EE Categories and Demographic and Family Variables

EE categories were unrelated to other maternal and family demographic variables including maternal age, SES, and size and intactness of family. There were no significant unique associations between EE categories and family environment variables. There was a trend in the univariate analysis for criticism to be negatively associated with family cohesion. DISCUSSION

HIRSHFELD ET AL.

or dissatisfaction requires further research, several interpretations might be considered. Patients with anxiety disorders may tend to be reactive to stimuli and easily aroused. As such, they may be more prone to respond to stresses with dissatisfaction and irritability. Moreover, patients with anxiety disorders (e.g., history of overanxious disorder) may be more perfectionistic and dissatisfied with imperfections. Finally, anxiety disorder patients tend to overappraise challenges or threats and underestimate their competence to cope (Beck et al., 1985). An inhibited, depressed, or oppositional child represents a significant challenge, and parents who feel ill-prepared to cope may respond with irritability and unhappiness with the child. The association in one sample between maternal mood disorder and high E01, while based on a very small number of cases, is consistent with Goodman and colleagues' (1994) report that depressed mothers were more likely to make statements reflecting overinvolvement with their children. Qualitative examination of our speech samples from depressed, high-EO I mothers showed indications of difficulties with limit-setting, suggesting depressive passivity (coded as self-sacrificing behavior). The interaction between BI or number of child diagnoses and maternal anxiety disorders indicates that both mother and child characteristics contributed to the higher level of criticism/dissatisfaction. However, the EE data in this study were not related to more general family measures. This finding suggests that EE by mother toward child may be regarded as a dyadic variable and not as an index of the family environment as a whole. Further research assessing EE between other dyads within the family is necessary to explore this possibility. Our results are tempered by several methodological limitations. The small size of our preexisting longitudinal samples and the absence of a normal comparison group diminished our ability to detect associations. It is possible, for example, that additional associations between child diagnoses (e.g., anxiety disorders) and EE might have been detected had we had available a sizable comparison group of children without psychiatric diagnoses. Another limitation was the fact that the diagnostic interview used with the mothers (the NIMH DIS) did not assess generalized anxiety disorder; hence the mothers rated as not having anxiety disorders may have included some women with generalized anxiety dis-

916

order. Our findings may, therefore, underestimate the strength of the association between criticism and maternal anxiety. Moreover, the fact that mothers were the sole informants about child diagnoses raises the possibility that associations between high EE and child characteristics may have been a function of mothers' global perception of the child. This limitation did not, however, affect the association with B1, which was assessed through independent, blind laboratory observations. An additional limitation was the collection of EE measures only from mothers. More full understanding of the associations noted could have been gained had we assessed paternal EE as well. The restriction of these samples to Caucasian subjects limits our ability to generalize to other populations. Finally, the limited diagnostic data available on the mothers in these samples leaves open the possibility that an unexamined variable might account for the association between maternal anxiety disorder and criticism. For example, it is not known whether mothers with anxiety disorders in the sample had characterological (Axis II) disturbances which might account for more strained relationships with offspring. Similarly, other unknown contextual factors might be responsible for the associations noted, such as possible disturbances in the fathers (e.g., substance abuse) which might influence both the mother's anxiety and irritability and the child's disruptive or inhibited behavior. However, the fact that both maternal anxiety disorders and child BI precede the EE argues against this possibility. Finally, it is possible that aspects of the assessment procedure (the Five-Minute-Speech-Sample measure ofEE) might differentially influence mothers with anxiety disorders. For example, women with a tendency to be anxious in the assessment setting might have less ability to inhibit expressions of dissatisfaction; or, if experienced in psychotherapy, such women might approach the openended task with the "set" of discussing problems or frustrations (A. Copeland, Boston University, personal communication). Despite these limitations, some important preliminary conclusions can be drawn. We found that mothers with anxiety disorders who had children who were challenging (i.e., who exhibited BI or psychiatric disorders) were at heightened risk for expressing maternal dissatisfaction and criticism. These attitudes may reflect difficulties in the parent-child relationship which might benefit clinically from evaluation and treatment. Pros-

J. AM. ACAD. CHILD ADOLESC. PSYCHIATRY, 36:7, JULY 1997

EXPRESSED EMOTION AND MATERNAL ANXIETY

pective, longitudinal studies of larger numbers of children, including normal controls, will be needed to confirm these conclusions and explore causal associations. Similarly, intervention studies that treat maternal anxiety disorder or child disorders or seek to reduce EE directly could shed light on which factors influence or are influenced by high EE.

REFERENCES Asarnow]R, Goldstein M], Tompson M, Guthrie 0 (1993), One-year outcomes of depressive disorders in child psychiatric in-patients: evaluation of the prognostic power of a brief measure of expressed emotion. j Child Psychol Psychiatry 34: 129-137 Asarnow ]R, Tompson M, Hamilton EB, Goldstein M], Guthrie 0 (1994), Family-exptessed emotion, childhood-onset depression, and childhoodonset schizophrenia spectrum disorders: is expressed emotion a nonspecific correlate of childhood psychopathology or a specific risk factor for depression? j Abnonn Child Psychol 22: 129-146 Beck AT, Emery G, Greenberg RL (1985), Anxi~ty Disordm and Phobias: A Cognitiv~ Pmp~etiv~. New York: Basic Books Biederman], Rosenbaum ]F, Bolduc-Murphy EA et al. (1993), A 3-year follow-up of children with and without behavioral inhibition. jAm Acad Child Adousc Psychiatry 32:814-821 Biederman], Rosenbaum]F, Hirshfeld DR et aI. (1990), Psychiatric correlates of behavioral inhibition in young children of parents with and without psychiatric disorders. Arch em Psychiatry 47:21-26 Brown GW, Birley ]LT, Wing ]K (1972), Influence of family life on the course of schizophrenic disorders: a replication. Br j Psychiatry 121 :241-258 Crowe RR, Noyes R, Pauls DL, Slymen 0 (1983), A family study of panic disorder. Arch em Psychiatry 40: 1065-1069 Garcia-Coli C, Kagan], Reznick]S (1984), Behavioral inhibition in young children. Child D~v 55:1005-1019 Goodman SH, Adamson LB, Riniti J, Cole S (1994), Mother's expressed attitudes: associations with maternal depression and children's self-esteem and psychopathology. jAm Acad Child Adousc Psychiatry 33: 1265-1274 Herjanic B, Reich W (1982), Development of a structured psychiatric interview for children: agreement between parent and child. j Abnonn Child Psychol1O:307-324 Hibbs ED, Hamburger SO, Kruesi MJP, Lenane M (1993), Factors affecting expressed emotion in parents of ill and normal children. Am j Orthopsychiatry 63: 103-112 Hibbs ED, Hamburger SO, Lenane M et al. (1991), Determinants of expressed emotion in families of disturbed and normal children. j Child Psychol Psychiatry 32:757-770 Hirshfeld DR, Biederman ], Brody L. Faraone SV, Rosenbaum JF (1997). Associations between expressed emotion and child behavioral inhibition and psychopathology: a pilot study. jAm Acad Child Adousc Psychiatry 36:205-213 Hirshfeld DR, Rosenbaum ]F, Biederman] et al. (1992), Stable behavioral inhibition and its association with anxiety disorder. jAm Acad Child Adol~sc Psychiatry 31: 103-111

J. AM. ACAD. CHILD ADOLESC. PSYCHIATRY. 36:7. JULY 1997

Hooley ]M, Orley ], Teasdale JD (1986), Levels of expressed emotion and relapse in depressed patients. Br j Psychiatry 148:642-647 Hosmer 0, Lemeshow S (1989), Appli~d Logistic Rrgrmion. New York: Wiley Kagan], Reznick ]S, Snidman N (1988), Biological bases of childhood shyness. Scimct 240: 167-171 Last CG, Hersen M, Kazdin AE, Francis G, Grubb HJ (1987), Psychiatric illness in the mothers of anxious children. Am j Psychiatry 144:1580-1583 Magana AB. Goldstein M], Karno M. Miklowitz OJ, Jenkins J. Falloon IRH (1986). A brief method for assessing expressed emotion in relatives of psychiatric patients. Psychiatry R~s 17:203-212 Miklowitz OJ, Goldstein MJ, Nuechterlein KH, Snyder KS, MintzJ (1988), Family factors and the course of bipolar affective disorder. Arch em Psychiatry 45:225-231 Moos RH, Moos BS (1974), Manual for th~ Family Environmmt Scau. Palo Alto, CA: Consulting Psychologists Press Moran C, Andrews G (1985), The familial occurrence of agoraphobia. Br j Psychiatry 146:262-267 Orvaschel H (1985). Psychiatric interviews suitable for use in research with children and adolescents. Psychophannacol Bull 21 :737-747 Parker G (l983). Pauntal Ovtrprouetion: A Risk Factor in Psychosocial Dro~lopmmt. New York: Grune & Stratton Robins LN. Helu:r ]E, Croughan J, RatcliffKS (1981), National Institute of Mental Health Diagnostic Interview Schedule. Arch Gm Psychiarry 38:381-389 Robinson]L. Kagan]. Reznick JS, Corley R (1992), The heritability of inhibited and uninhibited behavior: a twin study. D~v. Psychol. 28: 1030-1037 Rosenbaum ]F, Biederman J, Bolduc EA. Hirshfeld DR, Faraone SV. Kagan J (1992), Comorbidity of parental anxiety disorders as risk for childonset anxiety in inhibited children. Am j Psychiatry 149:475-478 Rosenbaum ]F, Biederman J, Gersten M et al. (1988), Behavioral inhibition in children of parents with panic disorder and agoraphobia: a controlled study. Arch em Psychiatry 45:463-470 Rosenbaum JF, Biederman J, Hirshfeld DR et aI. (1991), Further evidence of an association between behavioral inhibition and anxiety disorders: results from a family study of children from a non-clinical sample. j Psychiatr R~s 25:49-65 Schwartz CE, Dorer OJ. Beardslee WR, Lavori PW, Keller MB (1990). Maternal expressed emotion and parental affective disorder: risk for childhood depressive disorder, substance abuse, or conduct disorder. j Psychiatr R~s 24:231-250 Seifer R, Sameroff A], Baldwin CPo Baldwin A (1992), Child and family factors that ameliorate risk between 4 and 13 years of age. jAm Acad Child Adousc Psychiatry 31 :893-903 Stubbe DE, Zahner GEP, Goldstein M], Leckman JF (1993), Diagnostic specificity of a brief measure of expressed emotion: a community study of children. j Child Psychol Psychiatry 34: 139-154 Torgersen S (1983), Genetic factors in anxiety disorders. Arch em Psychiatry 40: 1085-1089 Turner SM. Beidel DC, Costello A (l987), Psychopathology in the offspring of anxiety disorders patients. j Consult Clin PsychoI55:229-235 Vostanis P, Nicholls J (1992), Expressed emotion in parents of non-referred children aged 6-11 years from two school populations: a pilot study. Child Car~ H~alth Dro 18:249-257

917