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Record: 136



Title:
Depression and conduct disorders
in children and adolescents: A
review of the literature.

Subject(s):
DEPRESSION in children -- Diagnosis; CONDUCT disorders in children -- Diagnosis;
CONDUCT disorders in adolescence --
Diagnosis; DEPRESSION in adolescence -- Diagnosis

Source:
Bulletin of the Menninger
Clinic, Spring92, Vol. 56 Issue 2, p188, 21p

Author(s):
Ben-Amos, Batsheva

Abstract:
Evaluates the explanatory models of the
relationship between childhood or adolescent depression and
conduct disorders by reviewing psychological
literatures. Direct causal relationship; Indirect causal relationship,
involving a third set of variables; `Final common pathway' hypothesis;
Other diagnostic problems; Theory and etiology, research, diagnosis and
treatment.

AN:
9603050236

ISSN:
0025-9284

Note:
This title is not held
locally

Full Text Word Count:

8586

Database:
Academic Search Premier


DEPRESSION AND CONDUCT DISORDERS IN
CHILDREN AND ADOLESCENTS: A
REVIEW OF THE LITERATURE


The psychological literature presents three explanatory models of the
relationship between childhood or adolescent depression and
conduct disorders: (I) a direct causal relationship; (2) an
indirect causal relationship, involving a third set of variables (i.e.,
personality disorders and developmental deficits);
and (3) the "final common pathway" hypothesis, which derives a relationship ex
post facto. Each of these models has dominated the literature at a different
period, each was affected by different research purposes, and each in turn
influenced further research. The author describes and critiques the three
models and concludes with suggestions for further exploration in the areas of
theory and etiology, research, diagnosis, and treatment. (Bulletin of the
Menninger Clinic, 56, 188-208)
The co-occurrence of depression and various types of antisocial behavior in
children and adolescents raises numerous questions.
At the theoretical level, why do these two sets of seemingly opposite symptoms
occur together and what are the causal ties between them? At the clinical level,
how can this group of symptoms be diagnosed and eventually treated? In the
literature, diagnostic criteria are sometimes based on conceptual assumptions
and at other times on clinical or other empirical evidence. A
review of theoretical developments and the empirical data
available in the literature provides the basis for some tentative answers to
these questions and indicates directions for further investigation.
The bulk of data and speculation from studies analyzed herein make clear the
nonfortuitous, nonrandom relationship between juvenile depression and juvenile
antisocial behavior. Several recent studies confirm that the relationship is
neither chance nor merely a reflection of the symptom orientation of the
American Psychiatric Association's (1980, 1987) diagnostic manual. Kovacs,
Paulauskas, Gatsonis, and Richards (1988) estimated that the prevalence of
comorbidity for depression and conduct disorders in
children and adolescents varies from 23% in their
sample to between 32% and 37% in other studies (Carlson & Cantwell, 1980;
Kashani, Carlson, Beck, & Hoeper, 1987; Marriage, Fine, Moretti, &
Haley, l986; Puig-Antich,1982). According to Kovacs et al. (1988), when these
two disorders occur together, they constitute a separate
diagnostic group. Other studies (Akiskal & Weller, l989; Puig-Antich,1982)
support this conclusion.
Given the evidence for an empirical connection between depression and conduct
disorders, an explanation of this co-occurrence seems all the more
necessary. Studies on this topic published since the 1950s can be organized into
three conceptual models that explain the relationship between the two
disorders: (1) the model of direct causal relationship (i.e.,
depression is the direct cause of antisocial behavior); (2) the model of
indirect causal relationship via a third set of variables (i.e.,
personality disorders and developmental deficits);
and (3) the model that derives a relationship ex post facto, or the "final
common pathway" hypothesis.
Each of these models has dominated the literature at different periods, each
was affected by different research purposes, and each in turn influenced further
research. Despite their different theoretical underpinnings, all the models shed
some light on the relationship between the two disorders. The
first model informs the historical background of this paper. The second model,
although now somewhat outdated, still influences professional consideration of
the subject. As for the third and most recent model, I have some questions about
it. But my conclusions and suggestions for further research are based on a
synthesis of all knowledge accumulated to date.
Direct causal relationship
As late as the mid-1960s, clinicians believed that youngsters cannot be
depressed because they lack a fully developed superego (Abraham, 1911/1948b,
1916/1948a; Bibring, 1953; Fenichel, 1945/1954: Freud, 1917/1963; Jacobson,
1946, 1954, 1961, 1971; Rie, 1966; Sandler & Joffe, 1965). Works that
attempted to deal with the co-occurrence of childhood or
adolescent depression and antisocial or delinquent acting out
represented a break from the psychoanalytic concepts of the time.
In the years that followed, accumulating clinical evidence began to
contradict the dominant theory. For example, Toolan (1962) wrote that
adolescent acting out and delinquency cover feelings of isolation,
loneliness, and depression. Others (Mattsson, Sees, & Hawkins, l969; Mosse,
1974) wrote that childhood depression is likely to express itself in symptoms
such as defiance, truancy, restlessness, boredom, and antisocial acts--all
masking the depression. At the same time, theoretical and clinical interest in
preoedipal processes increased sensitivity to the extent to which early
deprivation and adverse environmental conditions impair the ego development of
children (Kernberg, 1970a, 1970b, 1971; Mahler,
1971, 1972; Mahler, Pine, & Bergman, 1975; Masterson & Rinsley, 1975).
These trends suggested that juvenile antisocial acting out is related to
depression. However, although the relationship was noted, it was never clearly
and specifically formulated, nor was its significance analyzed. Consequently,
many questions have remained unanswered. Does one disorder cause
the other directly? Are the two related indirectly through an underlying set of
variables? How should the concurrent existence of the two
disorders be diagnosed ? Is it a part of a
personality disorder, and if so, which one? Or is it
one of the affective disorders, and if so, can it be treated as
such? How separate and independent is this diagnostic entity?
Early attempts to explain the co-occurrence of the two childhood
disorders perceived the youngsters' antisocial conduct as a
defense against a depressive core, low self-esteem, rejection, helplessness, and
hopelessness. These direct-cause explanations assumed that juvenile delinquency
was caused by depression: The delinquency follows the depression chronologically
and functions as a defense mechanism. Kaufman and Heims (1956), who conducted an
empirical research study, interpreted antisocial behavior of delinquent
juveniles as a restitutive, unrealistic attempt to find the sought-for parent
figure in the delinquent act, thereby avoiding the pain of unfulfilled
dependency needs. Theoretically, these researchers were ahead of their time in
that they attempted to relate the depression of juvenile delinquents to the
preoedipal environment and to ego impairments. Their explanation was similar tO
the theories of "masked depression" and "depressive equivalents" developed later
(Cytryn & McKnew, 1972; Glaser, 1967; Malmquist, 1971; Toolan, 1962). Some
of these theorists--notably, the proponents of a strict interpretation of the
masked depression theory--also saw the roots of children's
depression in early parental deprivation (Burke & Harrison, 1962; Glaser,
1967; Lesse, 1974, 1979). But they perceived childhood depression as masked
rather than as depression proper. They also postulated that the mask can take a
variety of forms, such as antisocial behavior, psychosomatic problems, school
underachievement, and general anxiety.
A variation of the theme of masked depression was proposed by Sandler and
Joffe (1965), and was later elaborated by Mendelson (1974). These writers
believed that parental loss and deprivation lead to delinquency as a defense
against the pain of loss felt by the child. When this defense fails, depression
follows. In this version, depression comes after the delinquency, not before it.
This change in the causal link also removes depression from the
characterological realm to the reactive-process sphere. Consequently, depression
becomes a state rather than a trait phenomenon.
Two empirical studies from the early 1970s provide data about the family
characteristics of depressed children with antisocial symptoms.
These youngsters tended to come from families with depressed relatives (Murray,
1970), or to have parents with characterological disorders (Cytryn
& McKnew, 1972). These two profiles of family background were not
investigated further at the time, nor was the possibility that several types of
childhood depression could interact with antisocial behavior.
All these earlier works deal mostly with characterological depression.
Kaufman and Heims (1956), for example, described gloomy colors in the Rorschach,
fantasies related to body and object emptiness, and themes of loss, dependency
needs, and fear of closeness. The lost object is not introjected but instead
externalized. Reality testing is impaired and fantasies of omnipotence dominate.
Toolan (1962) described the young delinquents diagnostically as having character
disorders. He distinguished character depression from neurotic
depression, with its hallmark of internalized conflict.
Such empirical data were accompanied by theoretical conceptualizations in the
area of child development, centering on ego development and mechanisms of
defense. Zetzel (1965/1970), for example, posited a developmental failure that
originated between the ages of z and 5. Because of this failure, the child is
unable (1) to accept the depression resulting from inevitable frustrations and
loss, and (2) to adapt through available areas of gratification. The
alternatives to constructive adjustment are acting out in general and
delinquency in particular. Rexford (1978) edited a volume on the causes of
antisocial acting out, focusing on the first 2 years of life. Rexford's own
contribution summarized the work of many earlier writers (Aichhorn, Alexander,
Bowlby, Friedlander, Healy), who viewed the origin and characteristics of
juvenile delinquent acting out as similar to those of acting out in general.
These writers identified such factors as repeated separations from the mother
and early deprivation in the relationship with the parents as leading to
impairment in adaptation to reality and a deficient superego, to chronic acting
out, and to impaired socialization and antisocial character formation.
In these analyses of acting out, Zetzel (1965/1970) and Rexford (1978), as
well as the proponents of the masked depression theory, made an important
distinction between impulsive acting out, or direct motor discharge, and acting
out as a defense mechanism. The latter is an organized ego activity with
defensive, compensatory, and adaptive purposes, as opposed to pure impulsive
behavior.
Today the findings and conceptualizations of this model are seen as invalid,
unoperational, and outdated (Carlson & Cantwell, 1980; Cytryn, McKnew, &
Bunney, 1980). Yet the thesis of masked depression was never falsified. It was
only abandoned in favor of new developments in the field. The second model,
which was emerging in the late 1970s, reflects a rejection of a simple linear
relationship between mood and behavior disorders.

Indirect causal relationship
By the late 1970s, researchers recognized childhood depression as a clinical
phenomenon and sought to establish reliable assessment techniques to identify
the disorder. Instruments included the Childhood Depression
Inventory (Kovacs & Beck, 1977), the "Kiddie SADS," or Schedule of Affective
Disorders and Schizophrenia for children (Chambers,
Puig-Antich, & Tabrizi, 1978), the Children's Depression
Rating Scale (Poznanski, Cook, & Carroll, 1979), and the Peer Nomination
Inventory for Depression (Lefkowitz & Tcsiny, l980). The thesis that
childhood is depression-free was abandoned in favor of the idea that childhood
and adult depression are one and the same phenomenon (American Psychiatric
Association, l 980,1987; Puig-Antich, Blau, Marx, Greenhill, & Chambers,
1978).
These new diagnostic Options changed the type of data that researchers found
in studies of juvenile depression and antisocial behavior. In addition to
symptoms of charactcrological depression in delinquent populations, the
researchers began to identify major depression as well (Alessi, McManus,
Brickman & Grapentine, 1984; Chiles, Miller, & Cox, 1980; Gibbs, 1981;
Kashani, Henrichs, Reid, & Huff, 1982; McManus, Alessi, Grapentine, &
Brickman, 1984; Schuckit & Morrissey, 1979). They also began to examine the
relationship between character disorders and affective illness,
becoming aware of the complexity of the disorders in question.
Akiskal and colleagues (Akiskal, Bitar, Puzantian, Rosenthal, Walker, 1978;
Akiskal et al., 1980) identified three types of chronic depression: (1)
late-onset chronic depression, which seems to have no characterological
involvement; (2) early-onset charactcrological depression, which is equivalent
to subaffective dysthymia with frequent superimposed major depressive episodes,
abnormal rapid-eye movement, and responsiveness to tricyclic medication and
lithium carbonate; and (3) characterological spectrum disorders,
which are a mixture of personality disorders with
depressive features complicated by alcohol and drug abuse, a family history of
sociopathy, and unfavorable response to medication.
More recently, Klein, Taylor, Dickstein, and Harding (1988) have confirmed
that early-onset dysthymia is a different clinical entity from double depression
(dysthymia and superimposed major depression, or Akiskal et al.'s type 2). The
dysthymic patient with superimposed major depression has a significantly higher
rate of lifetime substance abuse, personality
disorder, and early object loss than does the dysthymic individual
without major depression. The study also found a family history of antisocial
personality disorder in a higher proportion of
patients with dysthymia than in patients with episodic major depression.
Therefore the severe character pathology is probably not a simple result of
early-onset affective disorder.
Grinker (1979), Gunderson (1982), Gunderson and Elliott (1985),
Kernberg (1967), and Masterson (1972) saw major depression and
dysthymia as complications of borderline, narcissistic, and dependent
personality disorders; these disorders
cause difficulties in adaptation that lead to chronic dysphoria and depression.
An examination of the literature concerning the personality
profiles of offenders (including violent offenders) reveals that diagnostically
they best fit the character disorder Rosenbaum and Bennett (1986)
found that homicidal patients with major depression, compared with nonhomicidal
depressed patients, are more likely to have a personality
disorder to have been physically abused as children,
and to abuse alcohol and drugs. McManus et al. (1984) reported that in one
sample of juvenile delinquents, 25% were diagnosed as suffering from borderline
personality disorder and drug and alcohol abuse, in
addition to major depression or minor affective disorders. This
model of the relationship between depression and antisocial behavior, which sees
these disorders as secondary to the primary process of the
borderline personality disorder, has some support in
the clinical literature.
Studies of pharmacological treatments indicate an association among
borderline personality disorder, conduct
disorder, and affective disorders. For example,
borderline and conduct disorder patients respond to
pharmacological treatment in the same way as affective disorder
patients (Berg, 1983; Puig-Antich, 1982; Rinsley, 1980). Researchers have
repeatedly reported that more than one third of prepubertal and pubertal
patients have been diagnosed as suffering from major depression and conduct
disorder as well as from severe impulsivity and suicidal ideas and
acts (Carlson eF Cantwell, 1980; Kovacs et al., 1988; Marriage et al., 1986;
Puig-Antich,1982). This indirect-effect explanation suggests that depression and
delinquency are related because both, like character pathology, are the result
of severe ego impairment stemming from early deprivation.
From the perspective of object relations theory, Gunderson and Elliott (1985)
summarized two formulations of how depression can occur and lead to antisocial
conduct in borderline individuals. The first formulation focuses on abandonment
depression, as proposed and elaborated by Masterson (1972), Masterson and
Rinsley (1975), Hartocollis (1977), and Rinsley (1982). These authors suggested
that a traumatic separation from the parent during the rapprochement subphase
leads to depression, which is defended against with rage, acting out, and
withdrawal. The second formulation focuses on a feeling of inner badness and on
the bad self of the borderline individual (Buie & Adler, 1982; Goldstein,
1988; Gunderson, 1984; Gunderson & Elliott, 1985), and emphasizes anger
toward needed others. Depression results from a defensive reaction against
aggressive impulses that are perceived as dangerous, causing self-condemnation.
In a model that resembles the second formulation, Soloit (1982) addressed the
impaired object constancy of the borderline child. According to this model, the
attachment of a deprived child is aggressive, rather than libidinal, which
prevents the youngster from evoking pleasurable memories of a loving parent for
the purpose of learning and working. Coping mechanisms include aggressive
behavior and acting out.
The model of early deprivation leading to characterological pathology,
depression, and conduct disorder presents some problems. First,
even though it is generally known that early home and family instability leads
to character pathology (Akiskal & Weller, l989), there is as yet no evidence
that early deprivation is more important than parental psychopathology. Second,
this model is too general to deal with the full complexity of the phenomenon at
hand. For example, in this model it is irrelevant whether the depression is
major, characterological, or bipolar, or whether it is primary or secondary to
the conduct disorder. The third model attempts to deal with such
problems.

The "final common pathway" hypothesis
Thus far the picture has become quite complex. The clinical literature
reports that conduct disorder, major depression, and
characterological depression occur together with or without a
personality disorder. Therefore it is necessary not
only to understand why depressive and conduct disorders appear
together, but also t study whether characterological and major depressions have
the same cause.
The heterogeneity of the various symptoms has led clinical researchers to
develop the concept of a spectrum of disorders. Such
disorders are characterized by complexity, heterogeneity,
multidimensionality, and qualitative separability (Alarcon, & Walter-Ryan,
& Rippetoe, 1987). Much has been written about the borderline spectrum
(e.g., Akiskal, Yerevanian. Davis, King, & Lemmi, 1985; Cantor, Smith,
French, & Mezzich, 1980, Kernberg, 1979; Nelson et al., 1985:
Perry, 1985; Perry & Cooper, 1985; Pope, Jonas, Hudson, Cohen, &
Gunderson, 1983) and the affective spectrum (e.g., Akiskal, 1980, 1981. 1983a,
1983b; Akiskal et al., 1978; Akiskal, Djenderedjian, Rosenthal, & Khani,
1977; Akiskal, Khani, & Scott-Strauss, 1979; Akiskal et al., 1980). The
affective spectrum comprises the following clinical entities: cyclothymic
disorder; dysthymic disorder with characterological
depression; bipolar depression; hysteroid dysphoria; atypical depression; and
personality disorders, especially borderline
personality disorder.
The spectrum approach has fed to two opposite developments. One view (Alarcon
et al., 1987) suggests that because it is difficult to differentiate between the
various entities, taxonomic zeal should give way to a return to broader and more
inclusive categories until better nosological criteria are identified. The
second--and currently dominant--viewpoint is the final common pathway hypothesis
(originated by Akiskal & McKinney, 1975, and advanced by Whybrow, Akiskal,
& McKinney, 1984). This hypothesis suggests that although the factors that
cause the cooccurrence of depression and conduct disorder vary
among individuals, the final constellation of psychobiological dysfunction is
similar. This similarity suggests that there is a final pathway, a common
outcome, for the diverse predisposing variables.
A potential problem with this approach is that some researchers may focus on
the final common pathway of biological dysfunction in a reductionistic fashion,
losing sight of the complex etiology leading to it. At worst, this approach has
a dehumanizing effect on the field. Yet there is potentially much to be learned
from the study of the common biological dysfunction at this developmental
juncture.
An example of this approach is a clinical study by Puig-Antich (1982), who
serendipitously found that one third of a group of boys who fit both Research
Diagnostic Criteria (Spitzer, Endicott, & Robins, 1978) for major depression
and DSM-III (American Psychiatric Association, 1980) criteria for conduct
disorders responded to imipramine treatment. Followup confirmed
that conduct disorder behavior in most of the patients abated
following successful outcome of treatment for mood disorders.
Puig-Antich suggested that prepubertal boys who meet the criteria for major
depression and conduct disorder fall within the category of
antisocial personality in the depressive-spectrum disease
families. In these cases, a relationship between the two disorders
was inferred in reverse from treatment to etiology.
The role of medication in this theory was made clear in a study by Hudson and
Pope (1990), who identified eight disorders that may share a
pathophysiological abnormality: bulimia, panic disorder,
obsessivecompulsive disorder, attention deficit
disorder with hyperactivity, cataplexy, migraine, irritable bowel
syndrome, and major depression. They viewed the similar responses to
antidepressants by patients who suffer from these disorders as
indicative of an affective spectrum, and they argued that a causal chain of many
steps produces the full clinical picture of each disorder. Among
these steps, at least one is the same for all forms of affective spectrum
disorder, and antidepressants will act to interrupt the causal
chain of the disorder. According to Hudson and Pope, "The model
assumes that the organism is a black box" (p. 57), and that knowledge of
etiological factors--and even physiological processes--is irrelevant.
Although the ability to treat a disorder effectively does not
require complete understanding of its genesis or dynamics, the model of the
common path does not necessarily offer a definitive mode of treatment.
Researchers such as Puig-Antich (1982) and Hudson and Pope (1990) aspire to
ameliorate disorders as varied as bulimia, panic
disorder, obsessivecompulsive disorder, attention
deficit disorder with hyperactivity, cataplexy, migraine,
irritable bowel syndrome, and major depression. However, as these authors noted,
additional research is necessary to determine the effectiveness of medication
for treating such diverse disorders.

Pharmacological research as a diagnostic tool
Despite questions about the common pathway hypothesis, its emphasis on the
role of medication may throw some light on the disorders we are
examining. Information about response to medication can sharpen diagnosis. This
method is not new in medicine. Use of such information helps to liberate the
diagnosis from a priori conceptualizations and to base it primarily on empirical
facts. When studied in the context of an individual's development and family
history, response to medication could help identify the type of relationship
between the disorders in question, that is, whether it is one of
causality or association. Specifically, do the common manifestations of major
depression, characterological depression, conduct disorder, and
possibly borderline personality disorder indicate a
common etiology?
Earlier studies of response to medication already provide some answers.
Yerevanian and Akiskal (1979), who conducted research on differential response
of depressed patients to medication, identified two groups of patients.
Individuals in both groups had suffered from early object loss and deprivation,
but to different degrees. One group exhibited symptoms comparable to the
dysthymic characterological disorder, where early deprivation and
ego impairment are less severe. Superimposed major depression and a family
history of affective disorder were common in this group. These
patients responded to antidepressant medication and had a good social prognosis.
The second group comprised character-spectrum patients with depression. They
suffered severe early deprivation, and their functioning was seriously impaired.
They had alcoholic and antisocial relatives, did not suffer as often as the
first group from superimposed major depression, did not respond to
antidepressant medication, and had a poor prognosis for any type of therapy.
Rosenbaum and Bennett (1986) reported that violent individuals among such
patients have a history of child abuse and neurological impairment.
Can we meaningfully combine the results of these various studies? For
example, can we conclude that Puig-Antich's (1982) patients are a subgroup of
Yerevanian and Akiskal's (1979) treatment-responsive, dysthymic,
characterological disorder patients? Several issues must be
considered to answer such questions.
First, most of Yerevanian and Akiskal's character-spectrum depressive
patients were females; Puig-Antich's patients were all males. Second, Yerevanian
and Akiskal did not report conduct disorder occurring with
dysthymic depression; Puig-Antich did. Third, Yerevanian and Akiskal dealt with
subaffective dysthymia in adults; Puig-Antich studied prepubertal boys.
Furthermore, there is evidence that the disorders presented are
not the same diagnostic entity. Kovacs et al. (1986), in comparing
adolescent and adult dysthymia, concluded that although juvenile
patients with dysthymia are just as likely as adults to suffer from superimposed
major depression, juvenile dysthymia eventually remits. The adult subaffective
dysthymia observed by Yerevanian and Akiskal, however, is a lifelong primary
affective disorder. Kovacs et al. found it unclear whether the two
illnesses are the same diagnostic entity. However, they did identify many
adolescents diagnosed as having adjustment reaction with depressed
mood whose illness did not have such a favorable course.
Other diagnostic problems
Other outcome studies suggest the existence of another possible diagnostic
group conduct disorders related to bipolar illness. Akiskal et al.
(1978, 1980) reported that patients exhibiting early-onset characterological
depression with superimposed major depression responded to lithium carbonate.
Lithium is frequently used to treat children and teenagers who
themselves or whose parents have been diagnosed with bipolar illness, arid to
treat patients who are resistant to tricyclic antidepressants (Akiskal &
Weller, 1989). The early appearance of bipolar disorders is well
documented (e.g., Akiskal & Weller, 1989; Regier et al., 1988), as is the
fact that a child or an adolescent with any depressive
disorder is at high risk of developing bipolar illness (Akiskal
& Weller, 1989). But how is early bipolar disorder related to
conduct disorder?
Akiskal and Weller (1989) found that undiagnosed bipolar
disorder may be mistaken for conduct disorder or
hyperactivity. They reported that, of 65 youngsters with bipolar
disorder, 15 % were initially misdiagnosed as having a conduct
disorder, 35% as having an ad justment disorder, and
9% as being hyperactive. Mania is difficult to diagnose in
children and adolescents because the criterion of
increased involvement in pleasurable activities with negative consequences is
often confused with conduct disorder. Akiskal and Weller also
reported that, in a sample of hospitalized, prepubertal, manic
children, 50had been first diagnosed as having adjustment
disorder, conduct disorder, or schizophrenia, and
that similar numbers of misdiagnoses occur with adolescents.
DSM-III-R American Psychiatric Association, 197) differentiates conduct
disorder from bipolar disorder in
children and adolescents by the persistence of the
behavior. In conduct disorder, manic episodes are brief. DSM-III-R
further notes that manic episodes may be associated with antisocial behavior in
adults. But conduct disorder in childhood is a prerequisite for
the diagnosis of antisocial personality disorder.
Again, there is an emphasis on the nonepisodic nature of antisocial behavior.
On the other hand, Akiskal and Weller (1989) did find cases in which a
diagnosis of conduct and affective disorder was accurate. They
speculated that in cases of primary conduct disorder with
secondary depression in childhood, treatment of the depression may not influence
the conduct disorder. When the depression is primary, treating it
will alleviate the secondary conduct disorder. This contention is
only partially supported in the literature. For example, Puig-Antich's ( 1982)
research on prepubertal boys with major depression and conduct
disorder revealed that the onset of the major depression preceded
the onset of the conduct disorder. After pharmacological
treatment, the major depression disappeared before the conduct
disorder. When, as in some cases, a relapse occurred, the pattern
was for the depression to recur first, followed by the conduct
disorder. The same order was repeated after a second treatment
cycle.
Like Puig-Antich, Kovacs and her coworkers (1988) found that conduct
disorder behavior was secondary to mood disorder.
But contrary to Puig-Antich's findings, Kovacs et al. observed that the conduct
disorder behavior did not generally remit with the abatement of
the depression. Conduct disorder was associated with long-term
behavioral problems such as rule violations, fighting, truancy, stealing,
setting fires, and drug and alcohol abuse, which eventually led to suspension
from school and involvement with the police and the juvenile courts. The authors
concluded that temporal sequence alone does not convey the complex relationship
between comorbid conduct and depressive disorders in youth.
Looking for the interaction between childhood depression and conduct
disorder, Kovacs and her colleagues (1988) found no pattern of
association between type of depression and the presence of conduct
disorder. Age was associated with conduct disorder
comorbidity, because conduct disorder was most likely to become
manifest between ages 11 and 14, taking time to develop fully. The researchers
found that runaway behavior alone was associated with comorbidity of conduct
disorder and major depression. They were unable to find predictive
power in early childhood deprivation, but they suspected that their indicators
of early deprivation may have been nonspecific.
There is not enough evidence in the literature to determine whether violent
offenders exhibit depressive symptomatology related to a background of early
deprivation. Lewis and colleagues (Lewis et al., 1985; Lewis, Pincus, Feldman,
Jackson, & Bard, 1986; Lewis, Shanok, Grant, & Ritvo, 1983; Lewis,
Shanok, Pincus, & Glaser, 1979 ) found severe early deprivation in the
history of adolescents who later became murderers and death row
inmates. These delinquents had a history of physical and psychological abuse,
head injury, neurological problems, psychotic relatives, and violent behavior in
childhood to a significantly higher degree than nonviolent control groups. Lewis
(personal communication, September 14, 1987) observed "hatless
serious offenders tend to suffer from major depression more than do more violent
offenders. Yet she and her colleagues did not study the range of possible
affective disorders in their samples of violent offenders.
Tentative conclusions
This review of the literature reveals the need to reevaluate
our thinking in four major areas vis-a-vis the co-occurrence of depression and
conduct disorders in children and
adolescents: ( 1 ) theory and etiology, (2) research, (3)
diagnosis, and (4) treatment.
Theory and etiology
The co-occurrence of conduct disorder and juvenile depression
is a complex but distinct clinical phenomenon. This joint disorder
is heterogeneous in type, phenomenology, and course of illness, and its etiology
and dynamics are not yet clear. It remains unknown why two such qualitatively
different, if not opposite, disorders (Kovacs et al., 1988) occur
together. Although the literature suggests three models of possible relationship
as described in this paper (direct causal, indirect causal, and final common
pathway), it also seems to suggest another way to address issues of etiology and
dynamics, which further collapses these three models.
The literature on these three models reveals two major types of explanations,
reflecting two theoretical positions. The first viewpoint emphasizes
constitutional, genetic factors, and is presented in studies of the history of
familial psychopathology and in studies of response to medication. The
genetic/constitutional explanation views initial psychopathology as the cause of
later psychopathology. The second explanation focuses on the role of
social/environmental factors in the etiology of the disorder. This
viewpoint perceives certain disadvantageous social circumstances, including
early deprivation, as the cause of psychopathology. This dichotomy reflects the
old nature-nurture controversy in human development and behavior. To this day,
the relative influence of these factors remains unresolved (Dohrenwend, 1990).
Obviously, both factors are important. The tendency to exhibit the pathology
may have a genetic basis. Certain environments are more likely to favor
expression of the pathology. Once expressed, there will be a tendency to
perpetuate the pathology, psychologically through patterns of parental
deprivation, and socially through deviant socialization both in the family and
in the subculture at large.

Research
A more comprehensive theoretical explanation requires research in several
areas. First, the role of early deprivation and adverse family background in the
disorder needs to be explored further. Sensitive and specific
indicators of early deprivation should be developed through further research.
One such attempt was made by Walsh and Beyer (1987), who measured early
deprivation using the following indicators: physical and psychological abuse,
parents' substance abuse, the child's feelings of lack of love, official
designation as a runaway, truancy, illegitimacy, and a high performance over
verbal score on the Wechsler Intelligence scale. Their data confirmed that early
deprivation is a powerful variable in explaining violent criminal activity.
Second, broader studies of the effects of medication need to be undertaken.
Use of control groups, improvement of experimental design, and proper follow-up
techniques are essential for valid and reliable conclusions. Again,
quasi-experimental research design, through the use of the epidemiological
method with large samples of patients, or with whole populations, can be used to
explore causal connections on a wide sociocultural level (Dohrenwend, 1983;
Dohrenwend & Dohrenwend, 1976.
Third, an exploration of whether the co-occurrence of depression and conduct
disorder in children and adolescents
is actually a precursor of manic-depressive disorder in adults
would provide valuable insights. Such a study would, of course, be open to
conceptual and research pitfalls like those accompanying the notion of
delinquency as a mask for depression in children. Yet this
approach might illuminate the psychodynamic process in cases of violent
behavior, and possibly in cases of other antisocial behavior as well.
Diagnosis
With regard to diagnostic issues, there is, first of all, a general need for
reliable and valid measures of symptoms. Appropriate procedures for collecting
data on symptoms need to be selected, whether these are traditional methods or
newer techniques. Traditional clinical methods include the clinical interview,
psychological testing, construction of the dynamics of the patient, diagnoses on
all DSM-III-R axes, and determination of primary and secondary diagnoses. Other
traditional means are self reports, interviews with parents and teachers, and
family histories. Examples of newer epidemiological techniques of data
collection are the Schedule for Affective Disorders and
Schizophrenia (Endicott & Spitzer, 1978), the Symptoms Checklist, or
SCL-90-R (Derogatis,1977), and the Present State Examination (Cooper et al.,
1972; Sartorius, Jablensky, & Shapiro, 1978; Wing, Birley, Cooper, Graham,
& Isaacs, 1967; Wing, Cooper, & Sartorius,1974). Such instruments modify
the older traditions of clinical interview or self-reports in the use of large
population studies: They decrease measurement error and increase internal
consistency (Dohrenwend, 1990). A synthesis between the traditional and newer
techniques of data collection offers researchers wider scope. The choice could
be determined in part by the size of samples.
Second, the diagnostic criteria for characterological and major affective
disorders need to be sharpened and the distinctions between them
clarified. DSM-III-R lists bipolar disorder, major depression, and
dysthymia as mood disorders. Characterological depression is not
included here or among personality disorders. In the
testing literature, Exner (1990) constructed an index for clinical depression.
But similar formal testing criteria identifying characterological depression do
not exist. Although dysthymia, or neurotic depression, has an early onset and
seems to be associated with certain personality
disorders (APA, 1987), this diagnostic category has been
criticized as being a milder version of major depression (Goldstein &
Anthony, 1988), with similar diagnostic criteria (Kocsis & Frances, l987).
Such similarity may result in an erroneous diagnosis of double depression.
Akiskal (1981) pointed to a different possible source of error in the
diagnosis of mood disorders. Discussing the interchangeability of
diagnosis between affective and borderline personality
disorders in adolescents, he argued that the
affective component may be masked by stormy relationships with others, and is
often misdiagnosed as borderline personality
disorder. Go]dstein's (1988) view that one should distinguish
between the depressive, impulse-ridden character and the individual with a core
borderline personality supports this theory. Elsewhere, Akiskal
and Weller (1989) have contended that cyclothymic and bipolar II
disorders are particularly like]y to be labeled borderline.
In addition to problems in defining the components of depression, current
investigations have serious problems in specifying the components of antisocial
behavior in this disorder, some of which touch on its legal
dimension. First, current diagnostic procedures conceal the clinical association
of depression and antisocial conduct, violent or not, in children
as well as in adults. The failure of Lewis et al. (1979, 1983, 1985, 1986) to
investigate an association between violence and depression reflects a general
neglect in psychiatric research. Rosenbaum and Bennett (1986) attributed this
neglect to two factors: (1) Instruments for diagnosing depression do not include
questions about violence and violent ideas, and (2) legal proceedings are
unlikely to require violent offenders to undergo a detailed psychiatric study
that would elicit signs of depression.
Second, the distinction between juvenile delinquency and the psychiatric
classification of conduct disorder (and between adult criminal
behavior and antisocial personality disorder) is
blurred in current classification and research. Rutter (1987) believes that
antisocial acts define both the crime and the psychopathology, and he has
asserted that using antisocial behavior by young people as the defining
criterion for antisocial personality disorder in
adulthood is unjustified because conduct disorders may develop
into other types of personality disorders. These
problems have led Rutter to question altogether these diagnostic categories.
Third, the distinction between different levels of seriousness of antisocial
acts is also blurred in current research, and different levels of seriousness
are grouped under the same psychiatric label. McManus et al. (1984) have already
commented that to understand the relationship of delinquency and
psychopathology, one must specify type and severity of the antisocial behavior.
Finally, Rutter (1987) views antisocial personality
disorder--together with borderline, histrionic, and narcissistic
personality disorders--all as parts of a dramatic
cluster, which he has classified as a disorder of relationships.
The early literature indicated that conduct disorder often appears
with a codiagnosis of personality disorder. To
understand the etiology and define appropriate treatment, it is necessary to
determine whether conduct disorder and antisocial
personality disorder are indeed separate diagnostic
categories or are simply part of the character disorders spectrum.

Treatment
Pharmacology is one possible avenue for appropriate treatment of comorbid
conduct and depressive disorders in youth. However, studies using
antidepressants have yielded mixed results. Although Puig-Antich (1982) reported
the fortuitous discovery that imipramine produced an abatement of the two
disorders in the majority of a sample of prepubertal boys, such
results have not been replicated, and follow-up studies are scarce. Indeed,
there is evidence that conduct disorder tends to persist after the
remission of depression in children (Kovacs et al., 1988). Perhaps
the two component disorders should be treated separately.
Recently, there has been a renewed interest in psychological treatment of
youngsters suffering from major depression and personality
disorder (e.g., Black, Bell, Hulbert, & Nasrallah, 1988;
Kernberg, 1990). A combination of a elationship-oriented
psychological approach and medication would probably prove most beneficial. An
orderly and disciplined study of the literature can inform the continuing search
for the most effective treatment of comorbid depressive and conduct
disorders in children and adolescents.


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~~~~~~~~
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