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This is to certify that the

dissertation entitled

THE RELATIONSHIP BETWEEN ALEXITHYMIC TRAITS IN PRIMARY
CAREGIVERS AND A DIAGNOSIS OF ATTENTION‘DEFICIT/
HYPERACTIVITY DISORDER

presented by

James Denison Jones

has been accepted towards fulﬁllment
of the requirements for

Ph.D. Psychology

degree in

 

 

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Major professor

Date March 30, 2001

 

MS U is an Affirmative Action/Equal Opportunity Institution 0-12771

 

 

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em chlRWpG5—p.15

 

 

THE RELATIONSHIP BETWEEN ALBXI'I‘HYMIC TRAITS IN PRIMARY
CAREGIVERS AND A DIAGNOSIS OF
ATTENTION-DEFICIT/HYPERACTIVITY DISORDER
By

James Denison Jones

A DISSERTATION
Submitted to
Michigan State University
in partial fulﬁllment of the requirements
for the degree of
DOCTOR OF PHILOSOPHY

Department of Psychology
2001

Abstract
THE RELATIONSHIP BETWEEN ALEXITHYMIC TRAITS IN PRIMARY
CAREGIVERS AND A DIAGNOSIS OF
ATTENTION-DEFIClT/HYPERACTIVITY DISORDER
By
James Denison Jones
The relationship between alexithymic traits in primary caregivers and a

diagnosis of Attention-Deﬁcit/I-Iyperactivity Disorder (ADHD) in their children was
evaluated in this study. Seventy-ﬁve children and adolescents were assessed at a
small outpatient clinic. The children in the study completed a standard behavioral
and neuropsychological assessment battery and their primary caregivers were
administered standard behavior rating scales and the 20-Item Tomato Alexithymia
Scale (T AS-ZO). Results revealed that primary caregivers of children with ADHD do
not exhibit higher levels alexithymia than do primary caregivers of children who do
not carry this diagnosis. In addition, the TAS-20 was not signiﬁcantly correlated with
two neuropsychological measures of inattention and inhibition. Overall, there was no
support for the prediction of a positive relationship between children diagnosed with

ADHD and alexithymic traits in their primary caregivers.

This dissertation is dedicated to my. wife, Debra Jones, my family, and my ﬁ'iends.

Without their patience and support, this project would have been impossible.

ACKNOWLEDGMENTS
I want to acknowledge those colleagues and mentors who made this project
possible. I would like to recognize Dr. Bertram Karon for his kind, insightful, and
indispensable guidance. I would also like to mention my profound gratitude to Dr.
Greg Lamberty, a mentor and ﬁ'iend who made this project possible. I would also
like to recognize Dr. Jean Baker, Dr. Robert Caldwell, and Dr. Albert Rabin for their
constructive and insightful contributions to this ﬁnal product. All of the help is

deeply appreciated.

iv

TABLE OF CONTENTS
List of Tables
Introduction
Heritability and the inﬂuence of parenting on development

A contextual view of ADHD as an afternative to
biological determinism

Barkley’s neuropsycho logical model of ADHD

Alternatives to pharmacological treatment for ADHD
Alexithymia

Alexithymia as distinct ﬁom other forms of psychopathology
Further considerations of the alexithymia construct

Parental alexithymic traits, empathy, attachment,
and affect regulation

One contextual variable: Attachment and ADHD
Critical periods, brain development, and affect regulation
Conclusion

Hypotheses

Methods

Results

Discussion

Appendix A (T AS-20, Questionnaire, Consent)

References

12
14

15

18

21
23
24
29
29
31
38
52

58

LIST OF TABLES

Table l-Demo graphic variables by diagnostic groups analysis
of variance

Table 2-Diagnostic group by TAS-20 scores one-way ANOVA
Table 3-Diagnositc group by TAS-2O scores one-way ANOVA (boys)

Table 4-Intercorrelations among TAS-20 Total and Subscale Scores
and CBCL Scores

Table 5-Intercorrelations among TAS-20 Scores and demographic
variables

Table 6-Intercorrelations among TAS-20 Scores and CPT Scores

Table 7-Intercorrelations among TAS-ZO Scores and Stroop
Color-Word Scores

Table 8-Summary of independent samples t-tests for diagnostic
groups and TAS-20 Total Scores

Table 9-Classiﬁcation of TAS-20 Scores by diagnostic group

Table IO-Descriptive statistics by diagnostic group and TAS-20
Total Scores

42

43

45

48

51

INTRODUCTION

Attention-Deﬁcit/Hyperactivity Disorder (ADHD) is one of the most common
and disruptive behavior disorders of childhood and adolescence. Symptoms of
ADHD represent developmentally inappropriate levels of inattention, irnpulsivity, and
hyperactivity (American Psychiatric Association, 1994). Because ADHD is one of
the most commonly diagnosed and persistent of the childhood disorders, it carries a
substantial risk for escalating problems (Klein & Mannuzza, 1991). Consequently,
more research investigating potential risk factors for the disorder is needed.

As summarized in Robison, Solar, Skaer, and Galin (1999), cross-mtional
epidemiologic studies utilizing standardized diagnostic criteria suggest that 3% to 6%
of the school-age population may suffer with ADHD. Similarly, in a Quebec study of
prevalence rates of mental disorders, Breton et a]. (1999) found rates of ADHD
ranged ﬁom 3.8% to 9.8% for elementary school children; these rates decreased in
high school. Zito et al. (1999) found that physician visits for children aged 5-14 years
old with ADHD rose by 90% between 1989 and 1996 (as cited in Bonn, 1999).
Estimates have had a wide range of variability that may be explained by differences
in informants (parent or teacher), culture, and the degree of impairment needed for
diagnosis (Elia, Ambrosini, & Rapoport, 1999). However, studies conﬁrm an
increasing trend in the diagnosis of ADHI) (e.g., exceeding two million children;
Erdman, 1998) and an increasing trend in the prescribing of stimulant

plmrmacotherapy for its treatment (Robison, Solar, Skaer, & Galin, 1999). Though

there is general agreement regarding the prevalence and course of ADHD, the
etiology of this behavioral disorder remains in question. Consequently, treatment
recommendations are based upon arguable theoretical assumptions regarding the
origins of the behaviors and neuropsychological impairments found in children
diagnosed with ADHD.

Children with ADHD exhibit a wide range of problematic academic and
interpersonal deﬁcits, including poorer social skills than in children without this
problem (Merrel & Wolfe, 1998). These children were found “especially lacking in
social cooperation skills: the ability to follow rules, structure, and important social
expectations of both children and adults” (p. 101). It has also been reported that
noncompliance, interpersonal ﬁ‘iction with adults, peer rejection, aggression, and
school problems are associated impairments related to ADHD (Melnick & Hinshaw,
2000). Consistent with a plethora of research articles regarding neurological deﬁcits
in ADHD, Seidman et al. (1995) found that ADHD children performed more poorly
on tasks of attention, executive function, and learning and memory, than did normal
controls. Additionally, “executive function” measures of planning or controlling
motor output were more impaired in ADHD than in comparison boys (Nigg,
Hinshaw, Carte, & Treuting, 1998). Barkley (1998) offers a comprehensive model of
ADHD suggesting that ADHD is a developmental disorder of behavioral inhibition,
inattention, and self-regulation. The “developmental delay in inhibition gives rise to
deﬁcits in the executive functions that subserve self-regulation. It is these secondary
deﬁcits that result in inattentive, distractible, irnpersistent, and poorly regulated

behavior” (p. ix).

The most widely researched etiological models concerning the development
of ADHI) suggest that this disorder is one that develops because of genetic or
biologic factors or that it is “largely a result of neurological dysfunction” (Frick &
Lahey, 1991, p. 169). Information distributed to parents of children with ADHD
makes these claims clearly. For example, Harvey Parker, Ph.D., co-founder of the
largest national ADHD organization (Children and Adults with Attention Deﬁcit
Disorders; C.H.A.D.D.) reported that ADHD is a “neurobiological disorder.. .due to a
chemical imbalance” (Merrow, 1995).

Given the pervasive belief that ADHD is a genetic or biological disorder,
parenting problems, family factors, and traumatic life events in the lives of children
diagnosed with ADHD may actually be under-reported or under-estimated (e.g.,
Overmeyer, Taylor, Blanz, & Schmidt, 1999). Parenting characteristics, particularly
the role of the primary caregiver’s emotional availability and ability to be attuned and
empathic, may be one risk factor for the etiology or exacerbation of the
developmental struggles faced by children with ADHD. A disturbing trend was noted
by Gibbs (1998), in that the percentage of children with an ADHD diagnosis walking
out of a doctor’s oﬂice with a prescription for stimuhnts dramatically increased from
55% in 1989 to 75% in 1996. The number receiving psychotherapy fell ﬁ'om 40% in
1989 to 25% in 1996. This trend suggests that treatment options are being limited by
theoretical assumptions regarding the etiology and symptoms of ADHD. In this
proposal, I will review evidence supporting the hypothesis that a parental personality
trait, alexithymia (described below) might be one risk factor in the child’s

development of ADI-II). This contextual factor seems to more accurately represent

the current state of the developmental literature regarding the inﬂuence of early
parenting for later problematic behaviors.

The charge that many children are misdiagnosed, might be correct. The
DSM-IV requires that ADHD “must be distinguished ﬁ'om difﬁculty in goal-directed
behavior in children from inadequate, disorganized, or chaotic environments. . .”
(American Psychiatric Association, 1994, p. 83). It is felt by some that abnormal
psychosocial factors are under-detected in the lives of children with ADHD if
“clinicians. . .presurne a biological aetiology” (Overmeyer, Taylor, Blanz, & Schmidt,
1999, p. 262). They found that clinicians who knew the diagnosis of the child for
whom they were doing an assessment found diﬁerent rates of psychosocial adversity
in the histories of children with conduct disorder and children with hyperkinetic
problems. However, when clinicians blind to the diagnosis did the same interviews,
they found no difference in rates of psychosocial adversity between the two types of
disorders; this ﬁnding was contrary to the existing literature. Similarly, in a study of
parental attribution styles for child behavior, parents of ADHD children were less
likely to see themselves as the cause of child behavior and were more likely to
mention medication (Johnston, Reynolds, Freeman, & Geller, 1988). These authors
also reported that the attributions they found were consistent with current theoretical
views of ADHD as a primarily biological condition amenable to pharmacological
treatment and my reﬂect information parents have received ﬁom health care
professionals, parent support groups, and other sources. Finally, criticisms have been
leveled that “the diagnosis meets the needs of the parents more than it does that of the

child” (Smelter et aL, 1996, p. 430). Psychiatrist Peter Breggin, referring to materials

given to parents of children with ADHD which blame the child for causing parental
ﬁ'ustration and upset, reports that “there could be no better example of pedist [i.e.,
prejudice against children] child-blaming and mistaken parental exoneration”
(Breggin & Breggin, 1994, p. 89).

Crittenden (1992) stressed the importance of considering the behaviors of
these children in the context of their function, rather than to simply look at isolated
overt behaviors. Additionally, DeKIyen, (1996) found a link between childhood
disruptive behavior disorder, the quality of the mother-child interactions, and the
mother’s recollections of her attitudes toward her parents. Similarly, Hamish, Dodge,
and Valente (1995) reported that “children who experienced negative-quality
interactions with their mothers were more likely than children who experienced
positive-quality interactions to have increased levels of externalizing behavior
problems” (p. 749). Another study, looking at contextual factors, found that the
strongest factors in accounting for ADHD-type behaviors (and change in such
behaviors) were measures of relationship status at birth, social support for the parent,
and the direct measures of parental overstimulation (Carlson, Jacobvitz, & Sroufe,
1995).

eritab' ° the inﬂuence of ent’ on develo ment

Attention-Deﬁcit/Hyperactivity Disorder has been reported to be a genetic
disorder (Barkley, 1998). Despite some assertions that there is little evidence of
parents’ inﬂuence on behavior and personality in adolescence and adulthood (e.g.,
Harris, 1998; Rowe, 1994), recent evidence suggests that this may not be the ﬁnal

word (Collins, Maccoby, Steirrberg, Hetherington, & Bornstein, 2000). A recent

meta-analysis concluded that heredity rarely accounts for as much as 50% of the
variation in heritable traits among individuals in a particular population, perhaps even
less when personality characteristics are the focus (McCartney, Harris, & Bernieri,
1990). Lastly, even highly heritable traits can be highly malleable (Collins, Maccoby,
Steinberg, Hetherington, & Bomstein, 2000). For example, the Finnish adoption
study (Tienari et a1, 1994) suggests how a genetic predisposition can either manifest
itself or not, depending on whether certain environmental triggering events are
present.

Even though “parental behavior is inﬂuenced by child behavior, parents’
actions contribute distinctively to the child’s later development” (Collins et aL, 2000,
p. 222). The style and quality of parenting, to some extent, moderates associations
between early temperamental characteristics of diﬁicultness, impulsivity, and
unmanageability and later externalizing disorders (Bates, Pettit, Dodge, & Ridge,
1998; Rothbart & Bates, 1998). On the adaptive side, Collins et, aL, (2000) concluded

ﬁndings suggest that well-ftmctioning parents can buffer children

at genetic risk and circumvent the processes that might ordinarily lead ﬁom

genotype to phenotype. The more general point is that genetic

vulnerabilities (or strengths) my not be manifested except in the presence

of a pertinent environmental trigger such as parenting (p. 223).

The human infant is born with relatively few of its neural pathways committed
(Hoﬁ'er, 1984). Diﬁ‘erences in the social environment of an individual during
development can result in changes in the biology of the brain and body just as much

as in behavior (Lewontin, Rose, & Kamin, 1984, p. 142). “During its long infancy,

connections between nerve cells are formed on the basis not merely of speciﬁc
epigenetic programming but in light of experience” (p. 145). Endocrine, immune,
canﬁovamnﬂanIneuuxﬂkgandrunuochmmmwdvaﬁabkmaueaﬂlﬁddmnvﬁﬂnnthe
mother-infant interaction (Hofer, 1984). More speciﬁcally, Schore (1994) theorizes
that the degree to which the mother stimulates and modulates the infant’s affect-
annnwdsunesnnxiunﬁnuunsthenruidmnannodennerange,nunrudhunmcthe
balance between sympathetic and parasympathetic components of the autonomic
nervous system” (as cited in Fukinishi, Sei, Morita, & Rahe, 1999). Empirical
evidence suggests that brain development in young organisms is dependent, in part,
on experience in humans (e.g., Schore, 1994) and non-human animals such as rats
(e.g., Caldji et al., 1998; Liu et al., 1997) and Rhesus monkeys (Suomi, 1997; as cited
hICkﬂﬁnsetaL,2000)

Parental behavior has been shown to be highly stable across time (Holden &
Miller, 1999), however, changes in parenting practices are found to be associated
signiﬁcantly with changes in teacher-reported school adjustment and with changes in
both child-reported and parent-reported maladjustment (F orgatch & DeGarmo, 1999).
Parents also “mediate the association between broader social, cultural, economic, and
historical contexts and children’s behavior and personality” (Collins et al., 2000, p.

228).

Infants of mothers with psychosocial problems are found to be less likely to
develop secure attachments [as deﬁned by attachment theory] in the ﬁrst
place, suggesting both direct and indirect pathways for the inﬂuence of
maternal problems on later child adaptation (Lyons-Ruth, Alpem, &
Repacholi, 1993, p. 582).

The development of affects and aﬂ'ect-regulating capacities is facilitated early
in life by the experience of aﬁect sharing and “mirroring” of aﬂ’ective expressions
with the primary caregiver (Krystal, 1988; McDougall, 1988, Taylor, Bagby, &
Parker, 1997). The presence and activities of the infant stimulate a set of maternal
behaviors needed by the infant. . .and these reciprocal maternal behaviors serve to
facilitate the infant’s adaptation and development (Stern, 1985). Therefore, evidence
suggests that both genes and parenting aﬁ‘ect brain processes and neuroendocrine
systems (Collins et al., 2000). One current model of these processes will be explored
in detail in this study, though it my not be the only pathway.

A contextual model of ADHD as an alternative to biological determinism

In this proposal, I will offer a alternate consideration to the largely
biologically deterministic views within most ADHD researchers’ reports. In general,
adherents to biological etiological theories of emotional and behavioral disorders

answer that human lives and actions are inevitable consequences

of the biochemical properties of the cells that make up the individual;

and these characteristics are in turn uniquely determined by the constituents

of the genes possessed by each individual (Lewontin, Rose, & Kamin, 1984,

p. 6).

If the scientiﬁc and lay communities assume a genetic or purely
neurodevelopmental etiology of ADHD, then it becomes easy to dismiss important
contextual/environmental variables which may have direct impact on the
development of the symptoms associated with ADHD and treatment. In fact, it is
commonplace to read that the differences that are found in parenting styles and
practices are the result, rather than a possible cause, of the disordered behavior of
these children (e.g., Barkley, 1998). He writes,

ADHD is associated with an impairment in self-regulation and this

impairment must radiate into the social ecology of these children,

affecting others and the manner in which they may reciprocate (p. 143).

In view of the twin studies. . .that show minimal or nonsigniﬁcant

contributions of the common or shared environment to the expression

of symptoms of ADHD, theories based entirely on social explanations of the

origins of ADHD are diﬁicult to take seriously any longer (p. 175). Thus,

common parenting factors are not viewed as a major contributor to the
occurrence of ADHD symptoms or the disorder in children (p. 176). The
overly critical, commanding, and negative behavior of mothers of hyperactive
children is most likely a reaction to the diﬁicult, disruptive, and noncompliant

behavior of these children rather than being a cause of it (p. 176)

Hechtman (1996), in her review of families of children with ADHD, also reported
that negative parenting styles of mothers of hyperactive children were probably a
consequence of the child’s behavior. Barkley (1998) did report, however, that cases

of ADHD can also occur without a genetic predisposition, “provided the child is

exposed to signiﬁcant disruption or neurological injury to this ﬁnal common
neurological pathway (the preﬁontal cortical-striatal network;” p. 177). He felt,
however, that this would seem to account for a small minority of ADHD children.
Biedennan et al (1993) reported that indices of psychosocial adversity were
predictive of ADHD outcome (as cited in Seidman et al., 1995). Perhaps the role of
parental alexithymia and its inﬂuence on attachment behaviors is one example of
“signiﬁcant disruption” to which Barkley concedes. While there is little doubt that
there is complex interaction between parenting behaviors and children’s behavioral
and emotional problems, the tone of many articles and books regarding ADHD strikes
this reader as blaming the child. Fortunately, the scientiﬁc community is not of one
mind in this regard.

Erdman (1998), in her paper conceptualizing ADHD as a contextual response
to parental attachment, reported that even diagnoses of ADI-II) that are clinically valid
send a message to the parent and to the child that the problem lies within the child,
when in reality it is a Emily issue (p. 182). “The repercussions of viewing ADHD as
an individual problem to be treated solely with medication, behavioral management
techniques, or both, has serious implications” (p. 182). Speciﬁcally, “children who
are already frustrated and anxious over the lack of a parental bond will feel more
victimized if they are focused on as the problem” (p. 182). Similarly, on a more
philosophical level, Lewontin, Rose, and Kamin (1984) wrote:

The disordered brain is seen as the cause of an unacceptable interaction

of individuals and social organizations. The political consequence is that,

since the social institution is never questioned, no alteration in it is

10

therefore contemplated; individuals are to be altered to ﬁt the institutions

or else sequestered to suﬁer in isolation the consequences of their

defective biology (p. 21)

If we translate the notion of “social organization” into the more immediate Emily and
school organizations, the implications are clear. The consistent predictive power of
caregiving and contextual factors to distractibility and later hyperactivity, however,
suggests that there may be signiﬁcant psychogenic contributions to ADI-II) for many
children (Carlson, Jacobvitz, & Sroufe, 1995, p. 52). In their longitudinal analysis of
Emilies, they reported that relationship stability and external emotional support of the
primary caregiver emerged as particularly inﬂuential factors in the development of
ADHI) symptoms. (p. 52). Such contextual considerations may be crucial to the
prevention or amelioration of symptoms for some children and appear to be important
to an understanding of the course and treatment of the disorder regardless of etiology
(Carlson, Jacobvitz, & Sroufe, 1995, 54). Speltz (1990) explained conduct
problems—which he deﬁned as chronic noncompliance, aggressiveness, and ﬁequent
discontrol—as an outcome of the absence of immediate, consistent, and
developmentally appropriate parental responses to children’s behaviors.

Studies conﬁrm that parents of ADHD children are more likely to have
ADHD, or some residual characteristics (e.g., Alberts-Corush, Firestone, &
Goodman, 1986; Barkley, 1998). Additionally, parents of ADHD children are more
likely to experience a wide variety of other psychiatric disorders, including conduct
problems and antisocial behavior, alcoholism, and affective disorders (Cantwell,

1972; Faraone & Biedemran, 1997; Morrison & Stewart, 1973; Singer et al., 1981, as

11

 

exp

We}

 

cited in Barkley, 1998, p. 146). Parents who exhibit aﬁ‘ectionless control are more
likely to have children with anxiety disorders, obsessive—compulsive disorder, and
attention deﬁcit disorder (Hafner & Spence, 1988; Parker, 1984).
Barkley’s neuropgcholo gical model of ADHD

Barkley’s (1998) conceptual model of ADHD is a developmental
neuropsychological model of human self-regulation (p. 229). A comprehensive
review of this model and supporting literature is prohibitive in length; for a review
look to Barkley’s (1998) text. A deﬁcit in inhibition has become a theoretical
assumption, replacing the older importance placed on hyperactivity. Wender’s theory
(1971) of “minimal brain dysftmction,” a precursor to the more modem ADHD
diagnosis, gave a prominent role to the construct of poor inhibition. He believes it to
explain the activation diﬂiculties and the attentional problems that stem from them, as
well as the excessive emotionality, low ﬁ'ustration tolerance, and hot temperedness of
ADHD children (as cited in Barkley, 1998, p. 12). Irritability, hostility, excitability,
and a general emotional hyperresponsiveness toward others have been frequently
described in the literature (Barkley, 1990). Later he summarized ﬁndings that suggest
that emotional self-control may be problematic for children with ADHD (Barkely,
1998). Barkley’s (1998) model:

speciﬁes that behavioral inhibition, representing the ﬁrst and

foundation component of the model, is critical to the proﬁcient

performance of the four executive functions: non-verbal working

memory, internalization of speech (verbal working memory), the

self-regulation of aﬂ‘ect/motivation/arousal, and reconstitution (p. 229).

12

 

 

 

 

deﬁ

Deﬁcits in any particular executive function will produce a relatively distinct
impaimrent in self-regulation, different from that impairment in self-control produced
by deﬁcits in other functions (p. 234). On measures of sustained attention
(speciﬁcally of the goal-directed type) the prefrontal cortex and the executive
ﬁinctions that the cortex and its networks permit, are essential (p. 246). Behavioral
inhibition and at least three of the executive functions appear to be mediated by
separate but surely interacting regions of the preﬁontal lobes. Behavioral inhibition
and its component processes seem to be localized in the orbital-frontal regions and its
interconnections to the striatum.

Behavioral inhibition delays the decision to respond to an event. The

self-directed actions occurring during the delay in the response

constitute the executive ﬁmctions. . . .Over development, they may

become progressively more private or covert in form. The development

of internalized, self-directed speech seems to exemplify this process.

Although eventually “internalized,” these self-directed actions remain

essentially self-directed forms of behavior despite the Ect they have become

disengaged form their more obvious and public motor manifestations

(muscoloskeletal movements). Therefore, the term “executive ftmction”

refers here to those self-directed actions of the individual that are

being used to self-regulate (p. 233).

In summary, ADHD is not just a deﬁcit in behavioral inhibition, but also a
deﬁcit in executive functioning and self-regulation as a consequence of that inhibitory

impairment. “The deﬁcit results in a renegade motor control system that is not under

13

the same degree of control by internally represented information, time, and the
future” (249).
Altmivgs to plEnnacological treatment for ADHD

The most consistently recommended and implemented treatment for children
with ADHD is stimulant medications, such as methylphenidate. When considering
Barkley’s theoretical model of ADHD, he felt that only a treatment that improves the
underlying neuropsychological deﬁcit in behavioral inhibition is likely to result in an
“improvement or normalization of the executive function dependent on such
inhibition” (Barkley, 1998, p. 252). “To date,” he wrote, “the only treatment that
exists that has any hope of achieving this end is stimulant medication or other
psychopharmacological agents tlmt improve or normalize the neural substrates in the
preﬁontal regions that likely underlie this disorder” (p. 252). Given this belief,
pharmacological treatments for ADHD are far more widely employed, are less
expensive, and have much more short-term empirical support than psychosocial
treatments (Pelharn, Wheeler, & Chronis, 1998). However, Barkley also reminds us
that behavioral interventions and parent training programs are also useful for children
with ADHD and their Emilies (Barkley, 1998).

However, McGuiness (1989) reviewed follow-up studies showing that
children taking psychostirnulant medication for long periods of time fee] worthless
and have low self esteem. Another major limitation of stimulant therapy is that long-
term studies (up to ﬁve years) Eil to provide any evidence that the drugs improve
ADHD children’s long-term prognosis (Charles & Schain, 1981; Weiss & Hechtman,

1993).

I4

Widener (1998) found improvement in a patient’s ADHD symptoms when his
underlying feelings of depression, sadness, and loneliness have been addressed in
psychodynamic psychotherapy. She feels that the child’s hyperactivity may actually
be a way the child signals the presence of very painful aﬁ‘ects (p. 274). She also
reported that some of the changes in the child being treated were dependent on the
mother’s therapeutic work which resulted in her recognition of unresolved issues with
her own mother and her feelings about her self-as-mother. Orford (1998) offers one
therapeutic approach, by stating

what is effective with these children is help in organizing the terrifying

chaos of their inner worlds; it is a terrifying chaos that has been with

them since babyhood, which was not regulated at the time within the

maternal environment and which has led to subsequent habitual and

primitive responses of a hyperactive, hypervigilant kind (p. 264).

In my own clinical experience working with patients diagnosed with ADHD, I
have also found a dramatic and immediate attenuation of ADHD behavioral
symptoms when unacknowledged, uncomfortable feelings have been interpreted and
brought into the clinical exchange. When patients are able to ﬁnd words for and
express their underlying feelings, the behavioral symptoms, likely serving a
defensive/protective function, are no longer needed to cope with them (i.e., keeping

them at bay).

Al xrthm
The construct of alexithymia originally came ﬁom within the ﬁeld of

psychosomatic medicine, but was later described also by authors from within

15

psychoanalysis. According to his review (Taylor, 2000), this personality construct
has gradually captured the attention of “many psychiatrists and psychologists
throughout the worl ” (p. 134). He conducted a database review and found that 120
articles were published on alexithymia by the mid-1980’s, but since, well over 700
journal articles have been published on alexithymia. Alexithymia “reﬂects deﬁcits in
the cognitive processing and regulation of emotion” (p. 135). Sifrreos (1973) coined
the term alexithymia (ﬁ'om the Greek: a = lack, lexis = word, thymos = emotion) to
denote a cluster of cognitive and affective characteristics. Taylor et al. (1988)
described alexithymia, in accordance with formulations by Nemiah and Siﬁreos
(1970), as a “multidimensional construct deﬁned by the following cognitive-aﬂ‘ective
characteristics: a) a diﬂiculty in identifying and describing feelings, b) a diﬂiculty in
distinguishing between feelings and bodily sensations, c) a paucity of Entasies, and
d) a preoccupation with external events” (p. 500). Empirical evidence shows that
alexithymia is associated with dimculties in discriminating among different
emotional states (Bagby et al, 1993), and with a limited ability to think about and use
emotions to cope with stressﬁrl situations (Parker, Taylor, & Bagby, 1998; Schaﬁ‘er,
1993). Other features of alexithymia include: a tendency toward social conformity, a
tendency toward action to express emotion or to avoid conﬂicts, an inﬁ'equent
recollection of dreams, a somewhat stiff wooden posture, and a paucity of Ecial
emotional expressions (Krystal, 1979; Nemiah, Freyberger, & Siﬁreos, 1976; Ruesch,
1948;Siﬁ1eos, Apfel-Savitz, &Frankel, 1977).

This construct is best considered as a personality dimension, rather than as a

dichotomous category (Salrninen, Saarijarvi, & Aarela, 1995). There is “consensus in

16

the literature on the deﬁnition of the alexithymia construct, and there is now a
substantial body of empirical data supporting the validity of the construct” (Taylor,
1997, p. 267).

Alexithym’ as dg' inct ﬁom other forms of psychopathology

Individuals with alexithymic features have historically been labeled as
“normopaths” (McDougall, 1984) or “normotics” (Bollas, 1987), and are similar to
descriptions of people who have “inner blindness” (Homey, 1952). Despite its
origins from within psychosomatic medicine, alexithymia has not been found to be a
personality dimension that is speciﬁc to psychosomatic patients (Ahrens & Deﬁner,
I986; Sahninen, Saarijarvi, & Aarela, 1995). Alexithymic features have been found
to be common in patients suffering from: anorexia nervosa, bulimia, obesity,
substance abuse, depression, panic disorder, post-traumatic stress disorder, perverse
sexual behavior, and hypochondriasis and somatization (Taylor, Bagby, & Parker,
1997; Salminen, Saarijarvi, & Aarela, 1995). Importantly, however, alexithymia has
been found to be distinct ﬁom each of these disorders (Wise, Mann, & Randell, 1995;
Parker, Bagby, Taylor, 1991).

These deﬁcits in representing and regulating emotions cognitively are thought
to render alexithymic individuals more susceptible to a variety of medical and
psychiatric illnesses (Taylor, Bagby, & Parker, 1997). Studies comparing
alexithymia (as measured by the Toronto Alexithymia Scale; TAS) and depression (as
measured by the Beck Depression Inventory; BDI) have yielded consistent evidence
that alexithymia is a separate and distinct construct (Parker, Bagby, & Taylor, 1991).

“While there is some shared variance between measures of depression, anxiety, and

I7

 

 

alexithymia, the data from prospective studies with various medical and psychiatric
populations indicate that alexithymia is not simply a secondary response to anxious or
depressed states” (Parker & Taylor, 1997, p. 73). Treatment studies of persons with
substance or alcohol abuse problems show that after brief treatment periods, levels of
depression and psychological distress dropped signiﬁcantly, while mean alexithymia
scores were not signiﬁcantly lowered (Haviland, Shaw, Cummings, & MacMurray,
1988; Keller, Carroll, Nich, & Rounsaville, 1995; Pinard, Negrete, Annable, &
Audet, 1996). “These each lend support for the view that alexithymia is not merely a
state phenomenon secondary to depression or withdrawal” (Taylor, 1997, p. 188).
Further Qnsiderations of the alexithymia ' construct

Contemporary psychoanalytic theoreticians are of the opinion that serious or
long-term interferences in early life, such as the unavailability of an empathic and
responsive parent, rmy lead to stagnation in emotional development, which reveals
itself in later life as alexithymia (Taylor, Bagby, & Parker, 1997). While some
researchers believe alexithymia has a neurobiological basis (Dewaraja & Sasaki, ‘
1990; Zeitlin, Lane, O’Leary, & Schrift, 1989), others feel that alexithymia may be
caused by dysfunctional Emily environments, especially if the dysfunction was
experienced during critical developmental periods in the ﬁrst few years of life
(Crittenden, 1994). For example, in a study of Japanese college students (F ukunishi,
Sei, Morita, & Rahe, 1999), it was found that poor parental bonding is related to the
perceived difﬁculty in articulating feelings. They also found that alexithymia and
poor maternal care is related to high sympathetic activity during the resting period.

Additionally, Krystal (1988) has also written extensively about the alexithymic

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characteristics of people who have survived infantile or adult traum, such as being
interned at a Nazi concentration camp.

McDougall (1984) in her psychoanalytic paper on the “dis-aﬂ‘ected” patient
discovered that patients who were unaware of their affective reactions and internal
feeling states, would immediately disperse into action any emotional arousal.

In other words, these patients, instead of capturing and reﬂecting

upon the emotional crises that arose in their daily lives or in the

analytic relationship, would tend to act out their affective experiences,

discharging them through inappropriate action rather than ‘feeling’

them and talking about them in the sessions (p. 388).

In her work with patients with “dis-affected” presentations, she also reported that she
was able to reconstruct a paradoxical mother-chﬂd relationship in which the mother
seems to have been out of touch with the inEnt’s emotional needs, yet at the same
time has controlled her baby’s thoughts, feelings, and spontaneous gestures in a sort
of archaic “double-bind” situation (p. 391).

According to Taylor, Bagby, and Parker (1997), alexithymia is not a culture-
bound construct, as evidenced by both clinical and non-clinical populations in diverse
cultures, and by successﬁtl cross-validation studies of a self-report measure of the
construct in many different countries, including Italy, India, Japan, and Korea.
Additionally, there is strong support for alexithymia being a stable personath
feature, rather than just a consequence of psychological distress (p. 37). Alexithymia

was also found to be unrelated to age, gender, educational level, socioeconomic

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status, vocabulary skills, and general intellectual ability (Parker, Taylor, & Bagby,
1989)

People with alexithymic features have been found to have a host of
psychological adjustment problems associated with an impaired ability to know and
label their feelings. Individuals with alexithymic traits are in a “state of internal
alarm” (due to higher vegetative arousal), exhibiting high anxiety and high level
sympathetic reactivity, which is expressed somatically (Inﬁasca, 1997, p. 279). Also,
alexithymia is associated with primitive (Kooiman, Spinhoven, Trijsburg, &
Rooijmans, 1998) or immature (Parker, Taylor, & Bagby, 1998) defensive styles.
Alexithymic individuals are prone to use action-oriented behaviors such as binging on
food or abusing alcohol, seemingly in an attempt to regulate distressing emotional
states (Lane & Schwartz, 1987; Taylor, Bagy, & Parker, 1997). Schaﬂ’er (1993)
showed that highly alexithymic individuals tend to employ oral and somatic styles of
aﬁ‘ect regulation, such as bingeing on food or developing somatic symptoms.
Alexithymic individuals are prone to high levels of negative emotion and somatic
distress (Taylor, Bagby, & Parker, 1997; Bagby, Taylor, & Parker, 1990). They have
also been shown to have an impaired ability to recognize both verbal and nonverbal
emotional stimuli (Lane et al., 1994). For alexithymic people, there is not only a
diﬁculty in expressing emotions verbally but a deﬁcit in their cognitive processing
(Sahninen, Saarijarvi, & Aarela, 1995). This causes emotions to remain

undifferentiated and poorly regulated (Taylor, Bagby, & Parker, 1991).

20

 

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Parental alexith 'c features em ath attachment and affect re tion

Because of the dual process of acquisition of affect tolerance (by learning and
by identiﬁcation), children whose parents have diﬁculty in handling aﬁ‘ect also have
difﬁculty in developing advantageous ways of dealing with their emotions (Krystal,
1988). These difﬁculties are not likely to be under conscious control, as it has been
reported that parents vary in their own responsiveness and sensitivity to their babies’
communications depending on their own early experiences (Orford, 1998). Securely
attached individuals showed lower levels of alexithymia, and employed interpersonal
behavior and Entasies of talking to a caring person to help regulate aﬂ‘ect (Schaﬁer,
1993). According to Taylor, Bagby, and Parker (1997),

.. .the development of affect and affect regulating capacities is Ecilitated

early in life by the experience of affect sharing and “mirroring” of affective

expressions with the primary caregiver, and subsequently by engaging

in pleasurable playﬁrl interactions and being taught to name and talk

about feelings (p. 41).
Accurate empathic attunement has been found to be integral to the attachment
dynamic (McCluskey, Hooper, & Miller, 1999).

Empathy involves the ability to understand both selfand others. Tangey
(1991) reports that other-oriented empathy requires the ability to take another’s
perspective. reading the other’s internal emotional experiences, and being capable of
experiencing a range of emotional states. When the primary caregiver is emotionally
unavailable or when the child is subjected repeatedly to inconsistent responses

because of parental “rnisattunement,” the child is likely to manifest abnormalities in

21

affect development and affect regulation, as well as an insecure attachment style
(Emde, 1988a,b; Osofsky, 1992; Slade & Aber, 1992; Stern, 1985). Maternal
sensitive responsiveness is deﬁned by the attachment ﬁgures’ success in ﬁtting their
own response patterns to those of their offspring in ways that are mutually satisfying
(Crittenden, 1995). “Anything else must, by deﬁnition, be considered insensitive” (p.
389). Research studies on attachment styles in infancy and childhood have conﬁrmed
that the sensitivity and responsiveness of the primary caregiver to thechild’s
emotional states is a major determinant of the way the child learns to regulate
distressing affects and to relate to other people (Bretherten, 1985; Goldberg,
MacKay-Soronka, & Rochester, 1994).

Normal aﬂ'ect development does not occur when the parents are unable to read
the emotional cues of the infant, and Eil to ﬁmction as external regulators of the
inEnt’s emotional states (Taylor, Bagby, & Parker, 1997). Taylor (1992) links
Eilures in physiological self-regulation to psychological deﬁcits, particularly in
recognition of moods, that stem ﬁom early attachment problems. Insensitive mothers
impede an inEnt’s ability to modulate affective expression and arousal (Susman-
Stillrnan, Kalkoske, Egeland, & Waldman (1996). Successful affect development and
regulation of the experience of secure attachment provides “predictable positive
outcomes to affective communications, and thereby Ecilitates a satisfactory
integration of affective information with cognitive information” (Crittenden, 1994, p.
25). Primary caregivers who have alexithymic features, cannot imagine themselves
in another person’s situation and are consequently unempathic and ineffective in

modulating the emotional states of others (Goleman, 1995; Krystal, 1979; Lane &

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Schwartz, 1987). In a study where participants were asked to rate the emotional
content of ambiguous stimuli, it was reported that a general ability to perceive
consensual emotional content in visual stimuli was most strongly associated with the
ability to respond empathically (Mayer, DiPaolo, & Salovey, 1990).

One contemial variable: Attachment and ADHI)

According to Bowlby (1951), “the quality of the parental care which a child
receives in his earliest years is of vital importance for his future mental health” (p.
11). As reported in Bowlby (1988), prospective studies revealed that those children
who showed an anxious avoidant pattern (of attachment) are likely to be described
later as emotionally seeking of attention. Those who showed an anxious resistant
pattern are also likely to be described as unduly seeking of attention and either as
tense, impulsive, and easily ﬁ'ustrated or else as passive and helpless (p. 169).
Results indicate that stability in Emily of origin, emotional stability at three weeks,
and maternal empathy and conﬁdence at 18 months were signiﬁcantly related to
inEnt-mother attachment security. (Wieczorek-Deering, Greene, Nugent, & Graham,
1991).

The attachment relationship is widely believed to exert signiﬁcant inﬂuence
on a child’s later development (Susman-Stillman, Kalkoske, Egeland, & Waldman,
1996, p. 35). As is consistent with previous ﬁndings, they found a relationship
between distractibility at 3 '/2 years and ADHD symptoms at 6-8 years. However,
although attachment theory has been linked to conduct disorders and other behavioral

problems, it has not been linked to ADHD behaviors (Erdman, 1998, p. 184).

23

Critical pm’ods, brain development, and aﬁ°ect regu_la_tion
An inEnt’s genetic endowment (genotype) is transformed and modiﬁed,

through the brain’s plasticity, by environmental events. Evidence from the diﬁerent
domains of developmental neuroscience, neurobiology, behavioral neurology, and
developmental psychology suggests that the experiences within the early mother-
infant dyad are responsible for ﬁrnctional and structural brain maturation, particularly
in the frontal lobe structures that mediate the executive functions outlirwd in
Barkley’s (1998) model of ADHD. For example, there has been found a striking
similarity between ADHD symptoms and stress-induced prefrontal cortical deﬁcits
(Amsten, 1999). Below is a review of one current model of a mechanism by which
the infant gradually develops the ability to regulate its aﬁ‘ect. This model might
explain a mechanism involved in the development of ADHD.

During early inEncy, the infant is ill-equipped to effectively regulate its
aﬂ‘ect, leaving it prone to being overwhelmed, and “because it lacks the means for
modulation of behavior, which is made possible by the development of cortical
control.. .[t]he role of higher structures is played by the mother; she is the child’s
auxiliary cortex” (Diamond, Balvin, & Diamond, 1963, p. 305, as cited in Schore,
1994, p. 30). It is during infancy and early childhood that the brain is more malleable
to experience than the mature brain (Perry, Pollard, Blakely, Baker, & Vigilante,
1995).

In the developing brain, undifferentiated neural systems are

critically dependent upon a set of environmental and micro-environmental

cues (e. g., neurotransmitters, cellular adhesion molecules, neurohormones,

24

 

 

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amino acids, ions) to appropriately organize from their undifferentiated

form (Perry et al., 1995, p. 275)

For instance, Weber and Sackheim (1978) reviewed developmental neurobiological
studies and suggest that critical periods of development associated with signiﬁcant
changes in the environmental repertoire are correlated with shifts in nervous system
growth and reorganization (as cited in Schore, 1994, p. 29). Mutually interactive
experiencesintheﬁrstZyearsareoccurringwhilevarious sensorysystemsare
maturing, and, these experiences are internalized as ‘permanent idiosyncratic
modiﬁcations of the nervous system” (Freedman, 1981, p. 841).

Critical early affective transactions with the social environment are mentally
stored (internalized) in the form of representations of the self interacting with
signiﬁcant objects (Schore, 1994, p. 25); these representations are the same as
Bowlby’s (1988) “internal working models.” In a still-Ece paradigm, it was reported
that very young infants (by four months) begin to internalize aspects of the matemal
parenting environment in a rmnner that contributes to their response to stress and
interpersonal regulation strategies (Kogan & Carter, 1996). From an attachment
theory perspective, sensitive mothers are responsive to their children’s needs, which
helps inEnts modulate affective expression and arousal (Susman-Stillman, Kalkoske,
Egeland, & Waldman, 1996). Attachment theorists have argued that attachment
systems permit ﬂexible responses to environmental circumstances, influence the
regulation of emotion, and function through mental representations that children hold

of themselves and their relationships with others (Cassidy, 1994).

25

Neurobiological studies reveal that the dramatic onset of function in the ﬁrst
18 months of life reﬂects the immense synaptogenesis that occurs during this period
of inEncy. Indeed the speciﬁc period ﬁ‘om 7 to 15 months (roughly Bowlby’s period
for the establishment of attachment patterns) has been shown to be critical for the
myelination and therefore the maturation of particular rapidly developing limbic and
cortical association areas (Kinney, Brody, Kloman, & Gilles, 1988). ). At 18 to 20
months, representational processes mature rapidly and infants become substantially
more symbolic and verbal than they have been previously (Zeanah, Boris, Bakshi, &
Lieberman, 2000, p. 97). The onset of mature function in these corticolimbic
structures is instrumental to the emergence of inEnt aﬂ‘ective, affect regulatory, and
cognitive processes (Schore, 1994, p. 30). According to Gilbert (1989), there is now
convincing evidence indicating that this maturation is experience-dependent and
directly inﬂuenced by the caregiver-infant relationship (as cited in Schore, 1994, p.
30).

Perry at al. (1995) reported that “abnormal micro-enviromnental cues and
atypical patterns of neural activity during critical and sensitive periods. . .can result in
malorganization and compromised function in brain—mediated functions such as
humor, empathy, attachment, and affect regulation (p. 276).

Regarding the development of the ability to regulate one’s aﬂ‘ect, Wilson et
al., (1990) asserted that secure attachment Ecilitates the transfer of regulatory
capacities ﬁ‘om caregiver to inEnt. Thompson (1990) underscores the cardinal
principle that emotion is initially regulated by others, but as development proceeds it

becomes increasingly self-regulated as a result of neurophyisiological maturation (as

26

cited in Schore, 1994, p. 31). In surmnary, these observations suggest that “the
mother’s external regulation of the infant’s developing yet still immature emotional
systems during particular critical periods may represent the essential Ector that
inﬂuences the experience-dependent growth of brain areas prospectively involved in
self-regulation” Schore, 1994, p. 32). “The dyad’s response to stressﬁrl transaction,
such as occur in socialization experiences in the second year, are particularly
instrumental to the ﬁnal structural maturation of an adaptive cortical system that can
self-regulate emotional states” (Schore, p. 1994, p. 33). “Early object relational
experiences thus directly inﬂuence the emergence of a frontolimbic system in the
right hemisphere than can adaptively autoregulate both positive and negative aﬂ’ect in
response to changes in the socioemotional environment” (Schore, 1994, p. 33). These
functional advances reﬂect the structural nEturation of the right frontolimbic areas
and the emergence of more complex and emcient delay and inhibitory operations that
underlie regulatory capacities (p. 489). “Dyadic Eilures of affect regulation result in
the developmental psychopathology that underlies various forms of later forming
psychiatric disorders” (Schore, 1994, p. 33).

It is suggested that “a mother’s lack of aﬁ‘ective involvement thus produces a
growth-inhibiting environment which severely retards the experience-dependent
growth of right hemispheric temporal-ﬁontal and frontal-subcortical connections that
are necessary for the integrated functioning of the right cortex” (Schore, 1994, p.
485). Taylor (1987) describes:

It is likely that the right hemisphere contributes to the development

of reciprocal interactions within the mother-inEnt regulatory system,.

27

and when these are deﬁcient the child may Eil to develop a capacity

for being “in tune” with himself (p. 191).

He reports that deﬁciencies in the early mother-inEnt relationship result in an
alexithymic deﬁcit associated with a limitation of symbolic function and an impaired
capacity for self regulating emotional states and physiological functioning when
under stress. Schore (1994) concludes that maternal stress regulating verbalizations
are also internalized into the multirnodal interactive representations that encode the
self-caring functions of evocative memory. The child who is deprived of such
aﬂ’ective cormnunicational experiences in this critical period (second year) is in
danger of developing the regulatory disturbance of alexithymia (p. 489).

The orbitoﬁontal region is critically involved in attachment processes (Steklis
& Kling, 1985). Schore (1994) suggests that attachment experiences speciﬁcally and
directly inﬂuence the early maturation of the orbitofrontal cortex, a corticolimbic
structure that is critically involved in attachment processes (p. 255). Schore reports
that maternal stress regulating object relations transactions “act as a selection pressure
to critically shape. . .the maturing orbitoﬁ'ontal cortex” (p. 256).

Studies of adult animals (Kolb, 1974; Ruesch & Shenkin, 1943) have shown
that lesions in the orbital ﬁ'ontal cortex have resulted in hyperactivity (as cited in
Schore, 1994, p. 94). Similarly, Arntsen (1999) reported that both animals and
hurmns with lesions in the prefrontal cortex exhibit poor attention regulation,

disorganized and impulsive behavior, and hyperactivity.

28

Conclusion

The child’s nascent capacity to regulate its affect is dependent on an attuned
and empathic caregiver. Among other factors, affect regulation is a key component in
both cognitive and behavioral self-control, both of which are problematic for children
with ADHD. Problems associated with the development of self-regulatory capacities
are hypothesized to underlie some of the symptoms posed by current models of
ADHD. Given the empirical and theoretical models outline above, “good enough”
empathic attunement and mirroring of a child’s emotional states seems essential for
the successﬁrl development of the executive functions that underlie ADHD
symptoms. Accordingly, a parental characteristic, such as alexithymia, might
negatively affect the child’s developing regulatory capacities and place them at risk
for developing ADHD.
Hymtheses

In review of the current developmental literature and theoretical models of
Attention Deﬁcit-Hyperactivity Disorder (ADHD), alexithymia in prirmry caregivers
is hypothesized to be a risk Ector for the development of ADHD in their children.
The following speciﬁc hypotheses were investigated in this study.

1) Primary caregivers of children diagnosed with ADHD will evidence

greater levels of the alexithymia personality features as compared to
caregivers of clinic-referred children who do not have this diagnosis (e. g.,

mood disorders and conduct problems). I

29

2)

3)

4)

Alexithymic features in primary caregivers will be more strongly
correlated with subscales in the parent-rated behavioral measure consistent
with symptoms associated with ADHD, irrespective of diagnosis.
Speciﬁcally, alexithymic features will be more strongly correlated with the
“Attention Problems” subscale than with the “Anxious/Depressed”
subscale.

Alexithymic features in primary caregivers will not be found to correlate
highly with age, socioeconomic status, or education levels of the primary
caregivers.

Alexithymic features in primary caregivers will signiﬁcantly correlate

with the two neuropsychogical measures of sustained attention and

inlu'bition assessed for the participants with ADHD.

30

Methods
Partici ants

Participants for this study were drawn ﬁ'om a private psychological clinic in a
small midwestem city containing a major university. The children and adolescents
(age range of 6 to 18 years old, N = 75) were referred to this clinic for outpatient
psychotherapy and/or neuropsychological testing due to emotional, behavioral, and/or
academic difﬁculties. There were 19 females (12 in the ADHD group and 7 in the
Non-ADHD group) and 56 males (26 in the ADHD group and 30 in the Non-ADHD
group) included in this study. The sample was drawn from consecutive referrals to
the clinic, rather than from a randomized sample.

Therewere two groupsusedinthisstudy. Theﬁrstwascomposedofchildren
and adolescents who have a diagnosis of Attention-Deﬁcit/Hyperactivity Disorder
(ADHD). This diagnosis was made by examining parent and teacher behavioral
rating scales, clinical interview, and neuropsychological testing; this is a ‘rnulti-
method” approach to assessment and diagnosis recommended by Barkley (1998) and
others. The second (comparison) group was composed of clinic-referred children
who were being assessed, butwho do notcarryADHDasaprimarydiagnosis.
Parents or guardians of the referred patients were given a consent form prior to
becoming participants in this study. The clinic-referred children and adolescents also
carryaclhician-basedprhnaryDSMIVAxisIdiagnosisthatwasdetermined
independent of this research project. I

ThemeanagewithintheADI-ID groupwas9.l8 @=3.51),whilethemean

age within the Non-ADHD group was 11.05 (S_Q = 3.55). This is a signiﬁcant

31

difference between the two groups (p = .025; results shown in Table 1). The Non-
ADHD group was composed of children with the following diagnostic classiﬁcations:
mood/depressive

disorders (n = 6), conduct/oppositional disorders (n = 5), adjustment disorders (n = 8),
anxiety disorders (n = 5), learning disabilities (11 = 6), and neurological problems

(e.g., Asperger’s syndrome, n = 7).

Instruments

Child Behavior Checklist 4-18 (CBCL 4-18; Achenbach, 1991). This measure

 

provides an objective assessment of the identiﬁed child’s social and emotional
functioning. It is designed to record,in a standardized format, children’s
competencies and problems as reported by their parents. This measure is included in
the battery because a parent’s views of their children’s behavior is often crucial in
determining what will be done about the behavior (Achenbach, 1991). The primary
caregivers of clinic-referred children completed the CBCL 4-18. The measure can be
ﬁlled out by most parents who have at least ﬁfth grade reading skills; the measure
takes 10-15 minutes to complete. The CBCL 4—1 8 was normed on healthy children
(i.e., they had not recently received professional help for behavioral/emotional
problems) 4 to 18 years of age; they were chosen to be representative of the 48
contiguous states with respect to SES, ethnicity, region, and urban-suburban-rural
residence. This measure has solid psychometric properties in that both its reliability
and validity have been extensively supported.

The CBCL 4-18 has been found to have very high test-retest reliability (intraclass

correlation coeﬂicient (ICC) = .952) for the 118 speciﬁc problem items used in this

32

Table 1

Demoganhic variables by diagnostic groups analysis of variance (n=75)

 

 

ADHD
Variable Means ( SD)
Child’s Age 9.18 (3.51)
Grade Level 3.65 (3.64)

Mother’s Age 36.18 (7.48)

p<.05

1:3

38

37

38

Non-ADHD

Means (SD)

11.05 (3.55)

5.49 (3.70)

36.83 (7.46)

33

I3

37

37

36

t-value

-2.29*

-2.15*

-O.37

df

73

72

72

.025"I

.035“

.71

study. Additionally, the test-retest reliability of scale scores (test-retest rs) was .89
for the problem scales.

Content validity of the CBCL 4—1 8 is supported by the ability of nearly all
CBCL 4-18 items to discriminate signiﬁcantly between demographically matched
referred and nonreferred children (Achenbach, 1991). Construct validity has also
been supported by numerous correlates of CBCL 4-18 scales, including signiﬁcant
associations with
analogous scales on the Conners (1973) and Quay-Peterson (1983) scales (as cited in
Achenbach, 1991, p. 109).

Only two of the CBCL Problem Subscales (Anions/Depressed and Attention
Problems) were utilized for this study. The scale has several more Problem scales,
including: Withdrawn, Somatic Complaints, Social Problems, Thought Problems,
Delinquent Behavior, Aggressive Behavior.

Conners Comous Performance Test (Connors, 1995).. The standard
Conners’ Continuous Performance Test (CPT; 1995) is a test used to assess lapses in
attention or vigilance and irnpulsivity (Spreen & Stauss, 1998, p. 236). This test is a
computer-based assasment instrument that requires the test-taker to press the
appropriate key for any letter except the letter X. There are six blocks, each with
three 20-trial sub-blocks (letters presented, whether targets or not).

Therearetwo prirnarytypesoferrors includedintheCPT scoring system
The ﬁrst are errors of omission, which reﬂect deﬁcits in sustained attention or
vigilance (Halperin et al., 1991). The second are errors of commission, which appear

to reﬂect a deﬁcit of different underlying processes, including irnpulsivity and

34

inattention/memory (Halperin et al., 1991). Continuous performance tests have been
found to be reliable tests for discriminating groups of ADHD from normal children
(Corkum & Siegal, 1993). However, no single neuropsychological measure has been
found to adequate to arrive at a valid diagnosis of ADHD.

Demogmphic/SocQ/Metﬁgalgujm. The parents of the clinic-

referred children were asked to ﬁll out a detailed questionnaire regarding both the

 

referred child and themselves. The questionnaire elicits detailed demographic
information (e.g., age, sex, socioeconomic status, etc.) regarding both the referred
patient and his/her parents, pregnancy and birth history of the referred child, social
behavior questions, and medical/educational/psychological history questions.

Stroop Word-Colorkst (Stroop, I935). The Stroop Word-Color Test is a
timed test measuring the ability to suppress or inhibit automatic responses. The test
requires the test-taker to read the names of colors although the names are printed in a
different colored ink from the color speciﬁed in the name; for example, the word
“blue” is printed in green ink.

The Stoop test has generally been found to discriminate between ADHD
children and control groups of children (Barkley, 1998). However, it has also been
reported that this test has a Eirly high Else-negative rate of 53% (Barkley &
Grodinsky, 1994). Consequently, this measure is not used exclusively to assess or
diagnose ADHD, but is added to the test battery as one functional measure to tap
deﬁcits associated with ADHD. '

The Twenty-Item Toronto Alexithm' Sgge (TAS-20; Bagby, Taylor, &
Parker, 1994a,b). This instrument is a 20-item self-report measure of alexithymia.

35

Items are rated on a ﬁve-point_scale, ranging ﬁ'om “strongly disagree (1) to “strongly
agree (5). This measure contains three subscales measuring: (Ector 1) difﬁculty
identifying feelings and distinguishing them from the bodily sensations of emotions;
(factor 2) diﬂiculty describing feelings to others, and (Ector 3) an externally oriented
cognitive style of thinking (Parker, et al., 1993; p. 223). These subscales are
consistent with the theoretical underpinnings of the alexithymia construct.

The Toronto Alexithymia Scale (TAS), the measure upon which the TAS-20
improved and replaced, measured a personality dimension that is distinguishable ﬁom
neurotic psychopathology (Taylor et al., 1988). The modiﬁcations made to the
original scale did not change the basic utility of the original TAS, which was able to
discriminate between clinically designated alexithymic and nonalexithymic patients.
The authors reported internal consistency reliability coefﬁcients for the subscales of
.78, .75, and .66, respectively, good internal consistency (Crohnbach’s alpha = 0.81),
along with a three-week test-retest reliability of .77 for the total scale (Bagby, Taylor, '
& Parker, 1994). In this sample, the Crohnbach’s alpha level for the TAS-20 Total
Score was 0.79.

As with the original TAS (Taylor et al., 1988), the TAS-20 was also found to
have construct validity with clinical interview ratings of alexithymia (Parker, et al.,
1993) and with measures of psychological mindedness and need for cognition on the
NEO Personality Inventory (Costa & McCrae, 1985). In their investigation of the
TAS-20 and the mom, Bagby et aL, (1994), discriminant validity ofthe TAS-20
was supported by the ﬁnding of non-signiﬁcant correlations with the personality

dimensions of Agreeableness and Conscientiousness. Convergent validity was

36

supported in the same study by the ﬁnding of negative correlations between the TAS-
20 and the subscales assessing openness to feelings and openness to fantasy.
According to Bagby and Taylor (1997), provides evidence that the TAS-20 is
assessing deﬁciencies in emotional awareness and irnaginal activity — salient features
of the alexithymia construct” (p. 62).

Additional convergent validity of the TAS-20 has also been empirically
established. The TAS-20 was assessed by examining the relationship of the scale
with the Need for Cognition Scale (NCS; Cacioppo, Petty, & Kao, 1984) and the
Psychological Mindedness Scale (PMS; Conte et al., 1990, 1995) in a sample of
undergraduates (Bagby et al., 1994). This study found that the three factors of the
TAS-20 all correlated strongly and negatively with both the NCS and the PMS.

Pro ure

In this study, the prirmry caregivers of clinic-referred children ﬁlled out the
standard behavioral measures, history questionnaires, and the alexithymia scale
described above. Each was enlisted to participate in the study and had an informed
consent form explained to them by their clinician. They understood that participation
was voluntary and the data gathered will remain anonymous to the researcher.
Participant conﬁdentiality was maintained. The two neuropsychological measures
(CPT and Stroop) were included in the standard clinical assessment battery used in

the assessment of children and adolescents.

37

RESULTS

The statistics package STATISTICA was used for data analyses in this study.
An alpha level of .05 was used for all statistical tests. In order to maximize sample
size, each analysis was performed on the maximum number of cases (casewise
deletion) that contained relevant data for each hypothesis. In some case, the sample
sizes for individual analyses are smaller than the total sample due to casewise
deletion.
Alexithm’ and ADHD DMSIS Hypothesis

The hypothesis stated that primary caregivers of children diagnosed with
ADHD would evidence greater levels of the alexithymia, as measured by the 20-Item
Toronto Alexithymia Scale (TAS-20), as compared to primary caregivers of clinic-
referred children who do not have this primary diagnosis. This hypothesis was not
supported (see Table 2). One-way AN OVA results revealed a signiﬁcant main effect,
contrary to that hypothesized, between TAS-20 scores and diagnostic groups, F (1,73)
= 7.07, p = 0.01 . In order to control for the possible effect of gender, an additional
analysis was performed without including the girls in the sample. One-way AN OVA
results still revealed a signiﬁcant main effect between TAS-20 scores and diagnostic

groups, F (1,55) = 5.38, p = 0.024, as shown in Table 3.

Alexithmua’ and CBCL subscale (Anxious/Depressed Q, Attention Problem)

Hypgthesis

The hypothesis stated that alexithymic features in primary caregivers would
be more strongly correlated with subscales in the parent-rated behavioral measure

(CBCL) consistent with symptoms associated with ADHD, irrespective of diagnosis;

38

Table 2

Dggm' gic group by TAS-20 scores one-way ANOVA fN=75)

 

 

 

ADHD E38) Non-ADHD (n=37)
M MeansISD) MeanslSD) £1! E p
TAS-20 Total 39.45 (9.68) 46.92 (14.28) (1,73) 7.07" .010"
TAS-1 11.68 (4.93) 14.65 (6.99) (1,73) 4.52“ .037“
TAS-2 10.97 (4.32) 13.08 (5.02) (1,73) 3.80 .055
TAS-3 16.79 (4.29) 19.19 (3.84) (1,73) 6.50" .013“

TAS-Total = TAS-20 Raw Total; TAS-1 = Diﬁculty identifying feelings; TAS-2 = Dimculty
describing feelings; TAS-3 = Externally oriented thinking.
0 *p<.05, "p<.001

39

Table 3

Dragn' ostic group byTAS-ZO scores one-way ANOVA (bogs only. n=56)

 

 

 

ADHD (n=26) Non-ADHD (n=ﬂ)
my}; Means (SD) Means (SD) df E p
TAS-20 Total 38.46 (9.90) 46.40. (14.82) (1,54) 5.38“ .024*
TAS-1 11.23 (4.71) 14.20 (7.21) (1,54) 3.22 .078
TAS-2 10.92 (4.48) 12.93 (5.33) (1,54) 2.29 .136
TAS-3 16.31 (4.38) 19.27 (3.86) (1,54) 7.23* .010“

TAS-Total = Raw Total; TAS l = Dimculty identifying feelings; TAS 2 = Difﬁculty describing
feelings; TAS 3 = Externally oriented thinking
p < .05

40

this hypothesis was not supported. The correlation between TAS-20 Total Scores and
the CBCL “Anxious/Depressed” and “Attention Problems” subscales was .09 and .07,
respectively (see Table 4). The CBCL subscales were also not found to be
signiﬁcantly different from each other, given that they had positive correlations and
neither was signiﬁcantly different from zero.
Alexithm' and Demo gzaphics Hymthesis

The hypothesis stated that alexithymic features in primary caregivers would
not signiﬁcantly correlate with age (I = -.04) and socioeconomic status levels (2 = -
.11) of the primary caregivers; this hypothesis was supported (see Table 5).
Alexithmps' and Neuropsychologic_al Memes Hypothesis

The hypothesis stated that alexithymic features in primary caregivers would
positively correlate signiﬁcantly with the two neuropsychological measures of
sustained attention and inhibition; this hypothesis was not supported. The correlation
between the TAS-20 Total score and the Conners’ Continuous Performance Test
(CPT) Omission and Commission scores was .03 and -.14, respectively. The
correlation between'the TAS-20 Total score and the Stroop Color/Word subtest was -
.08, as shown in Tables 6 and 7, respectively. Simultaneous regression analyses were
performed with the CPT Omission and Commission and Stroop Color/Word scores to
predict TAS-20 Total score. Results indicate that these variables do not predict a

signiﬁcant amount of the variability in the dependent measure (TAS-20 Total score).

41

Table 4

lntercorrelations Among TAS-20 Total and Subscale Scores and CBCL Scores (N=75)

 

We 1 Z 2 i i Q

l. TAS-Total - .89“ .88“ .72“ .09 .07
2. TAS 1 - .72“ .41" .ll .08
3. TAS 2 - .47"' .01 .10
4. TAS 3 - .08 ~0.01
5. CBCL 3 -- .51"
6. CBCL 6 --

o TAS-Total = TAS-20 Raw Total; TAS-1 = Difﬁculty identifying feelings; TAS-2 = Difﬁculty
describing feelings; TAS-3 = Externally oriented thinking; CBCL 3 = Anxious/Depressed; CBCL
6 = Attention problems

"‘ p < .05

42

Table 5
IrltercorreLations AmongJAS-ZO Scores and dernpgrpphic variables (p=71)

MI; I Z .3. ‘1 i Q
1. Mother’s Age -— .26“ -.04 -.04 -. 13 .08
2. Income - -.1 l -.11 -.l l -.03
3. TAS-20 Total - .86" .87" .69"'
4. TAS-l -- .66“ .33"I
5. TAS-2 _ -- .46“
6. TAS-3 --

"‘ p < .05

43

Table 6

lntercorrlations Among TAS-20 Scores and CPT Scores (n=74)

ME I Z 3 ﬂ 5 .6. .7.

1. TAS-Total -- .87“ .88* .72* -.18 .03 -.14

2. TAS 1 -- .69" 39* -.15 -.03 -.09

3. TAS 2 .- .47* -. I7 .06 -.07

4. TAS 3 .- -.15 .07 -.2o

5. CPT Index .- .38" .06

6. car Ornision -_ __4-,....

7. CPT Commision --

o TAS-Total = Raw Total; TAS 1 = Diﬁculty identifying feelings; TAS 2 = Difﬁculty describing
feelings; TAS 3 = Externally oriented thinking; CPT Index = Continuous Performance Test (CPT)
Index Scores, CPT Omission = CPT Omission errors; CPT Commission = CPT Commission
errors

0 ‘p<.05, "p<.01,""p<.001

Table 7

lntercorrelations Among TAS-20 SCOI'QS_&[IC1 Stroop Color-Word Scores (n=5 8)

Variable

I. TAS-Total
2. TAS l
3. TAS 2
4. TAS 3
5. Stroop

1‘p<.05

'—

3

.89“

.71’

45

.4.

.77*

.48“K

.54'

Im

-.08
-.09
-.08

-.Ol

Additipnal was

The relationship between the ADHD group and the diagnostic subgroups
(those which were included in the Non-ADHD group) and the TAS-20 was examined
by independent samples t-tests (see Table 8). Group differences were observed
between the ADHD and Adjustment Disorder groups (1 (44) = -2.84, p. = .007) and
the ADHD and Anxiety Disorders groups(t (41) = -3.42, p. = .001).

Given the signiﬁcant diﬁerence in age between the two primary diagnostic
groups, an analysis of covariance of the TAS-20 was conducted. Results indicate that
age was not a signiﬁcant variable (F(1,72) = .025, p = .876).

Alexithjmps' and sa_mple characteristics

The developers of the TAS-20 report preliminary cut-off scores for research
purposes (Bagby & Taylor, 1997). A person with a TAS-20 score 5 51 is considered
non-alexithymic, while a person with a TAS-20 score 2 61 is considered alexithymic.
Descriptive statistics for the TAS-20 scores and diagnostic groups can be seen in
Table 9.

In this entire sample, nearly 76% of the caregivers scored in the non-
alexithymic range, nearly 12% scored in the mid-range between alexithymic and non-
alexithymic, and nearly 12% scored in the alexithymic range. These results show that
most caregivers in this clinical sample did not have alexithymia, as measured by the
TAS-20. I expected higher levels of alexithymia in this clinical sample, given that the
deﬁcits associated with alexithymia should interfere with a caregiver’s ability to be

emotionally available to their child. While these deﬁcits may negatively impact a

46

child, clearly others factors are no doubt responsible for the difﬁculties found in these

clinic-referred children.

47

Table 8

 

 

 

Sm of indemndent sanmle t-tests for diagpostic gzopps and TAS-20 Totsl
Gr9_up p Gr_o_up p t-value g1! gvalue
ADHD 38 Mood/Dep 6
39.45 (9.68) 38.5 (11.64) .217 42 .829
ADI-ID 38 Conduct/Opp 5
35.2 (9.20) .926 41 .359
ADHD 38 Adj Disorder 8
51.25 (14.86) -2.84 44 .007"b
ADHD 38 Anxiety 5
56.20 (14.86) -3.42 41 .001"b
ADHD 38 LB. 6
47.83 (13.73) -1.86 42 .069
ADHD 38 Neuro 7
49.86 (14.46) -2.42 43 .021

o p<.05,"p<.01
b = Bonferoni correction for multiple comparisons = .008

48

Table 9

_C_l_assiﬁcation of TAS-20 scores by dEgposticgroup CN=751

 

 

mp ADHD (n=3 8) Non-ADHD (n=37)
1. Non-Alexithymic 33 23

2. Mid-range Alexithynric 4 6

3. Alexithymic 1 8

As deﬁned for research purposes by Bagby and Taylor (1997) l = TAS-20 scores 5 51; 2 = TAS-20
scores between 52-60; 3 = TAS-20 scores 3 61

49

In the ADHD sample, nearly 88% of the caregivers scored in the non-alexithymic
range, 10% scored in the mid-range between alexithymic and non-alexithymic, and
nearly 3% scored in the alexithymic range. Whereas, in the Non-ADHD sample,
nearly

63% of the caregivers scored in the non-alexithymic range, 13% scored in the
mid-range between the two, and 21% scored in the alexithymic range (see Table 10).
The means of the ADHD and Non-ADHD TAS-20 Total scores fell within the
normative range (Taylor, Bagby, & Parker, 1992).

Only two of the diagnostic subgroups (Anxiety Disorders and Adjustment
Disorders) showed caregiver’s TAS-20 total mean scores above the non-alexithymic
range (see Table 10). Though the sample size for each was small (n=5), a brief
discussion is in order. Children with adjustment disorders are struggling in reaction
to some identiﬁable stressor. They no doubt struggle with both depressive, anxiety,
and/or conduct problems, but none in such quantity so that full criteria are met for
other disorders. Consequently, the stressors with which they are struggling outstrip
their capacities to cope effectively. Children with anxiety disorders are also clearly
struggling with symptoms that suggest fears, worries, and other internal states that are
outstripping their capacities to cope effectively. Although speculative, it may be that
children of caregivers who are unable to adequately know their feelings and regulate
their affect are more vulnerable to being overwhelmed with fears, worries, and

general uneasiness.

50

Table 10

Descriptive statistics by diagpostic g1_'oup and TAS-20 total scores (N=7SJ

Diagposis

m

Non-ADHD Group
Mood/Depressive Disorders
Conduct/Oppositional Disorders
Adjustment Disorders

Anxiety Disorders

Learning Disabilities

Neurological Problems

9

38

M( SD)
39.31 (9.68)

38.50 (11.64)
35.20 (920)

51.25 (14.86)
56.20 (14.86)
47.83 (13.73)

49.86 (14.46)

51

95% Cl

336—42

26—51
24—47
39—64
38—75
33—62

36-63

Min

24

25
26
32
36
31

33

Max

62

S9
48
75
76
63

72

DISCUSSION

The results of the present study Eiled to support the hypothesized relationship
between caregiver alexithymia and a diagnosis of Attention-Deﬁcit/Hyperactivity
Disorder (ADHD) in their children. Also, these same features were not signiﬁcantly
correlated with caregivers’ behavioral ratings of ADHD symptoms or
neuropsychological measures associated with sustained attention and inhibition. Each
result will be discussed in turn, followed by a general discussion and
recommendations.

The primary hypothesis of this study was that primary caregivers of children
with ADHD would evidence greater levels of alexithymia (as measured by the 20-
Item Toronto Alexithymia Scale; TAS-20) than would primary caregivers of clinic-
referred children who do not have this diagnosis. This hypothesis was not supported
and, in fact, the opposite ﬁnding was revealed. In other words, primary caregivers of
the Non-ADHD group showed signiﬁcantly greater levels of alexithymia than did
those of the ADHD group. Possible reasons for these ﬁndings remain unclear, though
the most conservative speculation is simply that alexithymia in caregivers is not a risk
Ector for the development of ADHD in children. However, in this sample, none of
the primary caregivers (in either primary group) had alexithymia scores in the
alexithymic range. Therefore, despite the hypothesized relationship, this sample does
not allow a deﬁnitive statement regarding the relationship between alexithymia and
ADI-ID because the primary caregivers were not, on average, alexithymic.

The caregivers’ empathic Eilures that were hypothesized to lead to ADHD

might still be an important risk Ector, but these empathic failures seem to be

52

unrelated to the presence of alexithymia in the caregivers. In other words, though
alexithymia is one problematic parental variable that leads to trouble with empathy, it
is not a necessary characteristic. It may be speculated, however, that an alexithymic
parent might be able to be empathic with an inEnt whose affects are not yet
differentiated, though the data in this study would not validate or invalidate this
speculation.

In this sample, the data suggest that caregivers of children with ADHD do not
report having the deﬁcits associated with alexithymia. Though greater levels of
psychopathology generally and psychiatric disorders speciﬁcally have been found in
parents of children with ADHD (Breen & Barkley, 1988), alexithymia does not
appear to be a risk Ector, according to these ﬁndings. Consequently, other
constitutional and environmental risk Ectors must be present in order for children to
develop ADHD.

Alexithymic features in primary caregivers were not signiﬁcantly correlated
with either the “Anxious/Depressed” or “Attention Problems” subscales of the Child
Behavior Checklist (CBCL). The hypothesis that alexithymic traits would be more
strongly correlated with parent ratings of attention problems versus ratings of anxiety
or depression ratings was not supported by the data. This ﬁnding is not surprising,
given that the primary hypothesis was also not supported, as described above.

Neuropsychological measures of sustained attention and inhibition (scores
ﬁom the Conners Continuous Performance. Test and the Stroop) were not
signiﬁcantly correlated alexithymia scores. Despite the theoretical model presented

above regarding the likely relationship between alexithymia and these laboratory-

53

based measures of these abilities, this hypothesis was not supported. Again, these
data suggest that the presence of alexithymia in primary caregivers does not
contribute to the development of neuropsychological difﬁculties as measured in this
sample.

Lastly, there was support for the secondary hypothesis that alexithymic
features in primary caregivers would not signiﬁcantly correlate with age and
socioeconomic status of the primary caregivers. This ﬁnding is consistent with
existing literature regarding the more general relationship between the alexithymia
construct and demographic variables.

Limitations and Recommendations

The theoretical model guiding this study would have been more directly
assessed if it included a direct measure of parent-cth attachment. Attachment was
not directly measured in this study due to the complexity and training required of
interviewers and time constraints. One focus of further research on ADI-ID should be
its relationship with attachment style and its implications for ADHD pathology.

A second limitation of this study was the heterogeneity of diagnoses within
the Non-ADHD group of children (see Table 9). While this type of heterogeneity is
common in clinical samples, future research would beneﬁt ﬁom larger and more
speciﬁc comparison groups. Furthermore, ﬁrture research would also beneﬁt by
looking at a non-clinical sample as a comparison group. This would allow an ADHD
group to be compared to a group of children whose symptoms do not overlap between

diagnostic categories.

54

Lastly, future studies would also greatly beneﬁt from an age-scaled
alexithymia measure, one that could be used with younger populations. At present,
no such scale has yet been validated (G. J. Taylor, personal communication,
sometime Spring 2000). Recent models suggest that affect dysregulation is a
fundamental mechanism of all psychiatric disorders (Taylor, Bagby, & Parker, 1997).

More generally, the results of this study parallel a diﬂicult problem plaguing
ADHD research. Over the years, complicated models have been developed to explain
the symptoms and underlying pathologies associated with ADHD, including
Barkley’s (1998) model outlined above. Aside from strictly behavioral ratings, we
have not been able to put forth a speciﬁc test or battery of tests that accurately and
reliably quantify ADHD. Despite the theoretical link between the behavioral
symptoms of ADHD and neuropsychological measures of sustained attention and
inhibition, none has been recommended to accurately diagnose children as having
ADHD (Barkley & Edwards, 1998). Barkley and Edwards (1998) write, “[I]t is hard
to establish whether an arrow hits the mark when the mark’s location is itself
uncertain” (p. 296).

The theoretical model relating ADHD with attachment problems is still one
that deserves further investigation. In their chapter on treating ADHD as
“AttacMnt Deﬁcit Hyperactivity Disorder,” Ladnier and Massanari (2000) report
that the two main areas of deﬁcits identiﬁed in ADHD children (self-regulation and
relating skills) were consistent with the classic symptoms of an attachment-disordered
chil ” (p. 29, italics added). This position is similar to that outlined above. Empirical

investigation of this relationship and the further development of theoretical models is,

55

no doubt, an area that will be important to investigate ADHD and more effectively

treat these children.

56

APPENDIX A

57

“P1313520

Udngﬂuscabmdasaguuamrdleohhowmuchyouwormmm
dummmmwmmuwmmw. mmm
you are nﬂrrgmleellngsandstylespgyowcﬂld’s. leeonlyonemtor

each W
Circle 1 If you STRONGLY DISAGREE
Circle 2 It you MODERATELY DISAGREE
Clrcle 3 If you NEITHER DISAGREE NOR AGREE
Circle 4 It you MODERATELY AGREE
Circle 5 It you STRONGLY AGREE

W
w W m manly My
also" Dim Nam m ‘0”
1. lanoﬂenoodwedaboutwhat

emoionlanfeallng 1 2 3 4 5
2 ltlsdﬂletltformetotindthenmt

wu'dsformyteeinoa 1 2 3 4 5
3. lhavephysiealsereationsthalevm

doaa'sdm’tmderstmd. 1 2 3 4 5
4. Ianablatodascnbemyfeelings

easily. 1 2 3 4 5
5. lprdertomdyzepmblemsrather

mmjustdasalbethem 1 2 3 4 5
3. MenlamupeetJdon‘tknowiflam

sad,trlmtened,orano'y. 1 2 3 4 5
7. lanoftenpuzzledbysensatlonsin

mybody. 1 2 3 4 5
8. lpletertojtralattlungshappenrather

thmtomclerstandwhytheytmred

otrltttatmy. 1 2 3 4 5
9. lhavefeallngsthatlem’tqite

identify. 1 2 3 4 5
10. Being lntouehwlthen'tollonsls

assailant 1 2 3 4 5
11.ltinditha'dtodesenbehowlfeel -

aboutpaoue. 1 2 3 4 5
12. Peopletallmetodeseribamy

tedlnosmore. 1 2 3 4 5

13. ldon’t lmowvuhat’s going on
inside me. 1 2 3 4 5

58

14.1mmdon'tlemmylamm. 1

15.

16.

17.

18.

19.

lpntertdldnatopeopleaboutthak
dﬂyactlvltluratharttm
thelrteellnos 1

lpretartountehﬂdrt’entatdment
immoral)

monologue-1m 1

ltlsdllorlttormetomedmylmarmod
memdooefrlenda 1

lmtealdosetomm,avenln
Metamucil. 1

111011deme
lnsotvhoperaondpmﬂema 1

. Looklmforhlddmmemlnoelnmovles

ordaysdatrwtslmm
MW 1

S9

Child and Adolescent History Questionnaire

 

 

 

 

Grild’sage Prunindroolyadelevd
*AgeafPatiua’smoma Oeapatian
Ageafl’atia’sfatha Oeupuim

 

 

Pm are: (circle one) SINGLE MARRIED SEPARATED DIVORCED DECEASED

Isdraeastqrparulindrepatial’shomﬂdrdeme) YES NO

Putin is (drde are) NATURAL ADOPTED FOSTER

Doesthepatiartlnvcsiblinp? YES NO
Ifyes, pleaselistgardamdagesofsiﬂing

 

 

Dobothparmvmrlr?YES NO mm PARTmothenFULLPART
Approximate family income: 044,999

15,000-34,999

35,000-54,999

55,000-74,999

75,0000rhidu _—
Aramaeanysigriﬁcamfmrilyormar'mlcmﬂias? YES NO

 

Is there a family history of alcohol or drug abme?(atplain)

W

Ageofmaheratdelivery— Matermlhalthproblanachningprmy? YES NO

Deliverywas: VAGINAL (ESAREAN

Babywas: FULLTERM PREMATURE ( Myanmar)

Washborpmlonged?YES NO .

ﬁdmepliugohaneﬁummehoqrinlwithyw? YES NO
Ifno,howmmydayunilthepatiueunehome

Anymddwoﬂ-mdaﬁstvksJamﬁcefwmfaﬁnamﬂmul YES NO

Ifyaorplairr

 

 

Mg ““2! r
Doesywrdrildgualmgwellwithcthadrildrm? arhlt'.’
Have ﬂinch? Keep friends?

I-Iaveproblanswirhpeuprunnuegmleoholorthugme)?

 

 

 

 

 

 

 

 

 

 

A‘I'l NAL RY
Any grades that were skipped or repeated?
Tacitus rqiort pmblans in (circle)
Raodrng min/concentration lpdlmg
Bdnvror anthmdic social adjuatmurt
Writing

Wasﬁsyourdrildmnllyhypmdive? YES NO Maxim? YES NO
Doteadrersrqrortproblemsthatyoudonotnotice? YES NO
Mydrild‘simdligmeelevel is likely (circle one)

Below average among high average apaior
PRIOR EXCHOLSEIQ E1ﬂY

Ibwympnvimnlylnddireacanawithmywdalagamymmnalhalmprofasimal?

(orplain incl. (has)

61

 

CONSENT AGREEMENT

We are conducting a study to examine parent’s feelings and styles of coping
in order to better understand the difﬁcult process involved in caring for children
and adolescents who are having academic, emotional. antﬂor behavioral problems.
We are asking for your participation.

Your participation requires ﬁlling out one or two additional questionnaires
that take approximately 15 minutes. Your participation is entirely voluntary. Your
decision to participate will not change any aspect of your child’s assessment or
treatment and you can withdraw permission at any time without penalty. Aside
from a few extra minutes of your time, there is no risk of injury or costs associated
with participating. In adth'tion to the questionnaires you complete, we may be
analyzing assessment data from your child’s assessment battery. Your child will not
be given any tests or questionnaires that are not part of the standard clinical
battery.

Your privacy will be protected to the maximum allowable by law. All data
will be kept strictly conﬁdential. Participant identiﬁcation numbers will be asa'gucd
to each test form. The only form that contains both the identiﬁcation number and
your name will be this consent form; it will be kept separate from all other data.

Your participation is greatly appreciated. You indicate your voluntary
agreement to participate by completing the returning the enclosed questionnaires.

If you have any questions regarding this study, you can speak to Greg Lamberty,
Ph.D., at the Alpine Clinic (765/446-9394) or James Jones. MA.’ (248165091 41).
David E. Wright. Ph.D. (517/355-2180) can be contacted for questions about your
role and rights as a subject of research.

 

 

Parent/Guardian Signature date Witness date

62

 

 

REFERENCES

63

REFERENCES

Achenbach, T. M. (1991). Manual for the Chil_d Behavior Checklist/4-18 and
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