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thesis entitled

HYPERACTIVITY-IMPULSIVITY-ATTENTION DEFICIT
AND AGGRESSION IN RELATION TO
VIOLENT AND CHRONIC OFFENDING

presented by

Brian D. Setzler

has been accepted towards fulfillment
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Master of ScienceJegI-eein Criminal Justice

 

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HYPERACTIVITY—IMPULSIVITY—ATTENTION DEFICIT AND
AGGRESSION IN RELATION TO VIOLENT AND CHRONIC OFFENDING

By

Brian D. Setzler

A THESIS
Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree of

MASTER OF SCIENCE

Department of Social Science

1998

ABSTRACT

HYPERACTIVITY-IMPULSIVITY-ATTENTION DEFICIT AND
AGGRESSION IN RELATION TO VIOLENT AND CHRONIC OFFENDING

By

Brian D. Setzler

The diagnosis of hyperactivity-impulsivity—inattention deficit (HIA-deficit) and its
comorbid relationship with other dysfunctional behaviors such as aggression have found to
exist fi'equently in the delinquent population. In this study the interaction of HIA—deficit
and aggression was hypothesized to increase the amount of violence and chronic ofi‘ending
compared to individuals with HIA-deficit or aggression alone. Using the Cambridge
Study in Delinquent Development by Dr. David Farrington, inconclusive evidence was
found on the significance of comorbid HIA-deficit and aggression on a boy’s violent and
chronic ofi‘ending. While the interaction of HIA-deficit and aggression increased more
violence in the boys during their teenage years, analysis of variance provided no evidence
of the interaction having caused more chronic offending or violence in the childhood and
adult years compared to a diagnosis of BIA-deficit or aggression alone. The findings
suggest the need for longitudinal treatment of those diagnosed with HIA-deficit or

aggression.

Copyright by
BRIAN DONALD SETZLER
1998

ACKNOWLEDGMENTS

This thesis would not be complete without the support fiom my committee
members. I am privileged to have had the opportunity to work with Dr. Vincent Hoffman
and Dr. Charles Corley. I thank them for their insight and guidance into juvenile
delinquency. A special thanks goes to Dr. Christina DeJong, who during this work has
given me direction, taught me the value of persistence, and above all, showed me

kindness.

iv

TABLE OF CONTENTS

LIST OF TABLES .................................................................................. vii
INTRODUCTION .................................................................................... 1
KIA-DEFICIT ......................................................................................... 6
Definition of HIA-deficit ................................................................... 6
Problems with HIA-definition .............................................................. 7
HIA-deficit Relationship to Ofi’ending ..................................................... 9
Aggression Relationship to Ofi‘ending ................................................... 10
DEVELOPMENTAL THEORY .................................................................. 12
Theory’s Importance to My Hypothesis ................................................. 14
Comorbid HIAodeficit and Aggression ................................................... 15
DATA ................................................................................................. 19
Dependent Variables ....................................................................... 20
Measures of Violence ............................................................ 20

Measures of Chronic Ofi‘ending ................................................. 22

Independent Variables ..................................................................... 24
Measures of HIA-deficit .......................................................... 24

Measures of Aggression .......................................................... 25

Control Variables ........................................................................... 26
METHODS .......................................................................................... 27
ANALYSIS ........................................................................................... 36
Bivariate Correlation Relationships ....................................................... 36

AN OVA: HIA-deficit and Aggressiveness at 12-13 Years ........................... 39

AN OVA: HIA-deficit and Aggressiveness at 14-15 Years ........................... 42
DISCUSSION ............ ' ........................................................................... 4 5
Summary of Findings ....................................................................... 45

Future Implications ......................................................................... 50
APPENDD( .......................................................................................... S3

BIBLIOGRAPHY ................................................................................... 58

vi

LIST OF TABLES

Table 1. Mean Measures of HIA-deficit and Aggression ..................................... 29
Table 2. Mean Measures of Violence ............................................................. 31
Table 3. Mean Measures of Chronic Ofi‘ending ................................................ 3 5
Table 4. Bivariate Correlations of the Independent and Dependent Variables ............ 37
Table 5. Two-way ANOVA: HIA-deficit and Aggression at 12-13 Years ................ 40
Table 6. Two-way ANOVA: HIA-deficit and Aggression at 14-15 Years ................ 43
Tables in Appendix

Table 1A Violence Classifications and Codings .............................................. 54
Table 2A Chronic Ofi‘ending Classification and Codings .................................... 56
Table 3A Independent Variable Classifications and Codings ............................... 57

vii

INTRODUCTION

Social science research contends that there exists at least two identifiable points of
interest with respect to childhood behavior. First, research suggests that childhood
behavior seems to have a high degree of continuity over time (Loeber & Dishon, 1983).
The second point of interest which exhibits itself through research is that there are
consistent social situations which pose the greatest risk for delinquent behavior (Loeber &
Dishon, 1983). The Significance of these two discoveries is that we should presumably be
able to determine childhood delinquency risk factors. Furthermore, we could infer that by
determining those delinquent risk factors that not only could we quell delinquent activity
considerably, be we would also have gained the capacity to thwart childhood delinquent
activities fiom amplifying into acts of violence. Unfortunately, research has presented us
with another conclusion about childhood risk factors: reliable childhood behavior,
accompanied by Situations that are consistently risky in terms of delinquent activity, does
not necessarily yield valid risk factors.

Indeed, risk factors for childhood delinquency are criticized as often as they are
researched. However, amidst all the scrutiny of viable risk factors, the search for these
childhood factors has Shown to provide a fair number of convincing and reliable factors
for different types of crimes. Both violent and chronic ofl‘ending are two particular areas

which have identified a large number of risk factors. The search for, and confirmation of,

childhood risk factors as they relate to violence and chronic offending is the general focus
of this thesis.

Hyperactivity-impulsivity-attention deficit (HIA-deficit) disorder iS one risk factor
that has been found to predispose children to delinquent behaviorl. Indeed, HIA-deficit
has been a growing topic of debate as of late. However, this disorder has not become an
interest by virtue of an ubiquitous nature. According to the American Psychiatric
Association (1994), HIA-deficit has a prevalence rate among schoolchildren at around 3-
5% of the general population. Although these numbers point to the rare occurrence of
this neurological deficit in the general population, in the delinquent population HIA-deficit
has been found to occur exceedingly more ofien (aleinteberg, Anderson, Magnusson, &
Stattin, 1993; Barkley, Anastopoulos, Guevremont, & Fletcher, 1991; Gittleman,
Mannuzza, Shenker, & Bonagura, 1985; Loeber, Stouthamer-Loeber, & Green, 1991;
Scatterfield, Hoppe, & Schell, 1982). This augmented prevalence of those diagnosed as
HIA-deficit, within not only the delinquent population but the adult criminal population as
well, will be an area of concentration for my study.

When using HIA-deficit as a predictor variable for violent and chronic offending, it
is necessary to consider other variables that might relate significantly to an HIA-deficit
diagnosis. The reasoning behind this lies with the fact that there is a common occurrence
of comorbidity, or combined existence, of two or more disorders in those diagnosed with

HIA-deficit.

 

‘ The American Psychiatric Association (APA) diagnostic manual describes this neurological disorder as
ADI-ID, or Attention-Deficit/Hyperactivity Disorder (1994). However, I prefer using what Loeber et al.
(1991) has described as the symptom factors that make up ADI-ID as I-IIA-deficit (hyperactivity-
impulsivity-attention deficit). Thus, I will be using this HIA-deficit nomenclature primarily for the
remainder of my thesis.

One construct which research has found frequently to exist in conjunction with
HIA-deficit is aggression. Aggression has been defined as various forms of behavior, from
a physical, violent response to a more verbally abusive, non-physical type of conduct.
Magnussen, Stattin, & Duner (1983) used a definition of aggression which supports the
non-physical mode of aggressive behavior, and is comparable to this study’ 5 concept of
aggression:

They (the boys) were aggressive against teachers and classmates. They may be

impertinent and impudent, actively obstructive or incite to rebellion. They like

disturbing and quarrelling with classmates (p.284).

Found within the realm of conduct disorder (APA, 1994), aggression has been found to be
a risk factor for violent crimes as well. The literature that exists on aggression and
violence will be reviewed, along with the significance of comorbid HIA-deficit and
aggression as risk factors for delinquency and violent ofi‘ending.

A theory which is of particular importance to the test of HIA-deficit, aggression,
and delinquency is Mofitt’s Developmental Theory (Mofiitt, 1993). In her theory,
Mofitt asserts there are two types of criminal ofi‘enders: Iife-course-persistent and
adolescent-limiting individuals. Mofitt’s Theory is intended convey the fact that
“antisocial behavior is remarkably stable across time and circumstance for some persons
but decidedly unstable for most other people” (1993, p.676). It is a group of life-course-
persistent ofl‘enders which tend to engage is a continuous level of antisocial behavior
throughout their lifetime. Conversely, the adolescent-limiting individuals are those who
commit crimes for a shorter duration (primarily during adolescence), and basically are

considered to have more temporary involvement in antisocial behaviors. Mofitt’s

Developmental Theory will be used as the theoretical basis to test my hypotheses, and will
be discussed later in firrther detail.

The variables used in the analyses are taken from the Cambridge Study in
Delinquent Development by Dr. David Farrington (F arrington, 1994). This longitudinal
study allows for adequate operationalization of HIA-deficit, aggression, and violent and
chronic ofi‘ending. Additionally, this study allows me to test the levels of ofi‘ending in
differing age groups. Past research using the Cambridge Study’s data has compared
aggression and violence (Farrington, 1989), while another has looked at the relationship of
hyperactivity and conduct disorder in childhood and its long-term criminal outcomes
(F arrington, Loeber, & Van Kammen, 1990). Indeed, it seems research from the
Cambridge Study is lacking in the area of HIA-deficit and aggression interaction.
Therefore, I conclude the Cambridge Study will allow my findings to bring a flesh and
practical angle to the research world of violence and chronic ofi‘ending. A more thorough
description of the Cambridge Study will be presented in the “DATA” chapter.

Once again, the hypotheses I will be testing include the concepts of HIA-deficit,
aggression, and violent and chronic ofi‘ending. An exorbitant amount of research has
covered the link between HIA-deficit, aggression, and criminal behavior. Nonetheless, the
diverse nature of operationalization in concepts such as HIA-deficit and aggression in
existing research leads to my interest in conducting another study on this topic.

My hypotheses for the study will be as follows:

Hypotheses # 1: Those diagnosed with comorbid HIA -deficit and aggression will commit
more violent crimes than those diagnosed with HIA deficit or agression alone.

Hmotheses #2: Those diagnosed with comorbid HIA-deficit and aggression will be more
likely to be chronic offenders than those diagnosed with HIA -deficit or agression alone.

Included in hypothesis #2 is the assumption that chronic ofi‘ending encompasses not only a
high number of crimes, but a long period of time as well. I am contending that because
HIA-deficit is diagnosed in most cases early in life (before age seven) (APA, 1994), and
this in turn augments aggressive behavior (Barkley, DuPaul, & McMurray, 1990), that the
bulk of early deviant behavior will consist of children with HIA-deficit and aggression.
Subsequently, the early offending in life as a result of comorbid HIA-deficit and
aggression will persist and amplify, thrusting those children into a life of chronic, or life-

course-persistent offending.

HIA-DEFICIT

Over the years, the definition of HIA-deficit has fluctuated quite often in DSM-III
(APA, 1980), DSM-III-R (APA, 1987), and into today’s DSM-IV (APA, 1994). Because
of this, there has been tremendous variation across studies in their operationalization due
to the changing diagnostic criteria (Barkley, Fischer, Edelbrock, & Smallish, 1990). To
compound this incongruity, researchers have been far fiom consistent with respect to their
labeling of hyperactivity-impulsivity-attention deficit. Although in recent studies it has
been referred to as hyperactivity (Bartusch, Lynam, Mofitt, & Silva, 1997), ADI-ID
(August et al., 1996), and HIA-deficit (Loeber et al., 1991), the symptoms and diagnoses
of the disorder by the researchers have remained virtually the same.

Currently, HIA-deficit is diagnosed with the essential features of inattention and/or
hyperactivity-impulsivity. The APA (1994) defines HIA-deficit, or ADI-ID, with five
criteria. First, HIA-deficit has the characteristic of “a persistent pattern of inattention
and/or hyperactivity-impulsivity that is more fiequent and severe than is typically observed
in individuals at a comparable lever of development (Criterion A)” (p.78). The second
criterion to HIA-deficit is that some of the symptoms that cause impairment must have
been present before age seven (Criterion B). Third, some impairment from the symptoms
must be present in at least two difi‘erent settings (e.g. at school and at home) (Criterion C).

Fourth, to be diagnosed as HIA-deficit, there must be clear evidence of the disturbance

interfering with the ability of the youth to express appropriate social, academic, or
occupational functioning (Criterion D). Lastly, the disturbance caused can not occur
exclusively with other Psychotic Disorders, and HIA—deficit can not be better accounted
for by another mental disorder (Criterion E).

Found within Criterion A are the symptoms defining inattention and/or
hyperactivity/unpulsivity. A diagnoses of HIA-deficit (ADI-1D) can be characterized into
one of three subtypes according to Criteria A. These three subtypes include: ADI-ID
combined; ADI-ID predominantly inattention; and ADHD predominantly hyperactive-
impulsive. A diagnosis of ADHD combined type requires six (or more) symptoms of
inattention and Six (or more) symptoms of hyperactivity-impulsivity to have persisted for
at least six months (APA, 1994). This combined ADI-ID, with emphasis on both
inattention and hyperactivity-impulsivity, will be the focus of my hypotheses.

There are a wide range of symptoms that can be classified under inattention. Some
of these symptoms for which inattention could be diagnosed include: dificulty sustaining
attention to tasks; not completing schoolwork, chores, or duties in the workplace; often
losing things necessary for tasks or activities; and being easily distracted by extraneous
stimuli (APA, 1994). Symptoms consistent in individuals with a diagnosis of
hyperactivity-impulsivity include: fidgeting with hands or feet or squirming in seat; often
running, climbing, or leaving a room unexpectantly; talking excessively; blurting out
answers to questions not completely spoken; difiiculty in awaiting turn; and interrupting or
intruding on others (e. g. during conversation and games) (APA, 1994).

Researchers assert that problems do exist, however, in the symptoms defining

HIA-deficit. Indeed, the diagnostic validity of HIA-deficit has been questioned (Szatrnari,

Boyle, & Ofl‘ord, 1989). Specifically, some researchers believe that certain criterion are
not pertinent to the definition of HIA-deficit and its relationship to delinquency.
Inattention is one such symptom that has been attacked. It has been concluded that
inattention is not unique to those diagnosed with HIA-deficit (Halperin et al., 1992). This
point leads to the issue of mislabeling. The fact that inattention is characteristic of youth
with cognitive deficits may lead clinicians to mislabel children with other psychotic
disorders as being HIA-deficit (Halperin et al., 1992). This finding bring to light the
considerable argument as to whether HIA—deficit is a “taxonomically valid disorder distinct
fi'om other, better established diagnosis, such as conduct disorder” (Szatrnari et al., 1989,
p.865). Consequently, some contend that, for purposes of difi’erential diagnosis, clinicians
need to concentrate more on the presence of hyperactivity and impulsive symptoms
(Halperin et al., 1992).

Another symptom factor of HIA-deficit which has been discussed vehemently is
hyperactivity. Research has compared the various subtypes of HIA-deficit, specifically
with or without hyperactivity (ADD+H and ADD-H), to test their distinct predictability to
delinquency. It was found that those with hyperactivity, compared to those without the
hyperactive characteristic, had more pervasive conduct problems at home, seemed more
impulsive, and were more aggressive and delinquent (Barkley, DuPaul, et al., 1990). This
finding lends support not only to the fact that hyperactivity should be concentrated on
more when diagnosing this disorder, but perhaps HIA-deficit is not a taxonomically
distinct disorder fi'om other firmly established disorders.

Previously reviewed literature has provided evidence that the symptom factors

such as inattention and hyperactivity are not particularly distinct to HIA-deficit. However,

other examinations have found certain HIA-deficit symptoms, such as hyperactivity, to be
“independent” with respect to other cognitive deficits. One study provided evidence that
hyperactivity is indeed a syndrome which exists absent of aggressiveness, disobedience,
and antisocial behavior (Stewart, Cummings, Singer, & de Blois, 1981). Other research
lends support to the distinctness of HIA—deficit by concluding that measures of aggression
do not difi‘erentiate among HIA-deficit and normal controls (Thompson, Riggs, Mikulich,
& Crowley, 1996). Beyond the clinical properties, it has been asserted that HIA-deficit
not only varies with other amictions such as conduct disorder in terms of their clinical
features, but also external variables (Biederman, Newcorn, & Sprich, 1991). For example,
HIA-deficit has the outcome of cognitive dysfunction, whereas conduct disorder has the
outcomes of aggression, antisocial behaviors, and delinquency (Biederman et al., 1991).
Similarly, HIA-deficit tends to vary with other disorders in terms of etiological factors and
psychosocial and developmental correlates (Biedennan et al., 1991).

In conclusion, it seems there is much debate as to the validity of HIA-deficit as a
clinically specific disorder. Inherently, if we are to circumvent any arguments as to the
validity of an HIA-deficit diagnosis, we must develop appropriate conceptualizations of
this and similar disorders to obtain a valid clinical diagnosis. This in turn can only help to
avoid future rnisdiagnoses and mislabeling (Barkley, 1990).

There have been significant findings that symptoms associated with HIA-deficit are
correlated with delinquency and violence. One symptom in particular, hyperactivity, has
been found to Significantly predict violence (af Klinteberg et al., 1993). In retrospective
studies it has been found that multiple ofi‘enders, characterized as hyperactive in

childhood, were rated as both antisocial and hard-to-handle by both parents and teachers

(Loeber et al., 1991; Scatterfield, 1987). Other behaviors which are characteristic of those
with HIA-deficit are a lack of concentration (inattention) and a need to be daring
(hyperactive). Both of these HIA-deficit defining behaviors have been found to
significantly predict violence in boys aged 12-14 years (Farrington, 1989). Furthermore,
in this same study of adolescent boys it was found that high restlessness (a criteria for
defining HIA-deficit) Significantly predicted all three measures of violence (teenage
violence, adult violence, and convicted violence) (F arrington, 1989).

The components of HIA-deficit have not only been found to be a childhood risk-
factor for more violent crimes, but also a risk for increased adult instituitionalization rates
(Scatterfield et al., 1982). It seems those who are characterized as being hyperactive,
impulsive, and inattentive in childhood are at a greater risk for activities leading to an
arrest, conviction, and incarceration in late adolescence and into early adulthood
(Mannuzza, Klein, Konig, & Giampino, 1989). In another Study of 110 hyperactive and
normal controls if was found the ofl’ender rates for serious ofi‘enses (robbery, burglary,
grand theft, grand theft auto, and assault with a deadly weapon), multiple ofi‘enses, and
institutionalization were all statistically significant for the hyperactives compared to the
normal controls (Scatterfield, 1987).

Although the symptoms of HIA-deficit have been found to be risk factors for later
violent crimes, other childhood variables play a role in violent crime as well. One distinct
variable that Should be reviewed in the company of HIA-deficit is childhood
aggressiveness (Loeber & Dishon, 1983). Paralleling HIA-deficit’s relation to delinquent
and violent ofi‘ending is aggression’s likelihood as a risk factor antisocial and problem

behavior (Pulkkinen, 1983). In a Study of adolescent boys, Magnussen et al. (1983) found

10

that high test scores of aggression significantly related to not only to criminal convictions,
but were strongly correlated to more serious crimes as well. Similar results were found in
a longitudinal follow-up of 8 year-olds (Pulkkinen, 1983). This research documented that
at the age of 14 and 20, both alcohol and violent ofi‘enses were correlated significantly
with aggression (Pulkkinen, 1983). Further evidence of aggression’s relation comes from
the Cambridge Study of Delinquent Development. Once mOre aggression’s relation to

violent behavior was found to be significant (Farrington, 1989).

ll

DEVELOPMENTAL THEORY

The theoretical basis for the hypotheses in this paper is Developmental Theory as
composed by Terrie E. Mofiitt. The premise of Mofitt’s theory is that there are basically
two kinds of antisocial behavior: adolescence-limiting and Iife-course-persistent
behaviors (Momtt, 1993). Mofitt (1993) contends that this dual taxonomy is needed to
describe antisocial behavior because two incompatible facts exist: antisocial behavior
Shows continuity over age, but that “its prevalence changes dramatically over age,
increasing almost 10-fold temporarily during adolescence” (p.674). Therefore, with
respect to juvenile delinquency, two distinct categories of individuals exist, each with its
own theoretical explanation.

The first theoretical assumption in Mofitt’s Developmental Theory is that there is
a small group of individuals who engage in antisocial behavior at every stage of their lives.
This group, labeled life-course-persistent, reflects roughly 5-6% of the offender
population. This percentage was found to be true in other studies, where 6% of the
ofl‘enders in a sample accounted for more than 50% of the crimes committed (Wolfgang,
1972). It is theorized that early individual differences, such as poor neuropsychological
functioning, may persist fi'om infancy and continue into adulthood. It is these
neuropsychological difi‘erences that may instigate antisocial behavior. Combined with this

deficit is a “failed” social development. It is at each stage of human development that

12

 

these life-course-persistent individuals fail to practice, even acquire pro-social alternatives.
The point of this “failed” development is that if “social and academic Skills are not
mastered is childhood, it is very dificult to later recover lost opportunities” (Mofitt,
1993, p.684). In summary, it is the lack of development at an early stage in life which
makes life-course-persistent individuals behavior essentially inflexible and refiactory to
changing environments.

The other halfto this taxonomy is the antisocial behavior labeled as adolescent-
limiting. Unlike life-course-persistent, adolescence-limiting antisocial behavior is
theorized to be ubiquitous. These types of delinquents seem to Show no continuity to
their antisocial behavior, and their delinquent behavior is often abrupt across age. Mofiitt
(1993) contends this type of antisocial behavior is essentially a “social mimicry” of their
life-course-persistent ofl‘ending counterpart (p.686). Mofitt asserts that today’s teens are
trapped in a “maturity gap,” the difl‘erence between the biological and social age.
Similarly, it is between the ages of 10 to 15 that children’s self-perception of autonomy
and self-reliance takes a dramatic shift. Children at this time begin seeing their life-course-
persistent counterparts sufi‘ering less fiom the maturity gap. The adolescence-limiting
individual perceives the quick rewards (e. g. clothes, cars, drugs) obtained by the life-
course-persistent individual, albeit through illegitimate means, as coveted assets. The
adolescence-limiting individual wants to relieve the stress fiom maturity gap, and believes
this can be accomplished through the attainment of “mature” status and privileges.
Subsequently, in an attempt to cut the gap and reap the rewards, the adolescence-limiting
individuals begin to mimic the behavior of life-course-persistent individuals through

delinquent activity. However, unlike their life-course-persistent counterparts,

l3

adolescence-limiting individuals are able to limit and discontinue their delinquent
behaviors. Because of their “successfirl” development in childhood, the adolescent-
limiting individual is able to recognize reinforcement and punishment contingencies, thus
reducing, in fact ceasing, any pattern of delinquent and/or chronic ofl‘ending.

Mofitt’s Developmental Theory is important to my hypotheses for several
reasons. To reiterate, my hypotheses include the concepts of chronic and violent
ofl’ending. Bartusch et al. (1997) found in a study of Moflitt’s Developmental Theory that
the younger age of onset, the more likely an individual will be a chronic ofi‘ender. I am
hypothesizing that HIA—deficit and aggression play an imperative role in the age of onset
of criminal behavior. My hypotheses implicate a young age of onset, because as
Developmental Theory posits, and as other research has found, there is a marked
reduction of functional problems between the ages of 13 and 18 for those with HIA-deficit
symptoms (Gittelman et al., 1985; Moflitt, Lynam, and Silva, 1994). In terms of violent
offending, Bartusch et a1. (1997) found that “childhood antisocial behavior was
significantly associated with convictions for violence, while adolescent antisocial behavior
was significantly more strongly associated with convictions for nonviolent ofi’enses”
(p.14). Thus, much research has concluded that not only is early onset of delinquency
predictive of chronic offending, but is also an excellent predictor of seriousness (Loeber &
Dishon, 1983; Mofitt, 1993; Tolan, 1987; Wolfgang, 1972). These findings are
consistent with my hypothetical statements. With the early initiation of HIA-deficit and
aggression in childhood, and the early onset of crime leading to more violent ofi‘ending,

HIA-deficit and aggression will be Significant in predicting violence.

14

Moffitt’s Developmental Theory is also a key to my hypotheses in that this theory
asserts childhood neuropsychological problems are a key component to antisocial behavior
(Mofiitt, 1993). I have previously reviewed the literature on HIA-deficit’s relationship to
violence. However, a dominant feature emerges when researching HIA-deficit’s
relationship in predicting delinquent behavior. This feature is the prevailing nature of
HIA-deficit’s comorbidity with other disorders. There seems to be a high-risk for HIA-
deficit individuals to be diagnosed with other childhood disorders, some of which include
aggression, oppositional defiant disorder, and conduct disorder (August et al., 1996;
Barkley, DuPaul, et al., 1990). One study found those experiencing HIA-deficit to have
three times the likelihood of comorbid oppositional defiant disorder, and four times more
likely to have comorbid conduct disorder, compared to a control group of HIA-deficit
teens (Barkley et al., 1991). Of particular significance to this study is the diagnosis of
conduct disorder. A criteria of conduct disorder, aggressive behavior exhibited in children
at the strongest levels also tended to be diagnosed with hyperactivity (Prinz, Connor, &
Wilson, 1981). One study concluded that as much as three-fourths of children diagnosed
with hyperactivity also experienced aggressive conduct disorder (Stewart et al., 1981). In
another study it was found that of the 93 boys scoring the worst on measures of HIA-
deficit, almost 64% scored equally bad on measures of conduct disorder (F arrington et al.,
1990). Furthermore, there is evidence that those diagnosed with HIA-deficit not only self-
report more conduct disorders, but also experience conduct disorder at an earlier age,
compared to non-HIA diagnosed individuals (Thompson et al., 1996).

Since the fiequent nature of comorbid HIA-deficit and aggression in delinquent

individuals exists, a dichotomy of sorts with respect to predictability has emerged. On one

15

end of the spectrum are those researchers who are skeptical about the validity of HIA-
deficit to independently predict antisocial behavior. These researchers’ findings has led
them to concluded that the presence of HIA-deficit in delinquent cases is solely contingent
upon the existence of aggressive traits (Momtt & Silva, 1988; Vitelli, 1996). It was
found that as a predictor variable, aggression was the behavior that carried the greatest
risk for continued problems for preschool boys with hyperactivity (Storrnont-Spurgin &
Zentall, 1995). Additionally, in a study of schoolchildren aged one through five, it was
concluded those children characterized as not easy to handle by both mom and teacher
were represented only among those children with combined aggression and HIA, versus
HIA alone (Loeber et al., 1991).

Contradicting these researchers’ findings are those studies that have found it is the
continuation of HIA symptoms, and not aggressive behavior, that poses the greatest risk
factor for the development of antisocial behavior into adolescence (Gittelman et al., 1985;
Klein & Mannuzn, 1991; Thompson et al., 1996). It has been contended that early
conduct disorder is not only associated, but also initiated by, the development of HIA-
deficit (Lambert, 1988; Thompson et al., 1996). Likewise, should the original symptoms
of hyperactivity alone be maintained through adolescence, the chances of developing
conduct disorder were almost four-fold (Gittelman et al., 1985). Also supporting the
predictability of HIA-deficit is the fact that only when combined with HIA-deficit
characteristics was aggression found to be related to delinquency outcomes, as opposed to
aggression without the HIA-deficit characteristics (Loeber et al., 1991).

The argument as to the validity of Hledeficit as a risk factor is not limited strictly

to juvenile delinquency. The significance of HIA-deficit as it relates to criminal behavior

16

lies in the fact that research has found the continuation of hyperactivity-hnpulsivity-
inattention symptoms into young adulthood to be quite common (Weiss & Hechtrnan,
1986). Barkley (1990) found that up to 70 -80% of children with FHA-deficit are likely to
display some of these symptoms into adulthood “to an extent inappropriate for their age
group” (p.114). One study indicated the continuation of the full HIA-deficit syndrome in
about one-third of the cases (Gittelman et al., 1985). Once again, however, the
continuation of HIA-deficit again brings forth a contemptuous belief of HIA-deficit’s
inability to predict adult criminality. One study concluded that regardless of the
continuation of HIA symptoms into adulthood, that HIAodeficit does not incur greater risk
for law enforcement contact (Mannuzza et al., 1989). Therefore, some research has
contended it is the presence of antisocial and aggressive behavior in young adulthood, and
not HIA symptoms, that leads to criminal behavior (Magnussen, 1983; Mannuzza et al.,
1989). Yet, the bulk of the research has determined that in both childhood and
adolescence, the continuation of comorbid HlAcdeficit and aggression heightens the
probability of criminal outcomes into adulthood (Barkley et al., 1991; Lambert, 1988).

In conclusion, it seems that the “overlap” of HIA-deficit and aggressive conduct
disorder has been found to be quite high. Because the early onset of HIA-deficit is
consistent with Mofitt’s Developmental Theory, I am led to believe that this study will
also find fi'equent cases of comorbid HIA-deficit and aggressive behavior to appear early
in life. In terms of a risk factor for delinquent and violent ofi‘ending, there appears to be
disagreement as to HIA-deficit’s predictive capability towards ofi’ending. However, the
present hypotheses will support past findings (F arrington et al., 1990; Mofiitt, 1990),

those findings being that the combination of hyperactivity, irnpulsivity, and inattention can

17

substantially predict criminal and antisocial behavior independently of childhood
aggression. In addition, past research has found the attributes of hyperactivity-
impulsivity-attention deficit, when accompanied with aggression, to be strong correlates of
delinquency (Brier, 1995). Accordingly, it is my proposition that these two entities, when
combined, will promote greater predictability towards juvenile and adult violence.

I am confident my hypotheses work well within Mofitt’s Developmental Theory.
With an emphasis on violent and chronic offending, as well as comorbid HIA-deficit and
aggression, my thesis is well grounded in the roots of a widely researched and significant

theory of antisocial behavior.

18

DATA

This paper looked at the variables of HIA-deficit and aggression as they related to
violent and chronic ofi‘ending. Once again, the hypotheses I tested were as follows:

Hypothesis # I : Those diagnosed with combined HIA -deficit and aggression will commit
more violent crimes than those diagnosed with either HIA -deficit or aggression alone.

Hypothesis #2: Those diagnosed with combined HIA-deficit and aggression will be more
likely to be chronic oflenders than those diagnosed with either HIA -deficit or aggression
alone.
For this study, the research that was used to test the hypotheses is the Cambridge Study of
Delinquent Development by Dr. David F arrington (F arrington, 1994). This 20-year
longitudinal study of 411 males began with surveys of the boys at age 8-9 years. Primarily
a group of boys from the working class in London, this sample was drafted fi'om the
registers of the six state primary schools located near the researcher’s ofice. Included
with the 399 males fi'om these six'schools were 12 males from a local school for the
educationally subnonnal. The sample primarily comprised of white, urban, working class
boys of British origin.

The interview process consisted of the boys interviewed by psychologists near the
ages of 8, 10, and 14 years of age. The boys also tested in their school during these same
years. In addition to the interviews and testing, the researcher also interviewed the

parents of the boys, beginning at age 8 and continuing every year up to the boys’ age of

14-15 years. Teacher questionnaires were also obtained about the boys behavior in school

19

at the ages of 8, 10, 12, and 14 years. Both the parent and teacher questionnaires were
completed in great numbers, having 97.1 and 94 percent return rates, respectively.

The aim of the interview process, up to the age of 18 years, was to meet with
every one of boys. The second set of interviewing, beginning at the age of 21, was
intended for only those boys who had been convicted and a similar sized sample of

unconvicted boys.

DEPENDENT VARIABLES

The dependent variables used in this analysis are violence and chronic ofi‘ending.
There are three items which measured the amount of violence taken at the age of 14, while
the same items measured age 16 violence. Adult violence also incorporated four items
similar to those measuring childhood and teenage violence. After these items were
recoded into nominal level form they were put into a scale, with each scale measuring
violence at their respective “stage” of development.

asures o viole e

The edition of the Cambridge Study in Delinquent Development to which I had
access for use in this thesis did not include a list of specific ofi‘enses. Traditionally,
research has suggested that the phrase “violent behavior” include such crimes as physical
and sexual assault, robbery, and other such violent behavior. However, because of the
unavailability of such crime definition, my operationalization of violence was not as
specific. Nonetheless, I believe that the variables used to define my concept of violence in
this thesis were definitionally sound. Table 1A in the Appendix lists the original item

fiequencies and their recoded scale frequencies for violence.

20

Vi l nce t 14 16:

Carried a weapon. At the ages of 14 and 16 the boy was asked if he had ever
carried some kind of weapon like a knife or a cosh in case it was needed in a fight. If the
boy has ever carried some kind of weapon for fighting purposes he was considered
violent. The frequency of the boys carrying a knife at age 14 totaled 84, or 20.7% of the
sample, while at age 16, a greater number of boys said they had carried a weapon (101, or
25.4%) in case it was needed in a fight.

Used a weapon. At the ages of 14 and 16 the boy was asked if he had ever used
any kind of weapon (knife, cosh, razor, broken bottle) in a fight. This item was
considered violent if the boy had ever used such a device in a fight. At age 14, a total of
49 (12.1%) boys had used a weapon at least once, while 68 (17.1%) said they had used a
weapon in a fight at age 16.

Struggled/fought to get away fiom law ofiicial. As with the two previous
questions, the boy was asked at the ages of 14 and 16 if he had ever struggled or fought to
get away fiom a policeman. At both ages, a boy was considered violent in this respect if
he had ever struggled or fought to get away fi'om a policeman. The total number of boys
in this category for age 14 and 16 was 28 (6.9%) and 51 (12.9%), respectively.

V1 l

Involved in fights. This question was asked of the boy at the age of 18 years. This
item was used to measure violence if the boy had ever gotten into a fight at all (excluding
getting beaten up in a fight and not retaliating). A total of 145 (37.3%) of the boys had

said they had gotten into at least one fight in the past year.

21

Started fights. Also asked at the age of 18, this question was used as a measure
of adult violence if the boy had started a fight. In all, a total of 90 (23.1%) boys said they
had started at least one fight.

Carried a weapon. Taken at age 18, this item was measured as the number of
days the boy carried a weapon (knife, razor, cosh, hammer, gun, glasses, axes, for ,
example). Only 32 (.8%) of the boys had carried a weapon at least one day in case it was
needed in a fight.

Used a weapon. Also taken at age 18, this item was measured as the number of '
times the boy has used a weapon (as in above reference) in a fight. This item was used to
measure violence not only if the boy had ever used a weapon in a fight, but also if he had
ever used a weapon as a threatening device. In this sample, 32 (.8%) of the boys had used
the weapon in a fight or threatened to use a weapon as least one time.

Measures at chronic oflending

Much like violent offending, chronic ofi‘ending was divided into three stages of life:
ofi‘ending at the age of 14, age 16, and adult ofi‘ending covering the years 17-24. The two
variables of age 14 (Youth at 14) ofi‘ending and age 16 (Youth at 16) ofi‘ending
encompassed both self-reported delinquency and oficial convictions, while adult ofi‘ending
used ofiicial convictions as its sole measure of chronic ofi’ending. Table 2A in the
Appendix lists the original item fi'equencies and their recoded scale frequencies for chronic
ofl‘ending.

Oflending at age 14. Measured prior to and into age 14, this item included both
measures of self-reported delinquency and oficial convictions. The self-reported

delinquency item was measured at the age of 14. This item scored the number of different

22

of delinquent acts committed out of 38. Only those boys who self-reported “14 or more”
were included as a measure of chronic ofi‘ending. In addition to self-reported delinquency,
official convictions were used to measure violence at this age. The item “Convicted 10-
13” refers to convictions for ofi‘enses committed between the tenth and fourteenth
birthday. If the boy had any convictions during this time span, he was considered a
childhood offender. In this sample, a total number of 94 (23.2%) boys self-reported in the
“14 or more” category, while 35 (8.5%) had at least one official conviction.

Offending at age 16. This variable measured the amount of delinquency
committed at the age of 16. Similar to childhood ofi‘ending, both self-reported
delinquency and oficial convictions were used to gauge this level of chronic offending.
The self-reported delinquency item was measured at the age of 16 and again measures the
number of ofi‘enses committed out of 38 acts. Only those self-reporting “17 or more”
delinquent acts were defined as part of the chronic ofl‘ending group. Also measuring
violence at age 16 was the item “Convicted 14-16,” which refers to convictions after the
fourteenth birthday up to the seventeenth birthday. A total of 92 (22.3%) of the boys self-
reported delinquency in the “17 or more” category, while 74 (18%) had at least one
oficial conviction.

Adult ofl‘ending. This measure incorporated only official records, namely because
there was no self-reported ofi‘ending measure taken after the age of 18. Adult ofi‘ending
measured those acts which took place fi'om the ages of 17-24. Thus, the items “Convicted
1 7-20” and “Convicted 21-24” were used to measure the amount of adult ofi’ending. The
amount of boys reporting in the “Convicted 17-20” and “Convicted 21-24” items were 95

(23.6%) and 46 (11.6%), respectively.

23

INDEPENDENT VARIABLES
There were two independent variables analyzed in this research as well. Both
HIA-deficit disorder and aggression were operationalized according to the items listed

below. Table 3A in the Appendix lists the original item frequencies and their recoded

scale fi'equencies for both HIA-deficit and aggression.

 

Because of the early initiation of HIA-deficit, it was important to measure this
disorder early in childhood. The Cambridge Study collected information concerning
measures of HIA-deficit fi'om the boys at the ages of 8 and 10. Previously used in part to
operationalize HIA-deficit from the Cambridge Study (F arrington et al., 1990), these three
measures seemed to appropriately define what can be considered the symptoms of this
disorder.

Inattention. At the ages of 8 and 10, the teacher rated the boy in terms of amount
of concentration or restlessness the boy exhibited in the classroom. Used as a measure of
the boy’s inattention, this item contributed to the diagnosis of HIA-deficit if ‘yes” was the
response from the teacher. At age 8, 135 (33.7%) boys were seen as has having a lack of
concentration. At age 10, 145 (37.8%) boys were considered inattentive.

Hyperactivity. Based on a parent interview, this question gauged the amount of
physical activity (such as climbing, trafiic, exploring) by the boy at the age of 8. This item
was used to measure the amount of hyperactivity only if the parent’s response was “Takes
many risks.” Of the 379 responses, 75 (19.8%) of the parents believed their boy had taken

many risks.

24

Impulsivity. At age eight, the boys were given four tests of psychomotor
performance: the Porteus Q, Tapping, Spiral Maze Error, and Body Sway Ataxia. A sum
of the scores on these tests were scored as a 1(0-1), 2(2), 3(3), 4(4), or a 5(5 or above).
High scores on these tests were intended to reflect careless, clumsy, or impulsive behavior.
Poor impulse control was also measured at age ten. Adding the raw scores of the Spiral
Maze Errors combined, Porteus, Maze Q combined, and Tapping Score combined derived
the psychomotor clumsiness score at this age. For my thesis, poor impulse control was
considered applicable only if the boy scored a “5” (5 or above) at age 8 and a “high” at
age 10. A total of 77 (18.9%) of age 8 boys were considered having poor impulse
control, while 104 (25.3%) of the boys had poor impulse control at age 10.

Measures at amession

My intention was to measure aggression not only in the childhood years, when
HIA-deficit is traditionally diagnosed, but to measure aggression subsequent to a diagnosis
of HIA-deficit as well. The reason for measuring aggression at different ages was to see if
aggression stems out of HIA-deficit, as I have asserted previously. However, it was also
important to measure aggression in the years to which children are developing their social
networks and are controlling their environment much more than in their pre-adolescent
years. Thus, in addition to measuring aggression at the ages of 12 and 13, levels of
aggression were also operationalized at the ages of 14 and 15. The measure of aggression
before age 14 was considered “Childhood Aggression,” while aggression at age 14 and
beyond characterized “Adolescent Aggression.”

Agressiveness. This item measuring aggressiveness combined 6 areas of behavior

as rated by the teacher. These areas included disobedience, dificulty to discipline, unduly

25

rough, over-competitive, quarrelsome and aggressive, and resentful to criticism.

Measured at the ages of 12 and 14, these behaviors were all rated on a scale of 1-3 (with a
3 being aggressive) and then summed. My concept of aggressive behavior included only
those boys who scored as “most aggressive.” A total of 86 (21.3%) boys scored as
aggressive in childhood for this item (age 12), while 89 (23.5%) of the boys at age 14

were considered aggressive in adolescence.

CONTROL VARIABLES

The nature of this study will undoubtedly encompass many other social and
psychological factors. The primary variables that one should consider in most studies
dealing with humans are the variables of sex, age, race, and income. However, for this
study it was not be necessary to control for these variables because of the nature of the
sample. In the Cambridge Study, Dr. Farrington (1994) used a longitudinal sample
composed strictly of boys, all of who were initially interviewed when they were 8 and 9
years old. These boys were also predominately all white Caucasian (only 12 boys had at
least one parent of West Indian origin). Additionally, the sample was limited to those boys
who were fiom urban, middle class neighborhoods, with the majority of the families
classified as working class (93.7% of the families were located within the category of HI,
IV, or V on the registrar general’s scale of occupational prestige). Because of the
attributes of the sample, I did not need to control for the variables of age, sex, race, and

income.

26

METHODS

There are five items that constitute the scale measuring HIA-deficit. Scales are not
created to measure aggression because only one item is used to measure the amount of
aggression each boy exhibits in childhood (ages 12-13) and adolescence (ages 14-15).
Scales measuring violence and chronic ofi‘ending are also created. Childhood violence and
teenage violence are measured at the ages of 14 and 16, respectively, while adult offending
is measured at the ages of 17-24 years. There are three items measuring childhood
(Violence at 14) and teenage (Violence at 16) violence, while four items are used to
measure violence at age 18 (adult violence). Chronic offending encompasses six items
covering the span of childhood, teenage, and adult ofl‘ending. Both omcial and self-
reported delinquency are used to measure childhood (Youth at 14) and teenage ofi‘ending
(Youth at 16), while omcial convictions covering the years of 17-24 measure adult
ofi‘ending.

I am using bivariate correlation and analysis of variance (AN OVA) to assess the
relationship between variables. Bivariate correlations not only test the Significance of
HIA-deficit and aggression on violence and chronic ofi'ending, but test the relationship
between HIA-deficit and aggression as well. This examination is used to support or
counteract findings of aggressive behavior originating from early HIA-deficit symptoms

(Barkley, DuPaul, et al., 1990). Further tests involving analysis of variance allow for the

27

determination of how the interaction efi‘ect of HIA-deficit and aggression afi’ects violent
and chronic offending. These tests incorporating AN OVA are essentially the focus of my
analysis: that HIA-deficit and aggression have an interactive efl‘ect on delinquency.

The first scale created is the HIA-deficit scale (Table 1). A reliability analysis on
these five items shows fair reliability among the items (alpha = .5231), based on the
standard accepted value of .6. A factor analysis is performed on the items to examine
their strength in measuring HIA-deficit. This analysis Shows that the five items are not
very strong measures of the same concept. In particular, the items which measure a boy’ s
hyperactivity (adventureness) and inattention (lack of concentration) do not seem to be
strong measures of HIA-deficit. However, psychomotor irnpulsivity is very strong in
measuring the concept. Both the reliability and factor analyses lend support to perceived
difliculty in the operationalization of HIA-deficit. Although logically these items seem to
be good measures of HIA—deficit, they appear to be borderline insignificant as to their
reliability and strength in measuring the same factor. A fiequency distribution of the HIA-
deficit measures shows that very few of the boys test positive for three items (9.6%), four
items (5.8%), or all five items (1.5%).

To help clarify the low number of HIA-deficit symptoms, a logical step might be to
examine the items measuring “psychomotor clumsiness” and “lack of concentration.”
Because these two items are used as HIA-deficit measures at two difi‘erent ages, there is
the possibility of the behaviors manifesting themselves at difi‘erent times. Ifthis is the
case, then there are issues of age-specific initiation and cessation points for irnpulsivity
and/or concentration to be considered. A contingency table on the items finds them to be

somewhat evenly distributed. For example, 5.1% of the boys test “yes” for impulsivity at

28

Table 1. Man Mmugg 2; flQ-defigit and Amsjgn

 

 

 

Factor
m Mean Range Landings
TEA-QM;
Adventureness (age 8) .1979 0 — l .443
Psychomotor Clumsiness (8) .1887 0 — 1 .731
Lack of Concentration (8) .3367 0 - 1 .528
Psychomotor Clumsiness (10) .2530 0 — l .704
Lack of Concentration (10) .3776 O — 1 .506
HIA-deficit scale': 1.2653 0 — 5
No measures (valid %): 33.2%
One measure: 32.7
Two measures: 17.2
Three measures: 9.6
Four measures: 5.8
Five measures: 1.5
*Alpha = .5231
Aggressm
Aggressive 12-13: .2129 0 - 1
Aggressive 14-15: .2354 0 - l

 

 

29

age 8 but not age 10, while 11.8% score “yes” at age 10 but not age 8. A total of 13.7%
measure “yes” at both age groups. Similar findings occur for the item “lack of
concentration.” Because the crosstabs indicate the distribution of these items to be evenly
distributed, support is provided that these two symptoms are neither age specific when
they start nor when they end. However, the findings do support measures of irnpulsivity
and inattention which are more common at age 10 as compared to age 8.

Aggression is measured on two difi‘erent levels for this analysis: childhood
aggressive behavior at age 12-13 and adolescent aggression at age 14-15 (Table 1). These
two items seem to be good measures of aggression because they encompass six difi‘erent
types of aggressive behaviors. Frequency distributions of aggression at each age group
indicate that in both groups, over one-fifth of the sample has aggressive tendencies.

The Violence at age 14 scale consists of three items measured at the age of 14
(Table 2). Originally an item measuring the seriousness of fighting at age 14 was included
as a measure of childhood violence. However, upon firrther analysis, it was found that this
item does not measure violence as well as the other three items measured at age 14. A
factor analysis indicates that fighting at 14 does not load well with the other items of
carried a weapon, used a weapon, and struggled/fought with a police oficer. The three
items measuring Violence at 14 seem to be reliable, as indicated by an alpha of .6337.
Furthermore, a factor analysis finds these items to be good measures of childhood
violence, with loadings all above .6. A fi'equency distribution of Violence at 14 indicates
that a fair amount of boys score on measures of childhood violence (Table 2).

Much like the previous items used for childhood violence, the items measuring

Violence at 16 also appear to be reliable measures (alpha = .6197) (Table 2).

3O

 

Table 2. Man Mmum 9f Xiglenge

119m
i 1

Vi

e 4:
Carried a weapon

Used a weapon
Struggled/fought with police

Violence @ 14 scale":

No measures (valid %):

One measure:

Two measures:

Three measures:
*Alpha = .6337

6.
Carried a weapon
Used a weapon
Struggled/fought with police

Violence @ 16 scale":
No Measures:
One measure:
Two measures:
Three measures:

*Alpha = .6197

Mam;

Involved in fights (age 18)
Started fights

Carried a weapon

Used a weapon

Violence @ Adult scale“:
No measures:
One measure:
Two measures:
Three measures:
Four measures:
*Alpha = .7269

31

.2074
.1210
.0069

.3975

74.1%

15.3
7.4
3.2

.2544
.1713
.1285

.5542

65.2%

18.9
11.1
4.8

.3728
.23 14
.0082
.0082

1.4424
60.9%

12.9
18.3
4.4
3.6

M

0—1
0—1
0-1

0-3

Factor
Loading

.808
.843
.620

.799
.839
.610

.823
.826
.631
.685

Additionally, the items are strong factors of teenage violence, as indicated by a factor
analysis. As expected, the frequency of violence at this age is higher than violence
occurring at age fourteen.

The adult violence scale consists of 4 items. These items seem not only to be very
reliable (alpha = .7269), but each item’s factor loading is greater than .6 (Table 2). An
interesting point to view with the adult violence scale is the high level of ofl‘ending
indicated by the mean score (1.4424). Although specific to violent offending, this finding
seems contrary to Moflitt’s Developmental Theory, which supports a definition of
ofi’ending that occurs more in the teenage years compared to the adult years.

In conclusion, it appears that the items used in measuring the levels of violent
ofi‘ending are reliable and Strong measures of the concept. A central focus of this
conclusion lies with the items measuring violence. While the items of carried and used a
weapon are good factors of childhood and teenage violence, this is not the case for adult
violence. Conversely, fighting is a good measure of violence in adulthood, but not for
measuring childhood violence. Thus, a conclusion to take fiom the analyses is that it
appears violent children utilize weapons moreso than violent adults. This finding tends to
agree with the traditional view of childhood violent ofl‘enders using weapons to settle
disputes. Unaware of the dangers of such actions, children behave that carrying and using
weapons will give them a “dangerous” and “powerful” demeanor not to be reckon with.
The findings fiom the analyses do (not necessarily echo such sentiments, but they do help

to support the Significant relationship of violent children and weapons.

32

Chronic ofl‘ending incorporates the three measures of childhood, teenage, and
adult ofi‘ending. According to Moffitt’s Developmental Theory, a life-course persistent
offender will commit crime throughout the life-course, whereas an adolescent-limited
ofi‘ender will only commit crime in the adolescent or teenage years (Moflitt, 1994). Thus,
we expect a life-course persistent individual to commit crime in the childhood, teenage,
and adult years of their lives. For this analysis, a boy who scores “chronic” within the
childhood, teenage, and adult ofi’ending periods is considered a life-course persistent
ofi‘ender.

A contingency table of ofi‘ending in childhood (Youth at 14) finds that many boys
self-reported a “high” amount of delinquency and no convictions. Conversely, few of the
boys report a conviction and no “ 'gh” self-reported delinquency, and few score “ ° ” on
self-reports and have at least one conviction between the ages of 10-13. In all about a
fourth (26.7%) of the boys report a high amount of self-reported delinquency and/or have
at least one oficial conviction between the ages of 10 and 13 years.

As expected, teenage boys exhibit a greater percentage of ofienders compared to
childhood boys. However, the analysis does not find the teenage boys more willing to
self-report delinquent behavior compared to boys aged 10-13 years. In the sample, only
13.6% of the teenage boys are “ 'gh” on self-report delinquency with no conviction
(compared to 18.3% of childhood offenders). Although not willing to admit delinquent
behavior, a frequency distribution of teenage ofi‘ending indicates that nearly one-third
(31.5%) of the boys measure chronic ofi‘ending scores by having a high amount of self-

reported delinquency and/or at least one conviction between the ages of 14 and 16 years.

33

The last item to measure chronic offending is adult ofi‘ending (Adult 1). Unlike the
previous two measures, adult ofi‘ending only takes into account oficial convictions for the
two age groups of 17-20 and 21-24 years. The analysis finds that more convictions took
place in the earlier age group (17-20) compared to the later adult years (21-14). In total,
a fairly large number of boys (26.0%) score as “chronic” in their adult years by having at
least one conviction in either age group.

Once again, chronic offending is scaled to include all three life periods of offending
(Table 3). Reliability analysis of the recoded items Youth at 14, Youth at 16 and Adult 1
finds the items are reliable (alpha = .6805). Further analysis shows that the items are
compatible with one another, as a factor analysis of Chronic Ofl’ender scores the items all
above .6. A final distribution of Chronic Ofi’ender indicates that 44 (11.5%) of the boys
are considered ofi‘enders in all three periods (childhood, teenage, and adult), thus are

considered persistent, or chronic ofl’enders in this study.

34

Table 3. Mggn Mgggm of ghmnic Qflgnding

Item

Chrome Qflendg (Self-Remus):
Self-report 14(valid %)
(Score out of 38 acts)
Self-report 16
(Score out of 38 items)

WW
Convictions 10 — 13
Convictions 14 — l6
Convictions 17 -— 20
Convictions 21 - 24

Youth 14 (S-report 14 + Ofiicial 10/ 13)
Youth 16 (S-report 16 + Ofiicial 14/16)
Adult 1 (Oficial 17/20 + Oficial 21/24)

Chronic Offender Scale":

* Alpha = .6805

 

35

ANALYSIS

The analyses for the two hypotheses incorporated the use of both bivariate
correlation and analysis of variance (AN OVA) techniques to determine the relationship
between the independent and dependent variables. The bivariate correlations were the
first set of analyses performed on the variablesz. The correlations indicated that virtually
all of the variables were significant at the .01 level (Table 4). In view of the correlation
analysis on HIA-deficit, the findings support that relationships do exist between this
variable and both aggression variables. It is important to keep in mind that while this
significam relationship does suggest an interaction exists between HIA-deficit and
aggression, a correlation’s Significance does not explain an interaction’s influence upon
ofi‘ending.

According to the correlations, HIA-deficit was Significantly related to violence at
the childhood, teenage, and adult stages of life. With correlations of .179, .218, and .216,
respectively, the statistics point to the probability of HIA-deficit’s impact being more
Significant in terms of violence as a boy got older, rather than a risk factor in childhood
violence. In terms of chronic ofi‘ending, HIA-deficit was also Significantly related to all
“stages” of offending. Much like violent ofi’ending, HIA-deficit appeared to have a

stronger relationship to overall ofi’ending as a boy got older. The correlations performed

 

2 Analyses not presented indicated that all relationships were positive.

36

Table 4. B'

M
HIA-deficit
Aggressive 12-13
Aggressive 14-15
Violence 14
Violence 16
Adult Violence
Youth 14

Youth 16

Adult 1

Chronic ofi’ender

 

HIA-ggfigit m
1.000
200* .000
.159* .005
.179* .001
.218* .000
.216* .000
.169* .002
.236* .000
.227* .000
.232* .000

Aggressive

37

12-13
200*

1.000

.328*
.132*
.061

.192*
.199*
.198*
.149*

.161*

* Correlation is significant at the .01 level (2-tailed).

its!
.000

.000
.008
.226
.000
.000
.000
.003

.002

Aggressive
14-15

.159*

328*

1.000

.263 *

224*

.251*

.326“

313*

221*

263*

 

Sig;
.005

.000

.000
.000
.000
.000
.000
.000

.000

with HIA-deficit were stronger with respect to teenage and adult ofi‘ending than with
childhood ofiending. The final correlation to discuss includes overall ofi‘ending, in which
case HIA-deficit did indeed have a significant correlation with chronic ofi‘ending (.232).

The correlations performed on Aggression at 12-13 appeared to have more
variance compared to HIA-deficit’s relation to violence and chronic ofi‘ending. Although
a boy who has aggressive tendencies was correlated with early violence at 14 years and
adult violence, this finding did not hold true for violence measured at age 16. In fact, of
all the correlations performed, the childhood aggression and teenage violence correlation
was the only non-significant relationship to exist (Sig. = .226). This finding is even more
intriguing considering fact that adolescent aggression was significantly related to teenage
violence (Sig. = .000). Lastly, it appears that childhood aggression had a declining efi‘ect
on chronic ofi’ending. That is, aggression at the ages of 12-13 was more highly correlated
with childhood and teenage ofi‘ending than with chronic ofl‘ending in adulthood.

Aggression at the ages 14-15 measured the amount of adolescent aggression.
According to the correlations, aggression at this stage of life was more highly correlated
with all ages of violent ofi‘ending, and for the most part all ages of chronic ofi‘ending, than
either childhood aggression or HIA-deficit. The finding that a variable measured in
adolescence has more correlation to delinquency compared to concepts measured in
childhood tends to suggest that adolescent measures are stronger predictors of
delinquency and violent ofi'ending.

In conclusion, the bivariate correlations indicated that HIA-deficit was Significantly
related to all measures of aggression, violence, and chronic ofl’ending. This finding helps

to confirm previous literature that symptoms of HIA-deficit are Significantly related to

38

violence and general delinquency. . Further support was found between the relationship of
aggression and delinquency. That is, on most levels, aggression was Significantly related
to violence and chronic ofi‘ending. Finally, these findings provide evidence of a
relationship existing between HIA-deficit and aggression. This relationship alone does not
allow us to reject our null hypotheses. However, these findings do support my
anticipation of the HIA-deficit and aggression interaction increasing violent and chronic
ofi‘ending. Support for the increased efi‘ect of comorbid HIA-deficit and aggression on
violence and chronic offending was determined from the AN OVA tests.

There were two sets of AN OVA statistics run for the HIA-deficit and aggression
variables. HIA-deficit and childhood aggression was run against the dependent variables
of Violence at 14, Violence at 16, ' Adult Violence, and Chronic Ofi‘ender. Likewise, HIA-
deficit and adolescent aggression was run against these same dependent variables.

The analysis of variance did not indicate the same support as provided by our
previous correlation analyses as to the significance of the independent variables (Table 5).
While controlling for childhood aggression, HIA-deficit exhibited an F ratio that increased
with each level of violent ofi’ending. In other words, HIA-deficit was less related to
childhood violence (F = 1.742) compared to teenage (F = 2.280) and adult violence (F =
4.337). Furthermore, while HIA-deficit exhibited a significant relationship with teenage
and adult violence, this was not the case with childhood violence (Sig. = .125).

Controlling for aggression, HIA-deficit also did not increase the amount of chronic
ofi‘ending (Sig. = .085).
An overview of childhood aggression found that its Significant relationship to

violence and chronic ofi‘ending was just the opposite of what HIA-deficit’s findings

39

Table 5. Two- AN VA- - ficit n A ion at 12-13 Y rs

N o. of Cases
m Signifiggnce Ingluggg Excludg
Violence 14 333 79
HIA-deficit .125
Aggressive 12/13 .029*
2-Way Interaction .123

Violence 16
HIA-deficit .047*
Aggressive 12/13 .621
2-Way Interaction .028*

Adult Violence
HIA-deficit .001*
Aggressive 12/13 .101
2-Way Interaction .042*

Chronic Ofi‘ender
HIA-deficit .085
Aggressive 12/13 .000*
2-Way Interaction .229

* Significant at the .05 level.

 

40

provided. For instance, while controlling for HIA-deficit, childhood aggression was
significantly related to childhood violence (Sig. = .029) and chronic ofi’ending (Sig. = .000).
Conversely, childhood aggression was not found to increase the amount of teenage
violence (Sig. = .621) or adult violence (Sig. = .101). This last finding was similar to a
correlation’s finding in that AN OVA determined the relationship between childhood
aggression and teenage violence to be non-significant.

In view of the previous findings, the important statistics now involved the two-way
interaction effect of HIA-deficit and aggression on violent and chronic ofi‘ending. As
hypothesized, it appeared that the interaction of HIA-deficit and childhood aggression had
a Significant efi’ect on several variables (Table 5). In terms of violence at age 16, the
interaction of HIA-deficit and aggression increased the amount of teenage violence
compared to HIA-deficit or aggression alone. This interaction efi’ect was significant at the
.05 level (Sig. = .028). Another significant finding related to adult violence, in that the
interaction of HIA-deficit and aggression was Significantly related to violence at age 18
(Sig. = .042). However, the interaction efi'ect did not influence adult violence as much
compared to HIA-deficit alone (Sig. = .001). Finally, the influence of comorbid HIA-
deficit and aggression was not found to significantly influence the amounts of childhood
violence (Sig. = .123) or chronic ofl’ending (Sig. = .229). In fact, the influence of HIA-
deficit and aggression alone increased the amount of chronic offending, and for the most
part teenage violence, compared to the HIA-deficit and aggression interaction.

In summarizing the first set of AN OVA statistics, it is important to note several
findings. First, it is interesting to note the reciprocal nature of the significance of HIA-

deficit and aggression alone on violence and chronic ofiending. HIA-deficit alone was

41

found to be Significantly related to teenage and adult violence, but not to childhood
violence or chronic ofi’ending. Conversely, by itself aggression was significantly related to
childhood violence and chronic ofi‘ending, but not to teenage or adult violence. Another
interesting finding related to the interaction efi‘ect of the variables. As mentioned before,
singular HIA-deficit was found to be significantly related to both teenage and adult
violence. Similarly, the interaction efi‘ect of HIA-deficit and childhood aggression was
significantly related to teenage and adult violence. Furthermore, just as HIA-deficit alone
was found to be insignificantly related to childhood Violence and chronic ofi‘ending, so too
was the interaction of HIA-deficit and! aggression insignificant. Needless to say, the

AN OVA analysis conveyed just the opposite findings for childhood aggression. That is,
when childhood aggression alone exhibited significance, the interaction did not, and vice
versa.

The second set of AN OVA performed included the variables of HIA-deficit and
adolescent aggression (Table 6). In this set we found that HIA-deficit alone did not
appear to be statistically related to most dependent variables. In fact, when controlling for
adolescent aggression, HIA-deficit was only found to be significant with adult violence
(Sig. = .002). On the other hand, adolescent aggression was very much an influential
variable on delinquency. Aggression at ages 14-15 was significantly related to childhood
violence (Sig. = .001), teenage violence (Sig. = .048), and chronic offending (Sig. = .000),
when controlling for HIA-deficit. Furthermore, in terms of adult violence, although
insignificant, adolescent aggression Still displayed a strong F ratio (2.139) almost worthy

of a significant relationship (Sig. = .096).

42

Table 6. Two-way AN QVA; HIA-ggfigit and Amgion at 14-15 Ygrs

No. of Cases
M E Significance M Exglgged
Violence 14 313 99
HIA-deficit 1.227 .296
Aggressive 14/15 5.838 .001*
2-Way Interaction .902 .557
Violence 16 305 107
HIA-deficit 1.713 .132
Aggressive 14/ 15 2.672 .048*
2-Way Interaction 1.792 039*
Adult Violence 301 111
HIA-deficit 3.916 .002*
Aggressive 14/15 2.139 .096
2-Way Interaction 1.566 .088
Chronic Offender 295 117
HIA-deficit 1.722 . 130
Aggressive 14/15 7.807 .000*
2-Way Interaction .801 .668

* Significant at the .05 level.

 

43

The two-way interaction efi‘ect of HIA-deficit and adolescent aggression did not
appear to be as strong as the previous interaction efl’ect of HIA-deficit and childhood
aggression. The only interaction effect of HIA-deficit and aggression which increased
delinquency more compared to HIA-deficit or aggression alone was with teenage violence
’ (Sig. = .039). This relationship to teenage violence was the only significant finding of the
AN OVA analyses on comorbid HIA-deficit and adolescent aggression. The interaction
efi’ect of HIA-deficit and adolescent aggression was not significantly related to childhood
violence (Sig. = .557), adult violence (Sig. = .088), or chronic ofi‘ending (Sig. = .668). In
fact, on both measures of childhood violence and chronic ofi‘ending, the efi‘ect of HIA-
deficit and aggression alone increased the amount of delinquency moreso compared to
comorbid HIA-deficit and adolescent aggression.

One interesting point to mention on AN OVA is the resemblance of the two sets of
interaction analyses. Generally Speaking, in both instances the interaction efi’ect of HIA-
deficit and aggression did not increase the amount of childhood violence or chronic
ofi‘ending compared to HIA-deficit or aggression alone. However, the interaction effect
did increase the amount of teenage violence compared to HIA—deficit or aggression alone.
In terms of adult violence, the analyses found that the interaction of HIA-deficit and
childhood aggression, not adolescent aggression, was significantly related. Despite its
significance in both analyses, the interaction of comorbid HIA-deficit and aggression did
not increase the amount of adult violence compared to HIA-deficit alone. However, the
HIA-deficit and aggression interaction did increase the amount of adult violence more than

childhood or adolescent aggression alone.

DISCUSSION

It seems there exists some clear and consistent findings in these analyses.
According to the bivariate correlations, HIA-deficit has a Significant relationship with both
measures of aggression, violence at all three age groups, and chronic ofi‘ending. Likewise,
adolescent aggression measures Significant relationships on all measures of violent and
chronic ofi‘ending. The same holds true for childhood aggression, with the exception of
teenage violence, in which case the relationship is not significant.

Perhaps the most influential finding of the correlation analysis relates to the
aggression variables. It is my finding that on every correlation measure, adolescent
aggression is more strongly related to all variables compared to childhood aggression.
This is significant because the as one would anticipate, aggressive behavior developed
early in childhood would advance and amplify in adolescence. Stated more Simply, we
anticipate adolescent aggression will have more influence upon a boy’s life as he gets
older. In my case, the analyses finds aggression’s influence to exhibit itself through
increased levels of violent and chronic ofi’ending.

Adolescent aggression is included in this analysis because of the potential for the
findings just discussed. Perhaps the finding that adolescent aggression is more
significantly related to violence and chronic ofi‘ending compared to childhood aggression

signifies the importance of “social networking.” That is, as a boy becomes more

45

acclimated towards a group or network of fiiends, the influence of his aggressive behavior
becomes heightened due to the socialization process with those fiiends. Social networks
also introduce the concept of peer pressure. Thus, if a boy already has the characteristics
of disobedience, is overly competitive, and has a tendency to play rough, the network
system can be a venue for not only displaying those characteristics, but also compounding
them. At any rate, these findings support a behavior that, in relation to violent and chronic
ofi‘ending, becomes more Significant as a boy gets older.

According to AN OVA, there appears to be several conclusive statements about
the comorbid HIA-deficit and aggression influence on violent behavior. One conclusion
would be that those with comorbid HIA-deficit and aggression are more likely to commit
teenage violence than those diagnosed with HIA-deficit or aggression alone. This
conclusion is applicable toboth measures of aggression. However, these same
conclusions are not applicable to violence in the childhood years. I found that the
interaction of HIA-deficit and aggression at both age groups does not increase the amount
of childhood violence. In fact, the findings support definitions of aggression that influence
violent offending in childhood considerable more than does its interaction efl'ect with HIA-
deficit. The same finding holds true for HIA-deficit. Compared to its counterpart
comorbid HIA-deficit/adolescent aggression, HIA-deficit increases moreso the level of
childhood violence.

In terms of adult violence, I am able to make several conclusions based on the
analyses of the HIA-deficit and aggression interaction. In both analyses, the interaction
effect of HIA-deficit and aggression does not increase the amount of adult violence more

than HIA-deficit alone. However, the interaction in both analyses does lead to more adult

46

violence compared to childhood or adolescent aggression. Having many of the same
results when compared to teenage violence, it appears that HIA-deficit has much more
influence in adult violence compared to aggression.

Generally speaking, I conclude that those with comorbid HIA-deficit and
aggression will commit more violence in their teenage years compared to those with HIA-
deficit or aggression alone. Additionally, the relationship of comorbid HIA-deficit and
aggression to childhood and adult violence lends support to a definition of comorbid HIA-
deficit and aggression which may have more of an influence, in terms of violent ofi‘ending,
as a boy gets older. How much influence each variable has upon violent ofi‘ending can be
proposed from these findings as well. I find that comorbid HIA-deficit and childhood
aggression is stronger upon adult violence compared to comorbid HIA-deficit and
adolescent aggression. This finding lends support to aggression’s decreasing influence in
violent behavior. Because of this decreasing influence, it might be that a boy’s aggression
does not have as much influence on violent ofi‘ending as does his level of HIA-deficit,
regardless of his age. This proposal is backed from the finding that childhood aggression
alone is not significant to adult ofi‘ending, but its interaction with HIA-deficit is significant.

In terms of chronic ofi‘ending, a more general conclusion can be made regarding
the influence of comorbid HIA-deficit and aggression. I must fail to reject my null
hypothesis and conclude that those diagnosed with comorbid HIA-deficit and aggression
will not be more likely to be chronic, or life-course persistent ofi’enders. Using both
measures of aggression, the interaction efi’ect with HIA-deficit does not incur a greater
number of chronic ofi‘enders. Yet this conclusion does not necessarily contradict Mofiitt’s

Developmental Theory, that an early neuropsychological deficit increases the likelihood of

47

someone becoming a life-course persistent offender. Rather, it provides evidence to the
fact HIA-deficit may have more of an influence upon violent ofi‘ending rather than general
ofi‘ending. However, in terms of aggression there are significant findings relating to
Mofitt’s Theory. Based on the findings fiom the correlations and fiom AN OVA, I
conclude that those with childhood and adolescent aggression will increase the amount of
chronic ofi‘ending compared to comorbid HIA-deficit and aggression or HIA-deficit alone.
Thus, is appears that those having fit my definition of aggression, that being a non-physical
and verbally abusive type of behavior, are at risk for becoming chronic, or life-course
persistent offenders.

One point must be made with regard to these findings on violent and chronic
ofi’ending. The results on the influence of HIA-deficit and aggression on violence and
chronic ofi’ending almost seem contradictory to previous understandings of general
ofl’ending. It seems logical that those who are characterized as chronic ofi‘enders are
usually prone towards more violent behavior. This study does not support such traditional
understandings. The finding that comorbid HIA-deficit and aggression is significantly
related to violence and not with chronic ofl’ending is definitely a unique concept.

In light of the findings, one point must be made with regards to accepting or
rejecting my hypothetical statements. It appearsthat the evidence used in the decision to
reject or fail to reject the null hypothesis, which states those diagnosed with comorbid
HIA-deficit and aggression will not commit more violent crimes, is indecisive. Whereas
one finding holds the null hypothesis to be rejected because a significant relationship exists
between comorbid HIA-deficit and aggression upon teenage violence, other findings fiom

the interaction of HIA-deficit and aggression on childhood violence indicate otherwise. In

48

addition, the decision revolving around the adult violence measure is unclear. HIA—deficit
and childhood aggression interact significantly with adult violence, but HIA-deficit and
adolescent aggression do not. Because of these findings, I am not able to make
generalizing statements to the significance of comorbid HIA-deficit and aggression upon
violence. I am only able to say that comorbid HIA-deficit and aggression increases
teenage violent ofi‘ending compared to HIA-deficit and aggression alone, and for the most
part, is significantly related to adult violence.

In reaching these conclusions about our hypothetical statements, I Should point to
other directions researchers Should take with regards to fiiither Studies on this topic. A
first point to consider is the admittingly over-generalized hypothetical statements. It is my
contention that this study’s conclusions are better suited towards more distinct points of
interest, rather than overall violent ofi‘ending. This study also exposes the dificulty in
operationalizing a disorder such as HIA-deficit. For example, limitations in the data do
not permit for a “full-symptom” diagnosis of HIA-deficit at several age groups. The
current findings not only suggest other operationalization techniques for HIA-deficit, but
more importantly suggest that future studies of violence should include “full-symptom”
diagnoses of HIA-deficit at both an early and late childhood age. Another direction to
consider involves the operationalization of a chronic ofi‘ender. The rate of chronic
ofl‘ending used in this study was 11.5 percent. Previous findings have supported a chronic
ofi‘ending rate around 5-6% (Mofitt, 1993; Wolfgang, 1972). It could be that the use of
both self-reported delinquency and oficial convictions in measuring chronic offending
over-reported the actual amount of ofi’ending. There is no question as to the dangers in

using self-reported questionnaires to gauge delinquent activity, those dangers being the

49

under- and over-reporting of delinquent behavior. However, in some instances, as it was
in this case, the necessity to include more cases was imperative. Thus, in measuring the
childhood and teenage offender both self-reported ofi‘ending and oflicial convictions were
used. These items were not combined, however, to measure adult offending. This is no
doubt a limitation to my study. Further studies measuring levels of ofl‘ending should be
consistent with respect to the items used in measuring a variable.

What do my findings mean for practitioners who treat the young male offender? If
we consider the fact that anywhere fi'om 30 to 80 percent of children with HIA-deficit will
continue to display the symptoms into adulthood (Barkley, 1990; Weiss and Hechtman,
1986), then we should be greatly concerned with fiiture violence and offending from this
population. Since HIA-deficit appears to manifest itself more in teenage and adult
violence, it is sensible to conclude that any treatment for this neuropsychological deficit
should extend fiirther than the current repercussions of today’s juvenile ofi‘ending. For
example, if practitioners are to initiate treatment based on these findings, then those
delinquents diagnosed with HIA-deficit will receive regular check-ups from social workers
and medical professionals throughout adolescence. Furthermore, should the childhood
HIA-deficit symptoms continue to persist, as some researchers have found, then follow-up
checks should carry through into adulthood.

In terms of chronic ofi’ending, the findings conclude that we should be more aware
of those with aggressive behavior than with HIA-deficit. According to the findings,
aggressive behavior needs to be examined at a relatively early age (12 years). The
previous analyses point to the existence of aggressive traits in early childhood, which are

significantly related to early violence. Furthermore, the analyses also point to the

50

significant contribution of aggression to chronic ofl‘ending. Because of these findings, it is
my contention that those with aggressive characteristics will be more likely to be
committing crimes throughout their lifetimes. For this type of delinquency, I would
suggest that treatments involving aggressive boys must involve behavior modification.
Modification is necessary because the assumption is that anyone involved in a persistent
cycle of ofi‘ending needs to be taught how to break that cycle. In this case, the aggressive
individual will need to learn how to control his temper and verbal aggression in a conflict
situation. The findings also indicate that any type of treatment for childhood aggression
should notice the significance of adolescent aggression on all types of ofi‘ending. Thus,
treatments for childhood aggression should also incorporate follow-ups through
adolescence.

With that in mind, it is my contention that treating those with HIA-deficit will be
much more dificult than treating aggressive delinquents. My basis for this assumption is
that violence, for the most part, is an unpredictable act involving no premeditated thinldng.
Conversely, an individual who is a chronic ofi’ender makes a living through thought-out
methods of illegitimate opportunity. In other words, this type of behavior is predictable in
the sense we can assume the individual will continue to obtain privileges through illegal
means. In my view, it is much easier to change the predictable chronic offender than the
unpredictable violent ofl’ender. Include the fact that the violent offender has a
neuropsychological deficit and the potential for treatment will dissipate even more.

In conclusion, my findings support a diagnosis of comorbid HIA-deficit and
aggression which does not increase the amount of chronic offending, but does increase the

amount of teenage violence, compared to either HIA-deficit or aggression alone.

51

Whatever the direction taken in researching these topics, my conclusions point to several
objectives. First, the dificulty in operationalizing HIA-deficit and aggression encourages
more research in these areas, particularly in the childhood years. Second, an objective
Should be made to study the efi'ects of longitudinal treatment for those with HIA-deficit
and aggression. Finally, the influence of comorbid HIA-deficit and aggression upon
violence should also be viewed in relation to other variables which might have an influence

in the late childhood, early teenage years of development.

APPENDIX

Table 1A: Violen ifi

Variable
Violenge 14:
Carried a weapon (age 14)

Used a weapon (14)

Struggled/fought
w/police (14)

Violegg l6:
Carried a weapon (16) *

Used a weapon (16) *
Struggled/fought
w/police (16) *

Adult Violence:
Involved in fights (18)

Started fights (18)

Ms

(and fi'equencies)

0 = never (79.3%)

1 = once/twice (4.0)
2 = sometimes (8.9)
3 = fiequently (7.9)

0 = never (87.9)

1 = once/twice (4.4)
2 = sometimes (5.2)
3 = frequently (2.5)

0 = never (93.1)

1 = once/twice (4.0)
2 = sometimes (2.2)
3 = fi'equently (0.7)

l = no (74.6)
2 = yes (25.4)

1 = no (82.9)
2 = yes (17.1)

1 = no (87.2)
2 = yes (12.8)

0 = no fights (60.7)

1= 1 fight (13.6)
2 = 2 fights (10.5)

60 = 60 fights (0.3)
Beat up-no retaliation (2.1)

0 = no fights (76.9)
1= 1 fight (13.6)
2 = 2 fights (3.3)

‘25 = 25 fights (0.5)

* Recoding was not necessary.

54

3.29.1:

(and frequencies)
0 = no (79.3)

1 = yes (20.7)

0 = no (87.9)
1 = yes (12.1)

0 = no (93.1)
1 = yes (6.9)

0 = no (62.7)
1 = yes (37.3)

0 = no (76.9)
1 = yes (23.1)

Table 1A (cont’d):

A lVi len :
Carried a weapon (18)

Used a weapon (18)

W

Violence at 14

Violence at 16

Adult Violence

9519
(and frequencies)

0 = never (91.8%)
1 = 1 day (2.1)
2 = 2 days (0.5)

365 = 365 days (0.3)
0 = never (91.8)

1 = 1 time (3.3)

2 = 2 times (0.8)

25 = 25 times (0.3)

Recode

(and fi'equencies)
0 = no (91.8)

1 = yes (8.2)

0 = no (91.8)
1 = yes (8.2)

Only to threaten/not hurt = (2.6)

m

(and frequencies)

Carried a weapon (20.7%)
Used a weapon (12.1)
Struggled/fought

w/police (6.9)

Canied a weapon (25.4)
Used a weapon (17.1)
Struggled/fought
w/police (12.8)

Involved in fights (37.3)
Started fights (23.1)
Carried a weapon (8.2)
Used a weapon (8.2)

55

Mm

(and frequencies)

0 = no measures (74.1 %)
1= 1 measure (15.3)

2 = 2 measures (7.4)

3 = 3 measures (3.2)

0 = 0 measures (65.2)
= 1 measure (18.9)
2 = 2 measures (11.1)
3 = 3 measures (4.8)

0 = 0 measures (60.9)
= 1 measure (12.9)
2 = 2 measures (18.3)
3 = 3 measures (4.4)
4 = 4 measures (3.6)

 

Table 2A- W

Xylem:
Convicted 10/ 13 *

Convicted 14/ 16 *

Convicted 17/20 *

Convicted 21/24 *

Self-report delinquency (age 14)

Self-report delinquency (16)

Fin ri

Youth at 14

Youth at 16

Adult offending 17-24

Chronic Offender

 

* Recoding was not necessary.

god;

(and frequencies)
1 = no (91.5%)
2 = yes (8.5)

1 = no (82.0)
2 = yes (18.0)

1 = no (76.4)
2 = yes (23.6)

1 = no (88.4)
2 = yes (11.6)

1 = 0-5 (26.2)

2 = 6-8 (24.0)

3 = 9-13 (26.7)

4 = 14 or more (23.2)

1 = 0-9 (28.2)

2 = 10-12 (26.2)

3 = 13-16 (22.4)

4 = 17 or more (23.2)

Itgmg

(and frequencies)
Self-reported (23.2%)
Convicted 10/13 (8.5)

Self-reported (23.2)
Convicted 14/16 (18.0)

Convicted 17-20 (23.6)
Convicted 21-24 (11.6)

Youth at 14 (26.7)

Youth at 16 (31.5)
Adult Offending (27.1)

56

Ram

(and frequencies)

0 = no (76.8%)
1 = yes (23.2)

0 = no (76.8)
1 = yes (23.2)

MM
(and frequencies)

0 = no (73.3%)
1 = yes (26.7)

0 = no (68.5)
1 = yes (31.5)

0 = no (72.9)
1 = yes (27.1)

0 = no (88.5)
1 =yes (11.5)

Table 3A: In nd 11 V ri

Kimble
HIA-deficit:
Adventureness (age 8)

 

Psychomotor Clumsiness (8)

Concentration (8) *

 

Psychomotor Clumsiness (10)

Concentration (10) *

Fing! Vgfiablfi
HIA-deficit

Aggression 12-13 Years *

 

Aggression 14-15 Years *

* Recoding was not necessary.

 

sifi 'nad

Coding

(and fiequencies)

1 = cautious (16.1%)
2 = average (64.1)

3 = many risks (19.8)

1= 0-1 score (18.6)
2 = 2 (19.1)
3 = 3 (25.0)
4 = 4 (18.4)
5 = 5 or more (18.9)

1 = no (66.3)
2 = yes (33.7)

1 = low (25.3)

2 = low average (24.6)
3 = high average (24.8)
4 = high (25.3)

1 = no (62.2)
2 = yes (37.8)

Item;

(and frequencies)
Adventureness (19.8%)
Psychomotor 8 (18.9)
Concentration 8 (33.7)
Psychomotor 10 (25.3)
Concentration 10 (37.8)

1 = 6-9 — least aggressive (18.6)

2 = 10 (39.9)
3 = 11 (20.3)

4 = 12 + - most aggressive~(21.3)

1 = 6-9 - least aggressive (19.8)

2 = 10 (40.2)
3 = 11 (16.4)

4 -.- 12 + - most aggressive (23.5)

57

 

Recodg

(and fiequencies)
O = no (80.2%)
1 = yes ( 19.8)

0 = no (81.1)
1= yes (18.9)

0 = no (74.7)
1 = yes (25.3)

 

Measures

(and frequencies)

0 = no measures (33.2%)
1 = 1 measure (32.7)

2 = 2 measures (17.2)

3 = 3 measures (9.6)

4 = 4 measures (5.8)

5 = 5 measures (1.5)

 

BIBLIOGRAPHY

BIBLIOGRAPHY

aleinteberg, B., Anderson, T., Magnusson, D., & Stattin, H. (1993). Hyperactive
behavior in childhood as related to subsequent alcohol problems and violent
ofi‘ending: a longitudinal study of male subjects. WM
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American Psychiatric Association. (1980). D ' ' . ' ’ :_
Disorders (3“1 ed.) Washington, D. C.: American Psychiatric Press

American Psychiatric Association. (1937). W
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