Cognitive Behavioural Programm

TITLE: Cognitive-behavioural Programme for children with
Attention Deficit Hyperactivity Disorder.
BY
Larry David Hirschowitz
A dissertation to be submitted in fulfillment of the

requirements for the degree
MASTER OF ARTS IN PSYCHOLOGY
IN THE FACULTY OF ARTS
at
RAND AFRIKAANS UNIVERSITY
Supervisor: Dr. Alban Burke
NOVEMBER 1999
Cognitive-behavioural Programme for children with
Attention Deficit Hyperactivity Disorder
L. D. Hirschowitz
Acknowledgements
I am indebted to the following people who contributed to this
study. I wish to express my sincere gratitude to:
Dr. Alban Burke, for his input, guidance and encouragement
from the start of this study, through to its completion.
My parents, for their continued support and encouragement in
my studies.
Mrs. Joan Porter for all her assistance, which enabled me to
find a sample to work with.
The participants of the programme who were willing to give
up their time to take part in this study.
Larry David Hirschowitz
November 1999.
Abstract
Attention Deficit Hyperactivity Disorder (ADHD) affects between 1% and 20% of
school-aged children. Many aspects of the disorder remain largely speculative
including the treatment of it, and often these children experience significant learning,
social and emotional difficulties from their childhood years through to adulthood.
Pharmacological treatment of the disorder has gained wide acceptance and it has
achieved much success in bringing about positive short-term changes in the
behaviours of such children. However the long-term efficacy of medication still
remains questionable and many children do not respond well to or do not tolerate such
treatment.
The use of psychological interventions for this condition has not received as much
support as that of medication. While research shows that some psychological
approaches have virtually no effect others have shown limited benefits.
Taking into account the previous research conducted into the benefits of the
psychological treatment of ADHD and through examining the limitations of these
approaches, the present research aims to establish an effective psychological
intervention in the treatment of this condition.
This intervention follows the format of a Parent-training based Cognitive-Behavioural
programme making use of Barkley's theory that Behavioural Inhibition is the central
impairment in Attention Deficit Hyperactivity Disorder.
I
Therefore the hypotheses of this research are twofold. Firstly, that psychological
interventions can make a positive contribution to the treatment of this condition and
secondly, that this parent-training based cognitive-behavioural programme is useful in
the treatment of Attention Deficit Hyperactivity Disorder.
II
Table of Contents
Contents Page
Number
Abstract I
Table of Contents III
List of Tables VI
List of Figures VII
Chapter 1 1
1.1. Introduction 1
Chapter 2 5
2.1. Aetiology of ADHD 5
2.2. Treatment of ADHD 9
2.2.1. Pharmacological Treatment of ADHD 9
2.2.2. Behavioural Treatment of ADHD 12
2.2.2.1 Introduction to Behaviour Therapy 12
2.2.2.2. Reinforcement 15
2.2.2.3. The Home Token Economy 16
2.2.2.4. Response-Cost interventions 18
2.2.2.5 Time-out 19
2.2.2.6 Modelling 19
2.2.3. The Cognitive Dimension 20
2.2.3.1. Introduction to Cognitive Treatment 20
III
2.2.3.2. Impulsiveness, Attention and Self-Instruction 22
2.2.3.3 Self-monitoring and Self-reinforcement 24
2.2.4. The inclusion of parents in the intervention 24
2.2.4.1. The parents' impact on the child's intrinsic motivation 25
2.2.4.2. Supporting and educating parents 27
2.2.5. Environment Restructuring 29
2.2.6. The effects of added stimulation 31
2.3. ADHD and behavioural inhibition 32
Chapter 3 Research Methodology 37
3.1. Introduction to methodology 37
3.2. Sample Information 37
3.3. Measurements 39
3.4. The Intervention 40
3.5. Experimental Methodology 44
3.6. Statistical Procedures 47
Chapter 4 Results 48
4.1. Introduction to results 48
4.2. Descriptive Statistics 49
4.3. Inferential Statistics 53
4.3.1. Kruskal-Wallis Test 53
4.3.2. Mann-Whitney Test 56
4.3.3. t-Test 60
4.4. Summary of significant results 67
IV
Chapter 5 68
5.1. Discussion and Conclusion 68
5.2. Implications for further research 75
References 77
Appendix A Information Booklet submitted to parents 92
Appendix B ADHD Rating Scale 107

List of Tables
Table Description Page
Number
4.1. Pretest Frequency Table for Total Sample 49
4.2. Posttest Frequency Table for Total Sample 50
4.3. Pretest Mean and Standard Deviation scores for the Total Group 51
4.4. Posttest Mean and Standard Deviation scores for the Total Group 51
4.5. Pretest Mean Ranks of responses on the rating scale 53
4.6. Posttest Mean Ranks of responses on the rating scale 54
4.7. Chi-Square of each item of the pretest for the Total Group 55
4.8. Chi-Square of each item of the posttest for the Total Group 55
4.9. Pretest Mean Ranks of responses on the rating scale 56
4.10 Posttest Mean Ranks of responses on the rating scale 57
4.11. Mann-Whitney test statistics of the pretest scores for the Total group 58
4.12. Mann-Whitney test statistics of the posttest scores for the Total group 59
4.13. Mean and Standard Deviation for the Total Group 60
4.14. Paired Sample Descriptive Statistics for the experimental group 61
4.15. Paired Sample Test for the experimental group 61
4.16. Paired Sample Descriptive Statistics for the control group 62
4.17. Paired Sample Test for the control group 62
4.18. t-Test for equality of means at the pretest stage 63
4.19. t-Test for equality of means at the posttest stage 64
4.20. Descriptive Statistics 65
4.21. Levene's test for equality of variances 65
4.22. t-Test for equality of means 66
VI
List of Figures
Figure Description Page Number
Number
2.1. The caudate nucleus and other structures within the basal ganglia in the 8
frontal lobe of the brain
2.2. A schematic configuration of Barkley's theory of behavioural inhibition 35
and ADHD.
3.4. Flow chart of the experimental methodology employed 46
4.1. Graph comparing pretest and posttest means for the total group on each 52
item
4.2. Graph comparing means of pretest and posttest scores on impulsivity 63
and inattention for the experimental and control groups.
5.1. The septo-hippocampal region of the brain 74
VII
Chapter 1
1.1. Introduction
Attention Deficit Hyperactivity Disorder (hereafter referred to as ADHD) affects between
1% and 20% of school-aged children (August & Garfinkel, 1989; Bhatia, Nigam, Bohra
& Malik, 1991), with boys being over represented, on average 3:1 (Barkley, 1997; Bhatia
et al., 1991). However girls with ADHD have largely been neglected by clinicians and
researchers (Berry, Shaywitz & Shaywitz, 1985) and some community-based samples
have found male-female relationships to be as low as 2.1: 1 ( Sharp, Walter, Marsh,
Ritchie, Hamburger & Xavier Castellanos, 1998). The reason for the relative neglecting
of girls is that there is evidence of normative sex differences in the presentation of
ADHD symptoms and therefore if identical research criteria is used for both sexes, one of
the sexes would be excluded to some extent (Sharp et al, 1998). Most research has tended
to use the criterion that favours male symptom presentation (Sharp et al., 1998).
As a result of the relatively new and more stringent criteria set out in the Diagnostic and
Statistic Manual of Mental Disorders IV (American Psychiatric Association, 1994), it is
expected that the prevalence rates will decrease (Reason, 1999). According to Reason
(1999) individual differences may have become unduly pathologised by previous
research criteria and therefore implying that the disorder has been over diagnosed.
The time of onset of the disorder is typically before the age of seven (Barkley, 1997). The
essential feature of the disorder include a persistent pattern of inattention and/or
1
hyperactivity-impulsivity that is more frequent and severe than is typically observed in
individuals at a comparable level of development (American Psychiatric Association,
1994).
The term ADHD is a psychiatric category that originated in the United States. European
practice has preferred the term hyperkinetic disorder, which has more stringent
parameters and a lower prevalence (Reason, 1999). The definitional labels assigned to
this syndrome have changed repeatedly over the years (Richters, Arnold, Jensen, Abikoff,
Conners, Greenhill, Hechtman, Hinshaw, Pelham & Swanson, 1995). The terminology
used for the disorder thus far have included, hyperactivity and minimal brain dysfunction
(pre DSM II), attention deficit disorder and hyperkinetic reaction (DSM II), attention
- -
deficit hyperactivity disorder (DSM III-R) and attention deficit / hyperactivity disorder
(DSM-IV).
The fourth edition of the Diagnostic and Statistical Manual of Mental Disorders,
(American Psychiatric Association, 1994) labels the disorder as "Attention Deficit /
Hyperactivity Disorder" implying that it can occur with or without hyperactivity. The
present research is only concerned with the disorder accompanied by hyperactivity for it
is based on Barkley's (1997) model of behavioural inhibition (see section 2.3.) who
among other theorists, suggest that Attention Deficit Disorder without hyperactivity is a
distinct disorder from ADHD (Barkley, 1997, Barkley, DuPaul & McMurray, 1990,
Barkley, Grodzinsky & DuPaul, 1992).
2
ADHD has continued to occupy a great deal of attention of professionals, teachers and
parents. It has recently been estimated that 3-5% of school-age children experience
significant problems that are associated with ADHD (Cotugno, 1995). As children's
brains mature their ability to control and refine attention and activity will improve and
some will outgrow their problems (Reason, 1999), however many ADHD children do not
outgrow their symptoms (Teeter, 1991) and problems of ADHD in childhood suggest
potential long-term ramifications for vocational and psychological functioning in
adulthood (Wilson & Marcotte, 1996). Left untreated, ADHD children show higher
evidences of conduct disturbances, depression, academic under-achievement, aggression,
oppositional defiant behaviour, depression, enuresis and encopresis ( Burte & Leeds
Burte, 1994) as well as difficulties in adult social relationships, marriage and employment
(Barkley, 1997).
Anastopoulos, DuPaul and Barkley (1991) state that as of yet no treatment has proven to
cure this condition. At present medication appears to be the most effective treatment to
reduce symptoms in the short-term, however, cognitive-behavioural family/parent
training programs fill many of the gaps left unaddressed by medication alone (Burte &
Leeds Burte, 1994). Furthermore the stimulants are not always effective (Richters et al.,
1995) and potentially have a number of side - effects (Cocciarella, Wood & Graff Louw,
1995).
This research aims to establish a non-pharmacological approach that would contribute to
the treatment of ADHD, involving both the child and his or her parents. The treatment
3
will take the form of cognitive and behavioural interventions that have been supported by
previous research in their effectiveness in treating ADHD. Cognitive-behavioural therapy
involves using performance-based and cognitive interventions to produce changes in
thinking, feeling, and behaviour ( Kendall & Panichelli-Mindel, 1995). It concerns itself
with both the external environment and the individual's internal processing of the world
(Kendall & Panichelli-Mindel, 1995) and additionally, it attempts to combine the
strategies developed from cognitive psychology for enhancing the acquisition of
knowledge, with the self-application of behavioural techniques, such as self-assessment,
self-instruction and self-reinforcement (Mash & Barkley, 1989).
Cognitive-Behavioural therapy approaches have produced solid and growing enthusiasm
for their use as adjuncts or even alternatives to more traditional pharmacological and
behavioural strategies (Whalen & Henker, 1991). Furthermore the inclusion of a
cognitive dimension may help to circumvent the limited generalisation of treatment
effects over time and setting seen in behavioural treatments (Mash & Barkley, 1989).
In order to formulate a treatment programme, it is necessary to consider the aetiology of
the disorder as well as some of the most common treatment approaches employed. There
has been considerable debate over the causes of ADHD and the most widely accepted
explanations will be discussed in the following chapter.
4
Chapter 2
2.1. Aetiology of ADHD
Although the aetiology of this disorder remains largely unknown, family, genetic, twin
and adoption studies suggest a genetic origin for some forms of this disorder (Spencer,
Biederman, Wilens, Harding, O'Donnel & Griffen, 1996; Dulcan & Scott Benson, 1997;
Tannock, 1998). Scientists have found that if one twin has symptoms of ADHD, the risk
that the other one will have the disorder is as high as 80% to 90% (Barkley, 1995). There
are others who suggest that well-controlled twin studies show that genetic effects can
explain at least half the variance of hyperactivity and inattentiveness (Reason, 1999).
Other common theories on the aetiology of ADHD include physiological problems
(Lucker & Molloy, 1995) and neuropsychological dysfunctions (Leffert & Garfinkel,
1991).
Zametkin, Nordahl, Gross, King, Semple, Rumset, Hamburger and Cohen (1990)
reported that global cerebral glucose metabolism was 8,1% lower in ADHD adults than in
controls. The metabolic rate of glucose, which is the speed at which glucose is
metabolised in the brain, reflects the extent to which regions of the brain are working or
failing to work, however it does not explain the aetiology of the dysfunction (Daniel,
Zigun & Weinberger, 1992). It only serves to inform that the activity level of the brain in
ADHD adults is less active than in normal controls.
5
There are other studies that indicate a possibility that the neurotransmitters dopamine and
norepinephrine may also be involved in ADHD (Barkley, 1995; Reason, 1999).
Neurotransmitters are substances in the brain that allow communication between the
neurons and therefore any problems in these substances would indicate some
neurological dysfunction.
There are some theorists who have speculated that ADHD may arise as a result of
delayed brain maturation ( Barkley, 1990). The maturational-lag hypothesis postulates
that the cognitive functions involved in language, reading, and other complex behaviours
are organised hierarchically and those levels of the hierarchy develop sequentially (Kolb
& Whishaw, 1996). Should one level of the hierarchy be slow to develop, the entire
hierarchy is retarded in development, since the higher functions are dependant on the
development of the lower ones (Kolb & Whishaw, 1996). The male brain does mature at
a slower rate than the female brain (Semrud-Clikeman & Hynd, 1990), which would
explain the higher prevalence of ADHD among boys. The difficulty with this theory is
that ADHD is also found in adults, who have fully developed brains.
There are a number of indications that the right hemisphere of the brain plays a
significant role in ADHD. Brumback and Staton (1982) proposed that Attention Deficit
Disorder might be the result of an anatomically based right hemisphere dysfunction.
Indeed, Branch, Cohen and Hynd (1995) observed that children with Attention Deficit
Disorder exhibited a variety of subtle left-sided neurological signs indicative of a right
hemisphere dysfunction.
6
According to Malone, Kershner and Swanson (1994) ADHD reflects a dysfunction in the
left hemisphere and an inadequate regulation of an overactive right hemisphere. This
follows the Geschwind-Galaburda hypothesis (Kolb & Whishaw, 1996) on the aetiology
of learning disabilities. They suggest that testosterone delays the development of the left
hemisphere of the brain, allowing the right hemisphere both space and time for greater
development. This would lend an explanation to the higher prevalence of ADHD among
boys. However the proposed effect of testosterone was found to be inaccurate by
Galaburda, Corsiglia, Rosen & Sherman (1987) and the bulk of evidence does not
support the theory (Kolb & Whishaw, 1996). Furthermore there are some views that
argue that ADHD exists as a diagnostic entity apart from the Learning Disabilities
(Robins, 1992), suggesting that the hypothesis cannot automatically apply to ADHD.
Furthermore a study by McDonald, Benett, Chambers and Castiello (1999) revealed that
although signs are bilateral, it appears that greater dysfunction is of the right rather than
that of the left hemisphere.
These studies that implicate the right hemisphere may be consistent with the speculation
that behavioural abnormalities in patients with ADHD may reflect functional impairment
of the frontal, striatal system with which the right hemisphere has preferential
involvement ( Gross-Tsur, Shalev, Manor & Amir 1995; Filipek,1999).
7
The frontal lobes and the caudate nucleus, in the striatum have been implicated
(Tannock, 1998) particularly in the right hemisphere (Reason, 1999). Some studies have
shown that ADHD children have reduced blood flow to the frontal part of the brain,
particularly in the caudate nucleus (Barkley, 1995; Lou, Henriksen, Bruhn, Brner &
Nielsen, 1989). Furthermore it is known that when regions of the brain are activated, the
blood supply will increase correspondingly in these areas (Kolb & Whishaw, 1996;
Elfgren & Risberg, 1998).
Putamen
Motor
cortex Thalamus
Caudate Caudate
head tail
Substantia
Amygdata nigra
Figure 2.1. Displaying the caudate nucleus and other structures, within the basal ganglia
in the frontal lobe of the brain. (Kolb & Whishaw, 1996).
The frontal lobe basis has also been established by studies that have demonstrated
similarities between patients with ADHD and frontal lobe patients (Evans, Gualtieri &
Hicks, 1986). Furthermore a clinical syndrome similair to ADHD develops in children
8
who experience a traumatic brain injury to the frontal lobe (Gualtieri, 1994). This fact led
to the original description of the syndrome as minimal brain dysfunction.
In conclusion, Barkley (1995), a world renowned expert on ADHD suggests that the most
probable causes for which there is convincing evidence of association with ADHD
include:
Various agents that can lead to brain injury or abnormal brain development, such as,
trauma, disease, fetal exposure to alcohol and tobacco and early exposure to high
levels of lead.
Findings of diminished activity in certain brain regions.
Heredity.
It would be useful to consider some of the existing approaches to treating ADHD as these
not only allow greater insight into the possible causes of the disorder but also assist in
developing new and improved methods of intervention. In the following sections various
treatment approaches will be discussed including a number of medical and psychosocial
interventions.
2.2. Treatment of ADHD
2.2.1.Pharmacological Treatment of ADHD.
9
The stimulants are the most established treatment for this disorder, (Spencer, Biederman,
Wilens, Harding, O'Donnel & Griffin, 1996; Whalen & Henker, 1991) with
methylphenidate or Ritalin being the most frequently used (Whalen & Henker, 1991). As
many as 30% of affected individuals do not respond to or may not tolerate such
treatments (Spencer et al, 1996; Gomez & Cole, 1991, Cousins & Weiss, 1993).
Furthermore adherence to recommended pharmacological interventions is typically fair to
poor (Sleator, 1985) with non-compliance estimated at 25% to 50% and increasing over
the duration of the treatment ( Bennett, Power, Rostain & Carr, 1996). Research suggests
that this non-compliance may be because parents are often ambivalent about the use of
medication in ADHD (Liu, Robin, Brenner & Eastman, 1991).
Despite its dramatic short-term effects on the core clinical features of ADHD, for most
parents stimulant medication has been less reliable in bringing about lasting
improvements, especially in social-emotional and academic problems such as poor peer
and teacher relationships and school failure (Richters et al., 1995). The results of several
long-term follow-up studies have indicated minimal improvement beyond those obtained
at the onset of treatment (Anastopoulos, DuPaul & Barkley, 1991; Whalen & Henker,
1991). Furthermore, because these drugs are short-acting, their use is complicated by the
need to take medication at school, and by the re-emergence of symptoms on the evenings
and weekends when the medication is generally not given (Gomez & Cole, 1991,
Cousins & Weiss, 1993). This " rebound effect" as it is commonly referred to, may
involve a worsening of behavioural control beyond levels observed when the child is not
taking Ritalin (Anastopoulos et al, 1991).
10
Despite the controversy surrounding the side - effects of Ritalin, these are typically quite
mild relative to other classes of medication (Anastopoulos et al, 1991) and are usually of
minor importance (Gomez & Cole, 1991). Furthermore the frequency and severity of
these side effects are apparently dose-related and may diminish with reductions in dosage
and/or the passage of time (Anastopoulos et al., 1991).
A common concern for parents is whether their child can develop a dependency on
Ritalin. It should be noted that there is no evidence suggesting that Ritalin predisposes
children to become drug dependant, however research does show that ADHD is over
represented among adults and adolescents in treatment for substance abuse (Horner &
Scheibe, 1997) and hyperactivity in childhood has been implicated to predispose one
toward substance abuse (Aytaclar, Tarter, Kirisi & Lu, 1999). There are a number of
possible explanations for this overrepresentation of ADHD among drug dependant
populations. These include that high behavioural activity levels are a predisposing factor
for substance abuse, particularly where there is coexisting conduct disorder (Aytaclar et
al., 1999). Furthermore Tarter, Jacob and Bremer (1989) suggest that executive cognitive
functioning deficits have also been implicated to be associated with an increased risk for
substance abuse. These deficits according to Barkley (1997) are characteristic of ADHD
and they include difficulties in planning, self-monitoring, abstract reasoning and the
capacity to learn from experience (Aytaclar et al., 1999).
11
Bennett et al. (1996) notes that parents are often ambivalent about potential interventions,
particularly medication. This is largely due to the lack of ADHD education in many
parents (Bennett et al, 1996).
A possibly more significant concern is the potential psychological impact on the child
regarding the use of medications for behaviour regulation. This may send a message to
the child or others that he or she is unable to control behaviour without external aids,
which in turn can have a negative impact on parenting practices, teacher expectations and
on the child's developing sense of self-efficacy (Henker & Whalen, 1989; Gomez &
Cole, 1991).
The literature on stimulant medication and the emerging literature on psychosocial
treatment for children with ADHD suggest that no single treatments for children with
ADHD is likely to yield clinically significant long-term therapeutic gains. (Richters et al.,
1995). Many researchers argue that stimulant medication alone is likely to be insufficient
in the treatment of ADHD (Cousins & Weiss, 1993; Burte & Leeds Burte, 1994).
Where long-term outcomes are mentioned, researchers and practitioners agree over the
importance of combining medication with other forms of interventions that enhance
social adjustment and academic achievement (Reason, 1999).
2.2.2. Behavioural Treatment of ADHD
2.2.2.1. Introduction to Behaviour Therapy
12
The core characteristic of behaviourism, is its emphasis that it places on the role of
external events (Mazur, 1986), that is, behaviourism focuses on environmental stimuli
and on overt behaviours. According to this approach, the behaviours of animals or people
can be shaped through changing their environments (Mazur, 1986; Jordaan & Jordaan,
1989).
A number of the relevant principles of behaviourism will be discussed briefly.
The central principle originating in behavioural thought is that of Classical Conditioning.
In order not to get caught up in the academic jargon, it would be useful to cite the most
widely known experiment demonstrating this process, that is, of Pavlov's dog (Mazur,
1986, Jordaan & Jordaan, 1989). Pavlov noticed that his dog would salivate when food
was placed before him. The salivation he called an unconditioned response as it is innate
to the dog, and the food he called an unconditioned stimulus. The experiment continued
with Pavlov ringing a bell, which was a neutral stimulus, whenever he presented the dog
with food. After doing this for some time he noticed that the dog would salivate when he
heard the bell. This response became termed a conditioned response and the bell was now
transformed from a neutral stimulus to a conditioned stimulus. This is a typical example
of classical conditioning.
Therefore classical conditioning, involves training, in which an organism is exposed to a
neutral stimulus (which becomes a conditioned stimulus) and a non-neutral stimulus
13
(unconditioned stimulus) that naturally provokes a certain response (unconditioned
response). Through the learned association between the conditioned stimulus and the
unconditioned stimulus, the conditioned stimulus is able to evoke the conditioned
response (Rosenhan & Seligman, 1989).
The maintenance of this conditioned response is dependent on the amount of
reinforcement present (Mazur, 1986). Reinforcement refers to an event (reward on
punishment), which when made contingent on a response increases the responses
probability of occurring (Mazur, 1986).
The next principle to be considered is that of Operant Conditioning, which involves
training an organism to respond in a specific manner in order to obtain a reward or to
avoid punishment, that is for reinforcement (Rosenhan & Seligman, 1989). This will
form a large component of the interventions used in this research.
In life reinforcement is not always available immediately following all behaviours. A
reinforcement schedule is a rule that states under what conditions, a reinforcer will be
delivered (Mazur, 1986). The reinforcement schedule can be adjusted to meet the needs
of the particular person. The goal in the context of this research is to continuously
minimise the reliance on the reinforcement so that ultimately the desired behaviour will
be present in the absence of external rewards or punishment.
14
It should be noted that not all learning takes place through classical and operant condition
or even through reinforcement, but also through the observation of others. Behavioural
theory has extended somewhat beyond the traditions of classical and operant learning to
incorporate Social Learning theory, which asserts that in addition to the above-mentioned
principles of learning, children also learn through observation and imitation (Mazur,
1989). This will be discussed further in the section entitled modelling.
In the following sections a number of behavioural interventions that have been used in
the treatment of ADHD will be considered.
2.2.2.2. Reinforcement
Many researchers have speculated that ADHD children display somewhat unusual
reactions to consequences or they fail to maintain their responding when the
consequences for performance are weak, delayed or unavailable (Barkley, 1995).
Therefore interventions that directly alter the pattern and timing of consequences by
socially arranged means to improve ADHD symptoms, should be the treatment of choice
(Barkley, 1995).
Furthermore it has been found that settings which involve immediate reinforcement or
punishment result in a reduction of problem behaviour (Barkley, 1995). Herbert (1991)
notes that maladaptive actions that are rewarded tend to be repeated, whereas those that
are unrewarded or punished tend to be discarded.
15
In a study by Cocciarella et al. (1995) in which they used the following techniques;
reinforcing appropriate behaviours and punishing negative behaviours, skills training and
parental education, there was a significant decrease in impulsivity of ADHD children at
home and in the classroom. However, according to Barkley (1995) the difficulty with
reinforcement lies in generalising such changes to the natural environment. For this
reason the present research will make use of cognitive exercises as well as the inclusion
of the parents in the intervention in order to attempt to generalise these changes to the
natural environment.
The reinforcement technique that will be used in the programme is based on the Premack
principle which states that preferred activities can be used as reinforcers for engaging in
less preferred activities (Gage & Berliner, 1992). Simply put, the child will be rewarded
with something that he or she desires if a particular task, that is less desirable, is
completed.
2.2.2.3. The Home Token Economy.
One technique through which reinforcement can be applied is through the use of a token
economy (Anastopoulos et al., 1991; Burte & Leeds Burte, 1994). This method provides
a simple and effective means for reducing hyperactive behaviour (Schaefer & Millman,
1977). In this technique a contract is negotiated by the parents and the child concerned,
containing a list of behaviours that if the child performs, he or she will be rewarded with
a token. Furthermore the contract will stipulate how many tokens are required to obtain a
given reward. The exact nature of each reward will be stipulated in the contract.
16
The effects of token economies appear to be long lasting if attention is given to making
the programme more generalisable (Gage & Berliner, 1992). As a result of naturally
occurring reinforcers in the environment which include praise or special rewards, a good
level of performance can be maintained (Gage & Berliner, 1992).
Gomez & Cole (1991) illustrated by means of a case study of two boys, that through the
use of a contingent management programme they were found to be more self-controlled,
less disruptive and received higher grades.
There is a need to be cautious in the implementation of token economies and contracting
systems as these can be misused. If extrinsic rewards become excessive, they can destroy
or undermine the child's intrinsic motivation (Gage & Berliner, 1992), therefore the
authors recommend that extrinsic rewards should gradually be withdrawn as the child
learns the values of studying, and appropriate behaviour for its own sake. This gradual
withdrawal of rewards should also have a positive impact on the child's ability to delay
gratification, which is often found lacking in the ADHD child (Schweitzer, 1996).
Furthermore positive feedback by the parents should be used whenever behaviour that is
to be maintained or strengthened occurs, in conjunction with the use of extrinsic rewards
and should continue even after these rewards have been withdrawn (Cousins & Weiss,
1993). This positive feedback should include firstly, a positive statement, secondly, a
17
specific statement indicating what was done appropriately and finally it must be made
immediately after the behaviour (Cousins & Weiss, 1993).
2.2.2.4. Response-Cost interventions.
This technique involves the contingent removal of reinforcers (tokens) for bad or
inappropriate behaviour (Gage & Berliner, 1992). This is an alternative to the direct
implementation of punishment and it merely involves the removal of rewards from the
child. Such interventions require relatively little time and effort, are perceived as
effective and tend to be more acceptable to parents than punishment in the traditional
sense. (Bennett, et al., 1996).
Tymchuk (1974) recommends that punishment should be avoided, especially if it is
physical. He suggested that the removal of reinforcers is most effective and that the child
should have a chance to earn them back. This prevents escape or avoidance behaviours
that may occur in general punishment procedures. Furthermore by having a chance to
earn them back, the child realises that he or she is still loved, although he or she has to be
"punished" for certain behaviours (Tymchuk, 1974).
Research in Gage & Berliner (1992) involved two boys on Ritalin. It was found that they
had increased attention and faster rates of task completion when free time was taken way
from them when they did not do their academic work. This case study lends support to
the positive contribution that psychological interventions, and more specifically response-
cost techniques, can have in the treatment of ADHD, even when medication is taken.
18
2.2.2.5. Time-out.
According to Barkley (1995) time-out is a technique that should be incorporated in the
behavioural intervention. Time-out is a procedure whereby children are deprived of the
opportunity to obtain reinforcement (tokens) if they misbehave (Gage & Berliner, 1992)
as well as any social reinforcers that come from being with others (Tymchuk, 1974). This
kind of punishment often seems more acceptable because it does not impose negative
stimuli or events and only removes the child from positive ones (Gage & Berliner, 1992).
This procedure is implemented immediately following misbehaviour and is terminated
once the negative behaviour has stopped (Tymchuk, 1974).
2.2.2.6. Modelling
Modelling involves the systematic demonstration in actuality (or symbolically, on film)
of a model displaying the required behaviour; a skill, an appropriate prosocial action or a
coping strategy (Herbert, 1987). Through this process the child learns the response or
behaviour of a model by observing and imitating the model's performance (Hoghughi,
Lyons, Muckley & Swainston, 1988).
Modelling is considered by social learning theorists to be the cornerstone of learning and
a significant basis for therapeutic intervention (Herbert, 1987).
19
Furthermore, there is strong speculation that ADHD children are weaker in the verbal or
auditory modality (Lufi & Cohen, 1985) and role-playing or modelling will minimise
their reliance on the less efficient auditory processing modality.
For practical reasons one or both of the parents would most suitably fill the role of the
model. For this procedure to be effective the model (parent) must be accepted by the
child in terms of competence, prestige and status (Hoghughi et al., 1988). Therefore, this
procedure should not be used if there is conflict between the child and both of the
parents.
When the child performs inappropriate behaviour, either of the parents should
demonstrate to the child how the behaviour is correctly or adequately performed. This
procedure should also be used in conjunction with the "stop, think, look and listen"
exercise (see section 2.2.3.2.) in the cognitive dimension. The parent should verbalise this
statement when he or she is demonstrating to the child how to complete a specific
academic task. FurtherMore, modelling can be included in social skills training where the
parent demonstrates to the child the appropriate social response when this is perceived to
be lacking in the child (Lucker & Molloy, 1995).
2.2.3. The Cognitive Dimension
2.2.3.1. Introduction to Cognitive Treatment
A second technique that may be used to generalise the child's change in behaviour into
natural surroundings is that of Cognitive - Behavioural interventions. This type of
20
intervention attempts to combine the strategies developed from cognitive psychology
with the behavioural techniques used to improve the symptoms of ADHD. It involves the
self- application of behavioural techniques by the child through self-instruction, self-
reinforcement and self-assessment (Mash & Barkley, 1989).
In the treatment of ADHD, cognitive training has more face validity than perhaps any
other therapeutic model (Abikoff, 1991). However this expectation of its clinical utility
has now been tempered by a decade of research. None of these studies have generated
results to indicate or even suggest that cognitive training is a competitor to the stimulants
or that it enhances their beneficial effects (Abikoff, 1991, Burte & Leeds Burte, 1994,
Gomez & Cole, 1991).
However Cognitive-Behavioural interventions have been shown in some reports to
produce both increased self-control and an increased use of specific coping strategies by
hyperactive children - effects that in one study were neither enhanced by the addition of,
nor produced independently by, stimulant medication (Richters et al., 1995).
Furthermore there are those who suggest that Cognitive-Behavioural programs need to
place greater emphasis on the role of parents and the family of ADHD children in their
programme implementation, as well as to develop more individualised programmes for
the specific children (Kendall & Panichelli-Mindel, 1995). This is precisely the intention
of this study.
21
2.2.3.2. Impulsiveness, Attention and Self-Instruction.
The inability to postpone gratification, uncontrolled motor behaviour and a response
style, which favours action over reflection, are characteristics of impulsivity (Shea &
Fisher, 1996). White & Sprague (1992) note that ADHD children "make their choices
more quickly than non-hyperactive controls and give less consideration, in a less
organised fashion...to alternatives."
Furthermore Schachar, Tannock, Marriott and Logan (1995) found that ADHD children
exhibited marked deficits in inhibitory control. This was verified by Schweitzer (1996)
when she found that ADHD children were less able to persevere for larger, delayed
rewards and tended to choose more immediate, smaller rewards than did the control
group when completing tasks.
Self-instruction involves teaching the child a series of steps for approaching a given task.
The steps may include repeating directions, describing the task, and "thinking aloud"
(i.e. verbal rehearsal) how they might attempt the task while contemplating the
consequences of that approach (Schwiebert, Sealander & Tollerud, 1995). Barkley (1997)
stressed the importance of the self-direction and internalisation of speech and the
profound control it may exert on the individual's behaviour. A study in Schaefer &
Millman (1977) showed that operant verbal mediation training, which in essence is
teaching a child to talk him or herself through the task at hand, reduces the misbehaviour
of children who have continued to misbehave after traditional behaviour modification has
been employed.
22
Pollack (1968) presents a theoretical discussion of how internal speech (verbal
formulated rules) can help a child orient himself or herself and to gain some level of self
control. According to Barkley (1997) the internalisation of speech is one of the four
neuropsychological functions that is diminished in ADHD children. Furthermore this
procedure can also help the child to obtain some autonomy and responsibility in their
own recovery. Pollack (1968) explains that the child often feels helpless and depends on
adults to change the negative behaviours associated with ADHD. She argues that by
providing a method for children to employ offers them a clear message that they are not
helpless.
Hyperactive children do not focus on tasks and have difficulty paying attention when
there are distractions (Kendall & Panichelli-Mindel, 1995). White & Sprague (1992)
found support for the theory that hyperactive children are over inclusive in their attention
allocation. ADHD children tend deploy their attention more narrowly than normal
children in that they inspect fewer different alternatives. To treat this Douglas (1972)
attempted training hyperactive children to say "Stop, look and listen" before responding
to tasks. This was employed to encourage the child to be more reflective, to consider
alternatives and essentially be less impulsive
The words of "stop, think, look and listen" will be used in this programme. Furthermore
the child will be encouraged to use these words at home through means of token
23
reinforcement. The parents will also model this statement or other guiding verbalisations
when assisting the child with academic work as has already been explained.
Hoghughi et al. (1988) outline the following steps used to teach children verbal
mediation:
Perform the appropriate task while talking out loud, with the child watching
(cognitive modelling).
Get the child to perform the same task according to your instruction (overt, external
guidance).
Let the child perform the task while instructing himself aloud (overt self-guidance).
Ask the child to whisper instructions to him or herself as he or she goes through the
task again (faded overt self -guidance).
Encourage the child to perform the task while guiding his or her performance via
inaudible or private speech or non-verbal self-direction (covert self-direction).
2.2.3.3. Self-monitoring and Self-reinforcement.
According to Mash and Barkley (1989) it is useful to teach the ADHD child to observe
and record his or her own behaviour. This will promote autonomy and responsibility in
the child's involvement in his or her own treatment, which in turn should enhance
motivation.
2.2.4. The inclusion of parents in the intervention.
24
2.2.4.1. The parents' impact on the child's intrinsic motivation.
In order for the newly reinforced behaviours and cognitive exercises to be generalised to
the child's natural environment, it is useful to involve the parents in the intervention, by
means of techniques such as token reinforcement for appropriate behaviour at home.
When using reinforcement in children to increase desired behaviour and to diminish
undesirable behaviour, there is a need to be cautious of the procedures used.
Many researchers propose that motivational factors play a strong role in ADHD
behaviours (Burte & Leeds Burte, 1994). Lucker & Molloy (1995) concluded that
children with ADHD possess social skills deficits as well as motivational deficiencies
[emphasis added]. According to research cited in (Barkley, 1997) the association of
ADHD with less drive, motivation or effort in the performance of goal-directed
behaviour, frequently appears when the ADHD child has to perform repetitive tasks that
involve little or no reinforcement.
Furthermore, as a means, motivation becomes one of the factors, like intelligence or
previous learning, that determine achievement (Gage & Berliner, 1992). For the long-
term benefits of the programme it is important that the intrinsic motivation of the child be
considered. If the child lacks intrinsic motivation his or her performance will no doubt
deteriorate soon after the programme has been discontinued and when tangible rewards
are no longer available.
25
Gottfried, Fleming and Gottfried (1994) conducted research into parental motivational
practices in children's intrinsic motivation and achievement. They assessed two types of
motivational practices; one being the encouragement of children's task endogeny
(pleasure in and orientation toward learning and task involvement) and the other being
the provision of task-extrinsic consequences.
Intrinsic motivation is associated with pleasure derived from the learning process itself,
curiosity, the learning of challenging and difficult tasks, persistence and a high degree of
task involvement (Gottfried et al, 1994).
To the extent that parent's encourage task endogeny, intrinsic motivation should be
enhanced. However research in Gottfried et al. (1994) suggest that extrinsic rewards may
have a detrimental effect on young children's intrinsic motivation.
Task contingencies that are perceived as imposing external control or indicating task
incompetence, result in lower intrinsic motivation (Gottfried et al., 1994). Task
contingencies that are perceived as promoting self - engagement in tasks or task
competence, result in enhanced intrinsic motivation (Gottfried et al., 1994).
Tangible or salient rewards have typically been associated with lower intrinsic motivation
because they tend to promote external perceptions of reasons for task engagement.
However a contingency presented within an autonomy-supporting context may facilitate
intrinsic motivation (Gottfried et al., 1994). For this reason, tangible rewards that are
offered at the outset of the programme will be gradually withdrawn. Furthermore the
26
programme will be negotiated with the child, after which some form of a contract will be
drawn up between child and parents, stipulating which behaviours will be rewarded and
which will not. This will provide the child with a greater sense of autonomy and therefore
will promote intrinsic motivation.
2.2.4.2. Supporting and educating parents.
There is much research that indicates that educating parents about ADHD is potentially
an important aspect in the treatment of the disorder (Bennett et al., 1996; Burte & Leeds
Burte, 1994). Research by Lamminmaki, Ahonen, Todd de Barra, Tolvanen, Michelsson
and Lyytinen (1997) verifies the importance of emotional support and the inclusions of a
parent's group in the treatment for children with learning difficulties. According to
Cousins and Weiss (1993) parental training help most, but not all parents, reduce
disruptive behaviour of their children and family stress, in addition to increasing their
children's senses of competence and confidence.
According to Barkley (1995) referral for children for ADHD, in part, results from the
social distress they have created for their caregivers and an attempt to change the
interactions between children and their caregivers should be quite useful. Fletcher,
Fischer, Barkley and Smallish (1996) report higher rates of conflict between mothers and
their ADHD child, than in the relationships between mothers and non-ADHD children.
Furthermore ADHD children are said to be more compliant with their fathers than with
their mothers (Mash & Barkley 1989). This is most likely as a result that the children
27
usually spend more time with their mothers and therefore they are more habituated to
their mothers' discipline (Mash & Barkley, 1989).
The ADHD child is more likely to request assistance from his or her parents during task
performance (Fletcher et al., 1996). These same studies indicate that parents of children
having ADHD, give more commands, repeat their commands more frequently, and use
more hostile behaviour such as reprimands and punishment during their interactions with
their ADHD child than do parents of non-ADHD children (Fletcher et al., 1996). These
parents may also be less responsive to the interactions initiated by their child toward them
than parents of non-ADHD children (Fletcher et al., 1996).
Parents of ADHD children used more negative-reactive and fewer positive parenting
strategies than those of the control groups, and therefore altering parental strategies may
lead to an improvement in ADHD symptoms (Johnston, 1996). Furthermore, loud
reactions to aggressive behaviour results in an increase in aggression in the ADHD child
(Meyer & Zentall, 1995). These findings may have important implications in the
education of parents and caregivers and the strategies they use for behavioural
management.
In addition, Johnston (1996) suggests that ADHD symptoms may provide challenges to
parent's feelings of competence and satisfaction in the parenting role and usually these
parents experience significantly more stress than parents of normal children
(Anastopoulos, Guevremont, Shelton & DuPaul, 1992). Johnston (1996) also found that
parenting self-esteem is lower in ADHD parents that in parents of so-called normal
28
children. A study in Johnston & Freeman (1997) indicated that parents of ADHD children
viewed their influence over the child as relatively unstable and uncontrollable. Lucker &
Molloy (1995) argue that it is important to educate parents and help them to understand
what may be causing their child's behaviour and not blame themselves because their
child is inattentive, hyperactive or impulsive.
Furthermore, parent training in child behaviour management has been shown to improve
both the school and home behaviour of hyperactive children ( Richter et al., 1995).
Finally, Barkley (1990) suggests that cognitive-behavioural techniques are most likely to
be useful when they are taught directly to the child's caregivers for use within the daily
interactions with the child. This suggestion is followed in the present research.
2.2.5. Environment Restructuring.
All of the primary symptoms of ADHD show significant changes across various
caregivers and settings (Barkley, 1990).
Symptoms of ADHD may not be observable when the child is in highly-structured or
novel settings, engaged in an interesting activity, receiving one-to-one attention or
supervision, or in a situation with frequent rewards for appropriate behaviour (Dulcan &
Scott Benson, 1997). Tymchuk (1974) suggests that a list or chart of the desired
behaviours for which reinforcement will be supplied, be placed on the wall in the room
where the child is studying, to serve as a reminder for the child.
29
Mash & Barkley (1989) notes that ADHD children show fewer behavioural problems in
non-familiar surroundings than they do in familiar surroundings. This implies that it may
prove useful to take one's child to another place such as a public library to study for a
test.
Tymchuk (1974) recommends that distracting stimuli or any other stimuli other than
those that are relevant to the task at hand should be removed from the child and the place
in which he or she studies. Barkley, Koplowitz, Anderson and McMurray (1997) found
that distractions impair the ADHD child's sense of time. This may explain why it
frequently takes these children excessive lengths of time to do things such as getting
dressed in the morning.
The ADHD child is inferior in short-term visual memory, which is an important cognitive
ability in reading, writing and arithmetic (Lufi & Cohen, 1985) as well as in verbal
learning (Webster, Hall, Brown & Bolen, 1996). Furthermore, research cited in Riccio,
Hynd, Cohen, Hall and Molt (1994) found that ADHD children were functioning at lower
levels than their chronological ages in areas of auditory attention, auditory processing and
receptive language, and it is speculated that ADHD children mediate visual input
spatially rather than verbally (Lufi & Cohen, 1985). If this is true, it very significant,
given that the primary mode of presentation in schools and in behaviour management is
through the auditory modality, implying that the ADHD child as a result, is very
disadvantaged (Webster et al., 1996).
30
Finally, fatigue and the time of day also seems to affect the severity of the ADHD
symptoms. A study cited in Barkley (1990) found that children do better in the classroom
and on various problem-solving tasks in the mornings than they do in the afternoons.
2.2.6. The effects of added stimulation.

Clinically, it is often reported that parents of children with ADHD often claim that their
children insist on doing homework while the television or radio is playing in the
background. Parents often worry that this distracts their children and interferes with
academic performance (Abikoff, Courtney, Szeibel & Kopleowicz, 1996). The reason for
this is explained by the underarousal/optimal stimulation theory explained in Abikoff et
al. (1996). According to this theory, the distractibility of children with ADHD, is an
attempt to compensate for their underarousal by seeking increased levels of stimulation or
novelty (Abikoff et al., 1996). This means that understimulation precipitates hyperactive
behaviour (Schaefer & Millman, 1977). It is postulated that in certain situations,
especially monotonous, routine tasks that are well - learned, the performance of ADHD
children will benefit from increases in self-induced or external stimulation (Abikoff et
al., 1996). However when the academic task is difficult, external stimulation will affect
the ADHD child's performance negatively (Abikoff et al., 1996). This is verified by
Schwiebert, Sealander and Tollerud (1995) who suggest that ADHD children may benefit
from novelty and stimulation on easy and repetitive tasks, but not on new or complex
tasks.
31
Improved academic attention has been documented for students with ADHD on simple
vigilance or writing tasks that add colour during initial training trials (Belfiore, Grskovic,
Murphy and Zentall, 1996) and on more complex tasks that add colour during later
training trials after practice (Belfiore et al., 1996). Furthermore Belfiore, Grskovic,
Murphy and Zentall (1996) found that non-specific colour added to the later part of a
lengthy task, but observable throughout the task, may help students with ADHD sustain
their attention through early training sessions and in the initial phases of tasks of long
duration.
2.3. ADHD and behavioural inhibition.
This section concludes Chapter 2, by organising all the information discussed so far into
a unifying theory of ADHD as proposed by Barkley (1997) (See figure 3.1.). It is on this
model that the intervention of this study is based.
In section 2.1. the frontal lobe basis to ADHD was discussed. In this section attention will
be placed on the prefrontal and striatal systems which are central to the neurology of
ADHD (Filipek, 1999). Gualtieri (1994) argues that frontal dysfunction is probably the
central event in ADHD. In order to expand on precisely what functions the frontal lobe
plays in ADHD, it is necessary to introduce the term executive cognitive functioning.
Lezak (1995) defines the executive functions as those capacities that enable a person to
engage successfully in independent, purposive, self-serving behaviours. Gualtieri (1994)
offers a similair definition; these functions refer to the capacity for autonomous
32
behaviour beyond the structures of external guidance (Gualtieri, 1994), that is to say,
these functions allow for an individual to behave independently in the absence of external
influence. Deficits in executive cognitive functions have been observed in children with
ADHD (Aytaclar et al., 1999). Furthermore the executive functions have been implicated
to reflect a dysfunction in the prefrontal cortex (Aytaclar et al., 1999).
In clinical terms the executive functions include initiative, motivation, spontaneity,
planning, judgement, insight, goal-directed behaviour, the ability to operate in favour of a
remote reward, the capacity for self-monitoring and the flexibility required for self-
correction (Gualtieri, 1994).
This model presumes that the central impairment in ADH.D is a deficit involving
response inhibition (Barkley, 1997). A fundamental component of the executive functions
is the ability to inhibit responding (Oosterlaan, Logan & Sergeant, 1998). Many
researchers have found behavioural inhibition to be at least a significant deficit in ADHD
(Schachar et al., 1995; Tannock, 1998; Oosterlaan et al., 1998) if not the hallmark
symptom (Robins, 1992; Barkley, 1997). In fact, it is not so much inattention that
distinguishes ADHD children from children with other disorders or from normal children,
as much as it is their hyperactive, impulsive and disinhibited behaviour (Barkley, 1990;
Robins, 1992) and furthermore tests of response inhibition reliably distinguish these
children too (Barkley, 1992).
33
This deficit in response inhibition leads to a secondary impairment in four of the
executive functions, working memory, self-regulation, internalisation of speech and
reconstitution (Barkley, 1997). These, in turn, lead to disturbances in self-control and
goal-directed behaviour, which ultimately result in the behaviours observed in ADHD
(Oosterlaan et al., 1998).
Therefore according to this model, the deficit in response inhibition of ADHD patients
causes a disruption to some of the executive functions, resulting in the disorder's
symptoms.
It is interesting to note that in 1980, Gorenstein and Newman argued that hyperactivity,
among a few other psychiatric illnesses, belongs to a class of disorders they termed
disinhibitory psychopathology (Gorenstein & Newman, 1980).
Furthermore the inhibitory functions are anatomically ascribed to the orbital-frontal
regions of the prefrontal cortex and its reciprocal connections with the ventromedial
region of the striatum (Barkley, 1997). These are the same structures that have been
implicated in ADHD (Reason, 1999; Filipek, 1997).
A consequence of this hierarchical model is that if behavioural inhibition is improved, an
improvement in the four executive functions should be evident, resulting in a reduction of
ADHD symptoms (Barkley, 1997).
34
Rutter (1982) argues that inhibitory problems are likely to be particularly evident when
external controls are lacking and when the children have developed a strong set toward
stimuli or activities they find reinforcing.
Behavioural Inhibition
Inhibit prepotent response.

Stop an ongoing response.
Interference Control
Working Memory Self-regulation of Internalization of speech Reconstitution

Holding events in mind. affect/motivation/arousal Description and reflection. Analysis and synthesis of
Manipulating or acting on the Emotional self control behavior.
events. Rule-governed behavior (instruction).
Objectivity/social perspective taking. Problem solving/self questioning. Verbal fluency/behavioral
Initiation of complex behavior Self-regulation of drive and fluency.
Generation of rules and meta- rules.
sequences. motivation. Goal-directed behavioral
Moral reasoning.
Retrospective function (hindsight). Regulation of arousal in the service of creativity.
Prospective function (forethought). goal directed action. Behavioral simulations.
Anticipatory set. Syntax of behavior.
Sense of time.
Cross-temporal organization of
behavior.
Motor Control/fluency/syntax
Inhibiting task irrelevant responses.

Executing goal directed responses.
Execution of novel/complex motor sequences.
Goal-directed persistence.
Sensitivity to response feedback.
Task-re-engagement following disruption.
Control of behavior by internally represented
information.
Figure 2.2. A schematic configuration of a conceptual model that links behavioral inhibition with the four
executive functions that bring motor control, fluency, and syntax under the control of internally represented
information (Barkley, 1997).
35
It is on this model that the intervention is based. Through the cognitive-behavioural
strategies an attempt will be made to alter these patterns of reinforcement and to replace
the non-existent or maladaptive external structure with improved methods of control as
well as an internalised sense of control in the ADHD child, thereby improving the child's
inhibitory skills.
36
Chapter 3: Research Methodology
3.1. Introduction to methodology

The purpose of this study is to examine what affect psychological treatment and more
specifically, parent training in the use of Cognitive-Behavioural techniques, has on the
symptoms of ADHD.
Two groups of subjects were compared, only one of which received the psychological
treatment offered in this research. The hypotheses of this research are: Firstly, that
psychological treatment can offer a positive contribution to the treatment of ADHD and
secondly, parent training in the use of cognitive-behavioural techniques aiming at
improving behavioural inhibition, may result in an improvement in ADHD symptoms.
3.2. Sample Information
The sample objective was to obtain ten subjects, half of which were to serve as the
experimental group and the other half as the control group.
The subjects were to consist of at least one or preferably both of the parents or care givers
of children diagnosed with ADHD by a professional competent to make the diagnosis.
In all the experimental subjects, but one, only the mothers were able to participate as the
fathers claimed they did not have the time. This occurred despite the fact that it was
37
emphasised to the parties that it would be potentially more beneficial to have both parents
present and that if necessary after- hours sessions could be arranged.
A number of schools, psychiatrists, neurologists and institutions were approached to
obtain a sample. The response was largely poor, however eventually eighteen potential
candidates were obtained.
All of these potential candidates were approached, however six did not want to or were
unable to participate in the programme. A further three were excluded based on their
pretest results, in which they failed to meet the diagnostic criteria of ADHD as set out by
the rating scale. This may have been due to the medication they were receiving at the
time of testing, which had the effect of normalising their scores on the rating scale.
One subject dropped out during the course of the programme, which incidentally was the
one where both parents were participating.
Finally, this left a sample of eight candidates. Five were selected to enter the treatment
programme. This selection was done on a "first come — first serve" basis, that is, the first
five people who would commit to a starting date were selected to participate in the
programme. The remaining three was to serve as the control group.
38
All of the children, except for one, were taking Ritalin for the treatment of the disorder.
The exception had been a young girl who had stopped taking Ritalin about three months
prior to the programme.
The ages of the children ranged from seven years to thirteen years, with a mean age of
9,57 years. Finally, there were four boys and four girls in the sample.
3.3. Measurements.
The ADHD Rating Scale developed by DuPaul (1991) was used to screen the potential
candidates for a confirmed diagnosis of ADHD as well as to measure the changes, if any,
at the termination of the programme in both the experimental and control groups.
There were a number of reasons for the selection of this instrument. Firstly, the rating
scale provides a direct rating of the essential symptoms of the disorder from both parents
and teachers and has substantial normative data for each gender that are based on parent
and teacher reports (Barkley, 1990).
Secondly, the scale has been shown to discriminate ADHD children from learning-
disabled and normal children, as well as to differentiate children with Attention Deficit
Disorder (ADD), with and without hyperactivity (Barkley, 1990). This is particularly
important in reference to Barkley's theory of ADHD (Barkley, 1997) in which he argues
that ADD and ADHD may be different disorders with different treatment implications.
39
Finally, the scale differentiates between the constructs of inattention and impulsiveness,
which is useful for exposing the areas in which changes occurred.
The scale was found to be a highly reliable questionnaire with sufficient criterion-related
validity (DuPaul, 1991). The test-retest reliability on Pearson product-moment correlation
coefficients for parent ratings were: ADHD total score, 0.94; inattention-hyperactivity,
0.94 and impulsivity-hyperactivity, 0.90 (DuPaul, 1991).
Therefore the rating scale was found to have adequate psychometric properties as a
screening and as an assessment instrument (DuPaul, 1991).
3.4. The Intervention.
The intervention made use of existing behavioural techniques and in some cases a few
cognitive tools, that have been supported by previous research in their applicability
toward the treatment of ADHD. However in this intervention these techniques were used
to improve the behavioural inhibition of the children where such deficits were found to
occur. For example, rather than attempting to improve studying per se, an attempt was
made to enable the child to inhibit distraction better, thereby improving concentration and
ultimately leading to improved studying behaviour. Indeed it has been shown that
ADHD children are more severely affected by a distractor than are clinical control
children (Goldstein & Blumenthal, 1995).
40
The mothers of the children were trained to use these techniques as well as to monitor the
progress of these interventions as they were applied.
In each subject the behaviours to be inhibited were selected on the basis of their worst
scores on the ADHD rating scale as well as those deemed to be most problematic by the
parents. Therefore the programme was modified toward the specific needs of the
individual subjects, however the basic behavioural and cognitive principles were retained.
The objective of the first session was to obtain the necessary information for the design
of the programme. Therefore the intervention really started in the second session.
All programmes began with a home token economy (see section 2.2.2.3.) where the
behaviours requiring improvement were selected and these were made understood to the
children by the mothers. A chart was made to facilitate the token economy, in which a
list of the desired behaviours was specified as well as an area in which progress could be
indicated.Examples of this includes; the child being rewarded with a token for every ten
minutes that he or she remained seated while studying, and the earning of a token each
time the child was observed to be inhibiting their desire to interrupt others when
speaking. The progress was monitored through placing stars or other symbols aside the
specified behaviour when the child performed this behaviour appropriately. The chart
was usually placed on the wall of the child's bedroom or in another room where the child
studies or spends significant time. This chart served as a reminder for the child as to
41
which behaviours required attention. Furthermore it also served as motivating factor, in
that the child could see the accumulation of stars or other symbols as time progressed.
In some cases the child was able to receive rewards in exchange for the tokens earned.
The amount of tokens required for a reward and the time period in which the reward
would be given was explained to the child before the onset of the programme in order
that it should serve as an incentive. In some cases the potential rewards were repeated to
the child when motivation was lacking.
There were a few parents who did not like the idea of a material reward, for various
reasons and in these cases the tokens themselves were to serve as the only means of
reinforcement.
The availability of rewards was monitored carefully and after time, the periods between
rewards was gradually increased so that the child's intrinsic motivation (see section
2.2.4.1) would not be affected drastically. The mothers were instructed to tell the child
precisely what he or she did to earn each token and it was emphasised that praise and
affection should accompany the giving of each token. This would have the effect of
minimising the child's reliance on material reward for positive reinforcement. The
ultimate aim is for the praise and affection to suffice for the postive reinforcement,
without any need for material rewards.
42
In the first two weeks of the programme there was no negative reinforcement used and in
some cases it was not used at all. Time —out (see section 2.2.2.5.) was introduced only if
and when the existing programme did not appear to be working. The time-out tool would
be additionally beneficial, in that the threat of this punishment would hopefully be an
effective warning to the child as soon as he or she begins to misbehave, not to perform
that behaviour. That is to say that the time-out could be used as a reminder and a warning
that the behaviour embarked on is not suitable and that it should immediately be stopped.
If and when time-out was not successful in bringing about any significant changes in the
child's behaviour, response cost interventions (see section 2.2.2.4.) would be introduced.
The child would have tokens taken away for severe misbehaviour, however the
implementation of this technique was seldomly used as it was rarely necessary.
Modelling (see section 2.2.2.6.) of appropriate behaviours was also used whenever the
children misbehaved. The mothers were trained to role play with the child so that the
child could learn the required skills.
In addition, some children were trained by their mothers in some cognitive exercises such
as self-instruction (see section 2.2.3.2.) to assist with attention and concentration in
studying, excessive talking and impulsive responding.
Finally, it should be noted that the programme did not provide therapeutic support for the
emotional difficulties experienced within the family as a result of the child's ADHD,
43
neither did it supply much educational information to the parents about the disorder. For
these reasons a booklet (see appendix A) dealing with these aspects was provided to those
parents requiring assistance in these issues.
3. 5. Experimental Methodology.
The first stage in the experimental component of the study was the obtaining of
volunteers to participate in the programme (see section 3.2.). All volunteers were asked to
complete the DuPaul (1991) rating scale (see section 3.4.) in order to evaluate the extent
of the children's behavioural problems. The children who did not meet the diagnostic
criteria for ADHD were excluded from the samples. The remaining volunteers who did
met the criteria were selected to form the samples for the study. The completed rating
scales of those selected were to serve as pretests.
The selected candidates were divided into two groups (see section 3.2.), the experimental
and the control group. The experimental group were trained to implement the cognitive-
behavioural programme directed at reducing the behavioural disinhibition of the children.
The control group received no intervention at all.
After the intervention was completed for the experimental group, all participants,
including those in the control group, were asked to complete the rating scale again for the
purpose of obtaining posttest results.
44
Thr duration of treatment was usually six weeks, except in the case of one mother who
failed to comply with the recommendations in the beginning and therefore required a
duration of about nine weeks. All subjects within the control group were evaluated for the
posttest six weeks after completing their first rating scale. It should further be noted that
not all subjects receievd their treatment concurrently.
Finally, the pretest and posttest scores for each group were analysed and compared
through a number of statistical procedures, which will be discussed in the following
section.
45
Volunteers Fig. 3.4. Depicting a flow chart of the
experimental methodology employed.
4.
Screening for ADHD by Those who did not meet the
the use of the Pretest criteria for a diagnosis of
--• ADHD were excluded from
the study.
4. 1
Control
Experimental Group
Group
4,
Intervention No
Intervention
Nz Posttest
46
3.6. Statistical Procedures
The aim of the study was to determine whether the intervention resulted in any significant
behavioural improvements in the children in the experimental group. This was done by
comparing the results of the rating scales of the experimental group and the control group
at the pretest and posttest stages.
Between—groups and within groups' designs were employed for the statistical analysis.
The use of the between-groups' designs allowed for the evaluation of significant
differences between the pretest and posttest scores for the total sample on each item of
the rating scale. The Kruskal-Wallis, Mann-Whitney and t-Test were used for the
between-groups anlysis.
The within-groups' designs were used to determine whether there were any significant
improvements on any of the two scales measured by the DuPaul (1991) rating scale
between the pretest and posttests for each group. The two scales considered were
inattentiveness and impulsivity. The t-Test was used for this purpose and it evaluated
both independent and paired samples.
The results of these procedures will be discussed in the following chapter.
47
Chapter 4: Results.
4.1. Introduction to results.
The aim of this study is to determine whether psychological treatment and specifically,
cognitive-behavioural interventions aiming to reduce behavioural disinhibition, would
have any beneficial effect on ADHD children.
The statistics that follow will examine the differences between the experimental group
who received the intervention and the control group who received no intervention at all.
This analysis will evaluate the differences between the two groups at both the pretest and
posttest stages, as well as evaluating each group separately at the these stages. Therefore
between groups and within groups designs will be considered.

- -
It should be noted that the DuPaul (1991) rating scale (see appendix B) measures the
extent of behavioural problems associated with ADHD on a continuum from zero to
three. A score of zero indicates that the behavioural problem is absent and a score of
three indicates that it is very much present. Scores of one and two indicate that the extent
of the behavioural problems lie between these extremes. Therefore the lower the score on
an item of the rating scale, the less severe that behavioural problem is.
Finally, please note that in the tables that follow, where groups 1 and 2 are mentioned,
they refer to the experimental and the control group respectively.
48
4.2. Descriptive Statistics
4.2.1. Frequencies of responses on the DuPaul ADHD rating scale (1991).
Table 4.1. Pretest Frequency Table for Total Sample
Scores
Item 0 % 1 % 2 % 3 %
Inattention 0 0 3 37.5 4 50 1 12.5
2
Inattention 12.5 1 12.5 3 37.5 3 37.5
3
Inattention 0 0 1 12.5 3 37.5 4 50
4
Impulsivity 12.5 3 37.5 3 37.5 1 12.5
Impulsivity 0 0 1 12.5 5 62.5 2 25
6
Inattention 0 4 50 2 25 2 25
7
Inattention 1 12.5 3 37.5 0 0 4 50
8
Inattention 25 3 37.5 0 0 3 37.5
9
Impulsivity 25 1 12.5 3 37.5 2 25
10
Impulsivity 0 0 0 5 62.5 3 37.5
i-i
Impulsivity 0 0 1 12.5 4 50 3 37.5
12
Inattention 25 0 0 2 25 4 50
Inattention 2 25 3 37.5 1 12.5 2 25
Impulsivity 3 37.5 1 12.5 1 12.5 3 37.5
49
Table 4.2. Posttest Frequency Table for Total Sample
Scores
Item 0 %
Yo 1 % 2 % 3 %
1
Inattention 0 0 0 0 2 25 6 75
2
Inattention 1 12.5 2 25 4 50 1 12.5
3
Inattention 1 12.5 0 0 4 50 3 37.5
4
Impulsivity 3 37.5 3 37.5 2 25 0 0
Impulsivity 0 0 3 37.5 2 25 3 37.5
6
Inattention 1 12.5 5 62.5 1 12.5 1 12.5
7
Inattention 1 12.5 5 62.5 0 0 2 25
Inattention 3 37.5 2 25 2 25 1 12.5
9
Impulsivity 4 50 1 12.5 1 12.5 2 25
10
Im p ulsivity 0 0 2 25 2 25 4 50
11
Impulsivity 0 0 4 50 2 12.5 2 12.5
12
Inattention 0 0 6 75 0 0 2 25
::attention 2 25 4 50 0 0 2 25
14
I m pulsivity 3 37.5 3 37.5 1 12.5 1 12.5
Through examining the differences between the pretest and posttest frequency tables, a
shift in the spread of responses on most items of the rating scale is clearly evident. In all
items, with the exception of item 1, there was a reduction in the frequency of responses
on the higher scores from the pretest stage to the posttest stage. This potentially indicates
that there was an overall reduction in behavioural problems for the total group.
50
Table 4.3. Pretest mean and standard deviation scores for items on the DuPaul (1991)
rating scale for the Total Group.
Item NNalid Mean Std. Deviation

1-Inattention 8 1.750 0.707
4- Impulsivity 8 1.500 0.926
5-Impulsivity 8 2.125 0.641
10-Impulsivity 8 2.375 0.518
11-Impulsivity 8 2.250 0.707
12-Inattention 8 2.000 0.926
13-Inattention 8 1.375 1.188
14-Impulsivity 8 1.500 1.414
Table 4.4. Posttest mean and standard deviation scores for items on the DuPaul (1991)
rating scale for the Total Group.
Item NNalid Mean Std. Deviation

4- Impulsivity 8 0.875 0.835
10-Impulsivity 8 2.250 0.886
11-Impulsivity 8 1.750 0.886
12-Inattention 8 1.500 0.926
13-Inattention 8 1.250 1.165
14-Impulsivity 8 1.000 1.069
51
Figure 4.1. Comparison between pretest and posttest means
Series 1 are the pretest scores.

Series 2 are the posttest scores.
These results indicate that on average there is an overall (the experimental and control
groups combined) reduction in posttest scores for all items, except for item 1 which
remained the same. This implies that potentially there was an overall improvement in the
children's behaviours following the intervention. However the statistical significance of
these results remains to be established.
52
4.3. Inferential Statistics.
The statistics that follow will examine the differences between the experimental and
control groups at the pretest stage and at the posttest stage, as well as those differences
within each group between the pretest and posttest stages
4.3.1. Kruskal-Wallis Test.
Table 4.5. Pretest mean ranks of responses on the DuPaul (1991) rating scale.
Item Group N Mean Rank

1-Inattention 1 5 4.6
2 3 4.33
2 3 3.33
2 3 5.33
4- Impulsivity 1 5 4.80
2 3 4.00
5-Impulsivity 1 5 4.80
2 3 4.00
2 3 5.83
2 3 5.33
2 3 6.00
2 3 5.50
2 3 5.67
2 3 5.00
2 3 4.83
2 3 5.17
2 3 5.33
53
Table 4.6. Posttest mean ranks of responses on the DuPaul (1991) rating scale.
Item Group N Mean Rank

2 3 4.17
2 3 6.33
2 3 4.67
4- Impulsivity 1 5 3.70
2 3 5.83
2 3 6.17
2 3 6.33
2 3 6.33
2 3 6.33
2 3 5.83
2 3 4.83
2 3 5.83
2 3 6.17
2 3 6.50
2 3 6.00
The mean rank reflects the average score obtained on the item. The higher the average
score, the higher the mean rank will be.
The mean ranks for the experimental group were lower at the posttest than they were at
the pretest stage for all items, with the exception of items 1, 3 and 10. This is indicative
of an overall reduction in the scores for most items, after the intervention had taken place.
54
Table 4.7. Chi-Square of each item of the pretest for the total group.
Item Chi-Square Df Asymp. Sig

1-Inattention 0.027 1 0.870
4- Impulsivity 0.221 1 0.638
5-Impulsivity 0.267 1 0.606
10-Impulsivity 1.524 1 0.217
11-Impulsivity 0.240 1 0.624
12-Inattention 0.104 1 0.747
13-Inattention 0.383 1 0.536
14-Impulsivity 0.614 1 0.433
Table 4.8. Chi-Square of each item of the posttest for the total group.
Item Chi-Square Df Asymp. Sig

3-Inattention 0.027* 1 0.870
4- Impulsivity 1.593 1 0.207
6-Inattention 3.529 1 . 0.060
10-Impulsivity 0.104 1 0.747
11-Impulsivity 1.659 1 0.198
12-Inattention 3.889 1 0.049*
13-Inattention 3.733 1 0.053
14-Impulsivity 1.989 1 0.158
There are two important results from this test. Firstly, in the pretest the experimental
group scored significantly lower than the control group on item 1, which is one of the
* Denotes significant at P < or = 0.05
55
items that measures inattention. This may indicate that the experimental group already
had significantly less behavioural difficulties associated with item 1 than did the control
group. Secondly, and more importantly there was a significant improvement in item 3
and in item 12 on the posttest of the experimental group indicating an improvement in
attention for the latter group.
4.3.2. Mann-Whitney Test.
Table. 4.9. Pretest mean ranks of responses on the DuPaul (1991) rating scale.
Item Group Number Mean Rank Sum of Ranks

1-Inattention 1 5 4.60 23.00
2 3 4.33 13.00
2-Inattention 1 5 5.20 26.00
2 3 3.33 10.00
3-Inattention 1 5 4.00 20.00
2 3 5.33 16.00
4- Impulsivity 1 5 4.80 24.00
2 3 4.00 12.00
5-Impulsivity 1 5 4.80 24.00
2 3 4.00 12.00
6-Inattention 1 5 3.70 18.50
2 3 5.83 17.50
7-Inattention 1 5 4.00 20.00
2 3 5.33 16.00
8-Inattention 1 5 3.60 18.00
2 3 6.00 18.00
9-Impulsivity 1 5 3.90 19.50
2 3 5.50 16.50
10-Impulsivity 1 5 3.80 19.00
2 3 5.67 17.00
11-Impulsivity 1 5 4.20 21.00
2 3 5.00 15.00
12-Inattention 1 5 4.30 21.50
2 3 4.83 14.50
13-Inattention 1 5 4.10 20.50
2 3 5.17 15.50
14-Impulsivity 1 5 4.00 20.00
2 3 5.33 16.00
56
Table. 4.10. Posttest mean ranks of responses on the DuPaul (1991) rating scale.
Item Group Number Mean Rank Sum of Ranks

1-Inattention 1 5 4.70 23.50
2 3 4.17 12.50
2-Inattention 1 5 3.40 17.00
2 3 6.33 19.00
3-Inattention 1 5 4.40 22.00
2 3 4.67 14.00
4- Impulsivity 1 5 3.70 18.50
2 3 5.83 17.50
5-Impulsivity 1 5 3.50 17.50
2 3 6.17 18.50
6-Inattention 1 5 3.40 17.00
2 3 6.33 19.00
7-Inattention 1 5 3.40 17.00
2 3 6.33 19.00
8-Inattention 1 5 3.40 17.00
2 3 6.33 19.00
9-Impulsivity 1 5 3.70 18.50
2 3 5.83 17.50
10-Impulsivity 1 5 4.30 21.50
2 3 4.83 14.50
11-Impulsivity 1 5 3.70 18.50
2 3 5.83 • 17.50
12-Inattention 1 5 3.50 17.50
2 3 6.17 18.50
13-Inattention 1 5 3.30 16.50
2 3 6.50 19.50
14-Impulsivity 1 5 3.60 18.00
2 3 6.00 18.00
Tables 4.9 and 4.10 replicate the findings of tables 4.5 and 4.6, but in addition they
describe the sum of ranks of each item for each group.
The comparison of the sum of ranks for the experimental group at the prestest and
Posttest stages show that there was a decrease in most scores after the intervention. Items
57
1, 3 and 10 were again the exception, showing an overall increase in scores for these
items. The reciprocal pattern is evident for the control group, indicating a general
increase in scores at the Posttest stage, with the exception of the items mentioned above.
Table 4.11. Mann-Whitney test statistics of the pretest scores for the total group.
Item Mann- Wilcoxon Z Asymp. Exact Sig.

Whitney U W Sig. (2- [2*(1-tailed
tailed) Sig.)]
1-Inattention 7.000 13.000 -0.163 0.870 1.000
2-Inattention 4.000 10.000 -1.097 0.273 0.393
3-Inattention 5.000 20.000 -1.759 0.079 0.143
4- Impulsivity 6.000 12.000 -0.470 0.638 0.786
5-Impulsivity 6.000 12.000 -0.516 0.606 0.786
6-Inattention 3.500 18.500 -1.288 0.198 0.250
7-Inattention 5.000 20.000 -0.816 0.414 0.571
8-Inattention 3.000 18.000 -1.420 0.156 0.250
9-Impulsivity 4.500 19.500 -0.928 0.353 0.393
10-Impulsivity 4.000 19.000 -1.235 0.217 0.393
II-Impulsivity 6.000 21.000 -0.490 0.624 0.786
12-Inattention 6.500 21.500 -0.322 0.747 0.786
13-Inattention 5.500 20.500 0.619 0.536 0.571
14-Impulsivity 5.000 20.000 -0.784 0.433 0.571
58
Table 4.12. Mann-Whitney test statistics of the posttest scores for the total group.
Item Mann- Wilcoxon Z Asymp. Exact Sig.

Whitney U W Sig. (2- [2*(1-tailed
tailed) Sig.)]
1-Inattention 6.500 12.500 -0.394 0.693 0.786
2-Inattention 2.000 ' 17.000 -1.759 0.079 0.143
3-Inattention 7.000 22.000 -0.163 0.870 1.000
4- Impulsivity 3.500 18.500 -1.262 0.207 0.250
5-Impulsivity 2.500 17.500 -1.578 0.115 0.143
6-Inattention 2.000 17.000 -1.879 0.060 0.143
7-Inattention 2.000 17.000 -1.893 0.058 0.143
8-Inattention 2.000 17.000 -1.702 0.089 0.143
9-Impulsivity 3.500 18.500 -1.297 0.201 0.250
10-Impulsivity 6.500 21.500 -0.322 0.747 0.786
11-Impulsivity 3.500 18.500 -1.288 0.198 0.250
12-Inattention 2.500 17.500 -1.972 0.049* 0.143
13-Inattention 1.500 16.500 -1.932 0.053 0.71
14-Impulsivity 3.000 18.000 -1.410 0.158 0.250
These results show some improvements on a number of items (6, 7 and 13), however the
only significant improvement was found on item 12, which is a measure of inattention.
Denotes significant at P < or = 0.05
59
4.3.3. t-Test
Table 4.13. Mean and standard deviation for the Total Group.
Items Test Group N Mean Std. Dev. Std. Error
1-Inattention Pre 1 5 1.800 0.837 0.374

2 3 1.667 0.577 0.333
Post 1 5 1.800 0.447 0.200
2 3 1.667 0.577 0.333
2-Inattention Pre 1 5 2.200 1.304 0.583
2 3 1.667 0.577 0.333
Post 1 5 1.200 0.837 0374
2 3 2333 0.577 0.333
3-Inattention Pre 1 5 2.200 0.837 0374
2 3 2.667 0.577 0333
Post 1 5 2.000 1.225 0.548
2 3 2333 0.577 0333
4-Impulsivity Pre 1 5 1.600 1.140 0.510
2 3 1.333 0.577 0333
Post 1 5 0.600 0.894 0.400
2 3 1333 0.577 0333
5-Impulsivity Pre 1 5 2.200 0.837 0374
2 3 2.000 0.000 0.000
Post 1 5 1.600 0.894 0.400
2 3 2.667 0.577 0333
6-Inattention Pre 1 5 1.400 0.548 0.245
2 3 2333 1.155 0.667
Post 1 5 0.800 0.447 0.200
2 3 2.000 1.000 0.577
7-Inattention Pre 1 5 1.600 1342 0.600
2 3 2333 1.155 0.667
Post 1 5 0.800 0.447 0.200
2 3 2333 1.155 0.667
8-Inattention Pre 1 5 1.000 1.225 0.548
2 3 2333 1.155 0.667
Post 1 5 0.600 0.894 0.400
2 3 2.000 1.000 0.577
9-Impulsivity Pre 1 5 1.400 0.894 0.400
2 3 2.000 1.732 1.000
Post 1 5 0.600 0.894 0.400
2 3 2.000 1.732 1.000
l0-Impulsivity Pre 1 5 2.200 0.447 0.200
2 3 2.667 0.577 0333
Post 1 5 2.200 0.837 0374
2 3 2333 1.155 0.667
11-Impulsivity Pre 1 5 2.200 0.447 0.200
2 3 2333 1.155 0.667
Post 1 5 1.400 0.548 0.245
2 3 2333 1.155 0.667
12-Inattention Pre 1 5 2.000 1.225 0.548
2 3 2.000 1.732 1.000
Post 1 5 1.000 0.000 0.000
2 3 2333 1.155 0.667
13-Inattention Pre 1 5 1.200 1304 0.583
2 3 1.667 1.155 0.667
Post 1 5 0.600 0.548 0.245
2 3 2333 1.155 0.667
14-Impulsivity Pre 1 5 1.200 1.643 0.735
2 3 2.000 1.000 0.577
Post 1 5 0.600 0.894 0.400
2 3 1.667 1.155 0.667
60
Table 4.13. shows that the mean scores on each item were reduced in the experimental
group at the Posttest stage, except for items 1 and 10, in which the mean scores remained
the same.
The changes in the mean scores for the control group from the pretest stage to the posttest
stage was somewhat random. Some scores were reduced, some increased and others
remained the same.
4.3.3.1. Paired Samples, Within Groups comparison of inattention and

impulsivity.
Table 4.14. Paired Sample Descriptive Statistics for the experimental group.
Pair Pre/Post Mean N Std. Std. Error

Test Deviation Mean
Pair 1 Pretest 13.400 5 6.656 2.997
Inattention Posttest 8.800 5 3.114 1.393
Pair 2 Pretest 10.800 5 3.033 1.356
Impulsivity Posttest 7.000 5 3.808 1.703
These results indicate that the mean scores for the experimental group were improved on
the scales of inattention and impulsivity between the pretest and posttest stages. However
the statistical significance of these results remains to be determined.
Table 4.15. Paired Sample Test for the experiemental group.
df Sig. (2-tailed)
Pair 1
Inattention: Pretest-Posttest 4 0.140
Pair 2
Impulsivity: Pretest-Posttest 4 0.007*
61
The results in table 4.15. indicate that only the improvement in impulsivity, found in
table 4.14. is statistically significant. Therefore it can be asserted with confidence that
there was an improvement in impulsivity for the experimental group following the
intervention.
Table 4.16. Paired Sample Descriptive Statistics for the control group.
Pair Pre/Post Mean N Std. Std. Error

Test Deviation Mean
Pair 1 Pretest 16.667 3 5.774 3.333
Inattention Posttest 17.333 6.028 3.480
Pair 2 Pretest 12.333 3 3.055 1.764
Impulsivity Posttest 12.333 5.686 3.283
Table 4.16. indicates that for the control group there was a deterioration in attention at the
time of the posttest compared to the pretest stage. However the average level of
impulsivity remained the same.
Table 4.17. Paired Sample Test for the control group.
Df Sig. (2-tailed)
Pair 1
Inattention: Pretest-Posttest 2 0.691
Pair 2
Impulsivity: Pretest-Posttest 2 1.000
Table 4.17. indicates that the deterioration in attention for the control group described in
table 4.16. is not statistically significant.
62
Figure 4.2. Graph comparing means of pretest and posttest scores on impulsivity and
inattention of the experimental and control groups.
20
-0-Ctrl. °nett.)
15
=C=Ctrl.
(
(Impuls.)
10
mr_ImExp. (Inatt.)
5
(Impuls.)
0
Pretest Postest
These results clearly show an improvement in both inattention and impulsivity for the
experimental group. The improvement in impulsiveness is statistically significant as
shown above, however the improvement in inattention is non-significant.
4.3.3.2. Independent Samples Test of each item for the total group.
Table 4.18. t-Test for equality of means at the pretest stage.
t-Test for equality of means
Items t df Sig Mean

(2-tailed) Difference
1-Inattention Equal variances assumed 0.240 6 0.818 0.133
Equal variances not assumed 0.266 5.695 0.800 0.133
2 - Inattention Equal variances assumed 0.655 6 0.537 0.533
3- Inattention Equal variance assumed -0.841 6 0.433 -0.467
Equal variance not assumed -0.931 5.695 0.389 -0.467
4- Impulsivity Equal variance assumed 0.369 6 0.725 0.267
Equal variance not assumed 0.438 5.969 0.677 0.267
5-Impulsivity Equal variance assumed 0.401 6 0.702 0.200
6-Inattention Equal variance assumed -1.592 6 0.162 -0.933
9-Impulsivity Equal variance assumed -0.663 6 0.532 -0.600
12-Inattention Equal variance assumed 0.000 6 1.000 0.000
63
Table 4.18. indicates that there were no statistically significant differences between the
experimental and control groups on any items at the pretest stage.
Table 4.19. t-Test for equality of means at the posttest stage.
t-Test for equality of means
Items t df Sig Mean

(2-tailed) Difference
1-Inattention Equal variances assumed 0.369 6 0.725 0.133
2-Inattention Equal variances assumed -2.042 6 0.087 -1.133
Equal variances not assumed -2.262 5.695 0.067 -1.133
4- Impulsivity Equal variance assumed -1.251 6 0.258 -0.733
7-Inattention Equal variance assumed -2.762 6 0.033' -1.533
12-Inattention Equal variance assumed -2.739 6 0.034' -1.333
13-Inattention Equal variance assumed -2.957 6 0.025* -1.773
These results indicate significant improvements in items 7, 12 and 13, which are all
measures of inattention at the posttest stage.
* Denotes significant at P < or =0.05
64
4.3.3.3. Independent Samples, comparison of the subscales of
inattention and impulsivity.
Table 4.20. Descriptive Statistics
Test Group N Mean Std. Std.

Deviation Error
Mean
Pretest 1 5 13.400 6.656 2.977
Inattention 2 3 16.667 5.774 3.333
Posttest 1 5 8.800 3.114 1.393
2 3 17.333 6.028 3.480
Pretest 1 5 10.800 3.033 1.356
Impulsivity 2 3 12.333 3.055 1.764
Posttest 1 5 7.000 3.808 1.703
2 3 12.333 5.686 3.283
Table 4.20. shows an improvement in the mean scores on inattention and impulsivity for
the experimental group at the posttest stage.
The mean scores for the control group show a deterioration in attention at the posttest
stage, whereas impulsivity remained the same.
Table 4.21. Levene's test for equality of variances.
Levene's Test for Equality of

Variances
F Sig.
Pretest Equal Variances 0,012 0.918
Inattention assumed
Posttest Equal Variances 1.344 0.290
assumed
Pretest Equal Variances 0.000 0.988
Impulsivity assumed
Posttest Equal Variances 0.654 0.450
assumed
Table 4.21. indicates that the results suggested in table 4.20. were found to be non-
significant.
65
Table 4.22. t-Test for equality of means.
t-Test for Equality of Means

95% Confidence Interval of
the Difference
Std. Error Lower Upper
Difference
Pretest Equal Variances
assumed
4,656 -14.659 8.126
Equal Variances 4.469 -14.823 8.290
not
ot assumed
Posttest Equal Variances
assumed
3.148 -16.236 -0.831
Equal Variance 3.748 -21.380 4.313
not assumed
Pretest Equal Variances 2.220 -6.967 3.900
assumed
Impulsivity - not assumed
Posttest Equal Variances 3.302 -13.413 2.747
assumed
not assumedb
t-Test for Equality of Means

t df Sig. Mean
(2- Difference
tailed)
Pretest Equal Variances assumed -0.702 6 0.509 -3.267
Equal Variances not
assumed -0.731 4.903 0.498 -3.267
Inattention Equal Variances assumed
Posttest Equal Variance not
-2.711 6 0.035* -8.533
assumed -2.276 2.658 0.119 -8.533
Pretest Equal Variances assumed -0.691 6 0.516 -1.533
Equal Variances not
assumed -0.689 4.311 0.526 -1.533
Impulsivity Equal Variances assumed
Posttest Equal Variances not
-1.615 6 0.157 -5.333
assumedb 4.442 3.109 0.242 -5.333
These results indicate that there was a significant overall improvement in inattention after
the intervention. Therefore it can be asserted with confidence that there was an
improvement in attention after the intervention.
66
4.4. Summary of significant results.
Thus far, many speculations and conclusions have been discussed, however in order to
maintain the scientific integrity of this paper, it is important to focus only on the
statistically significant results obtained in the analysis. The following is a description of
these significant findings.
In terms of the individual items on the rating scale , statistically significant improvements
were found on item 3 and item 12 for the experimental group. These items are both
measures of inattention.
The analysis of the two scales of impulsivity and inattentiveness, which incorporate and
combine all the items on the scale that measures these constructs, show significant
improvements in both inattention and impulsivity for the experimental group.
There were no significant improvements found for the control group at the posttest stage.
This implies that the intervention had the effect of reducing impulsivity and
inattentiveness in the experimental group.
67
Chapter 5
5.1. Discussion and conclusion
The statistics in the previous chapter show that the Cognitive-Behavioural Parent
Training Programme aimed at improving behavioural inhibition resulted in a significant
improvement in inattention and impulsivity. These results are somewhat different from
previous research in that Cognitive-Behavioural treatment is usually effective in
improving impulsivity and not inattentiveness (Kendall & Panichelli-Mindel, 1995;
Cocciarella et al., 1995).
The results of the present research are to some extent similair to the effects that the
stimulants have on children with ADHD. The stimulants also have the effect of
improving both impulsivity and inattentiveness of ADHD children, among other
symptoms (Spencer et al., 1996; Anastopoulos et al., 1991).
These results give rise to questioning how this programme is different from previous
psychosocial interventions and more specifically Cognitive-Behavioural treatments.
On a practical level, this programme differs from regular Cognitive-Behavioural
approaches in that it used the Cognitive-Behavioural techniques toward improving
behavioural inhibition, rather than attempting to improve attention and impulsivity
directly. The premise was that through an improvement in behavioural inhibition there
would be a secondary reduction in inattentiveness and impulsivity. This is what is
believed to have occurred in the present research.
68
On a more theoretical level, the results are fairly consistent with Barkley's (1997) theory
of behavioural inhibition discussed in chapter two. Barkley (1997) argues that
behavioural inhibition is the central impairment in ADHD and it is to some extent
localised in the orbital-frontal region of the brain. Furthermore Barkley (1997) argues
that if behavioural disinhibition is reduced there will be an improvement in all other
ADHD symptoms. This theory could explain how the present results are largely similair
to those obtained by the stimulants. It is known that the stimulants increase activity in the
orbital-frontal regions of the brain (Anastopoulos et al, 1991; Barkley, 1995), the same
area that is believed to control behavioural inhibition. This implies that the present
programme stimulated the same area of the brain that the stimulants do.
This finding would have very significant ramifications for the treatment of ADHD, in that
it indicates that psychosocial interventions may be able to replicate the results obtained
by the stimulants. However there is a need to be very cautious in coming to this
conclusion. Firstly, there is no indication that the improvement in inattentiveness and the
reduction in impulsivity obtained in this research are as significant as those obtained by
the stimulants. Secondly, in this study most of the children were already taking Ritalin,
albeit for some time, and there is no knowledge of what role this played in the reduction
of these symptoms. Perhaps the Ritalin helped the children reach an adequate level of
functioning, beyond which they would not be able to comply with the cognitive-
behavioural programme.
69
It would be amiss not to cite and explain the original theorist on behavioural inhibition,
that is Gray (1985) and the follow-up work of this theory as it pertains to ADHD by Quay
(1997). The results of the present research lend support to these theories and greater
insight into these results can be obtained through the understanding of these theories.
Gray (1985) draws attention to three independent but interrelated systems within the
brain. The first is the fight/flight system, which responds to unconditioned pain and
punishment to produce fight or flight. The second and third systems are motivational
systems that mediate the effect of conditioned stimuli on behaviour (Fowles, 1993).
These latter two are of importance in the context of the present research.
The second system is an appetitive, reward-seeking or approach system, which responds
to positive incentives by activating behaviour and is called a "behavioural activation
system" (Fowles, 1993). This is abbreviated as BAS.
The third system is the most important for this research, as it pertains to ADHD. This
system is called the "behavioural inhibition system" or the BIS, and it inhibits behaviour
in the presence of conditioned stimuli that indicate that aversive consequences would
occur (Fowles, 1993).
In order to understand how this theory works it is necessary to consider four basic
paradigms (Fowles, 1993).
70
The first paradigm is a simple reward-learning paradigm with 100% reinforcement. In
this situation stimuli associated with reward (Rew-CS) exert their control over behavior
via the BAS. That is the BAS activates reward-seeking behaviour in response to Rew-
CSs.
The second paradigm is obtained by transforming the reward-learning situation into an
approach avoidance conflict by the introduction of response-contingent punishment,

-
once the reward response has been established. This introduction of punishment in
addition to the reward results in a reduction in the rate or a reduction in the probability of
responding. This is called passive avoidance. This is attributed to the inhibition of the
approach response by the BIS in response to conditioned stimuli for punishment (Pun-
CSs). Therefore it can be seen that the BIS and BAS are in opposition to each other. The
BAS tends to activate approach behaviour in response to Rew-CSs and the BIS tends to
inhibit these responses in the face of Pun-CSs. Whether an approach response will occur
will depend on which system is dominant, which in turn is influenced by the relative
strength of the Rew-CS and Pun-CS inputs.
A similar mutual antagonism between the two systems is found in the third paradigm,
that of extinction. In this case it is assumed that the non-occurrence of an expected
reward produces frustration, which is functionally equivalent to punishment as far as the
BIS is concerned. Stimuli in the extinction situation, then become conditioned stimuli for
71
frustrative nonreward ( Rew-CSs), which activate the BIS with a subsequent inhibition
of the approach response.
The fourth and final paradigm is the one-way active-avoidance task, in which a
conditioned stimulus is presented for several seconds prior to the onset of a shock. The
animal receives the shock if it does nothing, but if it makes a response during the
conditioned stimulus that takes it out of the compartment, it can avoid the shock
altogether. The avoidance response is maintained by the nonoccurrence of an expected
punishment, the functional equivalent of a reward. Consequently, the avoidance response
is activated by the BAS, in response to conditioned stimuli for relieving nonpunishment
( Pun-CSs).
It must be noted that if behaviour is activated, the BAS is involved, if behaviour is
inhibited the BIS is involved. In addition, which system is involved depends on the
appetitive or aversive nature of the unconditioned stimulus.
Gray (Fowles, 1993) offered four terms to refer to the emotional or motivational state
induced by each of these conditioned stimuli. The two aversive motivational states are
called "frustration" (for Rew-CSs) and "fear" or "anxiety" (for Pun-CSs). The two
appetitive motivational states are called "hope" (for Rew-CSs) and relief (for Pun-CSs).
Therefore it is postulated that the BIS responds to conditioned stimuli for punishment and
non-reward, to bring about passive avoidance and extinction (Quay, 1997). Its output
72
results in the ceasing of ongoing behaviour (Quay, 1997). The present programme made
use of techniques such as reinforcement, response-cost and time-out, which according to
this theory served as conditioned stimuli for punishment and non-reward, thereby
enhancing behavioural inhibition.
Gray argued that the BIS is essentially an anxiety system and that anxiety has an
inhibitory effect on behaviour (Fowles, 1993). Indeed it has been found that the use of
antianxiety drugs results in a reduction in the effectiveness of the BIS in inhibiting
behaviour (Fowles, 1993; Quay, 1997) and perhaps this is the reason that such drugs are
contraindicated in ADHD. Quay (1988) proposed that an overactive BIS underlies
anxiety disorders, whereas an underactive BIS characterises ADHD.
In reference to ADHD, Quay (1997) notes that it is the fight/flight system that responds
to unconditioned pain or punishment and an underresponsive behavioural inhibition
system would not serve to impair responses to unconditioned punishment. Therefore it is
not that ADHD children do not respond to punishment but it is that they are less
responsive to conditioned stimuli, indicating that punishment or non-reward is likely to
be contingent on their making a particular response.
Gray (Fowles, 1993) argues that the anatomical location for the BIS is in the septo-
hippocampal system (part of the Limbic system, see figure 5.1.) and its connections to the
frontal cortex (Quay, 1997). However Quay (1997) argues that the septo-hippocampal
system cannot be directly implicated.
73
Despite the uncertainty surrounding the precise anatomical location of this system, the
stimulants which act on the limbic system, striatum and orbital cortex, lower the
threshold of sensitivity to reinforcement (Anastopoulos et al., 1991). This prolongs
responding under conditions that previously would have led to behavioural extinction,
which ultimately results in a reduction in the symptoms of ADHD (Anastopoulos et al.,
1991).
Fig. 5.1. Depicting the Septo-hippocampal region. (Kolb & Whishaw, 1996).
To sum-up thus far, there is strong evidence indicating that behavioural disinhibition is a
core characteristic of ADHD and furthermore this deficit in inhibition is likely to be
responsible for the main symptoms of inattention and impulsiveness.
It is known that the stimulants and more specifically, methylphenidate produce a decrease
in behavioural disinhibition as well as a reduction in inattention and impulsive behaviour
(Anastopoulos et al., 1991). Furthermore, the present research as well as previous
research (Barkley, 1997; Quay, 1997) indicate that psychological interventions can also
74
bring about changes in behavioural disinhibition. According to the Quay/Gray model
(Fowles, 1993; Quay, 1997) the BIS responds to conditioned stimuli associated with
punishment as well as those stimuli associated with the frustration of not receiving a
reward.
Therefore in conclusion, the present research supports the theory of Barkley (1997) and
the Quay/Gray model (Fowles, 1993; Quay, 1997) of behavioural disinhibition as it
pertains to ADHD. Furthermore the study supports both hypotheses predicted in the
research. Firstly, that psychological interventions can offer a positive contribution to the
treatment of ADHD and secondly, cognitive-behavioural parent-training programmes
aimed at reducing disinhibition in ADHD children contribute toward a reduction of the
main symptoms of the disorder.
5.2. Implications for further research.
There are a number of interesting and potentially significant questions that result from
this research.
Firstly, the sizes of the samples in the study were very small, implying that these results
are at best tentative. A further study using larger samples would be required to verify
these results.
Secondly, it would be beneficial from a clinical perspective to investigate what role, if
any, Ritalin played in this research. It is highly likely that in the absence of such
75
medication, the children concerned would be unable to participate adequately in the
programme. This investigation would require a study that compares the effects of the
intervention on children with ADHD taking medication with those who do not.
Thirdly, a long-term follow up of these children would be valuable, in that a common
complaint is that ADHD children revert to baseline behaviour at the termination of
treatment (Barkley, 1990). Furthermore such a study would give insight into the duration
of the intervention time required for maximum effectiveness.
Fourthly, since ADHD is such a genetically loaded disorder (see section 2.1.) there is a
relatively high probability that at least one of the child's parents also suffers from the
disorder. It would be useful to know if the structure the programme provides to these
parents is of any direct benefit to them with respect to their parenting roles.
Finally, it may prove valuable to investigate whether this programme could be adapted
for teachers to implement within the school environment.
76
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Appendix A
ADHD
Information Booklet
Introduction to ADHD.
What causes ADHD?
The role of psychosocial factors and the environment in ADHD.
The Challenge for parents.
Common treatments of ADHD.
Conclusion.
92
1. Introduction to ADHD.
Symptoms associated with Attention Deficit Hyperactivity Disorder (hereafter referred
to as ADHD) affect between 3% to 5% of school-age children (Cotugno, 1995).
Current figures estimate the number of people with ADHD at over two million
school-age children and this is a conservative estimate (Barkley, 1995). The disorder
is far more common in boys than it is in girls (Bhatia, 1991).
The typical time of onset of ADHD is before the age of seven (Barkley, 1997) and it is
not a disorder that will be simply outgrown (Barkley, 1995). It is a developmental
disorder of self-control, consisting of problems with attention span, impulse control
and activity level (Bennett et al., 1996). The results of these symptoms include an
impairment in a child's ability and even desire to control his or her behaviour in terms
of future goals and consequences . (Barkley, 1995). For most people a test is a goal,
which motivates them to study (the behaviour), however ADHD children are often
unable to behave appropriately (in this case study) toward achieving this goal. This
difficult in regulating their own behaviour extends to many other dimensions in their
lives, including social relationships.
Parents of ADHD children often report very similar stories about their situations and
experiences associated with their ADHD child. There is clearly something wrong with
their child's behaviour and these parents feel frustrated and confused about what is
causing this to happen and what to do about it. Furthermore the child is not at peace
93
with him or her self or within the dynamics of the family. There is often much conflict
over chores, homework, and relations with siblings and behaviour at home and at
school.
Usually the ADHD child has few if any friends as other children will often avoid him
or her. In short the ADHD child is missing out on precious parts of his or her
childhood. Valuable years and experiences of childhood are being hampered by
something that cannot be seen but everyone knows that it is there.
The awareness of the child that he is not what he wants to be, that he cannot control
himself as well as others, that he is not achieving what he feels he should be, together
with the loneliness felt as a result of having few friends only serves to impact
negatively on the child's self-esteem.
Furthermore raising a child with ADHD can be incredibly challenging for any parent
and it often results in feelings of anger and disappointment toward the child. The
conflict between parents and their child further reinforces the already established
negative self -image of the child.
Parents know that if something is not done about these problems, their child will most
likely lead a troubled life of underachievement. ADHD is not just a temporary state
that will be outgrown nor is it a frustrating but normal phase of childhood (Barkley,
1995).
94
It is imperative that parents realise and acknowledge that ADHD is not caused by their
failure to discipline and control their child and most importantly, ADHD is not an
indication that the child is a bad or evil person.
It is easy to see why many people find it difficult to view ADHD as a disability like
deafness and blindness or other physical disabilities. ADHD children look normal.
There is no outward sign that there is something wrong with the child. However
ADHD is a real disorder that presents with real problems and it requires some form of
treatment.
95
2. What causes ADHD?
ADHD has a number of causes. Knowledge of these causes and of how they influence
the brain and behaviour has increased dramatically since the mid-1980's (Barkley,
1995).
It should be noted at the outset, just how difficult it is to produce direct scientific
proof that anything causes problems with human behaviour. To illustrate this Barkley
(1995) makes use of the following finding. Scientists believe that damage to the
frontal lobe of the brain may result in ADHD. However experiments required to verify
this claim directly would be impossible to do. It would require damaging children's
brains to see what happens, which no scientist would be allowed or be prepared to do.
Therefore scientists are often left searching for information that is highly suggestive of
a cause but may never be proven absolutely certain.
According to Russell Barkley (1995), the most probable causes for which there is
convincing evidence of association with ADHD can be divided into three groups:
I. Various agents that can lead to brain injury or abnormal brain development.
These agents include trauma to the brain, disease, fetal exposure to tobacco and
alcohol, and early exposure to high levels of lead.
At most 5% to 10% of ADHD children develop this disorder from circumstances
associated with the above. Although ADHD children tend to have more pregnancy or
birth complications than non-ADHD children (Bhatia et al., 1991) the evidence that
96
these complications caused any brain injury which in turn lead to ADHD is
inconclusive (Bhatia, 1991).
Findings of diminished activity in certain brain regions.
Many studies have measured brain activity in those with ADHD and have found it to
be lower in the orbital-frontal area of the brain.
Furthermore the more active brain regions are the more blood they require. In one
study it was found that ADHD children have less blood flow to the frontal areas,
particularly in the region of the Striatum, an area which is important in inhibiting
behaviour and sustaining attention. It is interesting to note that stimulant medications
like Ritalin have been found to increase blood flow to these underactive areas to near
normal levels in some ADHD children.
Some scientists have suggested that certain neurotransmitters, which are chemicals in
the brain that permit nerve cells to send information to other cells, are deficient in
people with ADHD. The evidence here seems to point to a possible problem in how
much dopamine and possibly norepinephrine is produced in the brains of those with
ADHD. This evidence remains promising but has not been proven.
III. Heredity.
Family-genetic, twin and adoption studies suggest a genetic origin for some forms of
this disorder (Spencer et al., 1996).
97
Scientists have found that if one twin has the symptoms of ADHD, the risk that the
other will have the disorder is as high as 80% to 90%.
The inherited factor is probably associated with the development of the frontal cortex
of the brain and the striatum. However this remains to be verified.
98
3. The role of psychosocial factors and the environment in ADHD.
The parents' roles are further complicated by the fact that the symptoms of ADHD,
change with the particular situation of the child, where the child is, what he or she is
asked to do and who must care for the child (Barkley, 1995).
Research indicates that ADHD children are less distinguishable from non-ADHD
children in less restrictive settings as well as when the tasks are less demanding (Mash
& Barkley, 1989). The practical implications of this research can be useful in that
parents are able to manipulate the environment and the tasks in ways that are suited to
the ADHD child. For example, parents can make the environment less restrictive by
allowing the child to do his or her homework in different places such as the garden.
Furthermore, by separating big tasks into a number of smaller tasks, less pressure will
be placed on the child.
There is further evidence that ADHD children do better in unfamiliar surroundings or
when the tasks are new (Barkley, 1995, Dulcan & Benson, 1997). Therefore it may be
beneficial to change the child's environment frequently by taking him or her to the
library to study, allowing him or her to study in different rooms within the house or
even by moving the desk to another part of the room. Furthermore colourful, highly
stimulating educational materials presented differently from the usual dry textbook or
workbook format may enhance performance. In addition coloured pens and
highlighters may prove more stimulating.
99
ADHD children perform better when special rewards are promised immediately on
completion of a task, perhaps even as well as non-ADHD children (Cocciarella et al.
1995). This premise will form a large component of our programme.
ADHD children may be less active, inattentive and impulsive during one-to-one
encounters (Barkley, 1995, Dulcan & Benson, 1997). They are often at their best with
grandparents who are likely to give them individualised attention. They work better
under close supervision (Dulcan & Benson, 1997) and when instructions are repeated
more frequently (Barkley, 1995).
The time of day and fatigue also has influences on the child's symptoms. ADHD
children seem to do better on schoolwork in the mornings. Therefore it may be
beneficial for boring, repetitive tasks to be completed in the mornings. Furthermore
where possible homework should also be completed in the mornings.
100
4. The challenge for parents.
The demands faced by parents of ADHD children are far greater that those
experienced by typical parents (Barkley, 1995). They have to constantly supervise,
teach, organise, plan, reward and punish their child. Furthermore they find themselves
meeting with school staff, paediatricians and mental health professionals frequently,
in addition to dealing with problems created in the outside community by their
misbehaved ADHD child.
These demands often create conflict within the family system, which in turn only
serves to increase the distress associated with the disorder on the child. The frustration
experienced by parents often leads to the use of more hostile behaviour towards the
child or in some cases parents tend to be less responsive to the needs of their child
(Barkley, 1995).
This is further complicated by the fact that the ADHD child has an increased need for
parental guidance and love, which is very often masked by his excessive, demanding
and obnoxious behaviour (Campbell, in Fletcher, 1996).
An additional issue to be considered involves the self-esteem of the parents of ADHD
children. The symptoms shown by the ADHD child may provide challenges to
parents' feelings of competence and satisfaction in the parenting role.
Some parents succumb to the stress an ADHD child can place on them, resulting in a
family that experiences constant crises or a family that breaks apart over time.
101
However if the parents can rise to the challenge, raising a child with ADHD can
provide a tremendous opportunity for self-improvement and fulfilment as a parent.
102
5. Common treatments of ADHD.
A variety of treatments has been attempted with ADHD over the past century, far too
numerous to review here. However those treatments with some proven effectiveness
at symptom reduction include:
Pharmacological therapy.
Behavioural therapy techniques in the classroom.
Parent training in behaviour management.
Cognitive-Behavioural training.
An assorted combination of these treatments.
(Anastapoulos et al., 1991).
No treatment has yet proven to cure this condition, however all of the above has
provided some symptomatic relief. Moreover no treatment has produced any enduring
effects with these children once the treatment has been withdrawn (Anastapoulos et
al., 1991).
The most common pharmacological interventions consist of stimulants. This group
primarily consists of Methyiphenidate (Ritalin), d-Amphetamine (Dexedrine) and
Pemoline (Cylert), with Ritalin accounting for approximately 90% of stimulant
utilisation (Burte & Leeds Burte, 1994). A review of the literature suggests that
approximately 70% to 80% of patients show improvement on Ritalin (Calhoun et al.,
1994). Although the stimulants are the medication of choice for ADHD children, their
use remains controversial because of their prevalence, concern about adverse effects,
lack of evidence of their long-term efficacy and the belief that other treatments may be
equally effective (Calhoun et al., 1994).

103
The second level of medication intervention is the tricyclic antidepressants. Most
typically Imipramine (Tofranil) and Disipramine (Burte & Burte, 1994). The
antidepressants may be slower acting and raise blood pressure. However they have
been found to be effective in situations where the stimulants have not, such as those
ADHD children who are highly anxious or are depressed.
Medication alone cannot correct ADHD. While the effects of medication are rapid and
sometimes dramatic, these are not likely to be maintained over the long-term unless
supported by significant psychosocial interventions (Cousins & Weiss, 1993).
A combination of stimulant medication and behaviour modification has been
demonstrated, with suggestions that Cognitive-Behavioural programmes in
conjunction with medication may be required (Burte & Burte, 1994).
Although some studies have suggested that Cognitive-Behavioural interventions may
not add up to the effects of medication alone, other have suggested that when
significant others (peers, teachers or parents) provide positive feedback for a child's
efforts and change their own perceptions and attributions about the child, the child's
behavioural change is likely to be maintained (Burte & Burte, 1994). This aspect has
been incorporated in the programme.
Behavioural interventions including reinforcement, environment restructuring and
time-outs have also been effective with ADHD children (Cocciarella et al., 1995). In
104
general recommendations are that such treatments be lengthy, comprehensive and
intensive (Cocciarella et al., 1995).
105
6. Conclusion.
There is a significant amount of research that indicates that educating parents about
ADHD is potentially an important aspect in the treatment of this disorder. It is for this
reason that this booklet was produced.
There are a number of essential points that have been raised that require re-iteration.
These include:
Once the child has been diagnosed by a competent professional as having ADHD,
it is imperative that parents acknowledge that this is a real disorder and that it is
not some phase that the child is going through.
The symptoms that the child displays are not an indication in any way that the
child is inherently bad. Acknowledging this point will assist parents in dealing
with the anger felt in the event of misbehaviour.
Parents of ADHD children often feel inadequate in their parental role because the
child does not behave well. It is essential that parents do not blame themselves for
the child's difficulties.
The child will probably not outgrow the symptoms and it is imperative that parents
seek professional assistance in treating the disorder.
Finally, parents should be optimistic, as there are a number of different
interventions that have proved useful in treating the disorder.
106
Appendix B
ADHD RATING SCALE
Child's Name Age Grade
Completed by
Circle the number in the one column which best describes the child.
Not at all Just a little Pretty Much Very Much

Often fidgets or squirms in seat. 0 1 2 3
Has difficulty remaining seated. 0 1 2 3
Is easily distracted. 0 1 2 3
Has difficulty awaiting turn in 0 1 2 3
groups.
Often blurts out answers to 0 1 2 3
questions.
Has difficulty following 0 1 2 3
instructions.
Has difficulty sustaining 0 1 2 3
attention to tasks.
Often shifts from one 0 1 2 3
uncompleted activity to another.
Has difficulty playing quietly. 0 1 2 3
Often talks excessively. 0 1 2 3
Often interrupts or intrudes on 0 1 2 3
others.
Often does not seem to listen. 0 1 2 3
Often loses things necessary for 0 1 2 3
tasks.
Often engages in physically 0 1 2 3
dangerous activities without
considering consequences.
Note. From The ADHD Rating Scale: Normative Data. Reliability, and Validity by G. J. DuPaul, 1991,
unpublished manuscript, University of Massachusetts Medical Center, Worcester. Reprinted by permission
of the author. This form may be reproduced for personal use.
107
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TITLE: Cognitive-behavioural Programme for children with

Attention Deficit Hyperactivity Disorder.

Larry David Hirschowitz

A dissertation to be submitted in fulfillment of the

MASTER OF ARTS IN PSYCHOLOGY

IN THE FACULTY OF ARTS

RAND AFRIKAANS UNIVERSITY

Supervisor: Dr. Alban Burke

Attention Deficit Hyperactivity Disorder

I am indebted to the following people who contributed to this

study. I wish to express my sincere gratitude to:

Dr. Alban Burke, for his input, guidance and encouragement

from the start of this study, through to its completion.

My parents, for their continued support and encouragement in

Mrs. Joan Porter for all her assistance, which enabled me to

find a sample to work with.

The participants of the programme who were willing to give

up their time to take part in this study.

Larry David Hirschowitz

Attention Deficit Hyperactivity Disorder (ADHD) affects between 1% and 20% of

school-aged children. Many aspects of the disorder remain largely speculative

achieved much success in bringing about positive short-term changes in the

behaviours of such children. However the long-term efficacy of medication still

support as that of medication. While research shows that some psychological

approaches have virtually no effect others have shown limited benefits.

psychological treatment of ADHD and through examining the limitations of these

approaches, the present research aims to establish an effective psychological

intervention in the treatment of this condition.

This intervention follows the format of a Parent-training based Cognitive-Behavioural

impairment in Attention Deficit Hyperactivity Disorder.

secondly, that this parent-training based cognitive-behavioural programme is useful in

the treatment of Attention Deficit Hyperactivity Disorder.

Table of Contents III

List of Figures VII

2.1. Aetiology of ADHD 5

2.2. Treatment of ADHD 9

2.2.1. Pharmacological Treatment of ADHD 9

2.2.2. Behavioural Treatment of ADHD 12

2.2.2.1 Introduction to Behaviour Therapy 12

2.2.2.3. The Home Token Economy 16

2.2.2.4. Response-Cost interventions 18

2.2.3. The Cognitive Dimension 20

2.2.3.1. Introduction to Cognitive Treatment 20

2.2.3.3 Self-monitoring and Self-reinforcement 24

2.2.4. The inclusion of parents in the intervention 24

2.2.4.1. The parents' impact on the child's intrinsic motivation 25

2.2.4.2. Supporting and educating parents 27

2.2.5. Environment Restructuring 29

2.2.6. The effects of added stimulation 31

2.3. ADHD and behavioural inhibition 32

Chapter 3 Research Methodology 37

3.1. Introduction to methodology 37

3.2. Sample Information 37

3.4. The Intervention 40

3.5. Experimental Methodology 44

3.6. Statistical Procedures 47

4.1. Introduction to results 48

4.2. Descriptive Statistics 49

4.3. Inferential Statistics 53

4.3.1. Kruskal-Wallis Test 53

4.3.2. Mann-Whitney Test 56

4.4. Summary of significant results 67

5.1. Discussion and Conclusion 68

5.2. Implications for further research 75