**Meet the editor**

Dr Somnath Banerjee is a Community Paediatrician in UK. His interests are ADHD and Epilepsy in children. He Chairs ADHD team meetings in his Trust. Dr Banerjee received the annual Trust Award 2004 for the 'Best Clinical Audit Project'. He has presented various papers/ posters and conducted workshops on ADHD in National and International conferences. He has been involved

with various Pan-European researches on ADHD drugs. Dr Banerjee has contributed chapters in many medical books. He is the co-founder of Kent ADHD Network and Convenor; George Still Forum (National Paediatric ADHD Network Group), a special interest group of Royal College of Paediatrics and Child Health in UK.

Contents

**Preface IX**

**Stimulant 51**

Eleanna Nianiou

**Can Help 71** Sarina J. Grosswald

Glaser

**Section 2 Role of Endocrine Hormones 93**

Chapter 1 **ADHD Through Different Developmental Stages 3**

Chapter 4 **Is ADHD a Stress-Related Disorder? Why Meditation**

Chapter 5 **The Potential Role of Neuroendocrine in Patients with Attention-Deficit/Hyperactivity Disorder 95**

Chapter 6 **Dopamine and Glutamate Interactions in ADHD: Implications for the Future Neuropharmacology of ADHD 109**

Erin M. Miller, Theresa C. Thomas, Greg A. Gerhardt and Paul E. A.

Liang-Jen Wang and Chih-Ken Chen

Chapter 2 **Neurodevelopmental Pathways of Childhood ADHD into**

**Adulthood: Maturational Lag, Deviation, or Both? 21**

Antigone Papavasiliou, Irene Nikaina, Anna Spyridonidou and

Chapter 3 **Difficulties in Recognizing ADHD in an Urban Population and Treatment Satisfaction with a Short and a Long Acting**

Hojka Gregoric Kumperscak

Alban Burke and Amanda Edge

**Section 1 Introduction 1**

### Contents

#### **Preface XIII**


Chapter 6 **Dopamine and Glutamate Interactions in ADHD: Implications for the Future Neuropharmacology of ADHD 109** Erin M. Miller, Theresa C. Thomas, Greg A. Gerhardt and Paul E. A. Glaser

#### **X** Contents

#### **Section 3 Assessment and Diagnosis 139**


**Section 6 Ethical Issues 305**

Debby Zambo

Chapter 14 **Ethical Concerns Raised by Neuroscience, Labeling, and**

**Intervening in the Lives of Individuals with ADHD 307**

Contents **VII**


#### **Section 5 Outcome 213**


Chapter 13 **A Comparison Between Life Quality and Weight-Height Measurements of Patients, Under Stimulant and Non-Stimulant Treatment due to Attention-Deficit and Hyperactivity Disorder, and Healthy Population 285** Esra Ozdemir Demirci, Merve Cikili Uytun, Rabia Durmus and Didem Behice Oztop

#### **Section 6 Ethical Issues 305**

**Section 3 Assessment and Diagnosis 139**

Chapter 7 **Clinical Phenomena of ADHD 141**

**Disorder (ADHD) 151**

Chapter 8 **Review of Tools Used for Assessing Teachers' Level of**

**Knowledge with Regards Attention Deficit Hyperactivity**

**Hyperactivity Disorder: A Comparison of Behavioral Results**

**African-Americans; Current Challenges Associated with**

Marian Soroa, Arantxa Gorostiaga and Nekane Balluerka

Chapter 9 **Effects of Methylphenidate in Children with Attention Deficit**

Chapter 10 **The Impact of Attention Deficit/Hyperactivity Disorder in**

Rahn Kennedy Bailey and Ejike Kingsley Ofoemezie

Chapter 11 **Attention-Deficit/Hyperactivity Disorder (ADHD) as a Barrier to**

**Learning and Development within the South African Context:**

**(Facilitating Adjustment of Cognition and Emotion): Theory,**

**Measurements of Patients, Under Stimulant and Non-Stimulant Treatment due to Attention-Deficit and Hyperactivity Disorder,**

Esra Ozdemir Demirci, Merve Cikili Uytun, Rabia Durmus and Didem

**and Event–Related Potentials 181**

Ren Yan-ling and Dong Xuan

**Diagnosis and Treatment 193**

**The Perspective of Teachers 215**

**Research and Practice 243**

**and Healthy Population 285**

Behice Oztop

Zaytoon Amod, Adri Vorster and Kim Lazarus

Chapter 13 **A Comparison Between Life Quality and Weight-Height**

Chapter 12 **ADHD Children's Emotion Regulation in FACE© – Perspective**

Smadar Celestin-Westreich and Leon-Patrice Celestin

Nitin Patel

**VI** Contents

**Section 4 Drugs in ADHD 179**

**Section 5 Outcome 213**

Chapter 14 **Ethical Concerns Raised by Neuroscience, Labeling, and Intervening in the Lives of Individuals with ADHD 307** Debby Zambo

Preface

and treatment with drugs that are life-threatening.

increasingly recognised entity is the need of the hour.

A few topics in child mental health have sparked continued interest and controversy. Atten‐ tion Deficit Hyperactivity Disorder (ADHD) is one of them. ADHD is a developmental disor‐ der of behavioural inhibition and self-regulation. Since its first description by George Frederick Still in 1902, this clinical diagnosis had many name changes as well as changes in the diagnosis criteria. Despite many researches the exact cause of ADHD is still not known. Epide‐ miological studies have estimated its prevalence between 5% and 10%. Many of our colleagues doubt if it even exists as an entity. There are stories in TV and media about its over-diagnosis

Despite this hue and cry, the diagnosis and management approach have very little changes over last 30 or 40 years. Despite some fine tuning in diagnosis and management, we still rely on clinical judgement to make the diagnosis and management plan. Children/ Adolescents with ADHD perceive the world differently from others. Awareness and understanding of this

ADHD is primarily a condition of brain dysfunction, involving many sites in the brain. There is much more to ADHD than just hyperactivity. This book aims to encourage further reading and research in ADHD. ADHD is a combination of "nature" versus "nature". The topics cov‐ ered in the book plan to improve quality of lives in children with ADHD and in their family members. This book is intended to provide an overview rather than act as an exhaustive guide. It is hoped that many readers among mental health professionals all over the world will find this book to contribute in the field of ADHD. Finally this book would not have been pos‐

**Dr Somnath Banerjee**

Dover, Kent, UK

Community Paediatrician

MBBS, DCH, MRCPCH, MSc community Paediatrics, FRCPCH

East Kent Hospitals University NHS Foundation Trust

sible without the able guidance of Ms Mirna Cvijic, the commissioning editor.

### Preface

A few topics in child mental health have sparked continued interest and controversy. Atten‐ tion Deficit Hyperactivity Disorder (ADHD) is one of them. ADHD is a developmental disor‐ der of behavioural inhibition and self-regulation. Since its first description by George Frederick Still in 1902, this clinical diagnosis had many name changes as well as changes in the diagnosis criteria. Despite many researches the exact cause of ADHD is still not known. Epide‐ miological studies have estimated its prevalence between 5% and 10%. Many of our colleagues doubt if it even exists as an entity. There are stories in TV and media about its over-diagnosis and treatment with drugs that are life-threatening.

Despite this hue and cry, the diagnosis and management approach have very little changes over last 30 or 40 years. Despite some fine tuning in diagnosis and management, we still rely on clinical judgement to make the diagnosis and management plan. Children/ Adolescents with ADHD perceive the world differently from others. Awareness and understanding of this increasingly recognised entity is the need of the hour.

ADHD is primarily a condition of brain dysfunction, involving many sites in the brain. There is much more to ADHD than just hyperactivity. This book aims to encourage further reading and research in ADHD. ADHD is a combination of "nature" versus "nature". The topics cov‐ ered in the book plan to improve quality of lives in children with ADHD and in their family members. This book is intended to provide an overview rather than act as an exhaustive guide. It is hoped that many readers among mental health professionals all over the world will find this book to contribute in the field of ADHD. Finally this book would not have been pos‐ sible without the able guidance of Ms Mirna Cvijic, the commissioning editor.

> **Dr Somnath Banerjee** MBBS, DCH, MRCPCH, MSc community Paediatrics, FRCPCH Community Paediatrician East Kent Hospitals University NHS Foundation Trust Dover, Kent, UK

**Section 1**

**Introduction**

**Section 1**

### **Introduction**

**Chapter 1**

**ADHD Through Different Developmental Stages**

Persistent and severe impairment of psychological development resulting from a high level of inattentive, restless and impulsive behaviour is classified according to the fourth Diag‐ nostic and Statistical Manual of Mental Disorders (DSM-IV) as attention-deficit/hyperactivi‐ ty disorder (ADHD) [1] and according to the Tenth International Classification of Diseases (ICD-10) as hyperkinetic disorder (HD) [2]. In both classifications the behaviours to be rec‐ ognized are very much the same, they differ mostly in the ways the symptoms are weighted and combined into categories. The diagnostic criteria are in general broader in DSM-IV, which is why ADHD is a more common diagnosis. The ICD-10 diagnosis of HD is a narrow‐

er category, where nearly all cases of HD fulfil the diagnostic criteria for ADHD [3].

ty. Children have difficulty waiting their turn and interrupt or intrude on others.

of hyperactive, impulsive and inattentive symptoms.

Hyperactivity is the most noticeable symptom group in ADHD. Children are running and climbing excessively, often in very inappropriate situations. They often fidget with their hands or feet when they should seat still. They are always on the go and often act as if driv‐ en by a motor. Inattention is the second markmal of ADHD. Children often fail to give close attention to details and make careless mistakes in their schoolwork or in other activities. They do not seem to listen when spoken to directly, they often do not follow through in‐ structions and they fail to finish their schoolwork or other duties. Also, they have difficulties organizing their tasks and activities. They are easily distracted by extraneous stimuli and they tend to be forgetful in their daily activities. The third group of symptoms is impulsivi‐

The term *hyperactivity* in this chapter is restricted to mean the combination of symptoms that define overactive behaviour. The term *ADHD symptoms* is used to refer to the combination

The onset of the disorder is in early childhood, nearly always before the age of 5 and fre‐ quently even earlier. It often persists into adolescence and adult life [4]. Up to 65% of chil‐

and reproduction in any medium, provided the original work is properly cited.

© 2013 Gregoric Kumperscak; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,

Hojka Gregoric Kumperscak

http://dx.doi.org/10.5772/53963

**1. Introduction**

Additional information is available at the end of the chapter

### **ADHD Through Different Developmental Stages**

Hojka Gregoric Kumperscak

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/53963

#### **1. Introduction**

Persistent and severe impairment of psychological development resulting from a high level of inattentive, restless and impulsive behaviour is classified according to the fourth Diag‐ nostic and Statistical Manual of Mental Disorders (DSM-IV) as attention-deficit/hyperactivi‐ ty disorder (ADHD) [1] and according to the Tenth International Classification of Diseases (ICD-10) as hyperkinetic disorder (HD) [2]. In both classifications the behaviours to be rec‐ ognized are very much the same, they differ mostly in the ways the symptoms are weighted and combined into categories. The diagnostic criteria are in general broader in DSM-IV, which is why ADHD is a more common diagnosis. The ICD-10 diagnosis of HD is a narrow‐ er category, where nearly all cases of HD fulfil the diagnostic criteria for ADHD [3].

Hyperactivity is the most noticeable symptom group in ADHD. Children are running and climbing excessively, often in very inappropriate situations. They often fidget with their hands or feet when they should seat still. They are always on the go and often act as if driv‐ en by a motor. Inattention is the second markmal of ADHD. Children often fail to give close attention to details and make careless mistakes in their schoolwork or in other activities. They do not seem to listen when spoken to directly, they often do not follow through in‐ structions and they fail to finish their schoolwork or other duties. Also, they have difficulties organizing their tasks and activities. They are easily distracted by extraneous stimuli and they tend to be forgetful in their daily activities. The third group of symptoms is impulsivi‐ ty. Children have difficulty waiting their turn and interrupt or intrude on others.

The term *hyperactivity* in this chapter is restricted to mean the combination of symptoms that define overactive behaviour. The term *ADHD symptoms* is used to refer to the combination of hyperactive, impulsive and inattentive symptoms.

The onset of the disorder is in early childhood, nearly always before the age of 5 and fre‐ quently even earlier. It often persists into adolescence and adult life [4]. Up to 65% of chil‐

© 2013 Gregoric Kumperscak; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

dren with ADHD continue to experience symptoms as adults, however they manifest differently in different age periods. Hyperactivity, for instance, is seldom a problem in adults. It diminishes through adolescence and causes minimal or manageable problems in adulthood. Impulsivity, on the other hand, can even increase in adolescence but diminishes slightly through adulthood. The majority of ADHD problems in adults is caused by inatten‐ tion. Adults with ADHD are disorganized, inaccurate, frequently experiencing difficulties in their relationships, at work and with finances [5,6].

**3. DSM and ICD categorization**

by age 7 but 95% recalled the onset by age 12 [11].

(home/school) [1,2].

in the DSM-IV classification [1]:

met for the past 6 months

approaches available [3].

scales and Conners' Rating Scales (CRS) [8].

The DSM-IV classification is mostly used in North America and UK, while the ICD-10 is more commonly used in Europe. DSM-V is to come in a year. There was a tendency to bring definitions of ADHD and HD closer together, and indeed the criteria for the identification of inattentive, hyperactive and impulsive symptoms are almost identical (see diagnostic crite‐ ria in Table 1). However, there are still significant differences in the number of criteria in each domain required for a diagnosis, the role of inattention, the definition of pervasiveness and the handling of comorbidity. The diagnosis of ADHD requires the presence of six inat‐ tentive or six hyperactive-impulsive symptoms, or both. The diagnosis of HD requires at least six inattentive and three hyperactive as well as one impulsive symptom. Both ‒ ICD-10 and DSM-IV ‒ stress that the symptoms must be present by age 7 and in at least two settings

ADHD Through Different Developmental Stages

http://dx.doi.org/10.5772/53963

5

In DSM-V, the age by which the symptoms should be present is to be changed from 7 to 12 years [10]. One of the reasons for this change is the concern about appropriate criteria for adults. Population survey data indicated that in adults with ADHD, only half recalled onset

Because of heterogeneity of symptoms in ADHD, three different subtypes are distinguished

**•** Attention-deficit/hyperactivity disorder, **combined type**: if both criteria A1 and A2 are

**•** Attention-deficit/hyperactivity disorder, **predominantly inattentive type (ADD):** if crite‐

**•** Attention-deficit/hyperactivity disorder, **predominantly hyperactive-impulsive type**: if

HD is a narrower category than ADHD, and it appears that nearly all cases of HD fulfil the diagnostic criteria of ADHD [3]. Most of the children fulfilling the ADHD diagnostic criteria are not particularly impaired [6]. On the other hand, children with HD constitute the most severe 20% of those with ADHD [6]. Both diagnostic schemes (DSM and ICD) have their ad‐ vantages and disadvantages. When assessing an individual child, first the fulfilment of the ADHD criteria is checked, and if the latter are met, the HD criteria fulfilment is checked as next. If the diagnostic criteria for HD are met, medication will be included in the treatment

Essential components of a full assessment process include a clinical interview, medical ex‐ amination and administration of rating scales to patients, parents and teachers. There are broad-band instruments that evaluate general behavioural and psychosocial functioning, among most used one being the Strengths and Difficulties Questionnaire (SDQ), Achenbach

rion A1 is met but criterion A2 is not met for the past 6 months

criterion A2 is met but criterion A1 is not met for the past 6 months.

Early recognition and treatment of ADHD is crucial, since longitudinal studies indicate that inattentive and restless behaviour is a developmental risk. Untreated ADHD is also a risk for a range of other mental disorders such as conduct disorder, oppositional defiant disor‐ der, depression, and substance abuse or addiction. Many children with ADHD present with school difficulties including poor classroom participation and associated learning disabili‐ ties in reading, written expression, or mathematics. As a result, they receive low grades, are retained in a grade level or do not complete the school at the level they started with [4-6].

Untreated ADHD is not only a burden for a person with the disorder and its family, but also for a society in many aspects. For example, young adults with ADHD are more likely to be apprehended for violations of traffic laws and to be cited more often for such violations [7].

The treatment of ADHD must be comprehensive and individually tailored. Psychological in‐ terventions, educational change, medication, education and support for parents and/or teachers should be available. Multimodal interventions are usually indicated [4-6]. Most children whose problems are severe enough to receive an ICD-10 diagnosis of HD will need a medication [3]. There are clear guidelines about ADHD treatment including pharmaco‐ therapy, which, however, will not be discussed further in this chapter. The most prescribed group of medication are psychostimulants and atomoxetine [8,9].

#### **2. History**

ADHD is not some new diagnosis made-up in these times when there is an increasing need for children to sit longer and learn more. Already back in 1844 H. Hoffman wrote a story about fidget Philip, and in 1890 W. James talked about the attention disorder as a deficit of inhibitory control. In 1932 Kramer and Pollnow introduced the term hyperkinetic syndrome. Only 4 years later (in 1937) the first psychostimulant was available. Strauss and Lethinen used the term minimal cerebral dysfunction to refer to the same symptomatic condition. World Health Organisation (WHO) introduced in ICD-8 hyperkinetic syndrome of child‐ hood, to change it in 1992 to hyperkinetic disorder. American Psychiatric Association (APA), on the other hand, introduced in 1980 the term attention deficit disorder and 7 years later Attention-deficit/hyperactivity disorder (ADHD) [4-6].

Originally, ADHD was thought to be a transient phenomenon because of the tendency for symptoms (especially hyperactivity) to diminish as children reached adolescence. It is now clear that the disorder persists into adolescence and into adulthood, but manifests different‐ ly in each developmental stage [6].

#### **3. DSM and ICD categorization**

dren with ADHD continue to experience symptoms as adults, however they manifest differently in different age periods. Hyperactivity, for instance, is seldom a problem in adults. It diminishes through adolescence and causes minimal or manageable problems in adulthood. Impulsivity, on the other hand, can even increase in adolescence but diminishes slightly through adulthood. The majority of ADHD problems in adults is caused by inatten‐ tion. Adults with ADHD are disorganized, inaccurate, frequently experiencing difficulties in

Early recognition and treatment of ADHD is crucial, since longitudinal studies indicate that inattentive and restless behaviour is a developmental risk. Untreated ADHD is also a risk for a range of other mental disorders such as conduct disorder, oppositional defiant disor‐ der, depression, and substance abuse or addiction. Many children with ADHD present with school difficulties including poor classroom participation and associated learning disabili‐ ties in reading, written expression, or mathematics. As a result, they receive low grades, are retained in a grade level or do not complete the school at the level they started with [4-6]. Untreated ADHD is not only a burden for a person with the disorder and its family, but also for a society in many aspects. For example, young adults with ADHD are more likely to be apprehended for violations of traffic laws and to be cited more often for such violations [7]. The treatment of ADHD must be comprehensive and individually tailored. Psychological in‐ terventions, educational change, medication, education and support for parents and/or teachers should be available. Multimodal interventions are usually indicated [4-6]. Most children whose problems are severe enough to receive an ICD-10 diagnosis of HD will need a medication [3]. There are clear guidelines about ADHD treatment including pharmaco‐ therapy, which, however, will not be discussed further in this chapter. The most prescribed

ADHD is not some new diagnosis made-up in these times when there is an increasing need for children to sit longer and learn more. Already back in 1844 H. Hoffman wrote a story about fidget Philip, and in 1890 W. James talked about the attention disorder as a deficit of inhibitory control. In 1932 Kramer and Pollnow introduced the term hyperkinetic syndrome. Only 4 years later (in 1937) the first psychostimulant was available. Strauss and Lethinen used the term minimal cerebral dysfunction to refer to the same symptomatic condition. World Health Organisation (WHO) introduced in ICD-8 hyperkinetic syndrome of child‐ hood, to change it in 1992 to hyperkinetic disorder. American Psychiatric Association (APA), on the other hand, introduced in 1980 the term attention deficit disorder and 7 years later

Originally, ADHD was thought to be a transient phenomenon because of the tendency for symptoms (especially hyperactivity) to diminish as children reached adolescence. It is now clear that the disorder persists into adolescence and into adulthood, but manifests different‐

their relationships, at work and with finances [5,6].

4 Attention Deficit Hyperactivity Disorder in Children and Adolescents

group of medication are psychostimulants and atomoxetine [8,9].

Attention-deficit/hyperactivity disorder (ADHD) [4-6].

ly in each developmental stage [6].

**2. History**

The DSM-IV classification is mostly used in North America and UK, while the ICD-10 is more commonly used in Europe. DSM-V is to come in a year. There was a tendency to bring definitions of ADHD and HD closer together, and indeed the criteria for the identification of inattentive, hyperactive and impulsive symptoms are almost identical (see diagnostic crite‐ ria in Table 1). However, there are still significant differences in the number of criteria in each domain required for a diagnosis, the role of inattention, the definition of pervasiveness and the handling of comorbidity. The diagnosis of ADHD requires the presence of six inat‐ tentive or six hyperactive-impulsive symptoms, or both. The diagnosis of HD requires at least six inattentive and three hyperactive as well as one impulsive symptom. Both ‒ ICD-10 and DSM-IV ‒ stress that the symptoms must be present by age 7 and in at least two settings (home/school) [1,2].

In DSM-V, the age by which the symptoms should be present is to be changed from 7 to 12 years [10]. One of the reasons for this change is the concern about appropriate criteria for adults. Population survey data indicated that in adults with ADHD, only half recalled onset by age 7 but 95% recalled the onset by age 12 [11].

Because of heterogeneity of symptoms in ADHD, three different subtypes are distinguished in the DSM-IV classification [1]:


HD is a narrower category than ADHD, and it appears that nearly all cases of HD fulfil the diagnostic criteria of ADHD [3]. Most of the children fulfilling the ADHD diagnostic criteria are not particularly impaired [6]. On the other hand, children with HD constitute the most severe 20% of those with ADHD [6]. Both diagnostic schemes (DSM and ICD) have their ad‐ vantages and disadvantages. When assessing an individual child, first the fulfilment of the ADHD criteria is checked, and if the latter are met, the HD criteria fulfilment is checked as next. If the diagnostic criteria for HD are met, medication will be included in the treatment approaches available [3].

Essential components of a full assessment process include a clinical interview, medical ex‐ amination and administration of rating scales to patients, parents and teachers. There are broad-band instruments that evaluate general behavioural and psychosocial functioning, among most used one being the Strengths and Difficulties Questionnaire (SDQ), Achenbach scales and Conners' Rating Scales (CRS) [8].

#### **A. Either (1) or (2):**

(1) six (or more) of the following symptoms of inattention have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level:

**4. ADHD through different developmental stages**

**4.1. ADHD in children**

*4.1.1. Epidemiology*

aged 6‒14 years [4].

*4.1.2. Clinical picture*

attention deficit disorder (ADD) [15] such as:

**•** tendency to avoid tasks

**•** difficulties in following instructions and organizing tasks

and impulsiveness become most impairing, especially in social situations.

The only constant of ADHD symptoms is that they are changing in each particular child. Not only from day to day, but also with development. In pre-school children, hyperactivity is most obvious and impairing. Inattention becomes more salient once a child confronts school demands. In adolescence and adulthood, hyperactivity diminishes, and inattention

ADHD Through Different Developmental Stages

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7

The prevalence of ADHD depends on the diagnostic measures used. In [12] survey, 10% of the children in one elementary school in North Carolina had been given the diagnosis of ADHD and 7% were taking medication [12]. An epidemiological study found a cumulative incidence of ADHD in the elementary and secondary school population of 7.5% [13]. The rate of lifetime childhood diagnosis of ADHD in another study [14] was 7.8%, 4.3% were treated with medication [14]. Prevalence for HD is of course smaller, it is 1‒3% for children

The ratio males : females is around 3 : 1, the prevalence is highest among school-aged boys,

Hyperactivity is the most obvious and impairing symptom in children. At playing, hyperac‐ tive children are more often off-task and spend less time on a particular activity than their non-hyperactive peers [6]. Hyperactive children are more active through the day [6]. Many children without ADHD are occasionally hyperactive to some extent and this normal hyper‐ activity should not be confused with the more severe and persistent hyperactivity seen in ADHD children. In ADHD hyperactivity is frequent, severe and persistent and most impor‐ tantly it interferes with a child's peer and parental relationships, impeding their school per‐ formance and undermining their psychological well- being [6]. Not to forget that there must be six symptoms from the hyperactivity domain present plus the criterion C (two or more settings) plus criterion D (clear evidence of clinically significant impairment in social, aca‐ demic, or occupational functioning) to fulfil DSM-IV diagnostic criteria for ADHD [1].

Lack of hyperactivity, on the other hand, does not mean that a child does not have ADHD. Inattentiveness is the most overlooked symptom, especially in pre-school children and in particular in girls. Inattentive children are quiet, day-dreaming, sitting in the last row of the classroom without bothering/disturbing anyone. They have "dreamy" symptoms, typical for

and lowest in girls. But the prevalence in girls is more stable across the age [6].

#### **Inattention**

(a) often fails to give close attention to details or makes careless mistakes in schoolwork, work, or other activities

(b) often has difficulty sustaining attention in tasks or play activities

(c) often does not seem to listen when spoken to directly

(d) often does not follow through on instructions and fails to finish schoolwork, chores, or duties

in the workplace (not due to oppositional behavior or failure to understand instructions)

(e) often has difficulty organizing tasks and activities

(f) often avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort (such as schoolwork or homework)

(g) often loses things necessary for tasks or activities (e.g., toys, school assignments, pencils,

books, or tools)

(h) is often easily distracted by extraneous stimuli

(i) is often forgetful in daily activities

(2) six (or more) of the following symptoms of hyperactivity/impulsivity have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level:

#### **Hyperactivity**

(a) often fidgets with hands or feet or squirms in seat

(b) often leaves seat in classroom or in other situations in which remaining seated is expected

(c) often runs about or climbs excessively in situations in which it is inappropriate (in adolescents

or adults, may be limited to subjective feelings of restlessness)

(d) often has difficulty playing or engaging in leisure activities quietly

(e) is often "on the go" or often acts as if "driven by a motor"

(f) often talks excessively

#### **Impulsivity**

(g) often blurts out answers before questions have been completed

(h) often has difficulty awaiting turn

(i) often interrupts or intrudes on others (e.g., butts into conversations or games)

B. Some hyperactive-impulsive or inattentive symptoms that caused impairment were present before age 7 years.

C. Some impairment from the symptoms is present in two or more settings (e.g., at school [or work] and at home).

D. There must be clear evidence of clinically significant impairment in social, academic, or occupational functioning.

E. The symptoms do not occur exclusively during the course of a pervasive developmental disorder, schizophrenia, or other psychotic disorder and are not better accounted for by another mental disorder (e.g., mood disorder, anxiety disorder, dissociative disorder, or a personality disorder).

**Table 1.** Diagnostic criteria according to DSM-IV for attention-deficit/hyperactivity disorder [1].

#### **4. ADHD through different developmental stages**

The only constant of ADHD symptoms is that they are changing in each particular child. Not only from day to day, but also with development. In pre-school children, hyperactivity is most obvious and impairing. Inattention becomes more salient once a child confronts school demands. In adolescence and adulthood, hyperactivity diminishes, and inattention and impulsiveness become most impairing, especially in social situations.

#### **4.1. ADHD in children**

#### *4.1.1. Epidemiology*

**A. Either (1) or (2):**

6 Attention Deficit Hyperactivity Disorder in Children and Adolescents

**Inattention**

or other activities

books, or tools)

**Hyperactivity**

(f) often talks excessively

(h) often has difficulty awaiting turn

**Impulsivity**

before age 7 years.

work] and at home).

disorder).

occupational functioning.

(1) six (or more) of the following symptoms of inattention have persisted for at least 6 months to

(a) often fails to give close attention to details or makes careless mistakes in schoolwork, work,

(d) often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace (not due to oppositional behavior or failure to understand instructions)

(f) often avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort

(g) often loses things necessary for tasks or activities (e.g., toys, school assignments, pencils,

(2) six (or more) of the following symptoms of hyperactivity/impulsivity have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level:

(b) often leaves seat in classroom or in other situations in which remaining seated is expected (c) often runs about or climbs excessively in situations in which it is inappropriate (in adolescents

a degree that is maladaptive and inconsistent with developmental level:

(b) often has difficulty sustaining attention in tasks or play activities

(c) often does not seem to listen when spoken to directly

(e) often has difficulty organizing tasks and activities

(h) is often easily distracted by extraneous stimuli

(a) often fidgets with hands or feet or squirms in seat

or adults, may be limited to subjective feelings of restlessness) (d) often has difficulty playing or engaging in leisure activities quietly (e) is often "on the go" or often acts as if "driven by a motor"

(g) often blurts out answers before questions have been completed

(i) often interrupts or intrudes on others (e.g., butts into conversations or games)

B. Some hyperactive-impulsive or inattentive symptoms that caused impairment were present

C. Some impairment from the symptoms is present in two or more settings (e.g., at school [or

D. There must be clear evidence of clinically significant impairment in social, academic, or

E. The symptoms do not occur exclusively during the course of a pervasive developmental disorder, schizophrenia, or other psychotic disorder and are not better accounted for by another mental disorder (e.g., mood disorder, anxiety disorder, dissociative disorder, or a personality

**Table 1.** Diagnostic criteria according to DSM-IV for attention-deficit/hyperactivity disorder [1].

(such as schoolwork or homework)

(i) is often forgetful in daily activities

The prevalence of ADHD depends on the diagnostic measures used. In [12] survey, 10% of the children in one elementary school in North Carolina had been given the diagnosis of ADHD and 7% were taking medication [12]. An epidemiological study found a cumulative incidence of ADHD in the elementary and secondary school population of 7.5% [13]. The rate of lifetime childhood diagnosis of ADHD in another study [14] was 7.8%, 4.3% were treated with medication [14]. Prevalence for HD is of course smaller, it is 1‒3% for children aged 6‒14 years [4].

The ratio males : females is around 3 : 1, the prevalence is highest among school-aged boys, and lowest in girls. But the prevalence in girls is more stable across the age [6].

#### *4.1.2. Clinical picture*

Hyperactivity is the most obvious and impairing symptom in children. At playing, hyperac‐ tive children are more often off-task and spend less time on a particular activity than their non-hyperactive peers [6]. Hyperactive children are more active through the day [6]. Many children without ADHD are occasionally hyperactive to some extent and this normal hyper‐ activity should not be confused with the more severe and persistent hyperactivity seen in ADHD children. In ADHD hyperactivity is frequent, severe and persistent and most impor‐ tantly it interferes with a child's peer and parental relationships, impeding their school per‐ formance and undermining their psychological well- being [6]. Not to forget that there must be six symptoms from the hyperactivity domain present plus the criterion C (two or more settings) plus criterion D (clear evidence of clinically significant impairment in social, aca‐ demic, or occupational functioning) to fulfil DSM-IV diagnostic criteria for ADHD [1].

Lack of hyperactivity, on the other hand, does not mean that a child does not have ADHD. Inattentiveness is the most overlooked symptom, especially in pre-school children and in particular in girls. Inattentive children are quiet, day-dreaming, sitting in the last row of the classroom without bothering/disturbing anyone. They have "dreamy" symptoms, typical for attention deficit disorder (ADD) [15] such as:


**•** forgetfulness and tendency to lose things

Among ADHD subtypes, combined type seems to be the most common (43%), and also the most severe and persistent one [15]. On the other hand, in [16] study the ADD type emerged as the most prevalent. This study also revealed lower male : female ratios in ADHD diagno‐ ses than other studies, which implies that females and the ADD subtype could be under‐ diagnosed and/or undertreated [16].

*4.1.4. Course and prognosis*

ment in adolescence [24].

**•** Disruptive behaviour

**•** Low self-esteem

**•** Poor social skills

**•** Physical injury

*4.2.1. Epidemiology*

and school functioning [25].

**4.2. ADHD in adolescents**

age years (ages 13-18 years) [26].

**•** Oppositional defiant disorder

**•** Parent-child relationship difficulties

**•** Poor academic performance and learning delay

of ADHD into adolescence and adulthood [5,24].

As normal children develop better impulse control, attention focus, other executive func‐ tions, and ability to remain calm as they mature, so do those with ADHD, just at slower pace, lagging behind their age mates – usually never reaching them [5]. Various factors have been suggested as predictors of persistence of ADHD symptoms into adolescence and adult‐ hood (among them family history of ADHD, childhood severity of ADHD, psychiatric co‐ morbidity and psychological adversity, impact of treatment ) [15]. Among all the factors, studies have found that the childhood ADHD severity is a strongest predictor of persistence

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9

Regarding the impact of treatment (intensity and type) on ADHD outcome, the MTA study found that neither the type nor intensity of 14 months of treatment for ADHD in childhood (at age 7.0–9.9 years old) does not predict functioning six-to-eight years later. Rather, early ADHD symptom trajectory regardless of treatment type is prognostic. This finding implies that children with behavioural and sociodemographic advantage, with the best response to any treatment, will have the best long-term prognosis [24]. The same study also found that as a group, however, despite initial symptom improvement during treatment that is largely maintained post-treatment, children with combined-type ADHD exhibit significant impair‐

Across the life span, unmanaged ADHD can contribute to problems in social and academic

A review study found that children treated with stimulants for as long as 2 years showed improvement in ADHD symptoms, comorbid oppositional defiant disorder and academic

ADHD does not remit with the onset of puberty. Follow-up studies show that a majority (60‒85%) of children with ADHD will continue to meet criteria for the disorder during teen‐

settings that coincide with the child's developmental level. These are:

Many children with ADHD present with school difficulties including failure to complete their homework, poor test preparation and test-taking skills, poor organizational skills, poor understanding of material, poor classroom participation and failure to ask teachers for need‐ ed help, disruptive behaviour in the classroom, and truancy. Children with ADHD who are constantly singled out by their teachers and parents to "sit down" and "be quiet," eventual‐ ly have a negative perception (low self-esteem) of themselves. By age 10, these children are often behind their peers in terms of social and academic skills [17].

The social and academic impairments of children with ADHD cause stress within the fami‐ ly. Parents can become worried and anxious. Confronted with frustration, anger and selfblame can present with lower self-esteem as parents and as a family. The family seeks a social isolation, often self-imposed. It is difficult to determine if these effects are a result of parenting a child with ADHD or if the parental psychopathology is contributing to the child's psychological reaction and disorder [6,17].

As ADHD is among most heritable of psychiatric disorders with a high risk for familial ag‐ gregation, it is quite common that ADHD children have parents with the same disease. This fact further complicates the assessment, treatment and the course of disease. ADHD parents may have impairment across a variety of domains, including parenting [18], which could be the reason why many needed changes in a daily life of a child and family cannot/are harder to be indorsed. 20% to 40% are likely to have the disorder themselves [19]. Families of chil‐ dren with ADHD display higher rates of alcoholism, substance abuse and depression than families of children with Down's syndrome [20].

#### *4.1.3. Comorbidity*

Over 50% of children with ADHD have also comorbid disorders [4-6]. 35–50% have opposi‐ tional-defiant disorder, 25% conduct disorder, 15% are depressed and 25% have anxiety dis‐ order [6]. Learning disorder occurs in 15–40% of children, particularly among ADD. Language impairment is present in 15–75% of children with ADHD [21,22].

Epilepsy is commoner in ADHD children compared with general population. 36% of children with epilepsy met DSM-IV criteria for ADHD. Neither seizure type nor focus of electroencephalographic (EEG) discharge predict the occurrence of ADHD, but there is a tendency for ADHD to occur more frequently in those with generalized seizures [23].

#### *4.1.4. Course and prognosis*

**•** forgetfulness and tendency to lose things

8 Attention Deficit Hyperactivity Disorder in Children and Adolescents

diagnosed and/or undertreated [16].

Among ADHD subtypes, combined type seems to be the most common (43%), and also the most severe and persistent one [15]. On the other hand, in [16] study the ADD type emerged as the most prevalent. This study also revealed lower male : female ratios in ADHD diagno‐ ses than other studies, which implies that females and the ADD subtype could be under‐

Many children with ADHD present with school difficulties including failure to complete their homework, poor test preparation and test-taking skills, poor organizational skills, poor understanding of material, poor classroom participation and failure to ask teachers for need‐ ed help, disruptive behaviour in the classroom, and truancy. Children with ADHD who are constantly singled out by their teachers and parents to "sit down" and "be quiet," eventual‐ ly have a negative perception (low self-esteem) of themselves. By age 10, these children are

The social and academic impairments of children with ADHD cause stress within the fami‐ ly. Parents can become worried and anxious. Confronted with frustration, anger and selfblame can present with lower self-esteem as parents and as a family. The family seeks a social isolation, often self-imposed. It is difficult to determine if these effects are a result of parenting a child with ADHD or if the parental psychopathology is contributing to the

As ADHD is among most heritable of psychiatric disorders with a high risk for familial ag‐ gregation, it is quite common that ADHD children have parents with the same disease. This fact further complicates the assessment, treatment and the course of disease. ADHD parents may have impairment across a variety of domains, including parenting [18], which could be the reason why many needed changes in a daily life of a child and family cannot/are harder to be indorsed. 20% to 40% are likely to have the disorder themselves [19]. Families of chil‐ dren with ADHD display higher rates of alcoholism, substance abuse and depression than

Over 50% of children with ADHD have also comorbid disorders [4-6]. 35–50% have opposi‐ tional-defiant disorder, 25% conduct disorder, 15% are depressed and 25% have anxiety dis‐ order [6]. Learning disorder occurs in 15–40% of children, particularly among ADD.

Epilepsy is commoner in ADHD children compared with general population. 36% of children with epilepsy met DSM-IV criteria for ADHD. Neither seizure type nor focus of electroencephalographic (EEG) discharge predict the occurrence of ADHD, but there is a tendency for ADHD to occur more frequently in those with generalized seizures [23].

Language impairment is present in 15–75% of children with ADHD [21,22].

often behind their peers in terms of social and academic skills [17].

child's psychological reaction and disorder [6,17].

families of children with Down's syndrome [20].

*4.1.3. Comorbidity*

As normal children develop better impulse control, attention focus, other executive func‐ tions, and ability to remain calm as they mature, so do those with ADHD, just at slower pace, lagging behind their age mates – usually never reaching them [5]. Various factors have been suggested as predictors of persistence of ADHD symptoms into adolescence and adult‐ hood (among them family history of ADHD, childhood severity of ADHD, psychiatric co‐ morbidity and psychological adversity, impact of treatment ) [15]. Among all the factors, studies have found that the childhood ADHD severity is a strongest predictor of persistence of ADHD into adolescence and adulthood [5,24].

Regarding the impact of treatment (intensity and type) on ADHD outcome, the MTA study found that neither the type nor intensity of 14 months of treatment for ADHD in childhood (at age 7.0–9.9 years old) does not predict functioning six-to-eight years later. Rather, early ADHD symptom trajectory regardless of treatment type is prognostic. This finding implies that children with behavioural and sociodemographic advantage, with the best response to any treatment, will have the best long-term prognosis [24]. The same study also found that as a group, however, despite initial symptom improvement during treatment that is largely maintained post-treatment, children with combined-type ADHD exhibit significant impair‐ ment in adolescence [24].

Across the life span, unmanaged ADHD can contribute to problems in social and academic settings that coincide with the child's developmental level. These are:


A review study found that children treated with stimulants for as long as 2 years showed improvement in ADHD symptoms, comorbid oppositional defiant disorder and academic and school functioning [25].

#### **4.2. ADHD in adolescents**

#### *4.2.1. Epidemiology*

ADHD does not remit with the onset of puberty. Follow-up studies show that a majority (60‒85%) of children with ADHD will continue to meet criteria for the disorder during teen‐ age years (ages 13-18 years) [26].

#### *4.2.2. Clinical picture*

At adolescence, symptoms of hyperactivity and impulsivity related to ADHD tend to dimin‐ ish in intensity and are replaced with an inner restlessness, unableness to relax and feelings of unhappiness when not occupied [5]. Impulsivity presents in adolescents as interruptions of others, quick decisions, multitasking and feeling down when not occupied and feeling up when something is happening [5]. Inattention presents as disorganization, poor time man‐ agement, not listening to what is being said and as forgetfulness.

*4.2.4. Course and prognosis*

activity/impulsivity [6,30].

sistence has been inconsistent across studies [4-6, 31].

mission rather than disorder's course [31].

ble rate of syndromatic remission by age 20 [32].

*4.3.2. Clinical picture*

**4.3. ADHD in adults**

*4.3.1. Epidemiology*

It remains difficult to predict persistence of ADHD into adulthood. Controlling for se‐ verity and excluding treatment, none of the other variables (sociodemographics, child‐ hood adversity, traumatic life experiences and comorbidity) significantly predicted persistence, even though they were significantly associated with childhood ADHD [30]. Many studies reported adult persistence was much greater for inattention than for hyper‐

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Being diagnosed with ADHD as an adult actually means that the condition has been present since childhood, it just was not recognized or diagnosed at that time. Many follow-up stud‐ ies consistently documented the persistence of ADHD into adulthood, but the level of per‐

The first reason is the methodological, which includes changes in informant (patient's pa‐ rents versus adult patient), use of different instruments to diagnose ADHD in adults, comor‐ bidity and diagnostic criteria [31]. Diagnostic criteria are designed for school-aged children with regard to the number of symptoms required to meet the diagnostic threshold, which can be developmentally inappropriate for adults. Adults can suffer significant impairment even though they have fewer than six of nine symptoms needed for the diagnosis. The sec‐ ond reason is that differences in reported remission rates reflected the definition used for re‐

The persistence of the full syndrome of ADHD in adulthood has been found to be between 2‒8% when self-report is used [31]. When parent report is used, the prevalence increases to 46% [28]. The [30] study reported that 1 in 3 childhood ADHD still met DSM-IV criteria when aged 18- to 44-years [30]. In [32] study 40% of 18- to 20-year-old "grown up" ADHD patients met full criteria for ADHD, but 90% had at least five symptoms of ADHD [32].

Taking all studies together, the rates of syndromatic remission of ADHD in adults are quite in agreement; from 60% [32] to 65%‒70% [33]. But majority of subjects continue to struggle with substantial number of ADHD symptoms and high levels of dysfunction despite a siza‐

ADHD symptoms in adults manifest quite differently from the way they manifest in chil‐ dren. Hyperactivity is not impairing any more. It is rare to see ADHD adults fidgeting and/or running around. But some adult ADHD patients seem jittery and have trouble sitting still. Some complain of having "ants in their pants" and may experience an irritating need to pace [34]. Adults can learn through time to manage to settle their hyperactivity through ex‐ ercise or hard physical work. But if they are temporarily immobilized (broken leg, somatic

The [15] study found variations within ADHD subtypes in children and adolescents in the clinical population. Combined subtype is the most common one in childhood (43%), but in adolescence ADD subtype is more common (64%) [15].

Symptoms of ADHD in adolescence most often manifest during instructional or vocational situations. ADHD adolescents show signs of procrastination and disorganization with schoolwork. 46.3% of them did not complete high school and 29.3% retained a grade level at least once and 10.6% have been suspended from school. Feelings of tension, apprehension, the need for reassurance, irritability, negative self-image, and physical complaints are re‐ ported in more than 70% of ADHD patients [7, 27].

#### *4.2.3. Comorbidity*

ADHD in adolescence, especially if not treated can result in further complication (school suspension and/or expulsion, social exclusion, poor motivation, teen pregnancy, driving ac‐ cidents) and comorbid disorders (substance abuse or dependence, mood disorders, conduct disorders) [7, 17, 28].

Adolescents with (untreated) ADHD are more prone to substance abuse than their peers. In a [29] study the cumulative incidence of substance abuse disorders throughout adolescence was compared in 56 medicated ADHD patients, 19 non-medicated ADHD patients, and 137 non-ADHD control subjects. The analysis was restricted to male subjects older than 15 years of age. Substance abuse disorder was defined as any diagnosis of any of the following: alco‐ hol abuse/dependence (A/D), marijuana A/D, hallucinogen A/D, stimulant A/D, and cocaine A/D [29]. Non-medicated ADHD patients were at a significantly higher risk for substance abuse than either controls or medicated ADHD patients during the follow-up period of 4 years. However, there was no significant difference between medicated ADHD patients and controls. Medication was found to be associated with an 85% reduction in the risk of sub‐ stance abuse in ADHD patients [29].

ADHD and substance use disorder (SUD) may share also biological factors. Familial as‐ sociation between ADHD and SUD is strong, which suggests that two disorders may share genetic or other familial factors. The offspring of SUD parents are at greater risk not only for SUD, but also for inattention, impulsivity, aggressiveness, hyperactivity and ADHD [28].

#### *4.2.4. Course and prognosis*

*4.2.2. Clinical picture*

*4.2.3. Comorbidity*

disorders) [7, 17, 28].

ADHD [28].

stance abuse in ADHD patients [29].

At adolescence, symptoms of hyperactivity and impulsivity related to ADHD tend to dimin‐ ish in intensity and are replaced with an inner restlessness, unableness to relax and feelings of unhappiness when not occupied [5]. Impulsivity presents in adolescents as interruptions of others, quick decisions, multitasking and feeling down when not occupied and feeling up when something is happening [5]. Inattention presents as disorganization, poor time man‐

The [15] study found variations within ADHD subtypes in children and adolescents in the clinical population. Combined subtype is the most common one in childhood (43%), but in

Symptoms of ADHD in adolescence most often manifest during instructional or vocational situations. ADHD adolescents show signs of procrastination and disorganization with schoolwork. 46.3% of them did not complete high school and 29.3% retained a grade level at least once and 10.6% have been suspended from school. Feelings of tension, apprehension, the need for reassurance, irritability, negative self-image, and physical complaints are re‐

ADHD in adolescence, especially if not treated can result in further complication (school suspension and/or expulsion, social exclusion, poor motivation, teen pregnancy, driving ac‐ cidents) and comorbid disorders (substance abuse or dependence, mood disorders, conduct

Adolescents with (untreated) ADHD are more prone to substance abuse than their peers. In a [29] study the cumulative incidence of substance abuse disorders throughout adolescence was compared in 56 medicated ADHD patients, 19 non-medicated ADHD patients, and 137 non-ADHD control subjects. The analysis was restricted to male subjects older than 15 years of age. Substance abuse disorder was defined as any diagnosis of any of the following: alco‐ hol abuse/dependence (A/D), marijuana A/D, hallucinogen A/D, stimulant A/D, and cocaine A/D [29]. Non-medicated ADHD patients were at a significantly higher risk for substance abuse than either controls or medicated ADHD patients during the follow-up period of 4 years. However, there was no significant difference between medicated ADHD patients and controls. Medication was found to be associated with an 85% reduction in the risk of sub‐

ADHD and substance use disorder (SUD) may share also biological factors. Familial as‐ sociation between ADHD and SUD is strong, which suggests that two disorders may share genetic or other familial factors. The offspring of SUD parents are at greater risk not only for SUD, but also for inattention, impulsivity, aggressiveness, hyperactivity and

agement, not listening to what is being said and as forgetfulness.

adolescence ADD subtype is more common (64%) [15].

10 Attention Deficit Hyperactivity Disorder in Children and Adolescents

ported in more than 70% of ADHD patients [7, 27].

It remains difficult to predict persistence of ADHD into adulthood. Controlling for se‐ verity and excluding treatment, none of the other variables (sociodemographics, child‐ hood adversity, traumatic life experiences and comorbidity) significantly predicted persistence, even though they were significantly associated with childhood ADHD [30]. Many studies reported adult persistence was much greater for inattention than for hyper‐ activity/impulsivity [6,30].

#### **4.3. ADHD in adults**

#### *4.3.1. Epidemiology*

Being diagnosed with ADHD as an adult actually means that the condition has been present since childhood, it just was not recognized or diagnosed at that time. Many follow-up stud‐ ies consistently documented the persistence of ADHD into adulthood, but the level of per‐ sistence has been inconsistent across studies [4-6, 31].

The first reason is the methodological, which includes changes in informant (patient's pa‐ rents versus adult patient), use of different instruments to diagnose ADHD in adults, comor‐ bidity and diagnostic criteria [31]. Diagnostic criteria are designed for school-aged children with regard to the number of symptoms required to meet the diagnostic threshold, which can be developmentally inappropriate for adults. Adults can suffer significant impairment even though they have fewer than six of nine symptoms needed for the diagnosis. The sec‐ ond reason is that differences in reported remission rates reflected the definition used for re‐ mission rather than disorder's course [31].

The persistence of the full syndrome of ADHD in adulthood has been found to be between 2‒8% when self-report is used [31]. When parent report is used, the prevalence increases to 46% [28]. The [30] study reported that 1 in 3 childhood ADHD still met DSM-IV criteria when aged 18- to 44-years [30]. In [32] study 40% of 18- to 20-year-old "grown up" ADHD patients met full criteria for ADHD, but 90% had at least five symptoms of ADHD [32].

Taking all studies together, the rates of syndromatic remission of ADHD in adults are quite in agreement; from 60% [32] to 65%‒70% [33]. But majority of subjects continue to struggle with substantial number of ADHD symptoms and high levels of dysfunction despite a siza‐ ble rate of syndromatic remission by age 20 [32].

#### *4.3.2. Clinical picture*

ADHD symptoms in adults manifest quite differently from the way they manifest in chil‐ dren. Hyperactivity is not impairing any more. It is rare to see ADHD adults fidgeting and/or running around. But some adult ADHD patients seem jittery and have trouble sitting still. Some complain of having "ants in their pants" and may experience an irritating need to pace [34]. Adults can learn through time to manage to settle their hyperactivity through ex‐ ercise or hard physical work. But if they are temporarily immobilized (broken leg, somatic illness) and are suddenly deprived of a coping method, their hyperactivity can present as aggression and/or agitation [34].

*4.3.3. Comorbidity*

As in children and adolescents, adult ADHD is often present with comorbid disorders, which makes an accurate diagnosis even more difficult. Studies suggest that up to 90% of adult patients with ADHD have one or more comorbid psychiatric disorders [37]. The most common comorbid disorders in adults are anxiety disorders, affective disorders, substance abuse and antisocial personality disorder. In [36] study, the most prevalent comorbid disor‐ ders were lifetime depression (37.8%), substance abuse (28.1%) and alcohol abuse (23.3%), 14.6% had anxiety disorder. More than 19% had received a diagnosis of personality disor‐ der. Interesting in this study was that more women then men had comorbid borderline per‐ sonality disorder [36]. It is important to know that comorbid psychiatrics disorders emerge

ADHD Through Different Developmental Stages

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Bipolar disorder coexists with adult ADHD in 6–20% cases. Many ADHD symptoms can be mistakenly attributed to and overlooked because of bipolar disorder [37]. Interesting results were found in [39] study, namely that ADHD brings significant impairment to bipolar pa‐ tients, especially in adaptation and social functioning, compared with bipolar patients with‐ out comorbid ADHD. Even more interestingly, the authors failed to detect a significant impact of substance abuse on those same functional outcomes. This stresses out importance of making an accurate diagnosis of ADHD also in patients where the symptomatology (im‐ pulsiveness, multitasking, not finishing work, changing partners etc.) can be incorporated in

The high prevalence of comorbidity complicates the diagnostic process as well as treatment and some studies indicate that high rates of comorbidity in adult ADHD contribute nega‐

Follow-up periods into adulthood showed that stimulant treatment in childhood also was beneficial for social skills and self-esteem. Higher doses and longer treatment period pre‐

ADHD in adults have striking similarities with paediatric samples regarding psychiatric and cognitive impairment [41]. Some study suggest that the effect of stimulants is similar in paediatric and adult samples, which is a reason to believe that adult patients also will have

8-year-old boy was admitted to Child and Adolescent Psychiatry Unit because he had been experiencing increasing behavioural problems in the school during the last 3 months. He al‐ so showed slowness in mental tasks, was very impulsive, self-willed, irritable and displayed enhanced verbal and physical aggression. *History of problems* revealed delayed schooling be‐ cause of expressive language disorder. He was in the first grade of the primary school at ad‐ mission, while his peers where in the second grade. His mother presented a list of complaints as if they were copied from the ADHD diagnostic criteria ‒ he was always "on

early on in development in childhood and adolescence [38].

dicted less comorbidity and better social functioning [25].

another diagnosis (bipolar disorder) [39].

tively to the treatment outcome [40].

long-term positive outcome [42].

**5. Case report**

Symptoms of inattentiveness and impulsivity in adults manifest as [34]:


Adults with (untreated) ADHD are at greater risk for further complications compared with general population: changing jobs and partners, unstable relationships, financial problems, involvedness in car accidents, injuries, crime, and substance abuse. 16-year follow-up study found that men who had ADHD as boys were significantly more likely to be financially de‐ pendent on their parents, less likely to graduate from college, and had a lower social class than controls. These functional deficits are likely to be aggravated by the higher levels of neuropsychological impairment, which was observed on psychometric tests and on behav‐ ioural measures of executive dysfunction [35].

In Norway study, only 22.2% adult ADHD patients had ordinary work as their source of in‐ come, compared with 72% in the general population [36]. Approximately 48% had junior high school as their highest degree of education, compared with 29.8% in the general Nor‐ wegian population. Thus, more than half had an educational level not suited for most do‐ mains in the work market. Only 8.9% had a college or university degree, compared with 20.8% in the general population. 33% of ADHD patients were receiving disability pension and 38% temporary social benefits. Maybe the most interesting founding in this study was the fact that only 17.4% of participants with adult ADHD had been treated with central stimulants by the age of 18. Results are suggesting that early recognition and drug treatment of ADHD might protect against occupational impairment in adulthood [36].

Young adult drivers with ADHD were found to be nearly twice as likely to be cited for un‐ lawful speeding and to be cited more than three times as often as young adult subjects in the control group. Drivers with ADHD had more than 5 times as many traffic citations on their records than did controls [7].

#### *4.3.3. Comorbidity*

illness) and are suddenly deprived of a coping method, their hyperactivity can present as

**•** forgetfulness, particularly if it involves remembering tasks or jobs that need to be done.

**•** making decisions impulsively, or on the spur of the moment, without thinking about the

**•** frequently misjudge how much time they have – or need – to do something. They express

**•** being unable to tear themselves away from something enjoyable to shift to a more urgent,

Adults with (untreated) ADHD are at greater risk for further complications compared with general population: changing jobs and partners, unstable relationships, financial problems, involvedness in car accidents, injuries, crime, and substance abuse. 16-year follow-up study found that men who had ADHD as boys were significantly more likely to be financially de‐ pendent on their parents, less likely to graduate from college, and had a lower social class than controls. These functional deficits are likely to be aggravated by the higher levels of neuropsychological impairment, which was observed on psychometric tests and on behav‐

In Norway study, only 22.2% adult ADHD patients had ordinary work as their source of in‐ come, compared with 72% in the general population [36]. Approximately 48% had junior high school as their highest degree of education, compared with 29.8% in the general Nor‐ wegian population. Thus, more than half had an educational level not suited for most do‐ mains in the work market. Only 8.9% had a college or university degree, compared with 20.8% in the general population. 33% of ADHD patients were receiving disability pension and 38% temporary social benefits. Maybe the most interesting founding in this study was the fact that only 17.4% of participants with adult ADHD had been treated with central stimulants by the age of 18. Results are suggesting that early recognition and drug treatment

Young adult drivers with ADHD were found to be nearly twice as likely to be cited for un‐ lawful speeding and to be cited more than three times as often as young adult subjects in the control group. Drivers with ADHD had more than 5 times as many traffic citations on their

of ADHD might protect against occupational impairment in adulthood [36].

**•** they describe themselves having quick temper and low tolerance for frustration

Symptoms of inattentiveness and impulsivity in adults manifest as [34]:

aggression and/or agitation [34].

difficulty with being on time.

ioural measures of executive dysfunction [35].

records than did controls [7].

consequences

important task

They are often losing household items.

**•** unableness to keep track of several things at once

12 Attention Deficit Hyperactivity Disorder in Children and Adolescents

**•** difficulties in keeping promises or commitments to others

As in children and adolescents, adult ADHD is often present with comorbid disorders, which makes an accurate diagnosis even more difficult. Studies suggest that up to 90% of adult patients with ADHD have one or more comorbid psychiatric disorders [37]. The most common comorbid disorders in adults are anxiety disorders, affective disorders, substance abuse and antisocial personality disorder. In [36] study, the most prevalent comorbid disor‐ ders were lifetime depression (37.8%), substance abuse (28.1%) and alcohol abuse (23.3%), 14.6% had anxiety disorder. More than 19% had received a diagnosis of personality disor‐ der. Interesting in this study was that more women then men had comorbid borderline per‐ sonality disorder [36]. It is important to know that comorbid psychiatrics disorders emerge early on in development in childhood and adolescence [38].

Bipolar disorder coexists with adult ADHD in 6–20% cases. Many ADHD symptoms can be mistakenly attributed to and overlooked because of bipolar disorder [37]. Interesting results were found in [39] study, namely that ADHD brings significant impairment to bipolar pa‐ tients, especially in adaptation and social functioning, compared with bipolar patients with‐ out comorbid ADHD. Even more interestingly, the authors failed to detect a significant impact of substance abuse on those same functional outcomes. This stresses out importance of making an accurate diagnosis of ADHD also in patients where the symptomatology (im‐ pulsiveness, multitasking, not finishing work, changing partners etc.) can be incorporated in another diagnosis (bipolar disorder) [39].

The high prevalence of comorbidity complicates the diagnostic process as well as treatment and some studies indicate that high rates of comorbidity in adult ADHD contribute nega‐ tively to the treatment outcome [40].

Follow-up periods into adulthood showed that stimulant treatment in childhood also was beneficial for social skills and self-esteem. Higher doses and longer treatment period pre‐ dicted less comorbidity and better social functioning [25].

ADHD in adults have striking similarities with paediatric samples regarding psychiatric and cognitive impairment [41]. Some study suggest that the effect of stimulants is similar in paediatric and adult samples, which is a reason to believe that adult patients also will have long-term positive outcome [42].

#### **5. Case report**

8-year-old boy was admitted to Child and Adolescent Psychiatry Unit because he had been experiencing increasing behavioural problems in the school during the last 3 months. He al‐ so showed slowness in mental tasks, was very impulsive, self-willed, irritable and displayed enhanced verbal and physical aggression. *History of problems* revealed delayed schooling be‐ cause of expressive language disorder. He was in the first grade of the primary school at ad‐ mission, while his peers where in the second grade. His mother presented a list of complaints as if they were copied from the ADHD diagnostic criteria ‒ he was always "on the go", running and climbing whenever possible, when needed to sit still he was fidgeting, he talked excessively, blurted out answers, he could not await his turn, he intruded on oth‐ ers, did not listen to what was being said, lost things daily, was easily distracted and his school work was a disaster.

secondary schools, without finishing the first year in any of them. He was staying at home during the day, but went out in the evening taking his parent's money. When he took 2000

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15

He acted quite aloof at admission. He sat quietly and admitted that he was smoking mari‐ huana regularly for 3 years. He also tried ecstasy and cocaine several times – for the last time the weekend before. He drank alcohol regularly when he was in a company of others, otherwise he was too anxious. He had been playing poker for 3 years twice a week. He com‐ plained about his inner restlessness, which disappeared when he was on drugs or at least when he drank something. He revealed that he had rather poor peer relationships – actually he had no friends. He was unable to concentrate in school but had no problems concentrat‐ ing at poker game or at other pleasure activities (computer games, TV). He felt that he was a

loser; obviously he would not finish the school and he thought of suicide quite often.

He had been taking the medication for ADHD for two years (from the age of 8 till the age of 10), but stopped during the summer holidays. As he was no longer as hyperactive as before, his parents decided that he did not need it anymore. With a lot of help of his parents and instructors he somehow managed to finish the primary school, but at great cost – he strug‐

He was depressed and suicidal; anxious and tense but opponent to parents and medical

*Neuropsychological tests* at second hospitalization found organic-cerebral dysfunction, psy‐ chomotor and visuospatial disturbances as at the first testing. Actual IQ was discrepant with above average on verbal and lower borderline on non-verbal scale. Tests revealed executive deficits with diminished inhibition, planning, controlling and anticipation. Depressive

He was fulfilling the DSM-IV diagnostic criteria for *ADHD – inattentive type and for major de‐ pressive disorder.* Again, bipolar disorder was considered as possible diagnosis, but was ex‐ cluded due to a constant pattern of inattention, impulsive and hyperkinetic problems, without any episodic changes in ADHD or affective symptoms. He was treated with atom‐ oxetine and antidepressants and he attended the program for addicted/at risk adolescents for a year. He managed to finish the first year of the secondary school. Then he stopped tak‐ ing the medication and attending the program and started with marihuana and occasionally

Reported case describes prototypic ADHD child regarding the symptomatic and its chang‐ ing over development, family attitude to medication and family stress, comorbidity in child‐

It often happens that parents endure with hyperactivity symptoms and seek help only when school performance is critical. In severe ADHD cases, which also fulfil more strict ICD-10 diagnostic criteria for HD, the problems in school performance and behaviour are

EUR, they started suspecting drug abuse for the first time

gled with extremely low self- esteem.

symptomatic was also found.

used other drugs again.

hood and adolescence, and the course of disease.

**5.1. Discussion**

staff at admission.

*Developmental history* revealed a risk pregnancy with malpresentation (not head down posi‐ tion of a fetus). He was the third child, prematurely born, with icterus and apnoeic attacks. He was lagging in motor development (he walked independently at the age of 20 months) and in language development (spoke the first words at the age of 3, he visited speech and language therapist).

*Family history* was interesting since his father had symptoms of ADHD in his youth. One of his two brothers uttered the first words at the age of five. *General assessment at admission* showed clumsiness and stuttering. *Further observations* showed that he was easily distracted, had lapses in attention, was overactive, impulsive and impatient. He usually acted without thinking, behaved inappropriately, was verbally and physically aggressive towards co-pa‐ tients and medical staff, testing the limits all the time and showing stubbornness. He also seemed unhappy, sad and angry with sudden changes in mood.

*Neuropsychological tests* found organic-cerebral dysfunction, psychomotor and visuospatial disturbances and profound attention deficit with hyperactivity. His IQ at the time of testing was borderline due to severe inattention and hyperactivity. He presented with diminished inhibition, showed personally and emotionally less mature compared with his peers and he has been found as quite egocentric. *Basic laboratory tests* (including thyroid levels) and EEG were normal.

The boy fulfilled DSM-IV diagnostic criteria for ADHD *–* combined type. Because of his changing mood and aggressive periods which were new in his behaviour, bipolar disorder was considered as a possible *differential diagnosis or comorbid disorder*. His hyperactivity exist‐ ed ever since he was born and was not episodic (which is typical for hyperactivity in bipolar disorder). He was easily distracted and mostly did not finish his tasks ‒ but not because of flight of ideas, thought racing or delusions as seen in manic episodes. He was impulsive, blurting answers and interrupting – again not because of pressured speech or impulsive poor judgment as seen in manic episodes. His school performance was bad because of his inattention and not because of the loss of interest – as seen in depressed episodes of bipolar disorder. He was never grandiose and had never any appetite or weight changes often seen in bipolar patients. He was diagnosed as *ADHD combined type with comorbid oppositional-defi‐ ant and expressive language disorder*. He received psychostimulants, we educated his parents and his school teachers about the disorder and advised them about the behavioural manage‐ ment techniques. He continued visiting the speech therapists. He responded well to all in‐ troduced measures and we followed him for about a year when he moved to another city.

Nine years later (as 17-year-old) he was admitted again to our child and adolescent psychia‐ try ward. Parents complained about severe behavioural problems lasting for two years. He threatened with suicide several times, had constant difficulties with authority, was disre‐ garding his safety and was involved in a series of injuries and accidents. He changed three secondary schools, without finishing the first year in any of them. He was staying at home during the day, but went out in the evening taking his parent's money. When he took 2000 EUR, they started suspecting drug abuse for the first time

He acted quite aloof at admission. He sat quietly and admitted that he was smoking mari‐ huana regularly for 3 years. He also tried ecstasy and cocaine several times – for the last time the weekend before. He drank alcohol regularly when he was in a company of others, otherwise he was too anxious. He had been playing poker for 3 years twice a week. He com‐ plained about his inner restlessness, which disappeared when he was on drugs or at least when he drank something. He revealed that he had rather poor peer relationships – actually he had no friends. He was unable to concentrate in school but had no problems concentrat‐ ing at poker game or at other pleasure activities (computer games, TV). He felt that he was a loser; obviously he would not finish the school and he thought of suicide quite often.

He had been taking the medication for ADHD for two years (from the age of 8 till the age of 10), but stopped during the summer holidays. As he was no longer as hyperactive as before, his parents decided that he did not need it anymore. With a lot of help of his parents and instructors he somehow managed to finish the primary school, but at great cost – he strug‐ gled with extremely low self- esteem.

He was depressed and suicidal; anxious and tense but opponent to parents and medical staff at admission.

*Neuropsychological tests* at second hospitalization found organic-cerebral dysfunction, psy‐ chomotor and visuospatial disturbances as at the first testing. Actual IQ was discrepant with above average on verbal and lower borderline on non-verbal scale. Tests revealed executive deficits with diminished inhibition, planning, controlling and anticipation. Depressive symptomatic was also found.

He was fulfilling the DSM-IV diagnostic criteria for *ADHD – inattentive type and for major de‐ pressive disorder.* Again, bipolar disorder was considered as possible diagnosis, but was ex‐ cluded due to a constant pattern of inattention, impulsive and hyperkinetic problems, without any episodic changes in ADHD or affective symptoms. He was treated with atom‐ oxetine and antidepressants and he attended the program for addicted/at risk adolescents for a year. He managed to finish the first year of the secondary school. Then he stopped tak‐ ing the medication and attending the program and started with marihuana and occasionally used other drugs again.

#### **5.1. Discussion**

the go", running and climbing whenever possible, when needed to sit still he was fidgeting, he talked excessively, blurted out answers, he could not await his turn, he intruded on oth‐ ers, did not listen to what was being said, lost things daily, was easily distracted and his

*Developmental history* revealed a risk pregnancy with malpresentation (not head down posi‐ tion of a fetus). He was the third child, prematurely born, with icterus and apnoeic attacks. He was lagging in motor development (he walked independently at the age of 20 months) and in language development (spoke the first words at the age of 3, he visited speech and

*Family history* was interesting since his father had symptoms of ADHD in his youth. One of his two brothers uttered the first words at the age of five. *General assessment at admission* showed clumsiness and stuttering. *Further observations* showed that he was easily distracted, had lapses in attention, was overactive, impulsive and impatient. He usually acted without thinking, behaved inappropriately, was verbally and physically aggressive towards co-pa‐ tients and medical staff, testing the limits all the time and showing stubbornness. He also

*Neuropsychological tests* found organic-cerebral dysfunction, psychomotor and visuospatial disturbances and profound attention deficit with hyperactivity. His IQ at the time of testing was borderline due to severe inattention and hyperactivity. He presented with diminished inhibition, showed personally and emotionally less mature compared with his peers and he has been found as quite egocentric. *Basic laboratory tests* (including thyroid levels) and EEG

The boy fulfilled DSM-IV diagnostic criteria for ADHD *–* combined type. Because of his changing mood and aggressive periods which were new in his behaviour, bipolar disorder was considered as a possible *differential diagnosis or comorbid disorder*. His hyperactivity exist‐ ed ever since he was born and was not episodic (which is typical for hyperactivity in bipolar disorder). He was easily distracted and mostly did not finish his tasks ‒ but not because of flight of ideas, thought racing or delusions as seen in manic episodes. He was impulsive, blurting answers and interrupting – again not because of pressured speech or impulsive poor judgment as seen in manic episodes. His school performance was bad because of his inattention and not because of the loss of interest – as seen in depressed episodes of bipolar disorder. He was never grandiose and had never any appetite or weight changes often seen in bipolar patients. He was diagnosed as *ADHD combined type with comorbid oppositional-defi‐ ant and expressive language disorder*. He received psychostimulants, we educated his parents and his school teachers about the disorder and advised them about the behavioural manage‐ ment techniques. He continued visiting the speech therapists. He responded well to all in‐ troduced measures and we followed him for about a year when he moved to another city.

Nine years later (as 17-year-old) he was admitted again to our child and adolescent psychia‐ try ward. Parents complained about severe behavioural problems lasting for two years. He threatened with suicide several times, had constant difficulties with authority, was disre‐ garding his safety and was involved in a series of injuries and accidents. He changed three

seemed unhappy, sad and angry with sudden changes in mood.

school work was a disaster.

14 Attention Deficit Hyperactivity Disorder in Children and Adolescents

language therapist).

were normal.

Reported case describes prototypic ADHD child regarding the symptomatic and its chang‐ ing over development, family attitude to medication and family stress, comorbidity in child‐ hood and adolescence, and the course of disease.

It often happens that parents endure with hyperactivity symptoms and seek help only when school performance is critical. In severe ADHD cases, which also fulfil more strict ICD-10 diagnostic criteria for HD, the problems in school performance and behaviour are obvious already in the first grade of primary school and are so severe that parents are faced with the necessity for special assessment and treatment. Comprehensive treatment that includes education and support to parents and teachers, and also pharmacotherapy is very effective. As in presented case, children manage developmental tasks quite well as long the treatment is provided. Hyperactivity symptoms diminish with development and many parents understand this as a signal that the child has grown up of the ADHD and they stop with the treatment.

**References**

tion, Geneva, 1993.

[1] American Psychiatric Association. [1994]. Diagnostic and statistical manual of mental

ADHD Through Different Developmental Stages

http://dx.doi.org/10.5772/53963

17

[2] Classification of mental and behavioural disorders (ICD-10]. World Health Organiza‐

[3] Taylor E, Dopfner M, Sergeant J et al. European clinical guidelines for hyperkinetic

[4] Remschmidt H. Kinder- und Jugendpsychiatry. Stuttgart: Geirg Thieme Verlag; 2005.

[5] Martin A, Volkmar FR. Lewis's child and adolescent psychiatry. New York: Wolters

[6] Rutter M, Bishop D, Pine D et al. Rutter's child and adolescent psychiatry. Massachu‐

[7] Barkley RA, Murphy KR, Kwasnik D. Motor vehicle driving competencies and risks in teens and young adults with attention deficit hyperactivity disorder. Pediatrics

[8] National institute for health and clinical excellence. Attention deficit hyperactivity disorder. Diagnosis and management of ADHD in children, young people and adults. London: the British psychological society and the royal college of psychia‐

[9] Pliszka S, Bernet W, Bukstein O, Walter HJ et al. Practical parameter for assessment and treatment of children and adolescents with attention deficit hyperactivity disor‐

[10] APA DSM-5. A 10 attention deficit/hyperactivity disorder. http://www.dsm5.org/

[11] Barkley RA, Brown TE. Unrecognized attention-deficit/hyperactivity disorder in adults presenting with other psychiatric disorders. CNS Spectr 2008; 13[11]: 977-984.

[12] Rowland AS, Umbach DM, Stallone L et al. Prevalence of medication treatment for attention deficit hyperactivity disorder among elementary school children in John‐

[13] Bararesi WJ, Katusic SK, Colligan RC et al. How common is attention deficit hyperac‐ tivity disorder? Incidence in a population-based birth cohort in Rochester. Minn

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trists; 2009.

But in majority of ADHD cases, the symptoms only present differently but continue to interfere further in adolescent/adult life as inner restlessness, tension and irritability. Pa‐ tients have low school/work performance, are disorganized, have difficulties in social re‐ lationships, often abuse drugs, and are engaged in car accidences. As a further burden, the majority of them also have comorbid disorders such as depression, anxiety, bipolar disorder and personality disorder. The stress on family grows and the vicious circle of self-blame, avoidance of social contacts and low self-esteem repeats. In such cases, com‐ prehensive treatment enables better schoolwork, settles inner restlessness and tension, re‐ sulting in lower need for drug abuse.

#### **6. Conclusion**

ADHD disorder is predominantly diagnosed in childhood, persisting into adolescence and adulthood in majority of cases. With development the symptoms change, which is the rea‐ son why many of the adolescent and adult ADHD patients stay unrecognised. High comor‐ bidity in adolescence and adulthood is the second reason for ADHD unrecognition after childhood. The fact is that it is quite difficult to consider ADHD when patients complain about depressive symptoms, drug abuse or have a personality disorder. But with careful personal history which also involves patient's childhood (interview with patient's parents) and with the help of specialized ADHD questionnaires, ADHD can be properly diagnosed.

Comprehensive treatment is crucial in any developmental period. It is essential not only for reducing the core ADHD symptoms, but also for preventing many consequences of untreat‐ ed ADHD and for ensuring better quality of life for patients and their families.

#### **Author details**

Hojka Gregoric Kumperscak

Address all correspondence to: hojka.gregoric@guest.arnes.si

Department of Paediatrics, Child and Adolescents Psychiatry Unit, University Clinical Cen‐ tre Maribor, Maribor, Slovenia

#### **References**

obvious already in the first grade of primary school and are so severe that parents are faced with the necessity for special assessment and treatment. Comprehensive treatment that includes education and support to parents and teachers, and also pharmacotherapy is very effective. As in presented case, children manage developmental tasks quite well as long the treatment is provided. Hyperactivity symptoms diminish with development and many parents understand this as a signal that the child has grown up of the ADHD

But in majority of ADHD cases, the symptoms only present differently but continue to interfere further in adolescent/adult life as inner restlessness, tension and irritability. Pa‐ tients have low school/work performance, are disorganized, have difficulties in social re‐ lationships, often abuse drugs, and are engaged in car accidences. As a further burden, the majority of them also have comorbid disorders such as depression, anxiety, bipolar disorder and personality disorder. The stress on family grows and the vicious circle of self-blame, avoidance of social contacts and low self-esteem repeats. In such cases, com‐ prehensive treatment enables better schoolwork, settles inner restlessness and tension, re‐

ADHD disorder is predominantly diagnosed in childhood, persisting into adolescence and adulthood in majority of cases. With development the symptoms change, which is the rea‐ son why many of the adolescent and adult ADHD patients stay unrecognised. High comor‐ bidity in adolescence and adulthood is the second reason for ADHD unrecognition after childhood. The fact is that it is quite difficult to consider ADHD when patients complain about depressive symptoms, drug abuse or have a personality disorder. But with careful personal history which also involves patient's childhood (interview with patient's parents) and with the help of specialized ADHD questionnaires, ADHD can be properly diagnosed.

Comprehensive treatment is crucial in any developmental period. It is essential not only for reducing the core ADHD symptoms, but also for preventing many consequences of untreat‐

Department of Paediatrics, Child and Adolescents Psychiatry Unit, University Clinical Cen‐

ed ADHD and for ensuring better quality of life for patients and their families.

Address all correspondence to: hojka.gregoric@guest.arnes.si

and they stop with the treatment.

16 Attention Deficit Hyperactivity Disorder in Children and Adolescents

sulting in lower need for drug abuse.

**6. Conclusion**

**Author details**

Hojka Gregoric Kumperscak

tre Maribor, Maribor, Slovenia


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[37] Nutt DJ, Fone K, Asherson P et al. Evidence-based guidelines for management of at‐ tention deficit hyperactivity disorder in adolescents in transition to adult services and in adults: recommendations from the British association for psychopharmacolo‐

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**Chapter 2**

**Neurodevelopmental Pathways of Childhood ADHD**

Alban Burke and Amanda Edge

but not the symptoms of this disorder.

ferences in these neurobiological factors.

http://dx.doi.org/10.5772/53865

**1. Introduction**

Additional information is available at the end of the chapter

**into Adulthood: Maturational Lag, Deviation, or Both?**

The DSM-5 [1], which should be published in 2013, will in all likelihood have a category named Neurodevelopmental Disorders, under which ADHD will resort. This shift in nosol‐ ogy lays the foundation of the argument that will be put forward in this chapter, therefore the following points need to be emphasised and warrants further discussion. Firstly, this categorisation is based on shared aetiology, rather than shared symptoms or shared devel‐ opmental stage (as was the case with the DSM-IV-TR). Historically, disorders were classified according to shared aetiology (as was the case with DSMI and DSM-II), as opposed to shared symptomatology (as was the case with DSM-III and DSM-IVTR). The DSM-5 is to a greater, or lesser, extent a combination of these as it proposes a change to the categorisation,

The second point is that the shared aetiology is a *neurobiological based aetiology*. The name of the category implies that these disorders have a common, underlying, neurobiological cause. The question which arises is to what extent these disorders do have an underlying neurobiological cause, to what extent this is shared, and even to what extent these causes are shared within the sub-categories of disorders, for example ADHD. Grouping these disorders together implies a relatively homogenous group of disorders, and even further that the subcategories are homogenous within themselves. The DSM-5 makes provision for 4 sub-cate‐ gories of ADHD, i.e. the *Combined*, *Predominantly Inattentive*, *Inattentive (Restrictive)* and predominantly *Hyperactive/ Impulsive*, presentations. Does the grouping of these sub-catego‐ ries necessarily imply that they share the same neurobiological aetiology? The argument that will be put forward in this chapter is that although they all share a neurobiological cause, this cause is not common and that the sub- categories may have subtle or gross, dif‐

> © 2013 Burke and Edge; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

and reproduction in any medium, provided the original work is properly cited.

© 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,

### **Neurodevelopmental Pathways of Childhood ADHD into Adulthood: Maturational Lag, Deviation, or Both?**

Alban Burke and Amanda Edge

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/53865

#### **1. Introduction**

The DSM-5 [1], which should be published in 2013, will in all likelihood have a category named Neurodevelopmental Disorders, under which ADHD will resort. This shift in nosol‐ ogy lays the foundation of the argument that will be put forward in this chapter, therefore the following points need to be emphasised and warrants further discussion. Firstly, this categorisation is based on shared aetiology, rather than shared symptoms or shared devel‐ opmental stage (as was the case with the DSM-IV-TR). Historically, disorders were classified according to shared aetiology (as was the case with DSMI and DSM-II), as opposed to shared symptomatology (as was the case with DSM-III and DSM-IVTR). The DSM-5 is to a greater, or lesser, extent a combination of these as it proposes a change to the categorisation, but not the symptoms of this disorder.

The second point is that the shared aetiology is a *neurobiological based aetiology*. The name of the category implies that these disorders have a common, underlying, neurobiological cause. The question which arises is to what extent these disorders do have an underlying neurobiological cause, to what extent this is shared, and even to what extent these causes are shared within the sub-categories of disorders, for example ADHD. Grouping these disorders together implies a relatively homogenous group of disorders, and even further that the subcategories are homogenous within themselves. The DSM-5 makes provision for 4 sub-cate‐ gories of ADHD, i.e. the *Combined*, *Predominantly Inattentive*, *Inattentive (Restrictive)* and predominantly *Hyperactive/ Impulsive*, presentations. Does the grouping of these sub-catego‐ ries necessarily imply that they share the same neurobiological aetiology? The argument that will be put forward in this chapter is that although they all share a neurobiological cause, this cause is not common and that the sub- categories may have subtle or gross, dif‐ ferences in these neurobiological factors.

© 2013 Burke and Edge; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

The name of the category also implies a more fluid and dynamic process that starts in child‐ hood and may, or may not, extend across the lifespan into adulthood. This is in sharp con‐ trast to the more traditional, and rather rigid, distinction between adulthood and childhood pathologies. This category allows for the straddling between childhood and adulthood path‐ ologies. An important point, which warrants emphasis, is that these disorders typically *origi‐ nate in childhood,* which may then extend into adulthood. Again, in sharp contrast to the previous DSM classifications, the DSM-5 makes slightly more provision for ADHD in adult‐ hood. As far as the specific criteria, as well as the sub-categories, are concerned, the criteria for ADHD in adulthood are rather superficial as it does not include the rather extensive re‐ search that has been done on the clinical manifestation of this disorder in adulthood, nor is it explicit enough in terms of possible sub-categories of this disorder in adulthood. This cre‐ ates a picture of a rather homogenous disorder in adulthood which either influences, or is perpetuated by, research on this topic.

*mental deviation model,* appear to be particularly relevant to the syndrome of ADHD. In this

Neurodevelopmental Pathways of Childhood ADHD into Adulthood: Maturational Lag, Deviation, or Both?

http://dx.doi.org/10.5772/53865

23

While some evidence has suggested that the ADHD brain develops in fundamentally differ‐ ent ways to typical ones, other results have argued that they are just the result of a lag in the normal timetable for development, which is known as the maturational lag model [5]. This model of ADHD is organised around the notion that that the behaviours of a child with ADHD is abnormal merely in reference to his or her age [5]. This direction in thinking was initially based on observations that children with ADHD behave similarly to younger chil‐ dren who are more active, impulsive and exhibit a shorter attention span [6]. According to this model [5], "if the child was younger, the findings would be regarded as normal" (p. 268). He further postulates that the neurological factors that limit the performance of a child with ADHD are synonymous to that which typically limits the performance of younger chil‐ dren. Hence, the maturational lag model [5] stipulates that an individual with ADHD presents with a relative delay in certain aspects of their neurological maturation, but that maturation will eventually 'catch up'. On average, the brain of ADHD children matured about three years later than those of their peers, with 50% of their cortex only reaching maxi‐ mum thickness at age 10 years 6 months as opposed to 7 years and 6 months of those chil‐ dren without ADHD [7]. The lags in maturation seem to differ from one cortical area to the next, for example, the lag in the prefrontal cortex can be as high as 5 years. In other areas, the ADHD brain seems to mature faster than in a non-ADHD brain, an example being the primary motor cortex. These researchers draw the conclusion that their findings support the

Nearly 50 years of electrophysiological (EEG) research in the realm of ADHD suggest that children and adolescents who present with the disorder display abnormalities in their EEG [8]. The abnormalities observed are either organised according to the maturational lag or de‐ velopmental deviation model. From an EEG perspective, the maturational lag model sug‐ gests that an individual with ADHD should present with cortical activity that is similar to that witnessed in younger children [9, 10], since an increase in slow wave activity (delta and theta) and decreased fast wave activity (alpha and beta) is typical in younger children [11]. A number of researchers [12-16] interpret their findings of increased slow wave activity in children and adolescents with ADHD during an eyes closed resting condition as evidence of a maturational lag. Additional EEG support for the maturational lag is presented in Table 1.

The second neurodevelopmental model is that of the developmental deviation, also known as maturational deviance, which proposes that maturation is not necessarily lagging, but that it is not approaching normality or maturation, and that it is unlikely to do so at any stage during the lifespan. This model was built on EEG research where 90% of the ADHD sample presented with aberrances in their EEG activity [17]. Subsequently, the developmen‐ tal deviation model of ADHD came into play, which suggests that ADHD results from ab‐

section evidence supporting these two views will be reported.

hypothesis of maturational lag, not maturational deviance.

**2.2. Maturational deviance in ADHD**

**2.1. Maturational lag in ADHD**

As much as many Mental Health professionals would like to accept that the diagnosis of ADHD in adulthood is a valid one, there is also still much scepticism about both the validity of this disorder, as well as the clinical picture / diagnostic criteria. Some authors [2] postu‐ late that this scepticism may also be due to extensive, but poorly described, comorbid Axis I and Axis II disorders. Although some may consider ADHD and Personality Disorders (spe‐ cifically Cluster B) to be co-morbid conditions, there are also those that would argue that these Personality Disorders are often misdiagnosed as ADHD, or *vice versa* [3]. The roots of the dilemma are twofold, i.e. that Personality Disorders are a separate and distinct set of dis‐ orders that do not have a biological underpinning and the arbitrary distinction between childhood and adult pathology. If one removes both these problematic issues, and rather view a disorder in terms of the aberrant development of behaviour, (neuro)cognition and emotion (as opposed to "personality") over time (rather than in life stages), a different pic‐ ture, i.e. one of either maturational lag or maturational deviance, emerges. The neurodeve‐ lopmental disorders, such as ADHD, are associated with a unique temperament that is characterised by high novelty seeking, harm avoidance and low reward dependence [3]. The question that arises is whether the neurodevelopmental and personality disorders are the re‐ sult of the same underlying neurological process, or whether they are parallel processes that may or may not have reciprocal effects on each other [4]. On a theoretical level, i.e. the ma‐ turational lag theory, these two categories of disorders may be considered together, if it is indeed that the maturational lag theory holds true for both of them.

#### **2. Neurodevelopment of ADHD**

The use of the concept neurodevelopment in the categorisation and organisation of disor‐ ders in the DSM-5 suggests that variant disorders can be arranged according to specific neu‐ rodevelopmental pathways. It is understood that the developmental pathway may account for the neurobiological underpinnings, and thus aetiological foundation of the syndrome ob‐ served. Two neurodevelopmental models, namely the *maturational lag model* and the *develop‐* *mental deviation model,* appear to be particularly relevant to the syndrome of ADHD. In this section evidence supporting these two views will be reported.

#### **2.1. Maturational lag in ADHD**

The name of the category also implies a more fluid and dynamic process that starts in child‐ hood and may, or may not, extend across the lifespan into adulthood. This is in sharp con‐ trast to the more traditional, and rather rigid, distinction between adulthood and childhood pathologies. This category allows for the straddling between childhood and adulthood path‐ ologies. An important point, which warrants emphasis, is that these disorders typically *origi‐ nate in childhood,* which may then extend into adulthood. Again, in sharp contrast to the previous DSM classifications, the DSM-5 makes slightly more provision for ADHD in adult‐ hood. As far as the specific criteria, as well as the sub-categories, are concerned, the criteria for ADHD in adulthood are rather superficial as it does not include the rather extensive re‐ search that has been done on the clinical manifestation of this disorder in adulthood, nor is it explicit enough in terms of possible sub-categories of this disorder in adulthood. This cre‐ ates a picture of a rather homogenous disorder in adulthood which either influences, or is

As much as many Mental Health professionals would like to accept that the diagnosis of ADHD in adulthood is a valid one, there is also still much scepticism about both the validity of this disorder, as well as the clinical picture / diagnostic criteria. Some authors [2] postu‐ late that this scepticism may also be due to extensive, but poorly described, comorbid Axis I and Axis II disorders. Although some may consider ADHD and Personality Disorders (spe‐ cifically Cluster B) to be co-morbid conditions, there are also those that would argue that these Personality Disorders are often misdiagnosed as ADHD, or *vice versa* [3]. The roots of the dilemma are twofold, i.e. that Personality Disorders are a separate and distinct set of dis‐ orders that do not have a biological underpinning and the arbitrary distinction between childhood and adult pathology. If one removes both these problematic issues, and rather view a disorder in terms of the aberrant development of behaviour, (neuro)cognition and emotion (as opposed to "personality") over time (rather than in life stages), a different pic‐ ture, i.e. one of either maturational lag or maturational deviance, emerges. The neurodeve‐ lopmental disorders, such as ADHD, are associated with a unique temperament that is characterised by high novelty seeking, harm avoidance and low reward dependence [3]. The question that arises is whether the neurodevelopmental and personality disorders are the re‐ sult of the same underlying neurological process, or whether they are parallel processes that may or may not have reciprocal effects on each other [4]. On a theoretical level, i.e. the ma‐ turational lag theory, these two categories of disorders may be considered together, if it is

The use of the concept neurodevelopment in the categorisation and organisation of disor‐ ders in the DSM-5 suggests that variant disorders can be arranged according to specific neu‐ rodevelopmental pathways. It is understood that the developmental pathway may account for the neurobiological underpinnings, and thus aetiological foundation of the syndrome ob‐ served. Two neurodevelopmental models, namely the *maturational lag model* and the *develop‐*

indeed that the maturational lag theory holds true for both of them.

**2. Neurodevelopment of ADHD**

perpetuated by, research on this topic.

22 Attention Deficit Hyperactivity Disorder in Children and Adolescents

While some evidence has suggested that the ADHD brain develops in fundamentally differ‐ ent ways to typical ones, other results have argued that they are just the result of a lag in the normal timetable for development, which is known as the maturational lag model [5]. This model of ADHD is organised around the notion that that the behaviours of a child with ADHD is abnormal merely in reference to his or her age [5]. This direction in thinking was initially based on observations that children with ADHD behave similarly to younger chil‐ dren who are more active, impulsive and exhibit a shorter attention span [6]. According to this model [5], "if the child was younger, the findings would be regarded as normal" (p. 268). He further postulates that the neurological factors that limit the performance of a child with ADHD are synonymous to that which typically limits the performance of younger chil‐ dren. Hence, the maturational lag model [5] stipulates that an individual with ADHD presents with a relative delay in certain aspects of their neurological maturation, but that maturation will eventually 'catch up'. On average, the brain of ADHD children matured about three years later than those of their peers, with 50% of their cortex only reaching maxi‐ mum thickness at age 10 years 6 months as opposed to 7 years and 6 months of those chil‐ dren without ADHD [7]. The lags in maturation seem to differ from one cortical area to the next, for example, the lag in the prefrontal cortex can be as high as 5 years. In other areas, the ADHD brain seems to mature faster than in a non-ADHD brain, an example being the primary motor cortex. These researchers draw the conclusion that their findings support the hypothesis of maturational lag, not maturational deviance.

Nearly 50 years of electrophysiological (EEG) research in the realm of ADHD suggest that children and adolescents who present with the disorder display abnormalities in their EEG [8]. The abnormalities observed are either organised according to the maturational lag or de‐ velopmental deviation model. From an EEG perspective, the maturational lag model sug‐ gests that an individual with ADHD should present with cortical activity that is similar to that witnessed in younger children [9, 10], since an increase in slow wave activity (delta and theta) and decreased fast wave activity (alpha and beta) is typical in younger children [11]. A number of researchers [12-16] interpret their findings of increased slow wave activity in children and adolescents with ADHD during an eyes closed resting condition as evidence of a maturational lag. Additional EEG support for the maturational lag is presented in Table 1.

#### **2.2. Maturational deviance in ADHD**

The second neurodevelopmental model is that of the developmental deviation, also known as maturational deviance, which proposes that maturation is not necessarily lagging, but that it is not approaching normality or maturation, and that it is unlikely to do so at any stage during the lifespan. This model was built on EEG research where 90% of the ADHD sample presented with aberrances in their EEG activity [17]. Subsequently, the developmen‐ tal deviation model of ADHD came into play, which suggests that ADHD results from ab‐ normalities in CNS functioning [9]. It further denotes that the EEGs of children and adolescents with ADHD symptoms are not considered normal in children of any age and that it is also not likely to mature in a normal fashion [9]. Additional evidence for this model is provided by the adult ADHD (ADHD) studies which found that the presence of elevated slow wave activity, especially theta, persists into adulthood [18-19].

is also the foundation for on-going debates concerning the comorbidity between ADHD in adulthood and personality disorders. If one adopts a neurobiological / neurocognitive approach to personality, then the overlap between temperament, personality and person‐ ality disorders becomes more evident. Furthermore, given the mounting evidence that ADHD can persist from childhood into adulthood, it also follows that there should be more focus on the relationship between personality and ADHD [35]. Some authors [36] maintain that is important to describe ADHD in adulthood in terms of general personali‐ ty structures as it could contribute to a better conceptualization of the disorder. Further‐ more, there are suggestions that there is evidence that indicates that developmental factors may contribute to ADHD in ways that are separate from the associated behav‐ iour problems. One could go further by saying that it is important to describe personali‐ ty disorders (from a neurobiological perspective) in adults with ADHD, as this could aid in describing a possible shared aetiology. In fact one could go as far as to say that in‐ complete descriptions of Personality Disorders in ADHD continue to place pressure on the validity of the diagnosis in adulthood [2]. Although there have been a number of studies that have focused on the relationship between ADHD and personality, some au‐ thors [35] maintain that these studies have focussed on only a narrow range of personali‐ ty constructs. Table 2 provides a summary of personality constructs that have been investigated in relation to ADHD, as well as how these characteristics may feature in

Neurodevelopmental Pathways of Childhood ADHD into Adulthood: Maturational Lag, Deviation, or Both?

personality disorders.

maturational deviation

**Construct Characteristic of**

Sensation Seeking / External stimulation seeking [38, 39] Antisocial [49]

Externalizing problem behaviours [42] Antisocial [50] Emotional lability [41] Borderline [44]

Low reward dependence [43] Antisocial [47] Uncooperativeness [43] Borderline [46]

of disorders. The argument is based on the following postulates:

**ADHD**

Self-regulation [40] Borderline, Antisocial and Histrionic [50]

**Table 2.** Summary of personality constructs identified in ADHD and possible links with Cluster B disorders

There has traditionally been a great but, arguably unwarranted [43], emphasis on the preva‐ lence of Cluster B personality disorder in adults with ADHD. This study, in effect wants to investigate whether there is some shared neurodevelopmental process in both of these sets

**•** ADHD is a neurodevelopmental disorder and is the result of either maturational lag or

Behavioural disinhibition / Impulsivity [40, 41] Antisocial and Borderline [45]

**Characteristic of Cluster B Personality**

http://dx.doi.org/10.5772/53865

25

**Disorder**

Borderline [46, 48, 51]

Axis II disorders [52]

Antisocial and Borderline [45]

#### **2.3. Summary and conclusion**

The research referred to in this section was concerned with the investigation of cortical ac‐ tivity patterns in adults with ADHD via EEG methodologies. The research was specifically interested in the cortical activity patterns of adults with ADHD symptomatology at frontal, frontal midline and parietal sites seeing that these areas are often the most heavily implicat‐ ed in ADHD. From existing literature, it can be concluded that there is evidence that sup‐ ports both the maturational lag as well as the maturational deviance models (See Table 1).


**Table 1.** EEG support for the maturational lag and developmental deviation models

#### **3. Personality disorders**

Personality and psychopathology have, throughout the 20th century, been viewed as sep‐ arate but related domains. Although they have been viewed as related domains, the ex‐ act relationship remains largely unclear. In 1980, within psychopathology, clinical syndromes were separated from personality disorders [34]. Splitting these domains high‐ lighted the overlap between symptoms of clinical and personality disorders [34], which is also the foundation for on-going debates concerning the comorbidity between ADHD in adulthood and personality disorders. If one adopts a neurobiological / neurocognitive approach to personality, then the overlap between temperament, personality and person‐ ality disorders becomes more evident. Furthermore, given the mounting evidence that ADHD can persist from childhood into adulthood, it also follows that there should be more focus on the relationship between personality and ADHD [35]. Some authors [36] maintain that is important to describe ADHD in adulthood in terms of general personali‐ ty structures as it could contribute to a better conceptualization of the disorder. Further‐ more, there are suggestions that there is evidence that indicates that developmental factors may contribute to ADHD in ways that are separate from the associated behav‐ iour problems. One could go further by saying that it is important to describe personali‐ ty disorders (from a neurobiological perspective) in adults with ADHD, as this could aid in describing a possible shared aetiology. In fact one could go as far as to say that in‐ complete descriptions of Personality Disorders in ADHD continue to place pressure on the validity of the diagnosis in adulthood [2]. Although there have been a number of studies that have focused on the relationship between ADHD and personality, some au‐ thors [35] maintain that these studies have focussed on only a narrow range of personali‐ ty constructs. Table 2 provides a summary of personality constructs that have been investigated in relation to ADHD, as well as how these characteristics may feature in personality disorders.

normalities in CNS functioning [9]. It further denotes that the EEGs of children and adolescents with ADHD symptoms are not considered normal in children of any age and that it is also not likely to mature in a normal fashion [9]. Additional evidence for this model is provided by the adult ADHD (ADHD) studies which found that the presence of elevated

The research referred to in this section was concerned with the investigation of cortical ac‐ tivity patterns in adults with ADHD via EEG methodologies. The research was specifically interested in the cortical activity patterns of adults with ADHD symptomatology at frontal, frontal midline and parietal sites seeing that these areas are often the most heavily implicat‐ ed in ADHD. From existing literature, it can be concluded that there is evidence that sup‐ ports both the maturational lag as well as the maturational deviance models (See Table 1).

activity

and parietal sites

temporal sites.

Personality and psychopathology have, throughout the 20th century, been viewed as sep‐ arate but related domains. Although they have been viewed as related domains, the ex‐ act relationship remains largely unclear. In 1980, within psychopathology, clinical syndromes were separated from personality disorders [34]. Splitting these domains high‐ lighted the overlap between symptoms of clinical and personality disorders [34], which

**Description of Model EEG Findings References**

Increased relative and/or absolute slow wave activity and decreased relative and/or absolute fast wave

[8 -16, 20 – 27]

[9,19,26,28, 29]

Increased frontal relative and/or absolute theta Increased absolute and/or relative delta in temporal

Decreased relative and/or absolute alpha and beta

Increased absolute and/or relative theta activity in

Decreased relative alpha activity in parietal and

Elevated theta/beta and theta/alpha ratios

Decreased absolute and relative beta activity in frontal,

power in temporal and parietal sites

frontal and frontal midline sites.

parietal and temporal sites

slow wave activity, especially theta, persists into adulthood [18-19].

24 Attention Deficit Hyperactivity Disorder in Children and Adolescents

**2.3. Summary and conclusion**

Maturational Lag Individuals with ADHD symptoms

fashion.

**3. Personality disorders**

present with cortical activity patterns that is similar to that witnessed in younger children

ADHD symptoms result from abnormalities in CNS functioning. The EEGs of individuals with ADHD symptoms are not considered normal in individuals of any age and is not likely to mature in a normal

**Table 1.** EEG support for the maturational lag and developmental deviation models

**EEG Based Model**

> Developmental Deviation


**Table 2.** Summary of personality constructs identified in ADHD and possible links with Cluster B disorders

There has traditionally been a great but, arguably unwarranted [43], emphasis on the preva‐ lence of Cluster B personality disorder in adults with ADHD. This study, in effect wants to investigate whether there is some shared neurodevelopmental process in both of these sets of disorders. The argument is based on the following postulates:

**•** ADHD is a neurodevelopmental disorder and is the result of either maturational lag or maturational deviation

**•** In some cases ADHD does not continue beyond adolescence (which is in line with the ma‐ turational lag hypothesis), however

substantiate that this disorder is due to abnormal brainwave activity. Abnormal brainwave activity is only one of the many possible neurobiological factors in this disorder and other factors such as neurotransmitter systems, the endogenous opioid system [58] and various sub-cortical areas have been included as possible contributing causes to this disorder. De‐ spite numerous studies thyat have been done, the neurobiology of borderline personality disorder still remains largely unclear [58]. If there is evidence of neurobiological processes, and that symptoms do not appear to improve over time, one could deduce that these (nar‐ cissistic and borderline) are due to maturational deviation, rather than maturational lag.

Neurodevelopmental Pathways of Childhood ADHD into Adulthood: Maturational Lag, Deviation, or Both?

http://dx.doi.org/10.5772/53865

27

This study formed part of a much larger project, and this study itself was larger than what is reported here. The research question for this study is focused exclusively on maturational delay versus maturational deviation. Due to the fact that the existing literature seems to fo‐ cus mainly on Cluster B personality disorders, and that EEG studies in relation to the re‐ search question focus mainly on resting state EEG recordings, this study does the same. Therefore, although there is more information available than reported here, it will be limited

In order to address the research goals the study utilised purposive sampling methods to identify the ADHD sample. All participants had to be older than 18 years of age and as far as the other including characteristics are concerned, the researchers had to utilise their judgement to identify and select individuals from a target population that qualify for partic‐ ipation in the study, based on the sample characteristics [59]. During the initial phases of the sampling procedure the researchers verbally marketed the research undertaking to profes‐ sional practitioners (mostly psychiatrists and psychologists). Furthermore participants who were selected on the basis of purposive sampling also nominated acquaintances whom they believed may qualify for participation in the research. In the initial phase the target popula‐ tion was broadly defined by observed ADHD type behaviours that may be explained by the syndrome and may be potentially differentially diagnosed from other clinical conditions.

Participants who were subject to the exclusion criteria were not included in the study. The list of exclusion criteria are informed by similar EEG studies [18, 60-62] which included:

**•** Psychoactive medication, with the exception of methylphenidate (ADHD related medica‐ tion), in which case participants were asked to refrain from taking the medication for a

*3.2.1. Method*

*3.2.2. Participants*

to what is pertinent to the research question only.

minimum of 24 hours prior to the assessment.

**•** Evidence of another Axis I or Axis II disorder.

**•** Current diagnosis of hypothyriodism.

**•** History of a neurological disorder, head injury or CNS infection.

**•** History of substance use disorder in the previous two months.


If these postulates are correct, the question that arises is whether these two disorders could be the result of the same neurodevelopmental process. Most, if not all, of the characteristics mentioned in Table 2 have an underlying neuropsychological or neurobiological correlate. These neurobiological correlates may be the result of either a maturational lag or matura‐ tional deviance process, depending on which personality disorder one focuses on. One way of distinguishing between these two hypotheses, would be to consider the course and prog‐ nosis of the different personality disorders. Regarding the Cluster B personality disorders, two interesting pictures evolve when reviewing course and prognosis, and these may, argu‐ ably be classified as maturational lag or maturational deviation.

#### **3.1. Maturational lag**

The roots of the development of Antisocial Personality Disorder can be traced to early ado‐ lescence (i.e. Conduct Disorder) which then follows an unremitting course, with a variable outcome. There is some evidence that suggests that the symptoms decrease with age [53]. The fact that the symptoms may decrease with age, is somewhat suggestive of a delayed maturation process [54]. A further indication of a maturational lag is the fact that there is excessive theta wave activity, while awake, which is akin to what is evident in younger chil‐ dren [54]. One explanation for this could be the temporal discounting paradigm which quantifies the ability to favour larger, delayed rewards over smaller, more immediate re‐ wards. Temporal discounting matures with age, along with increased impulse control and self-regulation. This maturation seems to be associated with changes in activation of the ventromedial prefrontal cortex, anterior cingulate cortex, ventral striatum, insula, inferior temporal gyrus and posterior parietal cortex [55].

Although it is reported that adults with a histrionic personality disorder display less symp‐ toms as they age [53], it is uncertain whether this is truly due symptoms diminishing due to maturation, or whether this is merely due to a decline in energy levels due to aging.

#### **3.2. Maturational deviation**

In the case of both borderline and narcissistic personality disorders, the disorders are stable over time showing neither intensifying or decline in symptoms [53]. Unlike antisocial per‐ sonality disorder, the DSM does not make provision for early identification of these disor‐ ders; however, some research does provide some evidence for the early identification of specifically borderline personality disorder [56]. Although there is some evidence of epilep‐ tiform activity in borderline personality disorder [57], the prevalence is not high enough to substantiate that this disorder is due to abnormal brainwave activity. Abnormal brainwave activity is only one of the many possible neurobiological factors in this disorder and other factors such as neurotransmitter systems, the endogenous opioid system [58] and various sub-cortical areas have been included as possible contributing causes to this disorder. De‐ spite numerous studies thyat have been done, the neurobiology of borderline personality disorder still remains largely unclear [58]. If there is evidence of neurobiological processes, and that symptoms do not appear to improve over time, one could deduce that these (nar‐ cissistic and borderline) are due to maturational deviation, rather than maturational lag.

#### *3.2.1. Method*

**•** In some cases ADHD does not continue beyond adolescence (which is in line with the ma‐

**•** ADHD may continue into adulthood, which cannot be explained fully by the maturation‐

**•** There is evidence of both maturational lag and deviation processes in personality disorders. If these postulates are correct, the question that arises is whether these two disorders could be the result of the same neurodevelopmental process. Most, if not all, of the characteristics mentioned in Table 2 have an underlying neuropsychological or neurobiological correlate. These neurobiological correlates may be the result of either a maturational lag or matura‐ tional deviance process, depending on which personality disorder one focuses on. One way of distinguishing between these two hypotheses, would be to consider the course and prog‐ nosis of the different personality disorders. Regarding the Cluster B personality disorders, two interesting pictures evolve when reviewing course and prognosis, and these may, argu‐

The roots of the development of Antisocial Personality Disorder can be traced to early ado‐ lescence (i.e. Conduct Disorder) which then follows an unremitting course, with a variable outcome. There is some evidence that suggests that the symptoms decrease with age [53]. The fact that the symptoms may decrease with age, is somewhat suggestive of a delayed maturation process [54]. A further indication of a maturational lag is the fact that there is excessive theta wave activity, while awake, which is akin to what is evident in younger chil‐ dren [54]. One explanation for this could be the temporal discounting paradigm which quantifies the ability to favour larger, delayed rewards over smaller, more immediate re‐ wards. Temporal discounting matures with age, along with increased impulse control and self-regulation. This maturation seems to be associated with changes in activation of the ventromedial prefrontal cortex, anterior cingulate cortex, ventral striatum, insula, inferior

Although it is reported that adults with a histrionic personality disorder display less symp‐ toms as they age [53], it is uncertain whether this is truly due symptoms diminishing due to

In the case of both borderline and narcissistic personality disorders, the disorders are stable over time showing neither intensifying or decline in symptoms [53]. Unlike antisocial per‐ sonality disorder, the DSM does not make provision for early identification of these disor‐ ders; however, some research does provide some evidence for the early identification of specifically borderline personality disorder [56]. Although there is some evidence of epilep‐ tiform activity in borderline personality disorder [57], the prevalence is not high enough to

maturation, or whether this is merely due to a decline in energy levels due to aging.

**•** The is a reportedly high prevalence of personality disorders in adults with ADHD

ably be classified as maturational lag or maturational deviation.

temporal gyrus and posterior parietal cortex [55].

**3.2. Maturational deviation**

turational lag hypothesis), however

26 Attention Deficit Hyperactivity Disorder in Children and Adolescents

al lag hypothesis.

**3.1. Maturational lag**

This study formed part of a much larger project, and this study itself was larger than what is reported here. The research question for this study is focused exclusively on maturational delay versus maturational deviation. Due to the fact that the existing literature seems to fo‐ cus mainly on Cluster B personality disorders, and that EEG studies in relation to the re‐ search question focus mainly on resting state EEG recordings, this study does the same. Therefore, although there is more information available than reported here, it will be limited to what is pertinent to the research question only.

#### *3.2.2. Participants*

In order to address the research goals the study utilised purposive sampling methods to identify the ADHD sample. All participants had to be older than 18 years of age and as far as the other including characteristics are concerned, the researchers had to utilise their judgement to identify and select individuals from a target population that qualify for partic‐ ipation in the study, based on the sample characteristics [59]. During the initial phases of the sampling procedure the researchers verbally marketed the research undertaking to profes‐ sional practitioners (mostly psychiatrists and psychologists). Furthermore participants who were selected on the basis of purposive sampling also nominated acquaintances whom they believed may qualify for participation in the research. In the initial phase the target popula‐ tion was broadly defined by observed ADHD type behaviours that may be explained by the syndrome and may be potentially differentially diagnosed from other clinical conditions.

Participants who were subject to the exclusion criteria were not included in the study. The list of exclusion criteria are informed by similar EEG studies [18, 60-62] which included:


All participants were subject to the clinical interview, and screened for a 'best estimate' di‐ agnosis for ADHD by means of the ASRS-v.I.I. and also with the MCMI-III [63] for differen‐ tial diagnosis of other clinical syndromes. The nature of these assessment tools and rationale for their use are discussed below. The recruitment of participants resulted in a group of 51 adults with ADHD and a group of 43 adults with no clear indications of a clinical disorder.

*Adult ADHD Self-Report Scale (ASRS).* The ASRS is not a diagnostic tool but is used as a screening device to screen for signs and symptoms of adult ADHD. The Adult ADHD Self-Report Scale (ASRS) is a self-report 18 question questionnaire which screens adults for ADHD [67]. The ASRS is based on the criteria listed in the DSM IV, on ADHD [68]. Half of the questions focus on inattention and half of the questions focus on hyperactivity [69]. It is a paper pencil questionnaire which is self-scored and only takes 5 minutes to complete [67]. It has a five point Likert scale, where the testee ticks one of five responses, never, rarely, sometimes, often and very often [67]. The ASRS has demonstrated good reliability and val‐ idity in clinical and community samples [68]. The ASRS also has high-quality predictive power with values between 57 and 93%, showing that it can predict ADHD[70]. The ASRS proves good internal consistency with values between 0.75 and 0.89 [69]. Concordance was calculated by looking at the symptom responses of the ASRS and comparing the responses to clinical ratings, of which Cohen's k was used to assess this concordance [67]. The con‐ cordance however varied with a range of.16 to.81, which could be the result of error of measurement or the experience of the clinicians [67]. The total classification accuracy rated at 96%, however, the ASRS showed moderate levels of concurrent validity and sensitivity

Neurodevelopmental Pathways of Childhood ADHD into Adulthood: Maturational Lag, Deviation, or Both?

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29

*Millon Clinical Multi-axial Inventory-III*. This test is primarily a self-report questionnaire that assesses a wide range of information about an adult's personality and emotional adjustment [71]. Furthermore this instrument was designed as a diagnostic tool that yields information about personality disorders as well as clinical syndromes [72]. The test consists of 175 ques‐ tions that are forced-choice, true-false items [73]. The MCMI III has 28 sub-scales, of which are categorized into five different categories [71], i.e. Modifying Indices, Clinical Personality Patterns, Severe Personality Pathology, Clinical Syndromes, and Severe Syndromes. For the purposes of this study base rate scores below 75 were considered to be indications of no clinical significance, 75 – 84 as indicative of the presence of a personality trait, and 85 and

The results for the internal consistency was :66 for the compulsive scales and 0.90 for major depression, and the Cronbach alpha's for the remaining 26 scales exceeded.80, showing strong internal consistency [73]. Test-retest reliability scores indicated the lowest score of.82 for debasement and the highest was.96 for somatoform, of which the median test-retest coef‐

Construct and concurrent validity is tested by looking at how well the instrument performs in different populations and how much value it has in the real world [73]. The manner in which this is achieved was by comparing the MCMI to accepted standards achieved by other tests, comparing the scales on the MCMI to other scales on different tests [73]. It was identified that there is a high correlation between the scales of the MCMI-III and seven different tests, namely the symptom checklist-90, the Beck Depression Inventory, the State-Trait Anxiety Inventory, the General Behaviour Inventory, the Minnesota Multiphasic Personality Inventory (MMPI), the Michigan Alcoholism Screening Test and the MCMI-II [71]. The correlations on most of the scales where good, with some having negative scores, but these items were not related to the specific scales on the MCMI-III. Further evidence to assess how well the MCMI-III scales meas‐

ficient was.91, which shows stability of the instrument over time [71].

but high levels of specificity [69].

higher as persistent personality traits [73].

For the EEG study an initial 15 potential ADHD research participants were identified from the bigger pool, however, on further investigation 3 participants were excluded from further anal‐ ysis on the basis that they met the criteria for another clinical condition. Subsequently 12 partic‐ ipants met the operational criteria to constitute the ADHD EEG study population. These participants were first subject to the EEG assessment before the age- and gender- matched non-ADHD sample was identified. The reason for this was to ensure that no further participants needed to be excluded and that the non-ADHD sample could be matched on the characteristics of the final ADHD sample. Two individuals were further excluded from the study population on the basis that the one participant experienced excessive drowsiness and another participant presented with significant muscle movement that may confound the obtained results. Subse‐ quently, 10 participants were included in the research sample for the ADHD group. This sam‐ ple met the necessary operational criteria for the inclusion in the study and produced an EEG reading that is acceptable according to the quality standards. The mean sample age for the ADHD group was 34.4 years. The female to male ratio was 3:1.

Following the identification of the research sample for the experimental group the study set out to identify an age- and gender- matched healthy non-ADHD group. Matched sampling for this group took place by purposively selecting participants from the initial pool of poten‐ tial participants. The sampling of this group was matched exactly to gender and approxi‐ mately within a four year range of the target age criterion. Subsequently the non-ADHD research sample that was identified exhibited a mean sample age of 33.6 years with a similar female to male ratio as the experimental group.

#### *3.2.3. Measurement instruments*

One of the main challenges in this study was to accurately identify adults with a diagnosis of ADHD. Due to the fact that ADHD, specifically in adulthood, is not a widely accepted diagno‐ sis, or in other cases an over diagnosed disorder, one cannot rely only on formal diagnoses made by Mental Health Professionals. Added to this is the problem of a high rate of self-diag‐ nosis of this disorder amongst adults [64], which brings into question relying only on self-re‐ port questionnaires to identify possible participants. For this reason, over and above the MCMI-III, a semi-structured interview and a self-report questionnaire were also included.

*Semi-Structured Clinical Interview.* The interview was conducted by any one of the trained clini‐ cal psychologists that formed part of the research team. The purpose of the interview was to en‐ sure that participants met the sampling characteristics mentioned above and to make certain that none of the exclusion criteria were present in the respective population. The interview also obtained information regarding the biographical information of participants. Furthermore it served as a quick screening conformational tool by exploring the presence or absence of the cri‐ teria for ADHD in adulthood as proposed by a number of authors [65, 66].

*Adult ADHD Self-Report Scale (ASRS).* The ASRS is not a diagnostic tool but is used as a screening device to screen for signs and symptoms of adult ADHD. The Adult ADHD Self-Report Scale (ASRS) is a self-report 18 question questionnaire which screens adults for ADHD [67]. The ASRS is based on the criteria listed in the DSM IV, on ADHD [68]. Half of the questions focus on inattention and half of the questions focus on hyperactivity [69]. It is a paper pencil questionnaire which is self-scored and only takes 5 minutes to complete [67]. It has a five point Likert scale, where the testee ticks one of five responses, never, rarely, sometimes, often and very often [67]. The ASRS has demonstrated good reliability and val‐ idity in clinical and community samples [68]. The ASRS also has high-quality predictive power with values between 57 and 93%, showing that it can predict ADHD[70]. The ASRS proves good internal consistency with values between 0.75 and 0.89 [69]. Concordance was calculated by looking at the symptom responses of the ASRS and comparing the responses to clinical ratings, of which Cohen's k was used to assess this concordance [67]. The con‐ cordance however varied with a range of.16 to.81, which could be the result of error of measurement or the experience of the clinicians [67]. The total classification accuracy rated at 96%, however, the ASRS showed moderate levels of concurrent validity and sensitivity but high levels of specificity [69].

All participants were subject to the clinical interview, and screened for a 'best estimate' di‐ agnosis for ADHD by means of the ASRS-v.I.I. and also with the MCMI-III [63] for differen‐ tial diagnosis of other clinical syndromes. The nature of these assessment tools and rationale for their use are discussed below. The recruitment of participants resulted in a group of 51 adults with ADHD and a group of 43 adults with no clear indications of a clinical disorder. For the EEG study an initial 15 potential ADHD research participants were identified from the bigger pool, however, on further investigation 3 participants were excluded from further anal‐ ysis on the basis that they met the criteria for another clinical condition. Subsequently 12 partic‐ ipants met the operational criteria to constitute the ADHD EEG study population. These participants were first subject to the EEG assessment before the age- and gender- matched non-ADHD sample was identified. The reason for this was to ensure that no further participants needed to be excluded and that the non-ADHD sample could be matched on the characteristics of the final ADHD sample. Two individuals were further excluded from the study population on the basis that the one participant experienced excessive drowsiness and another participant presented with significant muscle movement that may confound the obtained results. Subse‐ quently, 10 participants were included in the research sample for the ADHD group. This sam‐ ple met the necessary operational criteria for the inclusion in the study and produced an EEG reading that is acceptable according to the quality standards. The mean sample age for the

Following the identification of the research sample for the experimental group the study set out to identify an age- and gender- matched healthy non-ADHD group. Matched sampling for this group took place by purposively selecting participants from the initial pool of poten‐ tial participants. The sampling of this group was matched exactly to gender and approxi‐ mately within a four year range of the target age criterion. Subsequently the non-ADHD research sample that was identified exhibited a mean sample age of 33.6 years with a similar

One of the main challenges in this study was to accurately identify adults with a diagnosis of ADHD. Due to the fact that ADHD, specifically in adulthood, is not a widely accepted diagno‐ sis, or in other cases an over diagnosed disorder, one cannot rely only on formal diagnoses made by Mental Health Professionals. Added to this is the problem of a high rate of self-diag‐ nosis of this disorder amongst adults [64], which brings into question relying only on self-re‐ port questionnaires to identify possible participants. For this reason, over and above the MCMI-III, a semi-structured interview and a self-report questionnaire were also included.

*Semi-Structured Clinical Interview.* The interview was conducted by any one of the trained clini‐ cal psychologists that formed part of the research team. The purpose of the interview was to en‐ sure that participants met the sampling characteristics mentioned above and to make certain that none of the exclusion criteria were present in the respective population. The interview also obtained information regarding the biographical information of participants. Furthermore it served as a quick screening conformational tool by exploring the presence or absence of the cri‐

teria for ADHD in adulthood as proposed by a number of authors [65, 66].

ADHD group was 34.4 years. The female to male ratio was 3:1.

female to male ratio as the experimental group.

28 Attention Deficit Hyperactivity Disorder in Children and Adolescents

*3.2.3. Measurement instruments*

*Millon Clinical Multi-axial Inventory-III*. This test is primarily a self-report questionnaire that assesses a wide range of information about an adult's personality and emotional adjustment [71]. Furthermore this instrument was designed as a diagnostic tool that yields information about personality disorders as well as clinical syndromes [72]. The test consists of 175 ques‐ tions that are forced-choice, true-false items [73]. The MCMI III has 28 sub-scales, of which are categorized into five different categories [71], i.e. Modifying Indices, Clinical Personality Patterns, Severe Personality Pathology, Clinical Syndromes, and Severe Syndromes. For the purposes of this study base rate scores below 75 were considered to be indications of no clinical significance, 75 – 84 as indicative of the presence of a personality trait, and 85 and higher as persistent personality traits [73].

The results for the internal consistency was :66 for the compulsive scales and 0.90 for major depression, and the Cronbach alpha's for the remaining 26 scales exceeded.80, showing strong internal consistency [73]. Test-retest reliability scores indicated the lowest score of.82 for debasement and the highest was.96 for somatoform, of which the median test-retest coef‐ ficient was.91, which shows stability of the instrument over time [71].

Construct and concurrent validity is tested by looking at how well the instrument performs in different populations and how much value it has in the real world [73]. The manner in which this is achieved was by comparing the MCMI to accepted standards achieved by other tests, comparing the scales on the MCMI to other scales on different tests [73]. It was identified that there is a high correlation between the scales of the MCMI-III and seven different tests, namely the symptom checklist-90, the Beck Depression Inventory, the State-Trait Anxiety Inventory, the General Behaviour Inventory, the Minnesota Multiphasic Personality Inventory (MMPI), the Michigan Alcoholism Screening Test and the MCMI-II [71]. The correlations on most of the scales where good, with some having negative scores, but these items were not related to the specific scales on the MCMI-III. Further evidence to assess how well the MCMI-III scales meas‐ ure what they say they measure is by calculating the positive predictive power, which was re‐ markable showing a range of.30 to.80 [71]. The MCMI-III has proven construct validity and diagnostic validity, by comparing test items with other tests and by comparing clinical judge‐ ment with the results indicated from the scales on the MCMI-III [73].

acquisition phase they will engaged in a three minute eyes-closed task. Participants were al‐ so instructed to remain as physically still as possible in order to limit muscle contamination throughout the entire assessment, and were requested to avoid speaking during the assess‐

Neurodevelopmental Pathways of Childhood ADHD into Adulthood: Maturational Lag, Deviation, or Both?

**Proof Corrections Form** 

**Chapter Title: Neurodevelopmental pathways of childhood** 

**ADHD into adulthood: Maturational lag, deviation, or** 

**PROOF CORRECTIONS FORM** 

T3 C3 Cz C4 T4

A1 A2

T5 P3 P4 Pz T6

O1 O2

10% 20% 20%

**Figure 1.** International 10-20 System of Electrode Placement (Adapted from [75])

20% 20% 10%

Fp1 Fp2

F7 F3 F8

Fz F4

10%

http://dx.doi.org/10.5772/53865

31

20%

20%

20%

20%

10%

**No. Delete Replace with** 

In the data acquisition phase subjects were fitted with an electrocap in accordance with the 10-20 International system of electrode placement. In order to tap the fronto-parietal atten‐ tion network, electrodes were grouped into three areas: frontal (F3 and F4), frontal midline (Fz) and parietal (P3 and P4) sites (see Figure 1.). EEG signal for all subjects was recorded under an eyes-closed condition. Eye movements were monitored by electrodes placed on the outer canthus of each eye for horizontal movements and by electrodes above the eye for vertical movements. EEG signal was recorded using *Acq*Knowledge software and BIOPAC MP Systems hardware. Impedance was kept below 5Kohm (kΩ) and a sampling rate of 200Hz was applied. Continuous EEG data was reviewed off-line. Segments containing head and eye movement as well as muscle artefact were removed from further analysis. Subse‐ quently, six two second epochs were extracted for the eyes-closed condition and for each of the cortical sites investigated and for the four frequency bands: delta (1-4Hz); theta (4-8Hz); alpha (8-13Hz); and Beta (13-20Hz). EEG data was Fast Fourier transformed (FFT) (Hanning

1

ment as a further attempt to avoid contamination of results.

**Author(s) Name(s): Alban Burke and Amanda Edge** 

**both?**

**Page No.** 

**Line** 

**11** 22 Figure

window) and subsequently log transformed (In).

**15** 17 ADHD, symptomatology ADHD symptomatology

**6** 24 children younger children

**1** 14 Along to

**9** 31 was.66 was .66

*Biopac MP Systems Hardware.* The research question is concerned with the nature of the intra‐ cranial electrical currents of adults with ADHD symptomatology. Therefore EEG recording is appropriate for this study in that it records the electrical activity of cortical nerve cells in the brain [74]. It is noteworthy to mention that cortical activity is presented in waveforms and is measured in terms of amplitude and frequency [75]. Amplitude is expressed in micro‐ volts (µV), EEG power is defined by the square of amplitude (µV2 ) and frequency is defined as the number of oscillations, or cycles, within a given time frame, or epoch, and is meas‐ ured in hertz (Hz) [76].

This study employed the Biopac MP Systems Hardware [77] for the assessment of cortical activity. The system is considered to be commercial EEG equipment utilised in the data ac‐ quisition and analysis for life science research. The recording technique utilised by this sys‐ tem is an ethically approved, non-invasive, safe and painless procedure [78]. In order to ensure the quality of research, the EEG methods employed in this study are informed by various other EEG studies that employed quantitative EEG techniques [75] as well as stand‐ ardised guidelines for the technologic recording and quantitative analysis of EEG activity in the research context [79].

A final matter to consider in this section is the reliability and validity of EEG recordings. Vari‐ ous researchers report that EEG recordings are reliable, in that the intra-individual stability of EEG is stable over time (over a period of 10 to 90 days) [80,81]. The validity of EEG research de‐ pends on the concepts of sensitivity and specificity [76]. In ADHD research, sensitivity refers to the percentage of ADHD individuals who present with an abnormal EEG while specificity re‐ veals the percentage of non-ADHD subjects who indicate a normal EEG [76]. In a literature re‐ view of several studies, it was concluded that EEG methods in ADHD research typically demonstrate good sensitivity (90% to 97%) and sound specificity (84%-94%)[76].

#### *3.2.4. Procedure*

All potential participants were required to complete the ASRS and MCMI for screening pur‐ poses. Based on the scores on these instruments they were allocated to different groups, or where they did not meet the criteria for any of the groups, were excluded from further stud‐ ies. As explained previously, the sample for the EEG study was drawn from this pool. Po‐ tential participants were approached to participate in the EEG study.

Upon arrival to the research laboratory participants were requested to sit in the allocated chair. The researcher and EEG equipment was situated outside of the participants direct line of sight. Participants were then oriented to the Biopac MP Systems Hardware equipment, and was further provided with an opportunity to ask questions. The researcher enquired about whether participants adhered to the instruction to refrain from the aforementioned substances 24 hours before the assessment. Participants were informed that during the data

acquisition phase they will engaged in a three minute eyes-closed task. Participants were al‐ so instructed to remain as physically still as possible in order to limit muscle contamination throughout the entire assessment, and were requested to avoid speaking during the assess‐ ment as a further attempt to avoid contamination of results. **Proof Corrections Form Author(s) Name(s): Alban Burke and Amanda Edge** 

ure what they say they measure is by calculating the positive predictive power, which was re‐ markable showing a range of.30 to.80 [71]. The MCMI-III has proven construct validity and diagnostic validity, by comparing test items with other tests and by comparing clinical judge‐

*Biopac MP Systems Hardware.* The research question is concerned with the nature of the intra‐ cranial electrical currents of adults with ADHD symptomatology. Therefore EEG recording is appropriate for this study in that it records the electrical activity of cortical nerve cells in the brain [74]. It is noteworthy to mention that cortical activity is presented in waveforms and is measured in terms of amplitude and frequency [75]. Amplitude is expressed in micro‐

as the number of oscillations, or cycles, within a given time frame, or epoch, and is meas‐

This study employed the Biopac MP Systems Hardware [77] for the assessment of cortical activity. The system is considered to be commercial EEG equipment utilised in the data ac‐ quisition and analysis for life science research. The recording technique utilised by this sys‐ tem is an ethically approved, non-invasive, safe and painless procedure [78]. In order to ensure the quality of research, the EEG methods employed in this study are informed by various other EEG studies that employed quantitative EEG techniques [75] as well as stand‐ ardised guidelines for the technologic recording and quantitative analysis of EEG activity in

A final matter to consider in this section is the reliability and validity of EEG recordings. Vari‐ ous researchers report that EEG recordings are reliable, in that the intra-individual stability of EEG is stable over time (over a period of 10 to 90 days) [80,81]. The validity of EEG research de‐ pends on the concepts of sensitivity and specificity [76]. In ADHD research, sensitivity refers to the percentage of ADHD individuals who present with an abnormal EEG while specificity re‐ veals the percentage of non-ADHD subjects who indicate a normal EEG [76]. In a literature re‐ view of several studies, it was concluded that EEG methods in ADHD research typically

All potential participants were required to complete the ASRS and MCMI for screening pur‐ poses. Based on the scores on these instruments they were allocated to different groups, or where they did not meet the criteria for any of the groups, were excluded from further stud‐ ies. As explained previously, the sample for the EEG study was drawn from this pool. Po‐

Upon arrival to the research laboratory participants were requested to sit in the allocated chair. The researcher and EEG equipment was situated outside of the participants direct line of sight. Participants were then oriented to the Biopac MP Systems Hardware equipment, and was further provided with an opportunity to ask questions. The researcher enquired about whether participants adhered to the instruction to refrain from the aforementioned substances 24 hours before the assessment. Participants were informed that during the data

demonstrate good sensitivity (90% to 97%) and sound specificity (84%-94%)[76].

tential participants were approached to participate in the EEG study.

) and frequency is defined

**both?**

**Page No.** 

**Line** 

**11** 22 Figure

**9** 31 was.66 was .66

ment with the results indicated from the scales on the MCMI-III [73].

30 Attention Deficit Hyperactivity Disorder in Children and Adolescents

volts (µV), EEG power is defined by the square of amplitude (µV2

ured in hertz (Hz) [76].

the research context [79].

*3.2.4. Procedure*

In the data acquisition phase subjects were fitted with an electrocap in accordance with the 10-20 International system of electrode placement. In order to tap the fronto-parietal atten‐ tion network, electrodes were grouped into three areas: frontal (F3 and F4), frontal midline (Fz) and parietal (P3 and P4) sites (see Figure 1.). EEG signal for all subjects was recorded under an eyes-closed condition. Eye movements were monitored by electrodes placed on the outer canthus of each eye for horizontal movements and by electrodes above the eye for vertical movements. EEG signal was recorded using *Acq*Knowledge software and BIOPAC MP Systems hardware. Impedance was kept below 5Kohm (kΩ) and a sampling rate of 200Hz was applied. Continuous EEG data was reviewed off-line. Segments containing head and eye movement as well as muscle artefact were removed from further analysis. Subse‐ quently, six two second epochs were extracted for the eyes-closed condition and for each of the cortical sites investigated and for the four frequency bands: delta (1-4Hz); theta (4-8Hz); alpha (8-13Hz); and Beta (13-20Hz). EEG data was Fast Fourier transformed (FFT) (Hanning window) and subsequently log transformed (In). **Chapter Title: Neurodevelopmental pathways of childhood ADHD into adulthood: Maturational lag, deviation, or PROOF CORRECTIONS FORM No. Delete Replace with 1** 14 Along to **6** 24 children younger children

1

**Figure 1.** International 10-20 System of Electrode Placement (Adapted from [75])

**15** 17 ADHD, symptomatology ADHD symptomatology

#### *3.2.5. Results*

#### *3.2.5.1. Personality disorder*

In order to gain a meaningful picture of Personality Disorders in ADHD, and therefore a better picture of maturational lag versus maturational deviation, the data gained from the MCMI-III was used in different ways. Firstly the average base rate scores (interval scale) were compared between the groups, thereafter the scores were categorised into 3 categories (Ordinal scale), i.e. <75, 75-84 and 85>, where after the groups were compared, and lastly, based on the categorisation of the data, number of personality disorders per individual, per group are reported.

In terms of the average base rate scores, Table 3 and Figure 2 reflected that the two groups were more or less equal in terms of Narcissism and that the non-ADHD group had a higher average score on the Histrionic, but significantly lower scores on both the Anti-Social and Borderline scales (See Tables 3 and 4). Of particular importance is that none of the average scores were higher than 75, indicating that neither of the two groups displayed typical per‐

Neurodevelopmental Pathways of Childhood ADHD into Adulthood: Maturational Lag, Deviation, or Both?

http://dx.doi.org/10.5772/53865

33

Interpreting only the differences in base rate scores of the MCMI can be misleading, there‐ fore the scores of individuals for each of the scales was categorised into one of three catego‐

Mann-Whitney U 861.0 980.5 502.5 612.5 Wilcoxon W 2187.0 1926.5 1448.5 1558.5 Z -1.791 -.882 -4.521 -3.678 p 0.07 0.38 *0.000\*\*\* .000\*\*\**

**Table 4.** Differences between ADHD and Normal groups for the interpersonal sub-scales

ries, i.e. Low (<75), High (75-84) or Significant (84>) (See Table 5).

**Histrionic Narcissistic Antisocial Borderline**

**Low score High score Significant score**

ADHD 42 5 4 51

ADHD 41 3 7 51

Total 76 5 13 94 ADHD 37 12 2 51

Total 76 16 2 94 ADHD 40 8 3 51

Total 81 9 4 94

Histrionic nADHD 30 4 9 43 Total 72 9 13

Narcissistic nADHD 35 2 6 43

Anti-social nADHD 39 4 0 43

Borderline nADHD 41 1 1 43

**Table 5.** Number of participants per category of Cluster B Personality scores

<75 75 - 84 85> Total N N N N

sistent personality traits.

Where: \*\*\*: p<0.001


**Table 3.** Descriptive statistics for the 4 groups for the interpersonal sub-scales

**Figure 2.** Mean scores of the 4 Cluster B Personality Scales for the 2 groups

In terms of the average base rate scores, Table 3 and Figure 2 reflected that the two groups were more or less equal in terms of Narcissism and that the non-ADHD group had a higher average score on the Histrionic, but significantly lower scores on both the Anti-Social and Borderline scales (See Tables 3 and 4). Of particular importance is that none of the average scores were higher than 75, indicating that neither of the two groups displayed typical per‐ sistent personality traits.


**Table 4.** Differences between ADHD and Normal groups for the interpersonal sub-scales

*3.2.5. Results*

*3.2.5.1. Personality disorder*

32 Attention Deficit Hyperactivity Disorder in Children and Adolescents

group are reported.

In order to gain a meaningful picture of Personality Disorders in ADHD, and therefore a better picture of maturational lag versus maturational deviation, the data gained from the MCMI-III was used in different ways. Firstly the average base rate scores (interval scale) were compared between the groups, thereafter the scores were categorised into 3 categories (Ordinal scale), i.e. <75, 75-84 and 85>, where after the groups were compared, and lastly, based on the categorisation of the data, number of personality disorders per individual, per

ADHD (n=51) Mean 50.6 58.5 61.4 55.4

Non-ADHD(n=43) Mean 60.1 55.9 43.6 38.4

Histrionic Narcissistic Antisocial Borderline

**Table 3.** Descriptive statistics for the 4 groups for the interpersonal sub-scales

**Figure 2.** Mean scores of the 4 Cluster B Personality Scales for the 2 groups

**Histrionic Narcissistic Antisocial Borderline**

ADHD non-ADHD

Std. Dev 23.6 21.7 14.3 21.7 Min 0 15 35 0.0 Max 95 110 90 92.0

Std. Dev 23.3 20.8 19.1 22.4 Min 4 15 8 0.0 Max 98 98 82 85.0 Interpreting only the differences in base rate scores of the MCMI can be misleading, there‐ fore the scores of individuals for each of the scales was categorised into one of three catego‐ ries, i.e. Low (<75), High (75-84) or Significant (84>) (See Table 5).


**Table 5.** Number of participants per category of Cluster B Personality scores

When investigating the data in this way, the results indicate that there were significant dif‐ ferences between the 2 groups on all of the subscales (See Table 6).

The study focused on two domains of investigation: power spectral and ratio coefficients. Pow‐ er spectral studies concerns the calculation of absolute and relative power estimates [20].

Neurodevelopmental Pathways of Childhood ADHD into Adulthood: Maturational Lag, Deviation, or Both?

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35

**•** Power spectral density or the power spectrum "… reflects the 'frequency content' of the signal or the distribution of signal power over frequency" [82, p. 806]. For the power spec‐

**•** Relative power is determined by the amount of EEG activity in a frequency band divided

**•** Absolute power is the amount for one specific frequency band without its relationship to

These two domains of investigation were selected on the basis that they are the most common and often preferred means of investigation for ADHD studies [20]. The mean values obtained for the ADHD and non-ADHD group, per area of the brain investigated and per frequency cluster were employed in obtaining the values for the domains of investigation. The above‐ mentioned equations were applied and subsequently, the absolute, relative and power ratios were determined. Note that for this study frequency parameters are set as follows: delta (1-4Hz); theta (4-8Hz); alpha (8-13Hz); and Beta (13-20Hz). The Greek symbols employed to de‐ note the different waves include: delta as δ; theta as θ; alpha as α; and finally beta as β. As far as

In order to address the research question a between-subjects analysis of diagnostic group differences was applied. Seeing that the small sample size was not representative of the greater population, nonparametric statistical procedures were employed [85]. Subsequently the Mann-Whitney U-test was applied with the use of SPSS software. The Mann-Whitney U test is the nonparametric alternative to an independent t-test. The Mann-Whitney U test is appropriate for the between-subjects analysis because it compares differences between two

frequency bands for the different cortical areas across the different conditions are reported. The table is formatted in this way as to compare the ADHD sample with the non-ADHD sample ac‐ cording to the four frequency clusters and according to the area of the brain investigated.

The results of the resting EEG reveal elevated ADHD relative theta activity at frontal mid‐ line sites. This finding is consistent with childhood and adolescent research that is sugges‐ tive of a maturational lag and developmental deviation profile. Increased relative theta activity is also indicated in the ADHD studies of [18,19] as well as Clarke et al. (2008b) at frontal midline sites. Although it was also expected that theta activity would be elevated in frontal sites, this was not confirmed in the present study. Moreover, the elevation or de‐ crease of theta activity is not documented widely for parietal sites in ADHD literature. How‐ ever, an interesting observation that was not indicated for the initial expectations for the current study is the presence of decreased absolute theta for the ADHD sample at parietal

) and Table 9 the relative mean power for the different

**•** Ratio coefficients refers to the ratio between power in different frequency bands [20].

the experimental condition is concerned, the abbreviation of EC is employed.

independent groups, in this case ADHD with non-ADHD [85].

In Table 8 the absolute mean power (µV2

tral domain the analysis was concerned with two spectral parameters, i.e.:

by the sum of the other bands [75].

the other bands [79].


**Table 6.** Chi Square for differences between the 2 groups

Given these results, a frequency analysis was done to determine how many elevated scores (85>) an individual participant had (See Table 7).


These results, from a maturational deviation perspective are meaningful in that the majority of the ADHD participants (76%) did not show any evidence of a Cluster B Personality Disor‐ der. If one assumes that ADHD is due to maturational lag, and that Cluster B Personality Disorders are also due to maturational lag, then these results seriously challenge this as‐ sumption. Given the fact that a higher percentage of ADHD (27.5%) showed indications of one or more Cluster B Personality Disorders than the non-ADHD group (9.3%), there seems to be evidence of a possible maturational deviation process.

#### *3.2.5.2. EEG results*

This part of the study focussed the brain's intracranial electrical currents and potentials, in other words cortical activity, of adults with ADHD, and those with no ADHD symptomatol‐ ogy. The patterns that are of particular concern are the activity (elevation or suppression) of the four frequency bands (delta, theta, alpha and beta).

The study focused on two domains of investigation: power spectral and ratio coefficients. Pow‐ er spectral studies concerns the calculation of absolute and relative power estimates [20].

When investigating the data in this way, the results indicate that there were significant dif‐

Given these results, a frequency analysis was done to determine how many elevated scores

0 39 (76.5%) 39 (90.7%)

1 9 (17.6%) 4 (9.3%)

2 2 (3.9%) 0 (0.0%)

3 1 (2%) 0 (0.0%)

Total 51 43

These results, from a maturational deviation perspective are meaningful in that the majority of the ADHD participants (76%) did not show any evidence of a Cluster B Personality Disor‐ der. If one assumes that ADHD is due to maturational lag, and that Cluster B Personality Disorders are also due to maturational lag, then these results seriously challenge this as‐ sumption. Given the fact that a higher percentage of ADHD (27.5%) showed indications of one or more Cluster B Personality Disorders than the non-ADHD group (9.3%), there seems

This part of the study focussed the brain's intracranial electrical currents and potentials, in other words cortical activity, of adults with ADHD, and those with no ADHD symptomatol‐ ogy. The patterns that are of particular concern are the activity (elevation or suppression) of

**Histrionic Narcissistic Borderline Anti-social**

ferences between the 2 groups on all of the subscales (See Table 6).

Where: \*\*\*: p<0.0001

**Table 6.** Chi Square for differences between the 2 groups

**Table 7.** Number of Personality Disorders per group

*3.2.5.2. EEG results*

to be evidence of a possible maturational deviation process.

the four frequency bands (delta, theta, alpha and beta).

(85>) an individual participant had (See Table 7).

34 Attention Deficit Hyperactivity Disorder in Children and Adolescents

Chi-Square 79.43 96.53 118.5 98.64 Df 2 2 2 2 Significance *.000\*\*\* .000\*\*\* .000\*\*\* .000\*\*\**

**Number of Personality Disorders ADHD nADHD**


These two domains of investigation were selected on the basis that they are the most common and often preferred means of investigation for ADHD studies [20]. The mean values obtained for the ADHD and non-ADHD group, per area of the brain investigated and per frequency cluster were employed in obtaining the values for the domains of investigation. The above‐ mentioned equations were applied and subsequently, the absolute, relative and power ratios were determined. Note that for this study frequency parameters are set as follows: delta (1-4Hz); theta (4-8Hz); alpha (8-13Hz); and Beta (13-20Hz). The Greek symbols employed to de‐ note the different waves include: delta as δ; theta as θ; alpha as α; and finally beta as β. As far as the experimental condition is concerned, the abbreviation of EC is employed.

In order to address the research question a between-subjects analysis of diagnostic group differences was applied. Seeing that the small sample size was not representative of the greater population, nonparametric statistical procedures were employed [85]. Subsequently the Mann-Whitney U-test was applied with the use of SPSS software. The Mann-Whitney U test is the nonparametric alternative to an independent t-test. The Mann-Whitney U test is appropriate for the between-subjects analysis because it compares differences between two independent groups, in this case ADHD with non-ADHD [85].

In Table 8 the absolute mean power (µV2 ) and Table 9 the relative mean power for the different frequency bands for the different cortical areas across the different conditions are reported. The table is formatted in this way as to compare the ADHD sample with the non-ADHD sample ac‐ cording to the four frequency clusters and according to the area of the brain investigated.

The results of the resting EEG reveal elevated ADHD relative theta activity at frontal mid‐ line sites. This finding is consistent with childhood and adolescent research that is sugges‐ tive of a maturational lag and developmental deviation profile. Increased relative theta activity is also indicated in the ADHD studies of [18,19] as well as Clarke et al. (2008b) at frontal midline sites. Although it was also expected that theta activity would be elevated in frontal sites, this was not confirmed in the present study. Moreover, the elevation or de‐ crease of theta activity is not documented widely for parietal sites in ADHD literature. How‐ ever, an interesting observation that was not indicated for the initial expectations for the current study is the presence of decreased absolute theta for the ADHD sample at parietal sites. The reduction of absolute theta at parietal sites is also not supported in the other six ADHD studies mentioned [10, 18, 19, 61,31,33].

**ADHD non-ADHD Mann-Whitney U Wilcoxon W Z Between group differences**

Neurodevelopmental Pathways of Childhood ADHD into Adulthood: Maturational Lag, Deviation, or Both?

δ 13.0985 13.5419 39.5 84.5 -0.45 0.50 θ 40.7944 40.6344 39.0 84.0 -0.49 0.66 α 33.4839 33.4904 40.0 85.0 -0.41 0.72 β 12.6232 12.3331 42.0 87.0 -0.25 0.80

δ 12.6778 11.7963 34.0 79.0 -0.91 0.40 θ 41.9948 40.9362 0.00 45.0 -3.68 **0.000\*\*\*** α 33.6352 35.0017 11.0 64.0 -2.94 **0.004\*\*** β 11.6922 12.2656 15.0 70.0 -2.45 **0.01\*\***

δ 14.0345 16.4011 20.5 75.5 -2.01 **0.04\*** θ 40.8777 40.1942 30.0 75.0 -1.23 0.24 α 33.1763 31.1389 29.0 74.0 -1.31 0.21 β 11.9112 12.2660 26.0 81.0 -1.55 0.13

**Table 9.** Relative Mean Power (µV2) for the ADHD (n=10) and the non-ADHD (n=9) Groups

**U**

θ:β 3.28 3.30 42.0 97.0 -0.25 0.84 θ:α 1.23 1.23 39.5 94.5 -0.45 0.66

θ:β 3.69 3.33 6.0 51.0 -3.19 **0.001\*\*** θ:α 1.28 1.17 2.0 47.0 -3.52 **0.000\*\*\***

θ:β 3.63 3.98 21.0 66.0 -1.96 0.05 θ:α 1.27 1.34 43.0 98.0 -0.16 0.91

**Table 10.** Mean Power Ratio Values for the ADHD (n=10) and the nADHD (n=9) groups

**ADHD non-ADHD Mann-Whitney**

The results of the resting EEG further reveal decreased absolute alpha and beta activity for the ADHD sample at parietal sites. These findings are observed in child and adolescent research that are consistent with the maturational lag and developmental deviation profile. The results however have not been indicated in the six ADHD studies identified in the literature search.

Frontal

Midline

Parietal

Frontal

Midline

Parietal

Where \*\* p<.01 and \*\*\* p<.001

p

http://dx.doi.org/10.5772/53865

37

**Wilcoxon W Z Between group**

**differences (p)**

The results of the resting EEG further reveal elevated theta/beta and theta/alpha ratios at frontal midline sites. These results are consistent with child and adolescent research that are suggestive of a developmental deviation profile. These results are also indicated in the ADHD studies of [18, 19, 33].

The resting EEG of the current study also indicates decreased relative beta power for the ADHD sample in the frontal midline area. These results are in line with child and adolescent research that are suggestive of a developmental deviation profile. Of the six ADHD studies [10, 18, 19, 31,33, 61] identified in the current author's literature search, none of the authors confirm such results. Also, although decreased beta power was expected for frontal and frontal midline sites, the finding was only apparent for the frontal midline area.


**Table 8.** Absolute Mean Power (µV2) for the ADHD (n=10) and the non-ADHD (n=9) Groups


**Table 9.** Relative Mean Power (µV2) for the ADHD (n=10) and the non-ADHD (n=9) Groups

sites. The reduction of absolute theta at parietal sites is also not supported in the other six

The results of the resting EEG further reveal elevated theta/beta and theta/alpha ratios at frontal midline sites. These results are consistent with child and adolescent research that are suggestive of a developmental deviation profile. These results are also indicated in the

The resting EEG of the current study also indicates decreased relative beta power for the ADHD sample in the frontal midline area. These results are in line with child and adolescent research that are suggestive of a developmental deviation profile. Of the six ADHD studies [10, 18, 19, 31,33, 61] identified in the current author's literature search, none of the authors confirm such results. Also, although decreased beta power was expected for frontal and

**ADHD non-ADHD Mann-Whitney U Wilcoxon W Z Between group differences**

p

frontal midline sites, the finding was only apparent for the frontal midline area.

δ 0.0191 0.0210 35.5 90.5 -0.78 0.44 θ 0.0549 0.0588 38.0 93.0 -0.57 0.60 α 0.0444 0.0476 34.5 89.5 -0.86 0.40 β 0.0171 0.0178 38.5 93.5 -0.54 0.59

δ 0.0106 0.0070 34.0 79.0 -0.91 0.40 θ 0.0304 0.0241 35.0 80.0 -0.82 0.45 α 0.0234 0.0206 38.5 83.5 -0.53 0.60 β 0.0082 0.0074 39.5 84.5 -0.454 0.66

δ 0.0171 0.0317 20.5 75.5 -2.01 **0.04\*** θ 0.0459 0.0696 20.5 75.0 -2.05 **0.04\***

α 0.0358 0.0513 21.0 76.0 -1.96 0.05

β 0.0129 0.0211 19.5 74.5 -2.09 **0.04\***

**Table 8.** Absolute Mean Power (µV2) for the ADHD (n=10) and the non-ADHD (n=9) Groups

ADHD studies mentioned [10, 18, 19, 61,31,33].

36 Attention Deficit Hyperactivity Disorder in Children and Adolescents

ADHD studies of [18, 19, 33].

Frontal

Midline

Parietal

Where: \*: p<0.05

The results of the resting EEG further reveal decreased absolute alpha and beta activity for the ADHD sample at parietal sites. These findings are observed in child and adolescent research that are consistent with the maturational lag and developmental deviation profile. The results however have not been indicated in the six ADHD studies identified in the literature search.


**Table 10.** Mean Power Ratio Values for the ADHD (n=10) and the nADHD (n=9) groups

#### *3.2.5.3. Conclusion*

The current study's results contribute to the neurobiological and pathophysiological infor‐ mation of ADHD and are important for the advancement of aetiological theorising in the field. Of particular relevance is the interpretation of data in accordance to the maturational lag and developmental deviation model. The abovementioned results are consistent with child and adolescent research that support both models. Hence this brings forth the question of which model more adequately describes the aetiological bases that may be related to the phenomenon of ADHD.

Given the overlap between the neurocognitive symptoms between ADHD and Personali‐ ty Disorders (specifically Cluster B), the first part of the study investigated the preva‐ lence of Personality Disorders in ADHD. The rationale for this was twofold, i.e. there is evidence to suggest that Cluster B disorders may be the result, as is the case with ADHD, of maturational lag, therefore, if this is true, all adults with ADHD should show signs of at least one Cluster B personality disorder. The results of the study indicated that the majority of the adults with ADHD did not show any significant signs of a Clus‐ ter B personality disorder. However, there were more ADHD adults showing signs of more than one personality disorder than those adults without ADHD. If one stays with the assumption that there is a neurocognitive component to personality disorders, this may be indicative of maturational deviation.

1 - 4 5 - 9 10-13 14-17 18-22 23-25

**Figure 3.** Comparison of normative, maturational lag and maturational deviation models of slow wave activity across

Neurodevelopmental Pathways of Childhood ADHD into Adulthood: Maturational Lag, Deviation, or Both?

**Figure 4.** Comparison of normative, maturational lag and maturational deviation models of fast wave activity across

As mentioned already, the results of the current study are in line with the ADHD results of [10, 18, 19, 33] who indicate elevated slow wave activity and increased theta/beta and theta/ alpha ratios. Seeing that EEG aberrances are clearly indicated in adult samples, it does not confirm the maturational lag's assumption that cortical maturation will eventually 'catch up'

Normative Lag Deviation

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39

**Maturation**

developmental stages

developmental stages

These findings seem to suggest that (1) ADHD cannot be viewed as a homogeneous disor‐ der with the same underlying neurodevelopmental processes, and (2) childhood ADHD does not necessarily progress into a personality disorder (see Figure 6), therefore there is room for both an Axis I and Axis II diagnosis in adults with ADHD. One of the problems considering ADHD as a homogenous disorder is that it may suggest a single course with a single outcome. Research, however, suggests that there may be multiple outcomes, i.e. re‐ mission in adolescence or continuation into adulthood. If there is an assumption of multiple outcomes, it should firstly indicate that this is not a homogenous disorder, and secondly it implies that there are different etiological pathways as well. Before one can draw a final con‐ clusiuon about these statements, it is important to also review the EEG results of the ADHD participants.

In order to further investigate the maturational lag vs. maturational deviation theory of ADHD, an EEG study, was done on a smaller sample. The maturational lag model sug‐ gests that ADHD behaviours are a consequence of a neurodevelopmental lag [8]. It fur‐ ther denotes that individuals with ADHD symptoms present with cortical activity patterns that are similar to that witnessed in younger children [8, 20]. Moreover it is ac‐ cepted that cortical development is expected to 'catch up' and remit in adolescence [6]. The developmental deviation model denote that the cortical activity of individuals with ADHD symptoms are not considered normal at any age and is not likely to mature in a normal fashion [20].

Neurodevelopmental Pathways of Childhood ADHD into Adulthood: Maturational Lag, Deviation, or Both? http://dx.doi.org/10.5772/53865 39

*3.2.5.3. Conclusion*

phenomenon of ADHD.

participants.

normal fashion [20].

may be indicative of maturational deviation.

38 Attention Deficit Hyperactivity Disorder in Children and Adolescents

The current study's results contribute to the neurobiological and pathophysiological infor‐ mation of ADHD and are important for the advancement of aetiological theorising in the field. Of particular relevance is the interpretation of data in accordance to the maturational lag and developmental deviation model. The abovementioned results are consistent with child and adolescent research that support both models. Hence this brings forth the question of which model more adequately describes the aetiological bases that may be related to the

Given the overlap between the neurocognitive symptoms between ADHD and Personali‐ ty Disorders (specifically Cluster B), the first part of the study investigated the preva‐ lence of Personality Disorders in ADHD. The rationale for this was twofold, i.e. there is evidence to suggest that Cluster B disorders may be the result, as is the case with ADHD, of maturational lag, therefore, if this is true, all adults with ADHD should show signs of at least one Cluster B personality disorder. The results of the study indicated that the majority of the adults with ADHD did not show any significant signs of a Clus‐ ter B personality disorder. However, there were more ADHD adults showing signs of more than one personality disorder than those adults without ADHD. If one stays with the assumption that there is a neurocognitive component to personality disorders, this

These findings seem to suggest that (1) ADHD cannot be viewed as a homogeneous disor‐ der with the same underlying neurodevelopmental processes, and (2) childhood ADHD does not necessarily progress into a personality disorder (see Figure 6), therefore there is room for both an Axis I and Axis II diagnosis in adults with ADHD. One of the problems considering ADHD as a homogenous disorder is that it may suggest a single course with a single outcome. Research, however, suggests that there may be multiple outcomes, i.e. re‐ mission in adolescence or continuation into adulthood. If there is an assumption of multiple outcomes, it should firstly indicate that this is not a homogenous disorder, and secondly it implies that there are different etiological pathways as well. Before one can draw a final con‐ clusiuon about these statements, it is important to also review the EEG results of the ADHD

In order to further investigate the maturational lag vs. maturational deviation theory of ADHD, an EEG study, was done on a smaller sample. The maturational lag model sug‐ gests that ADHD behaviours are a consequence of a neurodevelopmental lag [8]. It fur‐ ther denotes that individuals with ADHD symptoms present with cortical activity patterns that are similar to that witnessed in younger children [8, 20]. Moreover it is ac‐ cepted that cortical development is expected to 'catch up' and remit in adolescence [6]. The developmental deviation model denote that the cortical activity of individuals with ADHD symptoms are not considered normal at any age and is not likely to mature in a

**Figure 3.** Comparison of normative, maturational lag and maturational deviation models of slow wave activity across developmental stages

**Figure 4.** Comparison of normative, maturational lag and maturational deviation models of fast wave activity across developmental stages

As mentioned already, the results of the current study are in line with the ADHD results of [10, 18, 19, 33] who indicate elevated slow wave activity and increased theta/beta and theta/ alpha ratios. Seeing that EEG aberrances are clearly indicated in adult samples, it does not confirm the maturational lag's assumption that cortical maturation will eventually 'catch up' [6, 20]. Instead, the data suggests that ADHD symptoms do persist for some individuals into adulthood. The results further support the developmental deviation, which suggests that ADHD behaviours are related to the disorganisation of wave activity that deviates from nor‐ mal development [17, 20]. The deviation is revealed in the results wherein the cortical activi‐ ty patterns remain aberrant and have not normalised in the ADHD sample. Taken together, the results of the current study confirms [18] notion that since abnormalities of the EEG per‐ sists into adulthood for the ADHD sample, the data is indicative of a more *persistent* devel‐ opmental deviation for some individuals with the disorder and that not all individuals who present with the disorder will eventually outgrow it.

is because the observation of EEG activity, that is similar to that witnessed in younger chil‐ dren in one point in time, does not suggest that those patterns will eventually 'catch up'.

Neurodevelopmental Pathways of Childhood ADHD into Adulthood: Maturational Lag, Deviation, or Both?

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41

A further matter to consider in relation to the resting EEG of the current study is the posteri‐ or-anterior time course of cortical development. It is evident that the results of the current study yield EEG aberrances in parietal, frontal and frontal midline sites for the ADHD sam‐ ple. As discussed previously, the posterior-anterior time course of cortical development sug‐ gests that the cortical activity in posterior regions mature more rapidly than frontal regions [87]. When cortical development follows this pathway, delta, theta and alpha develop first from birth in occipital regions and only appear later in parietal and central regions and final‐

The results of the current study indicate deviations in the EEG for the ADHD from the con‐ trol group that are present in early-maturing (parietal area) and later-maturing (frontal and frontal midline area) sites. If maturation were seen to 'catch up' in the ADHD sample, then the greatest between- group differences would only have been indicated at frontal sites [26]. Hence, the data is not suggestive of development that is slow to 'catch up' but again sug‐ gests that development in the ADHD sample is indicating a more persistent deviation and disorganisation of wave activity [20, 30]. In Figure 5, a summary is provided of evidence for

ly in frontal regions [26].

both a maturational lag and deviance model.

**Figure 5.** Cortical Activity Patterns of ADHD in Resting Conditions

Up to this point the results of the resting EEG suggests that the data obtained is more sugges‐ tive of a developmental deviation than a maturational lag. However, as mentioned already, the results of the current study indicates increased relative theta and consequently elevated theta/ beta and theta/alpha ratios as well as decreased relative beta at frontal midline sites for the ADHD sample in comparison with controls. This profile displays an elevation in slow wave ac‐ tivity and a decrease in fast wave activity. Although this profile is clearly indicated in develop‐ mental deviation and maturational lag models, the maturational lag model provides the qualitative and aetiological information that links this profile with ADHD behaviours.

EEG support of the maturational lag model reveals in its findings cortical activity patterns that are similar to that witnessed in younger children [10, 20]. In accordance to Kinsbourne [5], the father of the model's ideas, the cortical activity patterns that limit the performance of younger children are synonymous to that which typically compromises the performance of individuals with ADHD symptomatology [10, 20]. Recent normative databases suggest that absolute and/or relative slow wave activity (delta and theta) is elevated in childhood and is the highest shortly before puberty, where after it declines by 60% and finally slows down in its decline af‐ ter the age of 17 [83, 84] (see Figure 3). Following puberty, fast wave activity (alpha and beta) re‐ portedly increases [86]. Finally, between the ages of 25 to 30 years the cortical thickening and thinning (myelination) stabilises and the process of growth spurts and oscillations in terms of cortical activity lessens and normalises [86]. In relation to normative EEG data it is evident that the increase in slow wave activity and decrease in fast wave activity would be more evident in younger children before puberty commences. Hence it appears that the ADHD type behav‐ iours of the current ADHD sample may be aetiologically related to the patterns of cortical activ‐ ity that typically limit the performance of younger children.

The abovementioned paragraphs elicit information that has implications for the interpreta‐ tion and advancement of aetiological theorising according to EEG-based models of ADHD. The developmental deviation denotes that the EEG aberrances observed in individuals with ADHD symptoms are not normal in individuals of *any* age [20]. However, as indicated above, the cortical activity patterns observed in the ADHD sample is synonymous to that which is often observed in younger children. Hence, the data supports the assumption that cortical maturation deviates from normal development and that the deviation is more per‐ sistent; however, it does not support the notion that the resting EEG observed is not similar to patterns witnessed at *any* particular age. Also, the presence of this profile in ADHD EEG research does not automatically serve as evidence of a maturational lag. The reason for this is because the observation of EEG activity, that is similar to that witnessed in younger chil‐ dren in one point in time, does not suggest that those patterns will eventually 'catch up'.

[6, 20]. Instead, the data suggests that ADHD symptoms do persist for some individuals into adulthood. The results further support the developmental deviation, which suggests that ADHD behaviours are related to the disorganisation of wave activity that deviates from nor‐ mal development [17, 20]. The deviation is revealed in the results wherein the cortical activi‐ ty patterns remain aberrant and have not normalised in the ADHD sample. Taken together, the results of the current study confirms [18] notion that since abnormalities of the EEG per‐ sists into adulthood for the ADHD sample, the data is indicative of a more *persistent* devel‐ opmental deviation for some individuals with the disorder and that not all individuals who

Up to this point the results of the resting EEG suggests that the data obtained is more sugges‐ tive of a developmental deviation than a maturational lag. However, as mentioned already, the results of the current study indicates increased relative theta and consequently elevated theta/ beta and theta/alpha ratios as well as decreased relative beta at frontal midline sites for the ADHD sample in comparison with controls. This profile displays an elevation in slow wave ac‐ tivity and a decrease in fast wave activity. Although this profile is clearly indicated in develop‐ mental deviation and maturational lag models, the maturational lag model provides the

qualitative and aetiological information that links this profile with ADHD behaviours.

EEG support of the maturational lag model reveals in its findings cortical activity patterns that are similar to that witnessed in younger children [10, 20]. In accordance to Kinsbourne [5], the father of the model's ideas, the cortical activity patterns that limit the performance of younger children are synonymous to that which typically compromises the performance of individuals with ADHD symptomatology [10, 20]. Recent normative databases suggest that absolute and/or relative slow wave activity (delta and theta) is elevated in childhood and is the highest shortly before puberty, where after it declines by 60% and finally slows down in its decline af‐ ter the age of 17 [83, 84] (see Figure 3). Following puberty, fast wave activity (alpha and beta) re‐ portedly increases [86]. Finally, between the ages of 25 to 30 years the cortical thickening and thinning (myelination) stabilises and the process of growth spurts and oscillations in terms of cortical activity lessens and normalises [86]. In relation to normative EEG data it is evident that the increase in slow wave activity and decrease in fast wave activity would be more evident in younger children before puberty commences. Hence it appears that the ADHD type behav‐ iours of the current ADHD sample may be aetiologically related to the patterns of cortical activ‐

The abovementioned paragraphs elicit information that has implications for the interpreta‐ tion and advancement of aetiological theorising according to EEG-based models of ADHD. The developmental deviation denotes that the EEG aberrances observed in individuals with ADHD symptoms are not normal in individuals of *any* age [20]. However, as indicated above, the cortical activity patterns observed in the ADHD sample is synonymous to that which is often observed in younger children. Hence, the data supports the assumption that cortical maturation deviates from normal development and that the deviation is more per‐ sistent; however, it does not support the notion that the resting EEG observed is not similar to patterns witnessed at *any* particular age. Also, the presence of this profile in ADHD EEG research does not automatically serve as evidence of a maturational lag. The reason for this

present with the disorder will eventually outgrow it.

40 Attention Deficit Hyperactivity Disorder in Children and Adolescents

ity that typically limit the performance of younger children.

A further matter to consider in relation to the resting EEG of the current study is the posteri‐ or-anterior time course of cortical development. It is evident that the results of the current study yield EEG aberrances in parietal, frontal and frontal midline sites for the ADHD sam‐ ple. As discussed previously, the posterior-anterior time course of cortical development sug‐ gests that the cortical activity in posterior regions mature more rapidly than frontal regions [87]. When cortical development follows this pathway, delta, theta and alpha develop first from birth in occipital regions and only appear later in parietal and central regions and final‐ ly in frontal regions [26].

The results of the current study indicate deviations in the EEG for the ADHD from the con‐ trol group that are present in early-maturing (parietal area) and later-maturing (frontal and frontal midline area) sites. If maturation were seen to 'catch up' in the ADHD sample, then the greatest between- group differences would only have been indicated at frontal sites [26]. Hence, the data is not suggestive of development that is slow to 'catch up' but again sug‐ gests that development in the ADHD sample is indicating a more persistent deviation and disorganisation of wave activity [20, 30]. In Figure 5, a summary is provided of evidence for both a maturational lag and deviance model.

**Figure 5.** Cortical Activity Patterns of ADHD in Resting Conditions

It must be emphasised that this study was exploratory in nature, and in many ways it result‐ ed in more questions than answers. What the study did do however, was to highlight some problems in our interpretation of quantitative data. The first of these is the problem of the *average*. The conclusion drawn from averages does not include a satisfactory explanation for the variance, i.e. in terms of maturational lag, as the findings suggest that there is a distinct possibility that some of these reach cortical maturity at the same rate as non-ADHD children (i.e. those at the higher end of the distribution), and that there are those who may reach this much longer after the 3 year average (i.e. those at the lower end of the distribution). At both ends of the distribution, it opens the possibility for maturational deviance as symptoms are present, but cannot be explained fully by the maturational lag theory (See Figure 6). In line with this above argument, even within studies, not all cortical areas are affected in the same way. This is, in essence, not problematic, however, formulating a general maturational lag model is, as it seems to imply that there is general maturational lag. Furthermore there are studies that report maturational lag, but include discrepant findings in cortical areas which are explained asymmetrical maturation. The question that arises is whether this should then be considered as maturational lag or maturational deviance.

this disorder, we need to review our research methodologies. It is argued that many of the confounding / contradictory results is the way in which studies are conceptualised. In this regard, the sampling of participants needs to be more focused, as current studies seem to include mainly the combined sub-type of ADHD [6].If this were true, it would not be inaccurate to state that very little is known about brain maturation in children with the inattentive subtype. It is therefore imperative that sampling be done much more specifically and that subtypes are compared to each other. Furthermore, one needs to de‐ viate from the common practice to exclude participants with both ADHD and comorbid conditions and rather group these participants together based on disorders that are alike

Neurodevelopmental Pathways of Childhood ADHD into Adulthood: Maturational Lag, Deviation, or Both?

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43

[2] Miller TW, Nigg JT, Faraone, SV. Axis I and II comorbidity in adults with ADHD.

[3] Anckarsäter H, Stahlberg O, Larson T, Hakansson C, Jutblad S-B, Niklasson L, Ny‐ den A, Wentz E, Westergren S, Cloninger R, Gillberg C, Rastam M. The Impact of ADHD and Autism Spectrum Disorders on Temperament, Character, and Personali‐

[4] Nigg JT, Goldsmith HH, Sachek J. Temperament and Attention Deficit Hyperactivity Disorder: The Development of a Multiple Pathway Model. Journal of Clinical Child

[5] Kinsbourne M. Minimal brain dysfunction as a neurodevelopmental lag. Annals of

[6] Rubia K. Neuro-anatomic evidence for the maturational delay hypothesis of ADHD.

[7] Shaw P, Gogtay N, Rapoport J. Childhood psychiatric disorders as anomalies in neu‐

[8] Clarke, AR, Barry, RJ, Dupuy, FE, McCarthy, R, Selikowitz, M, Heaven, PCL. Child‐ hood EEG as a predictor of adult attention-deficit/hyperactivity disorder. Clinical

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rodevelopmental trajectories, Human BrainMapping 2010; 31 917-925.

ty Development. American Journal of Psychiatry 2006; 163 1239-1244.

in both symptomotology and theoretical etiology.

Department of Psychology, University of Johannesburg, South Africa

Journal of Abnormal Psychology 2007; 116(3) 519-528.

and Adolescent Psychology 2004; 33(1) 42-53.

Neurophysiology 2011, 122 73-80.

the New York Academy of Sciences 2004; 205 268-273.

**Author details**

**References**

[1] www.dsm5.org

Alban Burke and Amanda Edge

A common theme which runs through all the studies, and may account for many of the comments above, is that ADHD is often considered to be a homogenous disorder. It is quite possible that maturational lag would best account for a certain sub-group, and de‐ viance for others (See Figure 6). If we are going to gain more insight into the etiology of this disorder, we need to review our research methodologies. It is argued that many of the confounding / contradictory results is the way in which studies are conceptualised. In this regard, the sampling of participants needs to be more focused, as current studies seem to include mainly the combined sub-type of ADHD [6].If this were true, it would not be inaccurate to state that very little is known about brain maturation in children with the inattentive subtype. It is therefore imperative that sampling be done much more specifically and that subtypes are compared to each other. Furthermore, one needs to de‐ viate from the common practice to exclude participants with both ADHD and comorbid conditions and rather group these participants together based on disorders that are alike in both symptomotology and theoretical etiology.

#### **Author details**

It must be emphasised that this study was exploratory in nature, and in many ways it result‐ ed in more questions than answers. What the study did do however, was to highlight some problems in our interpretation of quantitative data. The first of these is the problem of the *average*. The conclusion drawn from averages does not include a satisfactory explanation for the variance, i.e. in terms of maturational lag, as the findings suggest that there is a distinct possibility that some of these reach cortical maturity at the same rate as non-ADHD children (i.e. those at the higher end of the distribution), and that there are those who may reach this much longer after the 3 year average (i.e. those at the lower end of the distribution). At both ends of the distribution, it opens the possibility for maturational deviance as symptoms are present, but cannot be explained fully by the maturational lag theory (See Figure 6). In line with this above argument, even within studies, not all cortical areas are affected in the same way. This is, in essence, not problematic, however, formulating a general maturational lag model is, as it seems to imply that there is general maturational lag. Furthermore there are studies that report maturational lag, but include discrepant findings in cortical areas which are explained asymmetrical maturation. The question that arises is whether this should then

A common theme which runs through all the studies, and may account for many of the comments above, is that ADHD is often considered to be a homogenous disorder. It is quite possible that maturational lag would best account for a certain sub-group, and de‐ viance for others (See Figure 6). If we are going to gain more insight into the etiology of

be considered as maturational lag or maturational deviance.

42 Attention Deficit Hyperactivity Disorder in Children and Adolescents

**Figure 6.** Multiple outcomes of ADHD in adulthood

Alban Burke and Amanda Edge

Department of Psychology, University of Johannesburg, South Africa

#### **References**


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[26] Hobbs MJ, Clarke AR, Barry, RJ, McCarthy, R, Selikowitz, M. EEG abnormalities in adolescent males with AD/HD. Clinical Neurophysiology 2007; 118 363-371.

[27] Schmidt, RG, Tirsch, WS, Reitmeir P. Correlation of developmental neurological findings with spectral analytical EEG evaluations in pre-school age children. Electro‐

[28] Clarke AR, Barry RJ, McCarthy R, Selikowitz, M. Age and sex effects in the EEG: Dif‐ ferences in two subtypes of attention-deficit/hyperactivity disorder. Clinical Neuro‐

[29] Hermens DF, Soei EXC, Clarke SD, Kohn, MR, Gordon E, Williams LM. Resting EEG theta activity predicts cognitive performance in attention-deficit hyperactivity disor‐

[30] Alexander D M, Hermens DF, Keage, HAD, Clark CR, Williams LM, Kohn, MR, Clarke SD, Lamb C, Gordon E. Event-related wave activity in the EEG provides new

[31] Loo KS, Sigi Hale T, Macion J, Hanada G, McGough JJ, McCracken JT, Smalley SL. Cortical activity patterns in ADHD during arousal, activation and sustained atten‐

[32] Tian L, Jiang T, Liang M, Zang Y, He Y, Sui M, Wang Y. Enhanced resting-state brain activities in ADHD patients: A fMRI study. Brain and Development 2008; 30 342-348.

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**Chapter 3**

**Difficulties in Recognizing ADHD in**

**an Urban Population and Treatment**

Antigone Papavasiliou, Irene Nikaina, Anna Spyridonidou and Eleanna Nianiou

http://dx.doi.org/10.5772/53791

**1. Introduction**

Additional information is available at the end of the chapter

**Satisfaction with a Short and a Long Acting Stimulant**

Attention deficit hyperactivity disorder (ADHD) is an established neuropsychiatric disorder in children and adolescents with paediatric or mental health services available across most of Europe. In spite of major improvements in the availability of services for the diagnosis of ADHD and several therapeutic options, including medications, psychosocial and psychoeducational therapies, families of children with ADHD experience considerable emotional and social burden [1-2]. The presence and severity of the child's ADHD is a significant predictor of heightened parental stress and the diagnosis of ADHD can result in impairments in the Quality of Life in patients and their families [3-4]. Yet, there is a rather limited number of studies exploring parental perceptions of the diagnosis and overall treatment of this disorder. An American study determined that primary care physicians generally adhere to practices specified in the AAP guidelines [1] for the diagnosis and treatment of pediatric ADHD; some variations existed and improvements were possible. Poor access to mental health services, limited insurance coverage, and other potential system barriers to the delivery of ADHD care were noted [5]. An Australian study explored perceptions relating to the diagnosis, treatment and overall management of the disorder [6] in the families of 278 children with ADHD identified in a community sample of 11 184 children aged 10-12 years; only 66% of parents recalled the use of questionnaires or rating scales, drugs were tried in 82% and 66% of the children were still on them, behavioral intervention in 42% and alternative treatments, mostly elimination diet and/or fatty acid supplementation, were used in 71%. Overall, 55% of parents were satisfied or very satisfied with their child's care. The conclusion of this study was that adherence to recommended diagnostic guidelines was inadequate, behavioral intervention

> © 2013 Papavasiliou et al.; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

> © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,

and reproduction in any medium, provided the original work is properly cited.
