Attention Deficit Disorder

Diagnosis And Treatment From Infancy To Adulthood

Patricia O. Quinn

• Publisher: Routledge
• Year: 2013
• eBook ISBN: 9781135062965
• Edition: 1
• Topic: Education
• Subtopic: Inclusive Education

Published in 1996, Attention Deficit Disorder is a valuable contribution to the field of Psychiatry/Clinical Psychology.

Chapter 1

WHAT IS ADD?

Attention Deficit Disorder (ADD) is a neurobiological condition that affects learning and behavior and is present in 3 to 10% of the school-age population (Wender, 1987). It begins in childhood and was initially thought to be outgrown by adolescence. However, we now know that this is not the case and that 30 to 70% of adolescents with ADD continue to be affected by symptoms into adulthood (Silver, 1992). But what is the evidence that this condition has a neurobiological basis?

THE NEUROBIOLOGICAL BASIS OF ADD

One of the first models used to explain ADD was the catecholamine hypothesis (Kornetsky, 1970). This theory refers to the faulty functioning in the brain of the neurotransmitters dopamine and norepinephrine. In 1977, Shawitz and coworkers determined that concentrations of the metabolite of dopamine in the cerebrospinal fluid in children with ADD was significantly lower than in a control group of normal children, suggesting reduced turnover of dopamine in this group. Another study (Rapoport, Quinn, & Lamprecht, 1974) found that plasma dopamine β-hydroxylase (DBH) activity was elevated in a group of boys with ADD who had high scores for minor physical anomalies. In addition, both imipramine and methylphenidate significantly increased plasma DBH activity. While the dopamine system was clearly implicated in this disorder, serotonin levels were not found to differ significantly in hyperactive children versus controls (Rapoport, Quinn, Scribanu, & Murphy, 1974).

Wender, in his book Minimal Brain Dysfunction in Children, published in 1971, was one of the first to propose that children with this disorder had an abnormality in the metabolism of the monoamines serotonin, dopamine, and norepinephrine. Although the role of serotonin in ADD has not been established on a biochemical basis, the newer serotonergic agents such as fenfluramine and fluoxetine have proven useful in treating comorbid conditions, such as depression, but they do not appear to address the core symptoms of inattention, impulsivity, and hyperactivity. While we can postulate that these monoamines are involved in ADD, biochemical studies have had only limited success in correlating measures of norepinephrine, dopamine, and their metabolites with the ADD syndrome (Zametkin & Rapoport, 1987). Nonetheless, a tripartite model of ADD involving dopamine, norepinephrine, and serotonin as causing the inattentive, hyperactive, and impulsive types of ADD respectively has recently been postulated by Voeller (1991).

IMPAIRMENTS IN BRAIN FUNCTIONING

Recent technological advances and refinements in neuropsychological testing have led researchers to move beyond the catecholamine hypothesis in ADD and to look more seriously at anatomic structures in the brain and how impairments in their functioning could be related to symptoms of ADD. Further research has linked the frontal lobes, particularly the prefrontal cortex and limbic system, to motivation and emotional responsiveness. The executive functions, particularly attention and goal-oriented problem-solving behaviors, are also known to be dependent on the integrity of the frontal lobes and their subcortical connections, including the basal ganglia. Likewise, arousal states are modulated by interconnections with the reticular activating system within the deeper structures of the brain.

ADD has been described as a disorder of disinhibition and disregulation of the frontal cortex (Douglas, 1984; Gualtieri et al., 1985). In 1986, Chelune and coworkers also proposed a frontal lobe hypothesis for ADD. Neuropsychological studies were used to localize the disinhibition to the frontal lobes and resulted in the proposal that the symptom of hyperactivity was the direct result of a disturbed higher level of cortical inhibition. Since Chelune's work, other neuropsychological studies have confirmed frontal lobe disinhibition in individuals with ADD (Barkley et al., 1992).

More recently, neuroimaging techniques have allowed for further study of frontal lobe and striatal deactivation. Studies by Amen, Poldi, and Thisted (1993) reported significant prefrontal deactivation when individuals with ADD were asked to respond to an intellectual challenge. Some individuals in this study demonstrated decreased prefrontal activity even during rest. Lou and coworkers (1984) documented hypoperfusion in these same striatal areas of children with ADD, and Lubar and colleagues (1985) found abnormal brainwave activity in the frontal lobes of children with ADD when compared with controls.

Most exciting of all, however, were the landmark findings of Zametkin and colleagues at the National Institutes of Mental Health. In the New England Journal of Medicine (1990), these investigators reported convincing results from a study measuring glucose metabolism in the brains of adults who had histories of hyperactivity in childhood and who continued to be symptomatic. Each adult was the biological parent of a hyperactive child. Using positron emission tomography (PET) scanning techniques, this group measured regional cerebral glucose metabolism. Results indicated that this metabolism was lower in adults with ADD than in controls in both cortical and subcortical areas. Regions of greatest reduction were the premotor cortex and the superior prefrontal cortex. This study provided the documentation that these areas, which are responsible for control of attention and motor activity, were involved in the ADD syndrome.

Hynd and coworkers (1990), using magnetic resonance imaging (MRI) studies, have found differences in both the frontal areas and the corpus callosum of children with ADD. Results of an additional study in 1991 provided evidence of important differences in the morphology and size of certain areas of the corpus callosum in ADD children. More recent studies by Castellanos and colleagues at NIMH also indicate anatomic asymmetries on MRI scans of ADHD boys when compared to controls. Areas involved included the caudate, right frontal, globus pallidus and cerebellum (Castellanos et al., 1996).

AN INTEGRATED MODEL

These theories of frontal lobe disinhibition and the catecholamine hypothesis are not at odds but can be seen to complement each other. The prefrontal cortex has an abundant supply of catecholamines. In a review of the neurobiology of ADD by Zametkin and Rapoport (1987), dopamine was described as being localized in the limbic areas and assumed to be involved in the expression of ADD. Dopaminergic pathways are found between the motor cortex and the limbic center to the frontal areas. The prefrontal cortex also receives input from norepinephrine from lower brain structures. Thus the presence of both dopamine and norepinephrine in the prefrontal areas may be crucial to the functioning of the frontal lobes. Dysregulation of these systems impairs the capacity of the frontal lobes to perform properly. Consequently, both blood flow and metabolism appear to be depressed. Neuropsychological studies suggest that frontal areas are then unable to inhibit or control input from lower brain structures, resulting in the symptoms we see in ADD.

THE GENETICS OF ADD

Despite the varied clinical picture of ADD, investigators are now becoming more aware that ADD has a genetic basis. Studies of identical and fraternal twins (Gilles et al., 1992; Goodman & Stevenson, 1989) have found a significantly higher incidence of ADD in identical as compared with fraternal twins, suggesting a genetic predisposition. Other studies have discovered that relatives of ADD children are at greater risk for the disorder than are relatives of control children (Morrison and Stewart, 1971, 1973; Cantwell, 1972).

Research in molecular biology has also supported the concept of the heritability of ADD. Genetic studies of the dopamine D-2 receptor locus have found this to be a modifying gene in many neuropsychiatric disorders, including 46% of the patients with ADD. (Comings et al., 1991). Genetic transmission of ADD was also postulated, after research on a genetically inherited thyroid hormone disorder found that 70% of the children and 50% of the adults with generalized resistance to thyroid hormone also met the criteria for ADD (Hauser et al., 1993).

ADD IN GIRLS

Genetic factors clearly seem to be operating in the ADD syndrome, but the mode of transmission is not clear. Morrison and Stewart (1973, 1974) have proposed that polygenetic inheritance is the most likely mode of transmission for this condition. Gender differences do appear and ADD has always been reported to be more common in males than in females. Recently, however, girls have been diagnosed in increasing numbers as clinicians have become more aware of the disorder, particularly ADHD-I. In the latest DSM-IV field trials the ADHD-HI group contained 20% girls, with 27% diagnosed as ADHD-I and 12% found to be in the ADHD-C group (McBurnett, 1995). Recent predictions have even suggested that the male—female ratio may be as low as 3:1 or even 2:1, suggesting that hundreds of thousands of girls and women are affected by ADD.

Various factors may account for the phenomenon of missed diagnosis of ADD in females. Women with the disorder can escape even the best clinicians' detection, since they lack the typical symptoms of hyperactivity and impulsivity (Berry et al., 1985). In addition, girls tend to internalize more and develop the symptoms of anxiety and depression more often (Brown et al., 1989), thus presenting as patients with Mood Disorder as opposed to ADD. In their particular study Berry and coworkers found that girls with ADD further differed from males with ADD in that they demonstrated more cognitive impairments, particularly in the area of language function (Berry et al., 1985).

Differences were also seen in girls depending on whether the ADD was noted with or without hyperactivity. Girls with ADD without hyperactivity had poorer self-esteem and were usually older at the time of referral. All girls with ADD, regardless of whether they had hyperactivity or not, were reported to suffer more peer rejection; and research has shown that girls with ADD and hyperactivity tend to have more learning problems (O'Brien et al, 1994; Philips et al., 1993).

Girls with ADD may have increasingly severe problems beginning with the onset of puberty. These include increased emotional overreactivity, mood swings, and impulsivity thought to be due to an increase in hormones. Increased hormonal fluctuations throughout the phases of the menstrual cycle may also lead to more symptomatology (Hussey, 1990). In my practice I found that I was treating these girls with ADD for severe premenstrual symptoms (PMS) and mood swings with antidepressants as well as stimulants, long before the recent studies recommending the SSRIs to address these same symptoms were published.

Interest in these sex differences related to symptomatology and outcome led to a conference at the National Institutes of Mental Health in November, 1994. The purpose of the conference was to focus research attention on the presence of ADD in girls and women and to establish leading areas for future research. A summary of the recommendations and the data presented is yet to be published.

ADD WITHOUT HYPERACTIVITY

Recent research has now made clear that ADD without hyperactivity is a real entity and a valid diagnostic category. Lahey and Carlson's (1991) review of the literature on this topic established several points: First, factor analytic studies consistently indicate that covariation among the symptoms reflects two independent dimensions; second, ADD without hyperactivity exists as a clinical diagnosis; and third, children who meet the criteria for ADD without hyperactivity are be-haviorally different from children who have the hyperactivity component. The latter children have far less serious conduct problems; they are less impulsive, less rejected by peers, and more withdrawn. They are also more likely to be characterized as sluggish and drowsy. An increased comorbidity including depression and symptoms of anxiety disorders was also noted in this group (Lahey & Carlson, 1991).

Significant differences between hyperactive and nonhyper-active children with ADD were also noted in both neurologic and cognitive areas. The overall percentage of prenatal and perinatal complications, neurologic abnormalities, impairments in visual perception, visual and auditory memory, reading, and writing were found to be significantly increased in those children with the hyperactivity. Whereas both groups were found to have abnormalities in these areas, the group of children with ADD-H had an increased frequency of these deficits, leading ...

Table of contents

• Cover
• Half Title
• ABOUT THE BASIC PRINCIPLES INTO PRACTICE SERIES
• Full Title
• Copyright
• Contents
• Dedication
• ACKNOWLEDGMENTS
• INTRODUCTION
• Chapter 1 What Is ADD?
• Chapter 2 Atypical Infants and Toddlers
• Chapter 3 The Preschool Child with ADD
• Chapter 4 The Elementary School Child
• Chapter 5 The Adolescent/High School Student
• Chapter 6 The Postsecondary Student
• Chapter 7 Adults with ADD
• Chapter 8 Multimodal Treatment of ADD
• Chapter 9 ADD and the Law
• Chapter 10 Conclusion
• NAME INDEX
• SUBJECT INDEX