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ADHD: Context, Effects and Models of Intervention

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Examining Attention Deficit Hyperactivity Disorder (ADHD)

Introduction

Attention Deficit Hyperactivity Disorder has been recently acknowledged as a condition that affects the whole life experience of children with this disorder. The condition is chronic, no actual cures seem imminent. However, effective treatment interventions exist currently and more effective treatments are under development.

The following is an examination of ADHD from several perspectives. The historical concepts, issues and viewpoints regarding this disorder prove a rich ground for exploring advances, retrenchments and side roads along the timeline.

More in depth of discussion of diagnosis and treatment models for ADHD is provided. The complications introduced by the fact of comorbid conditions are discussed at some length. The details presented on models of treatment include portions of a medical and portions of a social model, well-suited to the coordination skills of a social worker to play a pivotal role.

The various impacts of ADHD, especially on the child, are discussed, together with implications for relieving these burdens.

In conclusion, a brief discussion of the social workers role in the ADHD constellation of requirements and opportunities is presented.

Historical Concepts, Issues and Perspectives

Largely due to changes in naming conventions, shifts in conceptualization and the spate of public and professional controversy, ADHD is perceived by many as a recently-identified disorder. In fact, however, the history of the concept is quite long, with a timeline stretching back to the mid-19th Century.

ADHD may have been first described by Dr. Heinrich Hoffman in 1845. A German physician who wrote on medicine and psychiatry, Dr. Hoffman also authored poetry for children. His verse concerning a fidgety young man named Philip made its way into the British medical journal Lancet in 1904. This is often cited as the first account of ADHD published in the medical literature:

The Story of Fidgety Philip

“Let me see if Philip can

Be a little gentleman;

Let me see if he is able

To sit still for once at the table.”

Thus Papa bade Phil behave;

And Mama looked very grave.

But Fidgety Phil,

He won’t sit still;

He wriggles,

And giggles,

And then, I declare,

Swings backwards and forwards,

And tilts up his chair,

Just like any rocking horse—

“Philip! I am getting cross!”

See the naughty, restless child

Growing still more rude and wild,

Till his chair falls over quite.

Philip screams with all his might,

Catches at the cloth, but then

That makes matters worse again.

Down upon the ground they fall,

Glasses, plates, knives, forks and all.

How Mama did fret and frown,

When she saw them tumbling down!

And Papa made such a face!

Philip is in sad disgrace . . . (Hallowell & Ratey, 1995, pp. 270-271).

Two years before the publication of this issue of Lancet, the pediatrician Sir George F. Still delivered a series of three lectures to England’s Royal Academy of Physicians, describing a group of twenty children whose behavior he characterized as impulsive, manifesting significant behavior problems. Given that children judged to be subject to poor child-rearing were excluded from these observations, Still concluded that the cause of these unbounded behaviors was likely genetic or a result of brain damage (Still, 1902).

Still’s proposition constituted a novel approach. Previously, objectionable behavior was assumed to be the product of voluntary choice on the part of the child and/or poor parenting, and physical punishment was the ‘treatment’ of choice. The offer of genetic and neurological dynamics as potential controlling factors ushered in a “kinder, more effective approach to child-rearing” (Hallowell & Ratey, 1995, p. 272).

As a result of the 1918 influenza pandemic, Still’s attribution of ADHD-like constellations of behavior to brain damage was reinforced by behavior patterns of many children recovering from encephalitis. These children were reported to exhibit “restlessness, inattention, impulsivity, easy arousability, and hyperactivity” (Wolraich, 2006, p. 86). Several publications, notably Kahn and Cohen’s 1934 article in the New England Journal of Medicine (Hallowell & Ratey, 1995, p. 272), provided the link between this neurological condition and the symptoms of distractibility, impulsivity and restlessness, now considered diagnostic of ADHD.

A few years later, in 1937, Dr. Charles Bradley demonstrated the apparently paradoxical effect of the stimulant Benzedrine in controlling hyperactivity in children. The finding that behavior problems improved with stimulant medication reinforced the notion of a biological basis. This link received convincing empirical support. In 1957, a technological boost arrived with the release of the stimulant methylphenidate (Ritalin; Hallowell & Ratey, 1995, p. 272; Wolraich, 2006, p. 87-88). Additional advances occurred in 1999, with the advent of extended-release stimulants and in 2003, with the approval of Atomoxetine (Strattera), a nonstimulant medication, for the treatment of ADHD in children and adults (see Troost et al., 2006). Coghill (2005) pointed out that “extended-release stimulant preparations and novel non-stimulant treatments for ADHD potentially offer real benefits for patient care” (p. 290).

When Ritalin became available in 1957, the disorder to be treated was termed Minimal Brain Damage. In 1966, the recognition that clear evidence of brain damage was absent in many cases prompted re-labeling the problem as Minimal Brain Dysfunction. The following year, DSM-II re-christened this diagnosis as the Hyperkinetic Reaction of Childhood Disorder, reflecting growing doubt regarding brain damage involvement. Also, research in the 1960s, including that of Stella Chase, placed an emphasis on hyperactivity as the major component of this disorder (Wolraich, 2006, p. 86-87).

Another potential cause of the disorder was introduced by the work of Dr. Ben Feingold in 1973. His argument that instances of hyperactivity were increasing as the levels of food additives rose promoted an alternative treatment literature based on diet and nutrition. This step along the ADHD timeline also reinforced the role of biology in the disorder through the mechanism of allergic reactions (Eigenmann & Haenggeli, 2004; Feingold, 1973).

The diagnostic labeled changed again with DSM-III in 1980. Reflecting a conceptual shift from hyperactivity to inattention as the focal deficit, the term Attention Deficit Disorder (ADD) replaced Hyperkinetic Reaction and two subtypes were defined: ADD with and without hyperactivity. Seven years later, DSM-III-R provided the current label of Attention Deficit Hyperactivity Disorder (ADHD), while scrapping the subtypes due to lack of evidence. DSM-IV retained the label ADHD and redefined three subtypes: predominantly inattentive, predominantly hyperactive-impulsive, and combined (Wolraich, 2006, p. 87). Wolraich (2006) speculated that recent research emphasizing impulse control, such as that reported by Barkley in 1997, may spur yet another reconceptualization of this diagnosis.

While the core diagnostic symptoms of inattention, impulsivity and hyperactivity have persevered across the timeline, the specific diagnostic criteria have changed to follow the focus of shifting conceptualizations of the disorder. Not only can shifts in concepts and labels be confusing, the concommitant adjustment of these criteria can alter incidence and prevalence statistics. For example, within the same sample, Wolraich (2006) cited an increase in ADHD prevalence rates from 2.6 % with DSM-III to 6.1% using DSM-III-R (p. 87).

All along the timeline, differences in concept and terminology flourish. These difference also include those that are cross-cultural in nature and those inspired by comorbidity. For example, the label DAMP (Deficits in Attention, Motor Control and Perception) is used only in Sweden and Denmark to designate ADHD co-occurring with dyspraxia (Gillberg, 2003).

The International Classification of Diseases (ICD) uses the label of HKD (Hyperkinetic Disorder) for symptomatology similar to ADHD in the DSM; for global discourse, the two are used interchangeably, although ICD-10’s stricter standards yield lower incidence rates (Remschmidt, 2005). Other examples abound.

Hallowell and Ratey (1995) characterized this journey through ADHD history as “riddled with false leads, multiple possibilities, contradictory findings, and many gut reactions of all kinds” (p. 274). It is no wonder that a fair number of frustrated stakeholders assert that ADHD is a mythic disorder, a social construct, without biological or psychological validity, perpetrated on society by profit-seeking drug companies and service providers (e.g., Neufeld & Foy, 2006; Timini & Taylor, 2004). Responses to these doubts regarding the validity and impact of ADHD constitute the final three points on this timeline.

Validity concerns, especially those related to low sample size, were addressed in 1999 by the multimodal treatment study of children with ADHD (MTA Study). Five hundred seventy-nine with ADHD, aged 7 to 10 years, were randomly assigned to four 14-month treatment conditions at six sites in the United States and Canada. The initial findings from this study indicated that medication alone was more effective than was only psychosocial treatment, and that the combination of treatments benefited some children more than medication only condition (MTA Cooperative Group, 1999). This substantial dataset has been used in the publication of more than forty studies.

In 2002, the world’s leading experts on ADHD joined together to publish the International Consensus Statement on ADHD, a strongly-worded document intended to put to rest the arguments against the validity and impact of this disorder, especially those propagated in the media (Barkley et al., 2002). This statement set out a two-part litmus test for a valid medical or psychiatric disorder: “…there must be scientifically established evidence that those suffering from the condition have a serious deficiency in or failure of a physical or psychological mechanism that is universal to humans…regardless of culture…and…that this serious deficiency leads to harm to the individual” (p. 89). Striving to meet, and exceed, both criteria, the statement relied on reference to research demonstrating deficits in specific neurological functions; cross-cultural twin studies, demonstrating the primary role of genetic contribution; and the abundance of data bearing on the lasting negative impact of ADHD for major life activities of the individual, as well as for the family, school, community and society (p. 90).

Following a similar mission, the Global ADHD Working Group set out to foster consensus on the validity and impact of this disorder, and to reach a consensus on best practice in diagnosis and treatment. The Group consisted of fifteen recognized experts from Australia, Brazil, France, Germany, South Korea, Mexico, Philippines, UK and USA. The outcome of their work was published as the Global Consensus on ADHD/HKD (Remschmidt, 2005). In addition to fleshing out the International Consensus Statement’s arguments for validity and impact, this Group addressed the importance of accurate diagnosis and measurement of impairment, highlighting the similarities and differences between ADHD (in DSM-IV) and HKD (in ICD-10). For example, the Group noted that a re-analysis of the MTA Study data to investigate the implications of using the ICD-10 classification system indicated that 25% of the sample diagnosed as ADHD would have received the HKD diagnosis under ICD-10 (p. 129).

The bulk of this Group’s work focused on achieving consensus treatment algorithms, designed to be used at a global level. These four algorithms are guidelines intended to aid clinical judgment in the multimodal treatment of ADHD alone, and ADHD with comorbidities present, including conduct disorder, major depressive disorder, and tic disorder (pp. 130-136). This highlights the pivotal role of comorbidity in conditioning the processes of ADHD diagnosis and treatment.

The next section examines the evidence and implications of some comorbidity findings, as well as other aspects of the diagnosis and treatment of ADHD.

Some Issues in Diagnosis and Treatment

Co-occurring Disorders

ADHD is associated with a high co-occurrence of other psychiatric disorders. More often than not, ADHD is accompanied by a learning disability. Each comorbid disorder serves to modify the clinical presentation of ADHD, challenging the diagnostic and treatment planning process.

For example, a review study by James et al. (2004) supported a connection between ADHD and suicide. Compared with USA national suicide rates and risk ratios for males between ages of five and twenty-four years, ADHD appears to increase this risk ratio for males via increasing the severity of comorbid conditions, especially conduct disorder (CD) and depression.

Common disorders that frequently co-exist with ADHD include:

  • Oppositional Defiant Disorder (and Conduct Disorder)
  • Learning and communication differences
  • Anxiety (state or trait)
  • Obsessive-Compulsive Disorder
  • Depression
  • Enuresis
  • Drug abuse
  • Bipolar Disorder
  • Sleep Problems
  • Tourettes Disorder
  • Pervasive Developmental Disorder
  • Many forms of physical illness (such as asthma)
  • Accidental injury

Faraone (2001) reviewed these patterns of comorbidity. The high instance of comorbidity has given rise to controversy as to whether ADHD exists as a primary disorder or only secondary to other psychiatric syndromes. The nosological system advocated in the DSM is a hierarchical one; that is, in the presence of two or more diagnoses, one is to be considered primary and should account for significant symptoms observed in the secondary disorder. There is mounting evidence, however, that many conditions exist concurrently with ADHD, and each modifies the overall clinical presentation and treatment response. Faraone argued that comorbid conditions should be considered simultaneously in order to broaden our understanding and maximize treatment.

Depressed patients may demonstrate diminished concentration and individuals with bipolar disorder often manifest psychomotor ‘hyperactivity’ and distractibility. It may be difficult to differentiate these symptoms from the core symptoms of ADHD. There are several ways to deal with symptom overlap in research and clinical settings. The “subtraction method” requires the same absolute number of symptoms to be present to diagnose either disorder, except that shared symptoms are “subtracted” or removed from diagnostic consideration. For example, 8 of 14 (57%) symptoms are needed for the diagnosis of ADHD in the DSM-IV. If two overlap symptoms are present between the two co-occurring disorders, then 8 of 12 (67%) symptoms would be required to make the diagnosis with the subtraction method. Alternatively, in the “proportional” method the same ratio of symptoms would be required. Milberger et al. (1995) reported that most patients with comorbid depression and ADHD still retained the diagnosis of ADHD whether the subtraction or proportional method was used. Long-term follow-up studies have demonstrated that individuals with ADHD and comorbid disorders have poorer prognoses and higher rates of hospitalization than those with ADHD alone (Biederman et al., 1998).

Pharmacologic “dissection” studies have been conducted to determine clinical contributions of each of the comorbid disorders and treatment strategies. For example, an individual with comorbid ADHD and bipolar disorder may first be treated with stimulants. Usually, little change occurs with this treatment intervention. Alternatively, if a mood stabilizer is initiated first, significant improvement may be expected. If symptoms of ADHD continue to persist after mood stabilization, this gives support for the diagnosis of two co-occurring diagnoses. The addition of a stimulant may then be indicated. Therefore, unless both comorbid conditions are adequately treated, the ADHD symptoms may not remit. Pharmacologic studies of bipolar disorder and ADHD suggest that the two disorders exist as discrete entities in many patients (Biederman et al., 1998).

ADHD with Asperger Syndrome. Asperger Syndrome (AS) is a pervasive developmental disorder characterized by deficits in social interaction and motor coordination, as well as by unusual or restricted patterns of interest and behavior. The clinical distinction between autism and AS has to do with severity and qualitative expression of the diagnostic criteria. Both are characterized by deficits in social interaction, impairment of communication skills, and the manifestation of unusual or bizarre behaviors. However, in AS, motor deficits are more pronounced, onset occurs later, and social deficits are present without grossly impaired speech and language (Frith, 1991).

There are relatively few studies of psychiatric disorders comorbid with AS. It is reported that 28% of AS subjects have co-occurring ADHD. The comorbidity of these two disorders vary according to developmental level; ADHD appears to be more common in the younger AS population (Klin & Volkmar, 1997).

ADHD with depressive disorders. The overlap between depression and ADHD is now well recognized. Given that the presence of an underlying or co-occurring mood disorder complicates the treatment of ADHD, proper recognition and treatment of this disorder is vital.

Recent evidence indicates that depressive disorders may be manifested in childhood in a variety of guises. Depressed children tend to present with irritability, negativism, social withdrawal, school dysfunction, and somatic disorders. AS with the core symptoms of ADHD, these symptoms can be attributed to normal childhood behaviors. Hence, the diagnosis may be overlooked.

The rate of comorbidity between ADHD and depression was examined in a long-term follow-up study by Biederman and colleagues (1996). The baseline rate of major depression in children diagnosed with ADHD was approximately 30%. At four years, the rate was over 40% in children with ADHD compared with approximately 5% in controls. The children with comorbid disorders manifested high rates of a variety of disorders including bipolar disorder and anxiety disorder. The comorbid group was more dysfunctional and had higher hospitalization rates as well as lower global functioning scores compared with children diagnosed with pure ADHD.

Results of other studies are consistent with these high comorbid rates. Butler et al. (1995) reported that among hospitalized children with ADHD, depression co-occurred for 36%, bipolar disorder for 22%, affective psychosis for 8% and dysthymia was comorbid for 3%. Only 31% had no concurrent affective diagnosis.

Family studies indicate a genetic link between depression and ADHD. Biederman and colleagues (1992) reported that rates of this disorder within the families of ADHD children (with or without comorbid depression) were significantly higher than among relatives of control children. This suggests that for some children, a particular genetic factor may contribute to ADHD, whereas in others this same factor may contribute to depression or to the co-occurrence of both disorders.

ADHD with bipolar disorder. There are many challenging issues in the treatment of children with comorbid bipolar disorder and ADHD. According to Janet Wozniak (2001), the rate of bipolar disorder in children has been underestimated. As with depression, the presentation of the disorder in children is different than in adults and may be difficult to distinguish from normal developmental issues. Manic children tend to demonstrate irritability, anger, and oppositional or aggressive behavior rather than euphoria. Symptoms such as grandiosity, racing thoughts, and pressured speech are often present, however. Manic outbursts in children may be intense but be relatively short-lived and have been termed “affective storms” for these reasons (Davis, 1979).

Because of symptoms shared between mania and ADHD, it may be difficult to discern whether the child has bipolar disorder, ADHD, or both. Specifically, mania and ADHD in children overlap with respect to distractibility, physical hyperactivity, and talkativeness. Because children with non-comorbid ADHD do not manifest mood disturbances, the presence of mood instability suggests the presence of bipolar syndrome.

Fifty percent of prepubescent depressed children in one sample manifested symptoms of bipolar disorder within ten years of the onset of depression (Geller et al., 2001). In a study of children referred for a psychopharmacologic evaluation, 16% of the children less than twelve years of age met the criteria for mania (Wozniak et al., 1995). Only one child who met the criteria for mania failed to justify the diagnosis of ADHD. When comparing the children with ADHD without mania, the manic children had significantly higher rates of major depression, psychosis, multiple anxiety disorders, conduct disorder, and oppositional defiant disorder as well as significantly greater impairment in psychosocial functioning.

ADHD with substance abuse. With or without comorbidity, ADHD is a risk factor for the occurrence of substance abuse among adults (Biederman et al., 1998B; Wilens et al., 1997). When an individual presents with both substance abuse and ADHD, clinicians should first attempt to stabilize and treat the substance abuse disorder. Depression should be treated next, followed by treatment of the ADHD.

Substance-abusing patients treated with methylphenidate evidenced a reduction in ADHD symptoms as well as an improvement in cocaine craving in some studies (Levin et al., 1998) or no increase in craving in other studies (Grabowski et al., 1997). Of course, the care giver must consider the degree of abuse potential associated a drug when choosing the most appropriate medication for this group.

A common concern is that the treatment of children with stimulants will increase the rates of substance abuse over time. However, findings from retrospective and prospective studies do not support this hypothesis, particularly when controlling for baseline severity. In fact, successful treatment of ADHD in childhood or adolescence appears to have dampening effects with respect to the later development of substance abuse. In a four-year follow-up study of ADHD and non-ADHD families, Biederman and colleagues (1999) observed that subjects with untreated ADHD had much higher rates of later substance abuse than did both treated ADHD patients and controls. Also, there is evidence that untreated ADHD is associated with higher rates of alcohol use at 15-year follow-up (Loney, 1998). Thus, although ADHD and substance abuse are highly comorbid among adults, treatment of ADHD in children or adolescents may offer a degree of protection from later substance abuse.

Treatment in the medical and the social model

Abundant data bear on the approaches to treatment for children with ADHD. Because this disorder can have lifelong consequences, interventions are designed to reduce the negative outcomes and increase functional capacities.

Only three modes of treatment have received substantial and consistent support as effective short-term interventions for ADHD: behavior modification, stimulants, and a combination of the two. Despite the evidence on efficacy, relatively little is known about the degree to which these interventions are employed in clinical and educational practice or in the family setting. Ther is scant evidence regarding the effectiveness of these treatments in non-research settings. Pharmacologic treatment is prevalent and short-term use has been shown to be effective in reducing ADHD symptoms. The longer-term efficacy of behavioral and pharmacological treatments has not been firmly established.

In the US particularly, the prescribing of stimulants for ADHD has increased quite dramatically. The use of Ritalin grew by 500% from 1990 through May 1995 (Diller, 1996). Epidemiological studies estimated that the 12-month prescription prevalence for school-aged children was at 6% in urban areas (Safer, Zito & Fine, 1996). In another study, family physicians estimated that 6.9% of children seen in their practice were using medications to treat ADHD. This estimate made by pediatricians was 10.8% and child psychiatrists estimated 55.6%of children in their practice were using medication as treatment for ADHD (Sax & Kautz, 2003).

Medications used in the treatment of ADHD act by inhibiting the dopamine transporter and/or increasing the release of dopamine into the synaptic cleft. Medications that increase the production of norepinephrine also have had success in treating the symptoms of ADHD. Research documents the improvement of the core symptoms of inattention, hyperactivity and impulsivity. Effects on the outcomes of intelligence and achievement tests are less significant (American Academy of Pediatrics, 2001).

The purely medical model intervention of psychopharmacology was well-entrenched. However, as a result of research findings, multimodal treatment interventions, including aspects of both the medical and the social model, became the gold standard for treating ADHD. One of the most widely-cited studies was touched upon earlier in laying out the historic timeline of ADHD; this is the Multimodal Treatment Study of Children with ADHD (the MTA Study) which was co-sponsored by the US National Institute of Mental Health and the US Department of Education. The purpose of this study was to investigate four different treatment conditions: medication only; medication and psychosocial therapy; psychosocial therapy only; and community care. At the end of a 14-month treatment period, results indicated that medication intervention alone and combined medication and psychosocial therapy provided greater treatment efficacy than did psychosocial intervention alone or community care (MTA Cooperative Group, 1999). At the end of 24 months, 68% of the combined treatment group, 56% in the medication only group, 34% in the psychosocial only group and 25% in the community care group showed improvement (Swanson et al., 2001). This is one among many examples of empirical endorsements for multimodal interventions, leaving little doubt that the social worker has a primary role to play in the treatment of ADHD.

Behavioral problems leave a legacy of low self-esteem for the child and high levels of stress for the family (Sekelman & Snyder, 2000). The risk of a deficit in social skills is greater in children with learning or attention problems (Kavale & Forness, 1996). Behavioral modification therapy includes interventions used to modify the physical and the social environment in order to alter the child’s behavior. Strategies involving social skills training and/or cognitive behavioral therapy may be effective in helping the child with ADHD gain control over target behaviors and promote a mastery of everyday routines through organizational strategies (Stein, 2002).

Parent training in behavioral modification and classroom behavioral interventions have been shown to be effective in changing the disruptive behavior of children with ADHD. Research provides evidence of the positive treatment effects of parent training, including increases in child compliance, in the use of recommended parental commands/communications, in the knowledge of appropriate parenting techniques, and in positive parental statements (McGoey, Eckert & Dupaul, 2002) Preliminary research evidence suggests that once effective parenting patterns are established and maintained, positive effects in the behavior of preschool-age children with ADHD may be observed in settings outside of the home and over an expanse of time (McGoey et al., 2002).

Increasing the parent’s knowledge regarding ADHD may also increase parental satisfaction and appraisal of competency. According to empirical evidence, the level of parental knowledge about this disorder has an effect on choices regarding the child’s treatment and long-term compliance with a treatment plan (Flannagan, Pillow & Wise, 2002). Without the requisite knowledge, parents are more prone to seek from ‘the family doctor’ and to follow the GP’s recommendations, however partial or incorrect this treatment may be (Malacrida, 2001; Sayal et al., 2002). The social worker can intervene in these situations to educate and guide the parents to a more appropriate first contact for treatment. Reinforcing this social work role is the fact that, because ADHD has a genetic component, one or both parents may have the disorder, making it difficult for them to regulate their own behavior and to provide the systematic support that the child requires (Voeller, 2004).

An alternative intervention

There are myriad claims of alternative that intervention, touting cures for ADHD, as well as symptom reduction. One of these is the Dore Programme. Through a series of exercises, mainly eye, balancing, and coordination, this program claims to cure the problems in the person’s cerebellum that Dore claims to be causal of ADHD. Unfortunately, no systematic, independent, well-controlled experimentation is reported to lend credence to the effects of being anything more than a placebo effect, boosted by wishful thinking and the high price of participation.

Outcomes and Impact of ADHD

Given the nature of ADHD, it is believed to have a clear impact on social, economic, educational and health care delivery systems. The associated burden of ADHD impacts the individual experiencing the disorder; the family members and caregivers; the school system; employers; systems of care, including medical, mental health and social work professionals; insurers; the justice system; the community and society at large (Hinshaw, 1999). The burden may be associated with extremes in behavior and the ramifications of that behavior, as well as the deficits in skill attainment and the resulting implications for lost productivity. Documentation of the magnitude of the social and economic burden in these areas has been limited. Additionally, there is a dearth of evidence as to what types of intervention can be effective in improving the real-world outcomes for children with ADHD.

Effects on the Individual

Several studies have investigated the functional impairments associated with ADHD in childhood, especially if the disorder remains untreated. These children can have compromised academic achievement and school performance. Up to 80% demonstrate academic performance problems, with a significantly higher rate of being ‘held back’ (i.e., retained at the same grade level whilst peers are promoted), a higher rate of special education placement, of suspension from school and of dropping out when compared to their peers (Rabiner et al., 2004). This study also indicated that the percentage of students with inattentive subtype ADHD who rated below grade level ranged from 76% in reading to 92% below in written language. As many as half the children with ADHD are suspended from school as a result of impulsive acts. The prevalence of children in special education with ADHD and a specific learning disability was 65%, compared to 46%

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