NIH Consensus Development Conference
on Diagnosis and Treatment of Attention Deficit Hyperactivity Disorder
November 1618, 1998
National Institutes of Health
The following is an abstract of the presentation of C. Keith Conners, Ph.D. giving an overview of current knowledge on Attention Deficit Hyperactivity Disorder (ADD / ADHD / AD/HD / Attention Deficit Disorder). The abstract is designed for the use of panelists and participants in the conference and as a reference document for anyone interested in the conference deliberations. We are grateful to the author, who has summarized his materials and made them available in a timely fashion.
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Attention deficit hyperactivity disorder (ADHD) refers to a developmental disorder of childhood characterized by a persistent pattern of inattention and/or hyperactivity-impulsivity that is more frequent and severe than is typically observed in individuals at a comparable level of development (American Psychiatric Association, 1994). The diagnosis requires that some of the inattentive or hyperactive-impulsive symptoms be present before age 7, and some impairment from these symptoms must be evident in at least two settings, such as home, school, or work. Clear evidence of impairment of developmentally appropriate social, academic, or occupational functioning must be present.
Although the name is new, the behavioral syndrome of ADHD has been recognized since the early 1900s. The features of this syndrome gradually emerged from observations over many years from professionals working in pediatric medicine, neurology, education, and pharma-cology. The core symptoms of hyperactivity, impulsivity, and inattention are a constant in the very earliest observations and throughout the numerous changes in terminology (Kessler, 1980). Changes in diagnostic terminology, definitional boundaries, conceptions of etiology, and preferred modes of treatment reflect changing scientific paradigms and professional allegiances, as well as empirical evidence derived from increasingly rigorous investigations (Conners, Erhardt, 1998).
Formal diagnostic criteria for the disorder underwent rapid changes as new syntheses and accumulation of data from field trials took place. The fact that the concept of ADHD has evolved with changing evidence should be taken as a strength, not as a sign of unreliability or vague conceptualization. Comprehensive review of the evidence regarding diagnosis and treatment carried out by independent expert medical reviewers concludes that diagnostic criteria for ADHD are based on extensive empirical research and, if applied appropriately, lead to the diagnosis of a syndrome with high interrater reliability, good face validity, and high predictability of course and medication responsiveness (Goldman, Genel, Bezman, et al., 1998).
ADHD appears to be among the most prevalent childhood disorders even when narrow and conservative criteria are employed. Estimates of prevalence vary with the particular criteria used to define the disorder. Past estimates have ranged from 1 to 20 percent. But when rigorous research criteria are employed, the figures range between 1 and 4 percent in North America. Despite some obvious differences in prevalence rates due to cultural variations, evidence from a number of studies now reveals that very similar rates appear in several other cultures, including China, Japan, Europe, India, and Latin America (Barkley, 1998a).
No single cause of ADHD has been discovered. Rather, a number of significant risk factors affecting neurodevelopment and behavioral expression have been implicated in ADHD. Several of these risk factors, often present at one time, lead to the assumption that the disorder frequently reflects a summation of independent forces impinging on early development (Biederman, Milberger, Faraone, et al., 1995). The expression of the disorder appears to depend on both these risk factors and individual protective factors and subsequent interactions with the environment. Evidence for genetic causes derives from consanguinity studies of hyperactivity, family genetic studies, and recent transmission studies from several laboratories. Normal variations in temperament (which are also likely to be genetically determined) must also be considered a risk factor for ADHD. Data suggest that some individuals are merely at the extremes of normal distributions for activity, impulse control, and attentional control. Medical causes, particularly those affecting early development of the fetal brain, such as maternal alcohol and tobacco use, are well-established as causes, as demonstrated by large collaborative studies of natal and perinatal development (Nichols, Chen, 1981). Injury to the developing brain from environmental toxins, lead, smoking, lack of crucial nutrients such as iron and calcium, and a host of other hazards have also been implicated in the etiology of ADHD-like symptoms.
Recent studies in neuroimaging of ADHD children, adolescents, and adults lend support to several possible anatomic substrates affected by the many risk factors to brain development. A variety of relatively small-sample studies with PET, SPECT, and MRI technologies have demonstrated impairments in ADHD relative to control in frontal, prefrontal, parietal, splenial corpus callosum, and right caudate nuclei (Ernst, Zametkin, 1995). These studies have now been supplemented by a large, well-controlled MRI study at the National Institute of Mental Health (NIMH) demonstrating deficits in the right-sided, prefrontal-striatal systems in ADHD. These findings include a smaller total cerebral volume, loss of normal right-greater-than-left asymmetry in the caudate, smaller right globus pallidus, smaller right anterior frontal region, smaller cerebellum, and reversal of normal lateral ventricular asymmetry in the ADHD group (Castellanos, Giedd, Marsh, et al., 1996).
ADHD is a chronic, lifetime disorder that exacts a considerable toll on those suffering from it as well as on the families of those who must care for them. Although as many as 40 to 50 percent of ADHD children may become indistinguishable from normal children by young adulthood, careful long-term prospective followup studies (Weiss, Hechtman, 1993) demonstrate that a significant proportion of those with ADHD end up with serious social, emotional, interpersonal, and economic limitations. The risks of death by misadventure; driving accidents; teenage pregnancy; sexually transmitted diseases; alcohol and other substance abuse; and academic underachievement are high. Profound impairment of self-esteem and personal identity are frequent sequelae in adults with a childhood history of ADHD.
Important strides in the treatment of ADHD have been made over the past several decades. The evidence for the short-term efficacy and safety of psychostimulants from controlled clinical trials is overwhelming (Swanson, McBurnett, Wigal, et al., 1995). Many studies of psychosocial treatment are also suggestive of positive benefits on the short-term status of ADHD. However, selective and careful review of the literature led Richters and colleagues (1995) to conclude the following:
This sobering conclusion led to the formation of the largest clinical trial in the history of NIMH (Arnold, Abikoff, Cantwell, et al., 1997) established through the mechanism of a Cooperative Agreement among seven university teams and NIMH. The results of that trial of a multimodal treatment strategy comparing medication management, psychosocial treatments, their combination, and a community-based control sample will form an important part of the empirical data presented in this consensus forum.
Important areas of our knowledge about ADHD remain to be clarified. Developments in cognitive neuroscience point to the multidimensional nature of both attentional processes and activity level, yet these concepts are poorly operationalized by current symptomatic criteria. Neuropsychological studies demonstrate a clear heterogeneity in samples of ADHD defined solely by symptomatic criteria (Conners, 1997). Doubts have been raised about the current nosological subtyping and the possibility that inattention and hyperactivity-impulsivity reflect separate disease entities (Barkley, 1998b). Current diagnostic criteria require that symptoms be more frequent and severe than are typically observed in individuals at a comparable level of development (American Psychiatric Association, 1994), but marked variations in the application of this rule lead to serious underdiagnosis or overdiagnosis, resulting in excesses or deficiencies of pharmacologic treatments (Angold, Costello, 1998). The embarassment of riches from neuroimaging studies reflects a poor understanding of any specificity for the neural basis of ADHD. The high levels of comorbidity of ADHD with oppositional, conduct, and mood disorders also call into question the specificity of the definition of the disease and whether current criteria are sufficient to allow further understanding of the neurobiology of the syndrome.
American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th ed. Washington DC: The Association; 1994.
Angold A, Costello EJ. Three-month prevalence rates for ADHD in the Great Smoky Mountains epidemiologic survey. Personal communication, 1998.
Arnold LE, Abikoff HB, Cantwell DP, Conners CK, Elliott G, Greenhill L, et al. National Institute of Mental Health collaborative multimodal treatment study of children with ADHD (the MTA): design challenges and choices. Arch Gen Psychiatry 1997;54:865-70.
Barkley RA. The prevalence of ADHD: is it just a U.S. disorder? The ADHD Report;1998a. p. 1-6.
Barkley RA. ADHD and the nature of self-control. New York: Guilford; 1998b.
Biederman J, Milberger S, Faraone SV, Kiely K, Guite J, Mick E, et al. Impact of adversity on functioning and comorbidity in children with attention-deficit hyperactivity disorder. J Am Acad Child Adolesc Psychiatry 1995;34:1495-503.
Castellanos FX, Giedd JN, Marsh WL, Hamburger SD, Vaituzis AC, Dickstein DP, et al. Quantitative brain magnetic resonance imaging in attention-deficit hyperactivity disorder. Arch Gen Psychiatry 1996;53:607-16.
Conners CK. Is ADHD a disease? J Attention Disorders 1997;l2:3-17.
Conners CK, Erhardt D. Attention-deficit hyperactivity disorder in children and adolescents: clinical formulation and treatment. Hersen M, Bellack A, editors. New York: Elsevier Science; 1998.
Ernst M, Zametkin A. The interface of genetics, neuroimaging, and neurochemistry in attention-deficit hyperactivity disorder. In: Bloom FE, Kupfer DJ, editors. Psychopharmacology: the fourth generation of progress. New York: Raven Press; 1995. p. 1643-52.
Goldman LS, Genel M, Bezman RJ, Slanetz PJ. Diagnosis and treatment of attention-deficit/ hyperactivity disorder in children and adolescents. Council on Scientific Affairs, American Medical Association. JAMA 1998;279:1100-7.
Kessler JW. History of minimal brain dysfunction. In: Rie HE, Rie ED, editors. Handbook of minimal brain dysfunctions: a critical view. New York: Wiley & Sons; 1980. p. 744. Nichols P, Chen T-C. Minimal brain dysfunction: a prospective study. Hillsdale (NJ): Lawrence Erlbaum Associates; 1981. p. 336.
Richters JE, Arnold LE, Jensen PS, Abikoff H, Conners CK, Greenhill LL, et al. NIMH collaborative multisite multimodal treatment study of children with ADHD: I. Background and rationale. J Am Acad Child Adolesc Psychiatry 1995;34:987-1000.
Swanson JM, McBurnett K, Wigal T, Pfiffner L, Lerner MA, Williams L, et al. Effect of stimulant medication on children with attention deficit disorder: a review of reviews. Except Child 1995;60:154-62.
Weiss G, Hechtman L. Hyperactive children grown up: ADHD in children, adolescents, and adults. New York: Guilford; 1993.
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