ATTENTION DEFICIT DISORDER

Children and adolescents who "act out" their feelings, frustrations, and emotional conflicts are said to exhibit externalizing behavior. Within the framework of the American Psychiatric Association's Diagnostic and Statistical Manual, 3rd edition, revised (DSM-III-R), once a certain level of severity is demonstrated, these youth qualify for the umbrella diagnosis of disruptive behavior disorder. Three disorders are encompassed within this general diagnostic category: (1) attention deficit/hyperactivity disorder (ADHD); (2) Conduct Disorder (CD); and (3) oppositional defiant disorder.

It should be noted that in recent years some controversy has developed concerning diagnostic techniques. It has been suggested that with the introduction of the American Psychiatric Association's Diagnostic and Statistical Manual, fourth edition (DSM-IV) in 1994, accurately diagnosing ADHD in adults has become problematic "because of the vague nature of the criteria" in DSM-IV (Higgins, 1999). Comparatively, in more recent studies, a different approach for administrating the Diagnostic Interview Schedule for Children (DISC), based on communication principles, has marked a shift from structured interviewing to a more open communication model. This communication model is defined by three factors: (1) a schematic representation of the areas to be covered; (2) a common language for the categories, diagnosis, and criteria; and (3) the respondent was permitted to chose the order of the diagnostic areas to be covered. This new method is a notable departure from the structured diagnostic interviews that have been implemented in the past. Significant developments have been made in these structured diagnostic interviews over more than two decades, but along with these improvements have come problems. This alternative diagnostic method may have potential for strengthening the authority of child psychiatric diagnosis (Edelbrock, Crnic & Bohnert, 1999).

Children who qualify for a diagnosis of ADHD often, but not invariably, meet criteria also for a diagnosis of conduct disorder or oppositional defiant disorder. In addition, attention deficit disorder does not always occur in conjunction with behavioral hyperactivity. These latter individuals are assigned the diagnosis of undifferential attention deficit disorder.

Characteristically, youth with ADHD demonstrate an excessively high level of behavioral activity across a wide variety of situations. The behavioral disturbance is most apparent, however, where the appropriate level of behavioral activity should be low, such as in a classroom where focused task-oriented cognitive demands are placed on the youngster. In naturalistic settings, ADHD children, although not overtly hyperactive, typically are impulsive, emotionally labile, restless, and distractible. They often act in a socially intrusive and inappropriate manner such that they are considered to be immature. Consequent to poor foresight and poor impulse control, combined with a high behavior level, ADHD children frequently get into social difficulties with adults and peers, which subsequently lead to rejection. Physical injury is common in ADHD because of poor self-control (e.g., dashing across the street without looking).

Because ADHD symptomatology is often present in children with poor coordination, reading and learning problems, and other neurodevelopmental disturbances, in the past labels such as "minimal brain damage" and "minimal brain dysfunction" were assigned, although no neurologic pathology or injury was detectable. The terms "hyperactivity" and "hyperkinesis" were subsequently introduced; however, these labels emphasize the motor aspects of the disorder. The current diagnostic label—attention deficit disorder—circumvents these problems by focusing on the core etiological determinant for the multifaceted expression of cognitive, behavioral, and emotional disturbances. For this diagnosis to be assigned, the disorder must first be expressed before age 7, have at least a 6-month duration, and not be the consequence of a pervasive developmental disorder (American Psychiatric Association, 1987).

EPIDEMIOLOGY

Approximately 10 percent of boys and 3 percent of girls in the general population qualify for a diagnosis of ADHD. The symptom presentation is different between the genders, with girls being somewhat older than boys at the time of first diagnosis. Girls manifest more mood changes, fears, and social withdrawal than boys but less aggressivity and impulsivity. Among children receiving psychiatric treatment, ADHD is estimated to be present in 40 to 70 percent of inpatient cases and 30 to 50 percent of outpatient cases.

GENETIC ETIOLOGY

Behavior-activity level is a heritable trait of temperament characterizing the human species. Individuals who are at the high end of this trait, compared to the average, are behaviorally highly active or hyperactive. Thus, although not necessarily implying pathology or a disorder, but rather normal variation in behavioral disposition, high-end active individuals demonstrate a rapid behavioral tempo and greater vigor and forcefulness than the average. For clinicians, it is important to distinguish between individuals with behavior-activity level as a temperament trait and extreme cases that comprise psychological and psychiatric disorder.

For many individuals, extremely high manifestations of behavior-activity level has a genetic basis. ADHD aggregates in families and twin studies show high concordance rates for this disorder. The neurobiological mechanisms underlying ADHD is an active topic of research. As of the mid-1990s, we assume that the neurochemistry in such people is likely to be disturbed; however, a candidate neurotransmitter system has yet to be identified. Most likely, multiple neurochemical systems are involved. Neuroimaging studies have revealed lowered brain metabolism, particularly in the frontal regions, in ADHD children (Zametkin et al., 1990).

NONGENETIC ETIOLOGY

Injury to the brain, particularly in the anterior region, can produce the symptoms of ADHD. For the developing fetus, malnutrition, exposure to toxins (especially alcohol), and medical illness during pregnancy augment the risk for ADHD symptoms to appear. Circumstances around birth, especially the occurrence of toxemia (toxins in the blood) or hypoxemia (not enough oxygen in the blood), increase the risk for neurological injury in the newborn, which ultimately could result in symptoms of ADHD. During childhood development, many factors, particularly head trauma (by accident or maltreatment), infection, toxic poisoning, and malnutrition can produce ADHD symptoms. Neurologic conditions (e.g., epilepsy) and neurodevelopmental disorders (e.g., dyslexia, autism) are also commonly associated with some symptoms of ADHD. Although all these latter conditions produce ADHD-type symptoms, according to DSM-III-R they must be excluded as etiologic factors to make the diagnosis of the ADHD syndrome. In other words, the diagnosis of ADHD is assigned only where there is no neurodevelopmental disability or injury.

NATURAL HISTORY

Recognizing that there is substantial variability in the etiology of ADHD, it is obvious that the lifetime course and outcome is also highly variable. Symptoms persist into adulthood in about 50 percent of cases. Under these circumstances, the person is assigned a diagnosis of attention deficit disorder-residual type.

RELATION OF ADHD TO DRUG ABUSE

Serious psychiatric disorder is common among adults with a history of ADHD. Antisocial Personality disorder, alcohol and substance abuse, depression, and anxiety are the most common associated disorders. These associated disorders should not be viewed as invariant outcomes of ADHD but rather as disturbances for which ADHD youth are at increased risk. Whether any of these psychiatric outcomes are manifested depends on a variety of factors besides ADHD, including the child's self-esteem, opportunity for normal socialization with peers, success in school, and level of social and family support (Tarter, 1988).

With respect to alcohol and other drug abuse, augmented risk appears to be circumscribed to youth who have both ADHD and a conduct disorder. The association, however, between ADHD and substance abuse is complex. Alcohol and other drugs may be more subjectively rewarding for ADHD youth and adults than in the general population. Drug use is commonly tied to a general pattern of social deviancy and nonnormative peer affiliation. Where the ADHD person has been ostracized by the normative peer group, the use of alcohol/drugs may be just another manifestation of generalized maladjustment. Furthermore, alcohol/drug use may be mediated by a coexisting psychiatric disorder, such as anxiety and depression, and thus reflect an attempt at self-medication. Therefore, although there is substantial evidence demonstrating an increased risk for alcohol/drug abuse in ADHD youth, this association is complex and is contingent on many factors.

TREATMENT

Because the psychological manifestations of ADHD are multifaceted, it is necessary that comprehensive treatment interventions that encompass multiple components be implemented (Danforth, Barkley, & Stokes, 1991).

Pharmacotherapy.

Psychostimulants are therapeutically beneficial for approximately 75 percent of ADHD children and adults. The most commonly used medications are Methylpheni-date (Ritalin), d -Amphetamine, and Pemoline (Cylert). Tricyclic antidepressants are also effective in many cases. These medications have been shown to be useful for reducing problem behavior of ADHD in more than 100 research studies; however, they do not improve school performance or eliminate a conduct disorder where this disturbance is present.

Additionally, it is interesting to note that recent studies of the effects of stimulant medication treatment have produced disparate results. A 1998 study by N. M. Lambert and C. S. Hortsough puts forward that stimulant medication treatment may be a "gateway to abuse", suggesting a connection between stimulant treatment and adult dependence on cocaine as well as tobacco. Alternately, a 1999 study by Joseph Biederman, Eric Mick, Stephen V. Faraone, T. Wilens, and T. Spencer found pharmacotherapy to be responsible for a significant reduction in substance abuse for young people with ADHD (Beiderman, Mick & Faraone, 2000).

Lifestyle.

Coordinated effort should be made to promote a healthy lifestyle, including scheduled regulation of bedtime, meals, homework, and recreation. Nutrition is important; however, contrary to popular belief and anecdotal reports, there is no substantive evidence linking diet or food allergies to the cause of ADHD. There is no scientific evidence indicating that a special diet or nutritional supplements can ameliorate ADHD.

Education.

Informing parents and school personnel about the causes of ADHD and the nature of the behavior disorder can constructively assist the child by evoking empathy rather than anger. Thus, family counseling and teacher education are integral components of treatment to help maximize the child's adjustment in the home and at school.

Environmental Engineering.

Structuring the environment so that the child is not easily distracted is an important intervention. In the home, this entails minimizing distracting stimulation from radio or television, especially while the youngster is doing homework. In the classroom, consideration should be given to the child's seat location to enable the teacher to ensure that the child persists at tasks, is not distracted by other students, or has no opportunity to be disruptive.

Behavior Modification.

Behavior-modification strategies are effective for training the youngster to control impulses and to monitor behavior cognitively. Behavior-modification methods, which help the child, are also useful in teaching effective parenting skills.

(See also: Psychomotor Stimulant ; Vulnerability As Cause of Substance Abuse )

BIBLIOGRAPHY

American Psychiatric Association (2000). Attention Deficit Disorder—Part I. Harvard Mental Health Letter, 17, issue 2.

Danforth, R., Barkley, R., & Stokes, T. (1991). Observations of parent-child interactions with hyperactive children: Research and clinical implications. Clinical Psychology Review, 11, 703-727.

American Psychiatric Association (1987). Diagnostic and statistical manual of mental disorders, 3rd ed. Washington, DC.

Biederman, J., Mick, E., & Faraone, S. V. (2000). Letter to the Editor. Journal of Learning Disabilities, 33, 4,314. Response to article by N. M. Lambert and C. S. Hartsough (1998). Journal of Learning Disabilites, 31, 533.

Edelbrock, C., Crnic, K., & Bohnert, A. (1991). Interviewing as Communication: An Alternative Way of Administrating the Diagnostic Interview Schedule for Children. Journal of Abnormal Child Psychology, 27 (6), 447.

Glicken, A. D. (1997). Attention deficit disorder and the pediatric patient: a review. Physician Assistant, 21 (4), 101-112.

Higgins, E. S. (1999). A Comparative Analaysis of Anti-depressants and Stimulants for the Treatment of Adults with Attention-Deficit Hyperactivity Disorder. Journal of Family Practice, 48 (1), 15-16.

Jensen, P. S., & Edelbrock, C. (1999). Subject and Interview Characteristics Affecting Reliability of the Diagnostic Interview Schedule for Children. Journal of Abnormal Child Psychology, 27 (6), 413.

Lambert, N. M., & Hartsough, C. S. (2000). Letter to the Editor. Journal of Learning Disabilities 31, 533. Resonse to Biederman, Mick & Faraone, 2000.

Nigg, J. T. (1999). The ADHD Response-Inhibition Deficit as Measured by the Stop Task: Replication with DSM-IV Combined Type, Extension, and Qualification. Journal of Abnormal Child Psychology, 27 (5), 393.

Tarter, R. (1988). Are there inherited behavioral traits which predispose to substance abuse? Journal of Consulting and Clinical Psychology, 56, 189-196.

Zametkin, A., et al. (1990). Cerebral glucose metabolism in adults with hyperactivity of childhood onset. New England Journal of Medicine, 323, 1361-1366.

Ralph E. Tarter

Ada C. Mezzich

Revised by Chris Lopez