Practice Parameters for the Assessment and Treatment

advertisement
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Practice Parameters for the Assessment and Treatment
of Children, Adolescents, and Adults
with Attention-Deficit/Hyperactivity Disorder
These parameters were developed by Mina Dulcan, M.D., principal author, and the Work Group
on Quality Issues: John E. Dunne, M.D., Chair and William Ayres, M.D., past Chair; Valerie Arnold, M.D.;
R. Scott Benson, M.D.; William Bernet, M.D.; Oscar Bukstein, M.D.; Joan Kinlan, M.D.; Henrietta Leonard,
M.D.; William Licamele, M.D.; and Jon McClellan, M.D. AACAP Staff: L. Elizabeth Sloan, L.P.C. and
Christine M. Miles. The authors wish to thank Diane Schetky, M.D. for her thoughtful review. These
parameters were made available to the entire Academy membership for review in October 1997 and were
approved by the Academy Council on February 14, 1997. They are available to AACAP members on the
World Wide Web (www.aacap.org). The first edition of the these parameters was developed by the AACAP
Work Group on Quality Issues chaired by Steven Jaffe, M.D., and was published in Journal of the American
Academy of Child and Adolescent Psychiatry 30:i-iii, 1991.
Reprint requests to AACAP Publications Department, 3615 Wisconsin Ave., N.W., Washington, DC
20016.
1997 by the American Academy of Child and Adolescent Psychiatry.
ABSTRACT
These practice parameters review the literature on children, adolescents, and adults with AttentionDeficit/Hyperactivity Disorder (ADHD). There are three types of ADHD: predominantly inattentive,
predominantly hyperactive-impulsive, and combined. All together they occur in as many as 10% of boys
and 5% of girls of elementary school age. Prevalence declines with age, although up to 65% of hyperactive
children are still symptomatic as adults. Frequency in adults is estimated at 2% to 7%. Assessment
includes clinical interviews and standardized rating scales from parents and teachers. Testing of
intelligence and academic achievement are usually required. Comorbidity is common. The cornerstones of
treatment are support and education of parents, appropriate school placement, and pharmacology. The
primary medications are psychostimulants, but antidepressants and alpha-adrenergic agonists are used in
special circumstances. Other treatments such as behavior modification, school consultation, family
therapy, and group therapy address remaining symptoms. Key words: attention-deficit/hyperactivity
disorder, psychopharmacology, methylphenidate, dextroamphetamine, practice parameter.
INTRODUCTION
Attention-Deficit/Hyperactivity Disorder (ADHD) is one of the most common psychiatric disorders of
childhood and adolescence. Recent clinical experience and research document the continuation of
symptoms into adulthood. These parameters, therefore, cover the full age spectrum, although far more is
known about this disorder in children and adolescents than in adults.
Terms that have been used historically for children with distractibility, impulsivity and usually also
overactivity include minimal brain dysfunction/damage (MBD), hyperkinetic reaction, and hyperkinesis.
1997 AACAP
1
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Diagnostic terminology and criteria have changed considerably since the publication of the DSM-III. For
purposes of these parameters, however, attention deficit disorder (ADD), attention deficit disorder with
hyperactivity (ADD-H), hyperactivity, and attention-deficit/hyperactivity disorder (ADHD) will be considered
to be interchangeable, unless specified otherwise. The DSM-III (American Psychiatric Association,1980)
term ADD without hyperactivity, the DSM III-R (American Psychiatric Association, 1987) term
undifferentiated ADD, and the DSM-IV category ADHD, predominantly inattentive type, are not identical,
but are roughly equivalent.
LITERATURE REVIEW
The literature on ADHD is voluminous. Books and journals published from 1985 through the first
half of 1996 were reviewed in detail, with older references included where pertinent. An asterisk in the
References section marks key references. Completeness of coverage was assured by the search of tables
of contents of the 100 journals in the Current Awareness series of Western Psychiatric Institute and Clinic
and by National Library of Medicine searches using keywords: ADHD, psychopharmacology, dexedrine,
methylphenidate, and pemoline. Finally, the authors drew on their own experience and that of expert
colleagues.
DIAGNOSTIC CRITERIA
There are two groups of nine symptoms each: inattention and hyperactivity-impulsivity (subdivided
into two groups). Inattention includes failing to give close attention to details or making careless mistakes,
difficulty sustaining attention, not listening, not following through, difficulty organizing, avoidance or dislike
of sustained mental effort, losing things, easily distracted, and forgetful. Hyperactivity includes six
symptoms: fidgety, out of seat, running or climbing excessively, difficulty playing quietly, on the go or as
if driven by a motor, and talking excessively. The three impulsivity symptom criteria are: blurting out
answers, difficulty awaiting turn, and often interrupting or intruding on others.
ADHD is divided into three types, according to the presence or absence of six or more symptoms
in each symptom group. These types are: predominantly inattentive, predominantly hyperactive-impulsive,
and combined (both sets of symptoms). At least some symptoms must have been present before the age
of seven years. The behaviors used to meet the criteria must be inconsistent with the patient’s
developmental level and intellectual ability and have been present for at least six months. Functional
impairment must be present in two or more settings, with clinically significant impairment in social,
academic, or occupational functioning. By definition, the diagnosis of ADHD cannot be made if the
symptoms occur exclusively in the presence of a pervasive developmental disorder, schizophrenia, or other
psychotic disorder or if they are better accounted for by another psychiatric disorder.
Signs of ADHD may not be observable when the patient is in highly structured or novel settings,
engaged in an interesting activity, receiving one-to-one attention or supervision, or in a situation with
frequent rewards for appropriate behavior. Conversely, symptoms typically worsen in situations that are
unstructured, minimally supervised, boring, or require sustained attention or mental effort (American
Psychiatric Association, 1994). Core deficits include impairment in rule-governed behavior across a variety
of settings and relative difficulty for age in inhibiting impulsive response to internal wishes or needs or
external stimuli (Barkley, 1994).
1997 AACAP
2
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
ADHD IN CHILDREN AND ADOLESCENTS
ASSESSMENT
The parent interview is the core of the assessment process. It is often difficult to confirm the
diagnosis of ADHD by the interview with the child or adolescent alone, since some children and most
adolescents with ADHD are able to maintain attention and behavioral control while in the office setting.
Many lack insight into their own difficulties and are not willing or able to report them accurately. Both the
parent and child interviews are used to rule out other psychiatric or environmental causes of symptoms.
Structured interviews of parents may be useful in assuring coverage of ADHD symptoms, or a DSM-IV
symptom checklist may be used (Baumgaertel et al., 1995). Standardized interviews of children and
adolescents are less useful for ADHD symptoms, but may aid in discovering alternative or comorbid
diagnoses. Queries about family history of ADHD, other psychiatric disorders, and psychosocial adversity
(e.g., poverty, parental psychopathology or absence, family conflict) are especially important because of
their relationship to prognosis (Biederman et al., 1996).
SCHOOL-RELATED ASSESSMENT
It is essential to obtain reports of behavior, learning, and attendance at school, as well as grades
and test scores. A standardized instrument is a convenient method for obtaining this information.
Teachers, school social workers, or guidance counselors can provide information on interventions that have
been attempted and their results. Psychoeducational testing is indicated to assess intellectual ability and to
search for learning disabilities that may be masquerading as ADHD or may coexist with ADHD.
Achievement testing will aid in educational planning.
RATING SCALES
Parent and teacher rating scales yield valuable information efficiently (Achenbach, 1991a; Barkley,
1990; Edelbrock and Rancurello, 1985; Edwards et al., 1995). Comparison to normative groups by age
and sex can help distinguish normal variants in levels of attention, activity, and impulse control from ADHD.
The broad-spectrum scales can also be used to screen for comorbidity. There are many choices (see
Barkley, 1990 and Klein et al., 1994, for reviews), but the most commonly used and best normed and
validated are the parent-completed Child Behavior Checklist (Achenbach, 1991a; Biederman et al., 1993b),
the Teacher Report Form (TRF) of the Child Behavior Checklist (Achenbach, 1991b; Edelbrock et al.,
1984), the Conners Parent and Teacher Rating Scales (Conners, 1969; Goyette et al., 1978), the ADD-H:
Comprehensive Teacher Rating Scale (ACTeRS) (Ullmann et al., 1985a), and the Barkley Home Situations
Questionnaire and School Situations Questionnaire (Barkley, 1990). The CAP (Child Attention Problems)
(Barkley, 1990; Barkley et al., 1989) is a brief teacher rating scale derived from the Teacher Report Form of
the Child Behavior Checklist (Achenbach, 1991b) that is convenient to use weekly to assess treatment
outcome. It covers both overactivity/impulsivity and inattention symptoms. The Conners Abbreviated
Teacher Rating Scale (Goyette et al., 1978) was developed to measure drug response. It is not ideal as a
diagnostic screen, because it misses children with attention deficits without hyperactivity (Ullmann et al.,
1985b) and is overinclusive of aggressive children. The IOWA Conners is a short form that was developed
to separate the inattention and overactivity ratings from oppositional defiance (Loney and Milich, 1982;
1997 AACAP
3
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Pelham et al., 1989a). It is useful in following treatment progress in children with both ADHD and ODD.
The AD/HD Diagnostic Teacher Rating Scale (ADTRS) uses DSM-IV criteria. Normative data are available
(Wolraich et al, submitted). Use of the Academic Performance Rating Scale (DuPaul et al., 1991) ensures
that academic achievement is not neglected in favor of behavioral performance.
In the absence of any intervention, rating scale scores tend to decline from the first administration
to the second (Milich et al., 1980; Zentall and Zentall, 1986), and then rise with frequent repeated
administration (Diamond and Deane, 1990). There appear to be halo and confounding effects between
ADHD and aggression. For example, a child who is defiant toward the teacher is more likely to be rated as
hyperactive or inattentive, regardless of the level of inattention or activity as measured by trained observers
(Abikoff et al., 1993; Schachar, et al., 1986). Regular class teachers rate the same behavior as more
hyperactive than do special education teachers (Abikoff et al., 1993).
OBSERVATION
Structured behavioral observation in naturalistic and laboratory settings (Barkley, 1990) may be
used, but typically contribute more in measuring medication response (Barkley et al., 1988) than in
diagnosis per se. Structured playroom observation may assist in distinguishing among boys who are
hyperactive, aggressive, or both (Roberts, 1990). Observational systems have been developed for the
classroom, lunchroom, and playground (Atkins et al., 1988, Gadow et al., 1990; 1996). An informal clinical
observation of the classroom and a less structured situation, such as the playground or lunchroom, can
provide important data regarding the child’s behavior, the teacher’s management style (Vitaro et al.,
1995), and the salient characteristics of the social and academic environment.
MEDICAL EVALUATION
Medical evaluation should include a complete medical history and a physical examination within
the past 12 months. A re-evaluation may be indicated if the clinical condition has changed since the
previous exam. History should include the patient’s use of prescribed, over-the-counter, and illicit drugs.
Vision or hearing deficits should be ruled out. Routine screening for blood lead is likely to have a low yield
(Kahn et al., 1995), and the clinical significance of even low lead levels is controversial and confounded by
socioeconomic status, home environment, and maternal IQ (Schonfeld, 1993). If clinical or environmental
risk factors are present, lead level should be measured, with treatment as necessary. Increased risk of
ADHD has been linked to a rare genetic syndrome: generalized resistance to thyroid hormone (Hauser et
al., 1993). Thyroid dysfunction does not, however, appear to be more common among clinically referred
children with ADHD (Elia et al., 1994; Spencer et al., 1994). Thyroid function tests are indicated only in the
presence of suggestive findings on the medical history or physical examination of clinical hypo- or
hyperthyroidism, goiter, family history of thyroid disease, or decreased growth velocity. Other possible
medical factors predisposing to ADHD include fragile x syndrome, fetal alcohol syndrome, G6PD
deficiency, and phenylketonuria. Risk factors, which account for only a small part of the variance, include
pregnancy variables such as poor maternal health, young age, use of alcohol, smoking, toxemia or
eclampsia, postmaturity, and extended labor. Health problems or malnutrition in infancy appear to
contribute. There are no data to support the use of hair analysis, and insufficient data to justify the routine
measurement of zinc (McGee et al., 1990).
ANCILLARY EVALUATIONS
1997 AACAP
4
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Speech and language evaluation may be suggested by the clinical findings. In special
circumstances, occupational or recreational evaluation may provide supplementary information regarding
motor clumsiness or adaptive skills.
TESTS
ADHD is a clinical diagnosis; there is no test for ADHD. Neuropsychological tests are useful to
evaluate specific deficits suggested by history, physical examination, or basic psychological testing, but are
not sufficiently helpful for diagnosis of ADHD to be routinely performed (Barkley and Grodzinsky, 1994;
Schaughency et al., 1989). Good performance on individually administered testing does not rule out
ADHD. EEG or neurological consultation is indicated only in the presence of focal signs or clinical
suggestions of seizure disorder or degenerative condition. Although some children with ADHD have
impaired motor coordination (Barkley, 1990), the measurement of neurological soft signs is not useful in the
diagnosis of ADHD. There are insufficient data to support the usefulness of computerized EEG measures
(neurometrics or brain mapping), event-related potentials, or neuroimaging as clinical tools, although they
have promise in research (Levy and Ward, 1995).
Computerized tests of attention and vigilance (CPTs) (Barkley, 1990; Conners, 1985; Greenberg
and Waldman, 1993; Swanson, 1985) are not generally useful in diagnosis because they suffer from low
specificity and sensitivity (Lovejoy and Rasmussen, 1990; Trommer et al., 1988). They are useful,
however, as research tools. Behavioral observations while performing the CPT discriminate ADHD children
from other groups as well as or better than the CPT scores (Barkley, 1991). The correspondence between
impulsive errors on the CPT and behavioral impulsivity has not been established (Abikoff and Klein, 1992).
When used for assessment of medication efficacy, the applicability of results to the patient s natural
environment is unproven (Aman and Turbott, 1991; Cohen et al., 1989) or even absent (Elia et al., 1991).
CPTs are not consistently sensitive to stimulant effects (Fischer and Newby, 1991). Also, task and
contextual factors, such as the presence or absence of an adult, the instructions given to the patient, and
the nature of feedback and contingencies, can substantially affect scores (Corkum and Siegel, 1993;
Power, 1992). Concerns have been expressed regarding commercial CPT products (Milich et al., 1986a).
A variety of techniques for measuring activity level exist (Conners and Kronsberg, 1985; Miller and
Kraft, 1994; Teicher, 1996) but are of limited clinical utility, since hyperactivity per se is not typically the
source of the most significant impairment (Tryon and Pinto, 1994). Usually, the important variable is not
the total amount of activity, but its situational appropriateness. Actometers, actigraphs, and other tools may
be useful for research purposes. An index combining characteristics of movement measured by infrared
motion analysis and accuracy and variability of response on a CPT accurately distinguished ADHD boys
from normal controls (Teicher et al., 1996).
CLINICAL FEATURES
Children with ADHD suffer from various combinations of impairments in functioning at school, at
home, and with peers (American Psychiatric Association, 1994; Barkley, 1990). School-based problems
include lower than expected or erratic grades, achievement test scores, and intelligence test scores,
caused by gaps in learned material, poor organizational and study skills, difficulty with taking tests due to
inattention and impulsivity, or failure to complete or turn in homework assignments. Grade retention may
result. Behavioral difficulties related to ADHD or to the combination with comorbid conditions often leads to
1997 AACAP
5
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
constant friction among the student, peers, the teacher, and the parents. The result may be special class
placement, suspension, or expulsion (Faraone et al., 1993). Peers often quickly reject ADHD children, due
to their aggression, impulsivity, and noncompliance with rules (Erhardt and Hinshaw, 1994).
Patterns of impairment vary considerably within the diagnostic category. Children with DSM-III
ADD without hyperactivity (roughly corresponding to DSM-IV ADHD inattentive type) are more likely than
children with ADD with hyperactivity (similar to ADHD combined type) to be characterized as sluggish and
drowsy or spacey, to daydream, to be socially withdrawn, to repeat a grade, and to exhibit depressed
mood and symptoms of anxiety disorder. They are less likely to have serious conduct problems,
aggression, or impulsivity or to be rejected by peers (Edelbrock et al., 1984; Lahey and Carlson, 1991).
Although early research suggested that clinically referred girls and boys with ADHD had different
risk factors and characteristics, more recent studies have found few differences related to gender (Breen,
1989; Horn et al., 1989; McGee et al., 1987). A recent meta-analysis found that ADHD girls have lower
rates of oppositional behavior and conduct problems than do boys in both community and clinical samples.
Among clinically referred ADHD children, girls have greater intellectual impairment than boys. In the
general population, ADHD girls have less inattention, internalizing behavior, peer aggression, and rejection
by peers than ADHD boys do, but in clinic samples boys and girls have equal levels of impairment in these
areas (Gaub and Carlson, in press).
DIFFERENTIAL DIAGNOSIS AND COMORBIDITY
A variety of other disorders can be mistaken for ADHD or can co-occur. Physical causes of poor
attention may include impaired vision or hearing, seizures, sequelae of head trauma, acute or chronic
medical illness, poor nutrition, or insufficient sleep due to sleep disorder or environment. Anxiety disorders
or realistic fear, depression, or the sequelae of abuse or neglect may interfere with attention. Patients with
Tourette s disorder may be distracted by premonitory urges or the effort to resist ticking. Various drugs
may interfere with attention, including phenobarbital (Burd et al., 1987) and carbamazepine, as well as
alcohol and illicit drugs. The data regarding whether the anti-asthma drug theophylline causes ADHD
symptoms are conflicting (Creer and Gustafson, 1989). It is possible that there is an effect only on children
who are already having attention or achievement problems (Schlieper et al., 1991). Parent report of
adverse behavioral side effects may not correspond to more objective data (Bender and Milgrom, 1992).
Some children may be at the high end of the normal range of activity, or have a difficult
temperament. Early-onset mania or bipolar mixed state may be particularly difficult to distinguish from
ADHD, or they may be comorbid. Helpful distinguishing features of ADHD may be earlier age of onset,
sustained clinical course, and family history. The Mania Rating Scale may be useful as an adjunctive
measure (Fristad et al., 1995).
Mental retardation, borderline intellectual functioning, and learning disabilities are commonly
mislabeled ADHD, even by teachers (Landman and McCrindle, 1986), although they often co-occur with
ADHD.
Comorbidity is present in as many as two-thirds of clinically referred children with ADHD, including
up to 50% for oppositional disorder, 30% to 50% for conduct disorder, 15% to 20% for mood disorders, and
20% to 25% for anxiety disorders (Biederman et al., 1991; Newcorn and Halperin, 1994). Tourette s and
chronic tic disorder are often comorbid with ADHD. In adolescents, substance abuse may be comorbid
with ADHD. Recent estimates of learning disorders in children with ADHD range from 10% to 25%,
1997 AACAP
6
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
depending on the population and on the criteria used (Richters et al., 1995). Speech and language delays
are also common. This high degree of comorbidity is not only a function of referral bias. A large New
Zealand community epidemiologic study found that of children with hyperactivity, 47% also had oppositional
or conduct disorder and 26% anxiety or phobic disorder. As many as 18% had two or more comorbid
conditions (Anderson et al., 1987). The Ontario Child Health Study found that in children aged 4 to 11
years, 53% of boys and 42% of girls who had ADDH (DSM-III) had at least one other Axis I diagnosis. For
children aged 12 to 16 years, the prevalence of ADDH subjects with at least one other diagnosis was 48%
for boys and 76% for girls (Szatmari et al., 1989). Clinical experience suggests that children referred to
specialized psychiatric health settings are more likely to have comorbid disorders than those treated by
pediatricians.
EPIDEMIOLOGY
Prevalence estimates vary according to the method of ascertainment, diagnostic system and
associated criteria (e.g. situational versus pervasive, degree of impairment), measures used, informants,
and the population sampled. The DSM-IV (American Psychiatric Association, 1994) estimates the
prevalence in school-aged children to be 3% to 5%. The Ontario Child Health Study (Szatmari et al., 1989)
found ADDH (DSM III) in 10.1% of males and 3.3% of females aged 4 to 11 years and in 7.3% of males
and 3.4% of females aged 12 to 16 years. In a community survey in upstate New York, Cohen et al. (1993)
found ADHD (DSM III-R) in 8.5% of girls and 17.1% of boys aged 10 to 13 years, 6.5% of girls and 11.4%
of boys aged 14 to 16 years, and 6.2% of girls and 5.8% of boys aged 17 to 20 years. Children with ADHD
are the most common category of referrals to child and adolescent psychiatric health services. In
elementary school-aged children, the ratio of boys to girls is typically 9:1 in clinical settings, but
approximates 4:1 in community epidemiological surveys (American Psychiatric Association, 1994).
Teachers identify fewer girls than boys with ADHD symptoms. The male to female ratio ranges from 4:1 for
the predominantly hyperactive-impulsive type, to 2:1 for the predominantly inattentive type. Interestingly,
even among children rated by teachers as meeting criteria for any subtype of ADHD, fewer girls than boys
receive an ADHD diagnosis or stimulant treatment (Wolraich et al., 1996).
PROGNOSIS AND OUTCOME
Overall, 30% to 80% of diagnosed hyperactive children continue to have features of ADHD
persisting into adolescence and up to 65% into adulthood (Barkley, 1996; Weiss and Hechtman, 1993). In
one recent study, over 70% of hyperactive children continued to meet criteria for ADHD as adolescents
(Barkley, 1996). A family history of ADHD, psychosocial adversity, and comorbidity with conduct, mood,
and anxiety disorders increase the risk of persistence of ADHD symptoms (Biederman et al., 1996).
Delinquent behavior or antisocial personality is seen on adolescent or adult follow-up in as many
as 25% to 40% of clinically referred ADHD children, especially boys with early conduct problems (Barkley
et al., 1990a; Gittelman et al., 1985; Weiss and Hechtman, 1993). Defiance toward adults and hostile
aggression are particularly poor prognostic signs (Abikoff and Klein, 1992; Fischer et al., 1993; Loney, et
al., 1981; Satterfield et al., 1994). Most studies find that antisocial behavior is rare in later life without early
conduct problems, although the New York State follow-up found increased risk of antisocial disorders in
adolescence even in ADHD subjects who did not have conduct disorder as children (Abikoff and Klein,
1997 AACAP
7
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
1992). The early conduct problems of some hyperactive children appear to desist in adolescence or
adulthood (Herrero et al., 1994). Children with ADHD are more likely than normal peers to experiment with
drugs and to use cigarettes in adolescence (Lambert, 1988; Mannuzza et al., 1991b; Barkley et al., 1990a).
ADHD adolescents who experiment with drugs may be more likely than normal peers to develop significant
substance abuse problems (Mannuzza et al., 1988). However, in one large longitudinal community survey,
the association between childhood ADD and adolescent use of tobacco, alcohol, and illicit drugs was
attributable only to associated conduct problems at age 8, rather than to ADD per se (Lynskey and
Fergusson, 1995). Specific predictors of poor prognosis include adult-directed oppositional and
aggressive behavior, low IQ, and poor peer relations and continuing ADHD symptoms (Hechtman, 1991).
The presence of comorbid oppositional-defiant disorder (ODD) in children with ADHD heightens their risk
for the development of conduct disorder (Farrington et al., 1990). In one sample, adolescents and young
adults who no longer had a DSM-III diagnosis were found to differ from controls only in academic
performance and school adjustment, suggesting a bimodal distribution of dysfunction in maturing
hyperactive children (Mannuzza et al., 1988). Although girls have been studied far less than boys, limited
data suggest similar outcomes (Klein and Mannuzza, 1991).
FAMILY STUDIES
Although family genetic studies suffer from methodologic limitations, including shared
environmental factors and potential referral bias in clinical populations, the evidence (as reviewed by
Faraone and Biederman, 1994) converges to suggest that there is a substantial genetic contribution to the
etiology of ADHD. Studies of adopted children support this conclusion. Siblings of children with ADHD
have two to three times the risk of having ADHD compared to siblings of normal controls. This risk may be
even higher in adults with ADHD. Concordance for ADHD is higher in full-siblings than in half-siblings and
in monozygotic than dizygotic twins. Although studies have inconsistent findings, the majority show an
increased risk of ADHD in the parents of ADHD children. The parents of clinically referred ADHD children
are at increased risk for other psychiatric problems as well. Children with ADHD without conduct problems
are more likely to have relatives with learning problems and dysthymia. Children with both ADHD and
conduct disorder are more likely to have relatives with conduct disorder, antisocial behavior, substance
abuse, depression, and marital dysfunction (Edwards et al., 1995).
Families with ADHD children are likely to have more stress, feelings of parental incompetence,
marital discord, marital disruption, and social isolation than controls (Edwards et al., 1995), although the
relative contributions of the stress of raising an ADHD child, non-specific effects of having a child with a
psychiatric disorder, parental ADHD, comorbid psychopathology in parents or child, and referral bias in
clinical settings have yet to be untangled. Mothers of ADHD boys may display more commanding and
controlling behavior and less positive affect than mothers of controls, but many of these differences resolve
when the boys behavior improves with stimulant medication (Barkley, 1988; Barkley and Cunningham,
1980).
TREATMENT
Comparing various treatments for ADHD is complex because of the heterogeneity of children and
adolescents with the disorder, the inconsistency of treatment effects on different domains of functioning, the
1997 AACAP
8
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
variation among methods of assessment, and the complexity of patients family, school, and peer social
environments. Psychosocial interventions frequently are insufficiently described, and vary dramatically
across studies, even within type of treatment (Whalen and Henker, 1991a). Whalen and Henker (1991a)
suggest an array of 12 ...abilities by which to evaluate the merits of a particular treatment. These are:
applicability across problems and developmental levels, adaptability to clinical and developmental
requirements, communicability/teachability of the basic therapeutic skills, availability in the community,
controllability for standards of delivery, compatibility with other interventions, durability over time,
generalizability beyond treatment targets and settings, constrainability (unintended side effects and
emanative effects), feasibility in time, cost, and difficulty for the child and family, visibility (potential for
stigmatization), and palatability to the child, family, and school. The direction and weighting of these
factors is likely to differ from patient to patient.
Comorbidity, specific target symptoms, and the strengths and weaknesses of the patient, family,
school, and community enter into the choice of intervention strategies. Parents, school personnel, and to
the degree appropriate, patients themselves are included in the discussion of treatment options, available
resources, parent and child motivation, potential risks and benefits of interventions, and the risks of no
treatment. An understanding of the patient’s and family s dynamics and knowledge base is essential for
facilitating their adherence to treatment (Stine, 1994). ADHD is a condition for which educational
accommodations are federally mandated. The child and adolescent psychiatrist must act as a consultant,
and even as an advocate, to ensure that the patient with ADHD obtains appropriate educational placement
and resources. Advocacy frequently is accomplished in collaboration with school psychologists and special
education personnel.
The evaluation and management of the treatments used for ADHD require input and cooperation
from the patient, the parents, and the school, making the clinician's role as coordinator or case manager
vital to the treatment. ADHD has an extended course, requiring continuous treatment planning to deal with
the effectiveness of current treatment and the emergence of new problems (Conners et al., 1994).
Treatment plans should be individualized, according to the pattern of target symptoms and strengths
identified in the evaluation (Satterfield et al., 1987). One way to conceptualize treatment planning is to
consider core symptoms of inattention, impulsivity, and hyperactivity which are likely to require and respond
to medication; behavioral symptoms to be addressed by environmental modification; and skills deficits in
academic, social, or sports domains, which require specific remediation and do not respond to either
medication (Swanson et al., 1993; Whalen and Henker, 1991b) or behavior modification. In addition,
psychotherapy of some nature may be required to address secondary relationship problems resulting from
the core ADHD deficits (Richters et al., 1995). Clinical experience suggests that more severe cases of
ADHD require an ongoing highly structured environment with contingencies that supplement the effects of
pharmacotherapy and psychosocial treatments. As patients mature, treatment plans must often be
adapted to respond to changing individual, family, and environmental conditions.
Although there are no studies systematically evaluating psychoeducational treatment in ADHD,
provision of information to patients, parents, and teachers is considered standard practice, in both
research protocols and clinical practice (Weiss, 1992). Content includes the symptoms of the disorder,
possible areas of impairment in individual and family functioning resulting from the disorder, etiology
(including heritability), treatment options, medication effects and side effects, expected course and
prognostic features, basic principles of behavior management, legal rights within the public school system,
and how to work with the child s school. It is useful to address persistent myths regarding ADHD and its
1997 AACAP
9
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
treatment. For example, ADHD does not vanish with puberty, and stimulant medications do not act
paradoxically, do not cause drug abuse, and do not stop working at puberty. Information may be
disseminated most economically in a group setting, through published books and newsletters (see
Appendix A) or custom-written information packets, or by referral to a support group such as Children and
Adults with Attention Deficit Disorders (CHADD) or National Attention Deficit Disorder Association.
Parent counseling may be done with individual parents or couples, or in groups. The goal is to
help parents understand their child and his or her problems, and to modify practices that may exacerbate to
the patient s difficulties. The therapist's understanding of the parents' point of view and of the hardships of
living with a hyperactive child or adolescent is crucial. For some parents who have serious difficulties of
their own, parent counseling may pave the way for individual treatment of the adult.
The most troubling difficulty with both psychosocial and pharmacologic treatments of ADHD is the
lack of maintenance of effects once treatment is discontinued and failure of generalization to settings in
which treatment has not been active. Treatment plans should be designed with these problems in mind.
Situations where symptoms cause the most impairment should be targeted for treatment.
Rating scales such as the CAP (Barkley, 1990), the Home and School Situations Questionnaires
(Barkley, 1990), the IOWA Conners (Loney and Milich, 1982), the Academic Performance Rating Scale
(DuPaul et al., 1991) or custom-designed target symptom scales or daily behavioral report cards may be
useful in monitoring treatment progress.
PHARMACOTHERAPY
The decision to medicate is based on the presence of a diagnosis of ADHD and persistent target
symptoms that are sufficiently severe to cause functional impairment at school and usually also at home
and with peers. Although medication is the most powerful and best-documented intervention, each of the
symptoms may not respond. Some parents and patients (especially adolescents) are resistant to the use
of medication, and some patients experience unacceptable side effects or limited efficacy. The careful
clinician balances the risks of medication, the risks of the untreated disorder, and the expected benefits of
medication relative to other treatments. A baseline for target symptoms is useful before starting
medication.
Medication should not be used as a substitute for appropriate educational curricula, student-toteacher ratios, or other environmental accommodations (Rapport, 1995). At times, the most appropriate
response to a behavioral problem is behavior modification, a change in classroom placement, or
modification of the teacher s classroom management style. This is particularly the case when there is
evidence that the disturbance is localized to one classroom situation, when it seems to be a reaction to a
change in teachers or to a particular teacher s approach with the patient, or when the patient has a
learning disability. In mild cases, parent education and appropriate school placement or resources are
often initiated before medication, although, on the other hand, a decision about special education may best
be deferred until the degree of improvement due to medication can be assessed. When severe
impulsivity, noncompliance, or aggression is present, initiation of medication may need to be more urgent.
Even children who respond positively to medication continue to show deficits in many areas.
Specific learning disabilities, gaps in academic knowledge and skills due to inattention, and impaired
organizational abilities may require educational remediation. Parent education and training in techniques of
behavior management are often indicated. Social skills deficits and family pathology may need specific
treatment.
1997 AACAP
10
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Administration of Medications
Faithful adherence to a prescribed regimen requires the cooperation of the parents, the patient,
school personnel, and often additional caretakers. Medications may be incorrectly used or not given at all
because of parental factors such as lack of perceived need for drug, carelessness, inability to afford
medication, misunderstanding of instructions, complex schedules of administration (Briant, 1978), and
family dynamics. Both developmental and psychopathological factors may impede the patient's
cooperation. Even in intensively monitored protocols, missed doses and unilateral discontinuation by a
parent (even when the child responds positively) are common (Brown et al., 1987; Firestone, 1982).
Recent media attention to alleged inappropriate use of Ritalin has increased the resistance of some
families and teachers to pharmacotherapy.
Children and adolescents should not be responsible for administering their medication, since they
are impulsive and disorganized at best, and usually dislike the idea of taking medication. They will often
avoid, "forget," or outright refuse medication. However, as an adolescent approaches adulthood, an effort
should be made to assist the patient to assume responsibility for administering his or her own medication.
Many children cannot or will not swallow pills. If necessary, a behavior modification program may be
implemented to shape pill-swallowing behavior (Pelco et al., 1987). Apparent tolerance or decreased drug
effect may also be due to a reaction to a change at home or school or the attenuation of a placebo
response. Lower efficacy of a generic preparation is another possibility, although supporting data for this
effect are only anecdotal.
Attention is required to avoid possible negative emanative effects of medication, i.e. indirect and
inadvertent cognitive and social consequences, such as lower self esteem and self efficacy; attribution by
child, parents, and teachers of both success and failure to external causes, rather than the child's effort;
stigmatization by peers; and dependence by parents and teachers on medication rather than making
needed changes in the environment (Amirkhan, 1982; Whalen and Henker, 1991b). On the other hand,
self-efficacy can increase as a result of environmental reinforcement of medication-related improvement in
behavior.
Monitoring Medication Efficacy
Multiple outcome measures are essential, using more than one source, setting, and method of
gathering data. Premedication baseline school data on behavior and academic performance should be
available (Fischer and Newby, 1991; Klein et al., 1994; Pelham and Hoza, 1987; Rapport et al., 1986). The
clinician should work closely with parents on dose adjustments and obtain annual academic testing and
frequent reports from teachers. A brief checklist such as the Child Attention Problems profile (CAP)
(Barkley, 1990) or the IOWA Conners Teacher Rating Form (Loney and Milich, 1982) is invaluable in
obtaining teacher reports of medication efficacy. A practical schedule includes weekly ratings from
teachers and two ratings per week from parents: one for Monday through Friday and one for weekends.
Curriculum-based measures and academic performance ratings are useful for monitoring progress in
academic subjects (DuPaul et al., 1991; Stoner et al., 1994). Measures of academic productivity and
accuracy administered in the office (Gadow and Swanson, 1985; Pelham, 1985), such as timed brief
reading and math tests, may be especially useful in assessing drug effect because of their similarity to
tasks expected of the child at school. Protocols have been developed for determining optimal dose in
ADHD children of normal IQ and those with mental retardation using direct observation and other measures
1997 AACAP
11
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
in the school setting (Gadow et al., 1991; Gadow et al., 1992b). A structured side effects checklist can be
used, such as the Stimulant Side Effects Checklist (Gadow et al., 1991).
If symptoms are not severe outside of the school setting, a medication-free trial may be arranged
for all or part of the summer. The purposes are to assess continuing efficacy of and need for medication,
as well as to minimize side effects. If school behavior and academic performance are stable, a carefully
monitored trial off medication during the school year (but not at the beginning) will provide data on whether
medication is still needed. The duration of medication treatment is individually determined by whether
drug-responsive target symptoms are still present. Treatment may be required through adolescence and
into adulthood.
Detailed discussion of the use of every medication that can be used in the treatment of ADHD is
beyond the scope of these parameters. The reader is referred to Appendix B for texts.
Stimulants
The literature on the stimulant medications: methylphenidate, dextroamphetamine, and pemoline,
is voluminous. See Greenhill (1995) for a recent detailed review. In most cases, a stimulant is the first
choice medication. Stimulants are clearly effective, at least in the short term, and, from large numbers of
research studies and sixty years of clinical experience in very large numbers of patients, more is known
about stimulant use in children than about any other drug. In addition, most side effects are mild and easily
reversed, the onset of action is rapid, the dose is easy to titrate, and positive response often can be
predicted from a single dose (Buitelaar et al., 1995). Although there is no evidence that drug abuse results
from properly monitored prescribed stimulants (Hechtman, 1985) (and abuse of methylphenidate or
pemoline is rare in any event), caution may be indicated in the presence of conduct disorder, preexisting
chemical dependency, or a chaotic family. If the risk of drug abuse by the patient or the patient s peers or
family is high, pemoline or a non-stimulant medication may be preferable to methylphenidate or
dextroamphetamine.
1997 AACAP
12
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
TABLE 1
SPECIFIC EFFECTS DOCUMENTED IN GROUPS OF ADHD STIMULANT RESPONDERS
Motor Effects
Reduce activity to the level of normal peers
Decrease excessive talking, noise, and disruption in the classroom
Improve handwriting
Improve fine motor control
Social Effects
Reduce off-task behavior in classroom
Improve ability to play and work independently
Reduce anger
Decrease intensity of behavior
Improve participation when playing baseball
Reduce bossiness with peers
Reduce verbal and physical aggression with peers
Improve (but not normalize) peer social status
Reduce impulsive stealing and property destruction (in a laboratory setting)
Reduce noncompliance, defiance, and oppositional behavior with adults
Improve mother-child and family interactions
Parents and teachers become less controlling and more positive
Cognitive Effects
Improve sustained attention, especially to boring tasks
Reduce distractibility
Improve short-term memory
Reduce impulsivity
Enhance use of cognitive strategies already in the repertoire
Increase amount of academic work completed
Increase accuracy of academic work
(Abikoff and Gittelman, 1985; Barkley, 1990; DuPaul and Rapport, 1993; Hinshaw, 1991;
Hinshaw et al., 1992; Pelham, 1983; Pelham et al., 1990b; Swanson et al., 1993; Whalen
and Henker 1991b; Whalen et al., 1981; Wilens and Biederman, 1992)
1997 AACAP
13
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
The majority of hyperactive children improve on stimulants. Although actual response rates vary
according to the measures used and the definition of positive response, a recent study using a wide range
of doses of methylphenidate and dextroamphetamine found that 96% improved behaviorally in response to
one or both drugs (Elia et al., 1991). Response to stimulants is not diagnostic, as hyperactive and normal
children have qualitatively similar cognitive and behavioral responses (Donnelly and Rapoport, 1985).
Contrary to common assumption, stimulants have a wide variety of social effects, in addition to improving
the core symptoms of inattention, hyperactivity, and impulsivity (see Table 1). Stimulant effects on
attentional, academic, behavioral, and social domains, however, are highly variable within and between
individuals (Rapport et al., 1994). Although most studies have found linear dose-response relationships in
group data (Pelham et al., 1985), individual dose-response curves vary in shape (Rapport et al., 1987). For
a particular child, a dose that produces improvement in one area of functioning may have no effect, or even
lead to worsening, in another (Rapport et al., 1988; Sprague and Sleator, 1977). Even more puzzling,
response may differ between measures, even in the same domain (e.g. math and reading). In general,
however, both behavioral and cognitive measures improve with increasing dose, within the usual
therapeutic range (Spencer et al., 1996). Whether an individual patient is considered a positive responder
depends on the balance of improvement in target symptoms with severity of side effects. Data on subjects
other than school-aged boys with classical hyperactivity are limited. Girls appear to respond similarly to
methylphenidate as boys do (Pelham et al., 1989b). Some children with ADD without hyperactivity may
have a positive response to stimulants (Famularo and Fenton, 1987).
Stimulant medication remains effective over many years. Stimulant treatment in childhood has not
yet been demonstrated to have long-term therapeutic effects, but existing studies have methodological
problems (Hechtman, 1985; Pelham, 1983; Schachar and Tannock, 1993). It is probably unethical to
conduct a sufficiently long-term study with random assignment of children to medication or placebo
(Hechtman, 1993), and widespread poor compliance with medication undermines the validity of studies
even as short as five months in length (Firestone, 1982; Kauffman et al., 1981).
Efforts to predict drug responsiveness among a group of hyperactive children have been largely
unsuccessful (Barkley, 1976). Neurological soft signs, electroencephalograms (EEGs), or neurochemical
measures do not predict stimulant responsivity (Halperin et al., 1986; Zametkin et al., 1986). In a three
week study of a mixed group of clinically referred children, greater hyperactivity, inattention, and
clumsiness and absence of emotional disorder predicted more positive response to methylphenidate
(Taylor et al., 1987). Children with more severe inattention and those with a better mother-child
relationship may have a greater positive response (Barkley, 1990). Although there have been suggestions
that auditory evoked potentials can predict stimulant response (Young, 1995), serious methodologic flaws
limit confidence in these conclusions.
A substantial empirical literature documents that stimulants are just as, or even more, effective in
children with ADHD and comorbid aggression as in those with pure ADHD (Hinshaw, 1991). Verbal and
physical aggressions are reduced. Covert antisocial behaviors have been demonstrated to be reduced, at
least in laboratory settings (Hinshaw et al., 1992). A small open case series suggests that pemoline may
have efficacy in the treatment of conduct symptoms that have not responded to methylphenidate (Shah et
al., 1994).
1997 AACAP
14
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Studies conflict on whether response to stimulants is reduced in children and adolescents with
comorbid anxiety disorders (DuPaul et al., 1994; Livingston et al., 1992). In one sample, although
methylphenidate reduced activity level in children with ADHD and anxiety, working memory improved in
children with ADHD only, but not in those with comorbid anxiety. There was no stimulant-related
decrement in performance (Tannock et al., 1995). Pliszka (1989) found fewer stimulant responders among
ADHD subjects with comorbid anxiety, and some had a placebo response as large as the stimulant
response (Pliszka, 1989). In that sample, none of the ADHD children with anxiety worsened on stimulant
medication. Other studies have found that children with comorbid anxiety respond as well as those without
(Gadow et al., 1995; Livingston et al., 1992).
Among mentally retarded children with ADHD, higher parent ratings of impulsivity and activity and
higher teacher ratings of activity, impulsivity, inattention, and conduct problems predict greater positive
response to stimulants. Laboratory measures of behavior have relatively poor predictive utility for
medication response (Handen et al., 1994). Children with an IQ of less than 45 are much less likely to
have a clinically significant positive response (Aman et al., 1991). In children and adolescents with mental
retardation and ADHD, stimulants reduce target symptoms of inattention, impulsivity, and overactivity
(Aman et al., 1993a, 1993b; Handen et al., 1990; Handen et al., 1992; Varley and Trupin, 1982). Measures
of learning and social interactions did not appear to improve in these children, however (Handen et al.,
1992).
No patient characteristics are helpful in suggesting which stimulant drug is best for a particular child.
Minimum ages approved by the Federal Drug Administration are not based on clinical or research data.
Methylphenidate is the most commonly used and best studied and may be more effective in reducing motor
activity than other stimulants (Borcherding et al., 1989). Dextroamphetamine often has a longer duration of
action than methylphenidate, permitting less frequent doses or reducing gaps in medication effect between
doses. Dextroamphetamine is less expensive, but it is not included in many third party formularies.
Disadvantages of dextroamphetamine include negative attitudes of pharmacists, including some who are
unwilling to stock it, greater risk of growth retardation (Greenhill, 1991), and higher potential for abuse by
the patient s peers and family. Dextroamphetamine may be more likely to cause appetite suppression and
compulsive behaviors. Twenty-five percent of a recent sample of ADHD boys tested on both
methylphenidate and dextroamphetamine responded positively to one of the drugs but not to the other.
Eighty percent of the methylphenidate non-responders were positive dextroamphetamine responders and
66% of the dextroamphetamine non-responders were positive responders to methylphenidate (Elia et al.,
1991). Therefore, if one stimulant is insufficiently effective, another should be tried before using another
drug class.
Both positive and negative placebo effects have been observed in medication trials for children with
ADHD (Gan and Cantwell, 1982; Ullman and Sleator, 1986). At times, parent, teacher, and child positive or
negative drug expectancies may be so significant that a blind placebo trial is required, even in the clinical
setting. This can be done at the time of initiating stimulant medication or in a placebo withdrawal paradigm
to determine if medication continues to be required and effective, or is no longer needed, ineffective, or
even exacerbating the condition. An individual placebo trial may also be useful in evaluating alleged
stimulant side effects (Ahmann et al., 1993; Barkley et al., 1990b; Fine and Johnston, 1993; Golinko, 1982).
Because of the short half-life of stimulants, these trials are easy to do in the clinical setting, and a number
of office-based protocols have been developed (Fine and Jewesson, 1989; McBride, 1988; Strayhorn,
1997 AACAP
15
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
1995; Ullmann and Sleator, 1986; Varley and Trupin, 1983). Parents report greater satisfaction with this
method than with typical clinical procedures (Johnston and Fine, 1993).
Long acting preparations are appealing for children for whom the standard formulations act briefly (2
to 3 hours), who experience severe rebound, or for whom administering medication every four hours is
inconvenient, stigmatizing, or impossible. The most commonly used and systematically studied long-acting
stimulants are Ritalin Sustained Release [SR], Dexedrine Spansule, and Cylert. (Others include Adderall
and Desoxyn Gradumet.) For some children, Ritalin SR is less reliable and less effective than two doses of
the standard preparation, although SR works better for a few children. Onset of action may be delayed up
to two hours, and may be more variable from day to day (Pelham et al., 1987). Only one pill strength is
available, and it cannot be cut to fine-tune the dose. On the other hand, Dexedrine Spansule appears to
have more consistent results than standard methylphenidate and to be more effective for some children
(Pelham et al., 1990a). An advantage of the spansule over Ritalin SR is its greater range of available
doses. Excessively high doses may result if a child chews a SR tablet or spansule instead of swallowing it
(Rosse and Licamele, 1984). An innovative strategy for difficult to manage cases is the combination of
short acting and longer acting medication forms (Fitzpatrick et al., 1992).
Magnesium pemoline has the least abuse potential of the stimulants. It may be given only once a
day, although absorption and metabolism vary widely, and some children need two daily doses. Although it
was previously believed that pemoline action was delayed, more recent research shows effects within the
first one to two hours after a dose, lasting for seven to eight hours after ingestion (Pelham et al., 1990a;
Pelham et al., 1995; Sallee et al., 1992). At current dose recommendations, it may be as effective as the
other stimulants. The half-life increases with chronic administration (Sallee et al., 1985). The frequency of
choreoathetoid movements (Sallee et al., 1989), insomnia, chemical hepatitis (Nehra et al., 1990), and
even (very rare) fulminate liver failure (Berkovitch et al., 1995), make pemoline rank behind the Dexedrine
Spansule. Liver enzymes should be assessed prior to treatment. Because the onset of hepatitis is
unpredictable, routine laboratory follow-up studies are not useful. Instead, parents should be alerted to
notify the clinician immediately if nausea, vomiting, lethargy, malaise, or jaundice appear, or if abdominal
discomfort persists for more than two weeks.
Stimulant medication is typically initiated with a low dose and titrated weekly according to response
and side effects. An alternate strategy is a systematic (open or single blind) trial of several different doses,
with ratings of efficacy and side effects. Giving medication after meals minimizes anorexia. Patients
without hyperactivity, or with ADHD and comorbid mental retardation, may benefit from and tolerate lower
doses of stimulants. Starting with only a morning dose may be useful in assessing drug effect, by
comparing morning and afternoon school performance. The decision of how many doses per day (BID
versus TID) and per week should be based on the severity and time course of target symptoms (Stein et
al., in press). A third dose after school improves behavior without increasing bedtime sleep latency (Kent et
al., 1995). The usual range for methylphenidate is 0.3 to 0.7 mg/kg/dose, rounded to the nearest 2.5 or 5
mg. Dextroamphetamine doses are usually half those of methylphenidate. Pelham et al. (1995)
recommend that pemoline be given in a single morning dose that is approximately six times the
methylphenidate single divided dose. Another rule of thumb is that the daily dose of pemoline is roughly
1.5 times the total daily dose of methylphenidate.
Studies show little evidence for tolerance (Safer and Allen, 1989; Sallee et al., 1992), although it has
been reported anecdotally. Because compliance is often irregular, missed doses should be considered
1997 AACAP
16
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
when medication appears to become ineffective. Tolerance may be more likely with the long-acting
formulations (Birmaher et al., 1989), and can be remedied by substituting another stimulant.
Although stimulants have an extremely high margin of safety, s ide effects are similar for all
stimulants and increase linearly with dose. In the individual patient, however, side effect severity may
differ among the stimulants. Often waiting for a few weeks or decreasing the dose eliminates or reduces
common side effects such as irritability, headaches, abdominal pain, and loss of appetite. Mild appetite
suppression is almost universal, and may be addressed by giving medication after breakfast and lunch
(Swanson et al., 1983), encouraging a high-calorie snack after dinner, and reducing the dose on weekends
and during the summer. Persistent or severe side effects may require changing drugs.
Rebound effects, consisting of increased excitability, activity, talkativeness, irritability, and insomnia,
beginning 4 to 15 hours after a dose, may be seen as the last dose of the day wears off, or for up to several
days after sudden withdrawal of high daily doses of stimulants. This may resemble a worsening of the
original symptoms (Zahn et al., 1980). Although rebound has not been convincingly demonstrated in
controlled trials (Johnston et al., 1988), it is frequently encountered by clinicians. Management strategies
include increased structure after school, a dose of medication in the afternoon that is smaller than the
morning and midday doses, use of a long-acting formulation, and the addition of clonidine or guanfacine to
the regimen.
Using a short-acting stimulant TID does not increase sleep problems over BID use (Kent et al., 1995;
Stein et al., in press). Difficulty falling asleep may be due to ADHD symptoms, oppositional behavior or
separation anxiety, drug effect, rebound, or a preexisting sleep problem. The remedy should address the
cause, and may include behavior modification, clonidine or a small dose of stimulant before bedtime, or
decreasing the afternoon stimulant dose or moving it to an earlier time.
Stimulants may either worsen or improve irritable mood (Gadow, 1992). Persistent stimulant-related
dysphoria may respond to a lower dose, but may require switching to a different stimulant or to an
antidepressant medication.
The use of stimulants in patients with tics has been controversial because of concern that new,
persistent tics might be precipitated. As many as 60% of children with ADHD develop transient, usually
subtle tics when one of the stimulant medications is initiated (Borcherding et al., 1990; Ickowicz et al.,
1992). For children who already have Tourette's disorder or chronic tics, low to moderate doses of
methylphenidate often improve attention and behavior without significantly worsening tics (Gadow et al.,
1989; Gadow et al., 1995). On the other hand, withdrawal of chronic methylphenidate in children with
ADHD and Tourette s disorder may result in a decrease in tic frequency and severity, with an increase
when methylphenidate is reinitiated (Riddle et al., 1995). Some studies have found worsening of tics in 2530% of patients (Castellanos, personal communication; Spencer et al., 1996). Stimulants should be used
with caution when there is patient or family history of tics. If ADHD symptoms cause functional impairment,
and other medications are ineffective or have unacceptable side effects, and if parents are capable of
close monitoring, a stimulant may be the first choice medication, even with a history of tics. If tics appear or
worsen, the usual response is to observe for a few days to a few weeks. If tics remain problematic, dose
reduction or a different stimulant may be tried. Clinical judgment is required to balance the relative
impairment from tics and from ADHD symptoms, considering efficacy and safety of stimulants versus other
medications or psychosocial treatments.
1997 AACAP
17
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Growth retardation resulting from stimulant use is a concern. Decrease in expected weight gain is
actually small, although it may be statistically significant. Effect on height is rarely clinically significant. The
magnitude is dose-related and appears to be greater with dextroamphetamine than with methylphenidate or
pemoline (Greenhill, 1981; Zeiner, 1995). It can be minimized by using drug-free periods (Klein et al.,
1988). Preliminary data on early adolescents show no significant deviation from expected weight and
height growth velocities (Vincent et al., 1990). Adult height has not been shown to be reduced following
methylphenidate treatment in childhood (Klein and Mannuzza, 1988).
Although in general there are no adverse cardiovascular effects of stimulants (Safer, 1992; Zeiner,
1995), black male adolescents may be at higher risk for mild chronic elevation in blood pressure (Brown
and Sexson, 1989). Low doses of methylphenidate have been shown to produce an elevation of heart rate
in ADHD children with comorbid anxiety (Tannock et al., 1995). There is no evidence that stimulants
produce a decrease in the seizure threshold (Crumrine et al., 1987; McBride et al., 1986; Wroblewski et al.,
1992) or that addiction results from the prescription of stimulants for ADHD.
Mentally retarded children may be at greater risk for side effects, including tics and social withdrawal
(Handen et al., 1991).
Buproprion
Buproprion may decrease hyperactivity and aggression and perhaps improve cognitive
performance of children with ADHD and conduct disorder (Conners et al., 1996; Simeon et al., 1986). One
blind controlled crossover study found efficacy of bupropion to be statistically equal to methylphenidate
(Barrickman et al., 1995). Bupropion is administered in two or three daily doses, beginning with a low dose
(37.5 or 50 mg) BID, with titration over two weeks to a usual maximum of 250 mg/day (300-400 mg/day in
adolescents). Experience with this drug in children and adolescents is limited. The most serious side effect
is a decrease in the seizure threshold, seen most frequently in patients with eating disorders or at doses
greater than 450 mg/day. Divided doses are recommended to reduce the risk of seizure. Bupropion may
exacerbate tics (Spencer et al., 1993b).
Tricyclic Antidepressants (TCAs)
Although far less studied than stimulants, controlled trials of TCAs in both children and adolescents
demonstrate efficacy in the treatment of ADHD (Spencer et al., 1996). Despite their narrower margin of
safety, they may be indicated as second line drugs for those patients who do not respond to stimulants or
who develop significant depression or other side effects on stimulants, or for the treatment of ADHD
symptoms in patients with tics or Tourette's disorder (Riddle et al., 1988; Spencer et al., 1993a; Spencer et
al., 1993c). Patients with ADHD and comorbid anxiety disorder or depression may respond better to TCAs
than to stimulants (Kutcher et al., 1992; Spencer et al., 1996). TCAs' longer duration of action averts the
need for a dose at school, and rebound is not a problem. Efficacy in improving cognitive symptoms does
not appear as great as for stimulants. Drawbacks include serious potential cardiac side effects (especially
in prepubescent children), the danger of accidental or intentional overdose, troublesome sedating and
anticholinergic side effects, and possible declining efficacy over time.
Initial studies of imipramine demonstrated efficacy, although often less than that of stimulants
(Rapoport et al., 1974; Winsberg et al., 1972). One controlled study found that imipramine was not
effective in children who had failed to respond to methylphenidate (Winsberg et al., 1980). Desipramine
has fewer anticholinergic side effects than imipramine, and well-documented immediate and sustained
1997 AACAP
18
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
efficacy in both children and adolescents (Biederman et al., 1989; Donnelly et al., 1986), although less than
methylphenidate (Garfinkel et al., 1983). In two open trials with children and adolescents, many of whom
had a poor response to stimulants, nortriptyline produced improved attitude, increase in attention span, and
a decrease in impulsivity (Saul, 1985; Wilens et al., 1993).
Pharmacokinetics for TCAs are different in children than in adolescents or adults. The smaller fat
to muscle ratio in children leads to a decreased volume of distribution, and they are not protected from
excessive dosage by a large volume of fat in which the drug can be stored. Children have larger livers
relative to body size, leading to faster metabolism (Sallee et al., 1986), more rapid absorption, and lower
protein binding than in adults (Winsberg et al., 1974). As a result, children are likely to need a higher
weight corrected dose of TCAs than adults. Prepubescent children are prone to rapid dramatic swings in
blood levels from toxic to ineffective, and should have divided doses to produce more stable levels (Ryan,
1992). Parents must be reminded to supervise administration of medication and to keep pills in a safe
place. If the history suggests head trauma or seizures, an EEG is indicated prior to starting treatment,
because TCAs lower the seizure threshold. A normal EEG, however, does not ensure the absence of a
seizure diathesis.
TCAs' quinidine-like effect slows cardiac conduction time and repolarization. Children and
adolescents may develop mildly increased pulse and blood pressure and small, statistically significant, but
usually clinically benign intraventricular conduction defects, seen on electrocardiogram (ECG) as
lengthened P-R interval that may progress to a first degree atrioventricular heart block, and occasional
widening of the QRS complex, especially at doses equivalent to greater than 3 mg/kg/day of imipramine or
desipramine (Bartels et al., 1991; Biederman et al., 1993a; Fletcher et al., 1993; Leonard et al., 1995;
Schroeder et al., 1989; Winsberg et al., 1975). In one carefully monitored sample of nearly 200 children
and adolescents, desipramine in doses up to 5 mg/kg/day produced increases in diastolic blood pressure,
heart rate, and ECG conduction parameters that were statistically significant but not clinically meaningful or
symptomatic (Biederman, 1991). Prolongation of the QTc interval may be a sensitive indicator of cardiac
effect (Wilens et al., 1991). The tendency of prepubescent children to have wider swings in blood levels
may place them at higher risk for serious cardiac conduction changes. A minority of the population has a
genetic defect in TCA metabolism, increasing risk for toxicity.
Five cases of unexplained sudden death during desipramine treatment, three of which were
following exercise, have been reported in three prepubescent children, one 12-year-old girl, and one 14year-old boy (Popper and Zimnitzy, 1995; Riddle et al., 1991; 1993). A causal relationship between the
medication and the deaths has not been established. The evidence appears to suggest that treatment with
desipramine in usual doses is associated with only slightly added risk of sudden death beyond that
occurring naturally (Biederman et al., 1995a). Desipramine may represent a greater risk than other TCAs,
however. Because of these concerns, clinical practice now favors nortriptyline and imipramine as the first
choices among the tricyclics in the treatment of prepubescent children. In any case, TCAs should be used
only for clear indications and with careful monitoring of therapeutic efficacy and of baseline and subsequent
vital signs and ECG. Revised parameters have recently been published (Wilens et al., 1996). Patient
history of cardiac disease or arrhythmia, or a family history of sudden death, unexplained fainting,
cardiomyopathy, or early cardiac disease may be a contraindication to TCA use.
1997 AACAP
19
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Behaviorally, toxicity may be manifested by irritability, mania, agitation, anger, aggression,
forgetfulness or confusion. A drug blood level is often required to differentiate central nervous system
toxicity from exacerbation of the primary condition.
Sudden cessation of moderate or higher doses results in a flu-like anticholinergic withdrawal
syndrome with nausea, cramps, vomiting, headaches, and muscle pains. Other manifestations may
include social withdrawal, hyperactivity, depression, agitation, and insomnia (Ryan, 1990). Therefore,
TCAs should be tapered over a two to three week period. The short half-life of TCAs in prepubescent
children can produce daily withdrawal symptoms if medication is given only once a day. These symptoms
may also indicate that poor compliance is resulting in missed doses. Because of the predictability of TCAinduced ECG changes, a rhythm strip is useful in monitoring compliance.
The clinician should be alert to the risk of intentional overdose or accidental poisoning, not only by
the patient, but by other family members, especially young children.
Other Antidepressants
Selective Serotonin Reuptake Inhibitors (SSRIs). Although there has been considerable clinical
interest in the use of the SSRIs in the treatment of ADHD, the only published data are from one open trial of
fluoxetine alone (Barrickman et al., 1991), an open case series in which fluoxetine was added to
methylphenidate because of inadequate response (Gammon and Brown, 1993), and one single case study
of the combination of fluoxetine and methamphetamine (Bussing and Levin, 1993). Anecdotal reports do
not support efficacy of the SSRIs for the core symptoms of ADHD.
Monoamine oxidase inhibitors (MAOIs). Tranylcypromine has been shown in one study to be as
effective as dextroamphetamine (Zametkin et al., 1985), but the risk of severe reactions due to dietary
indiscretions or drug interaction make its use impractical for children and adolescents. Use of deprenyl
averts these potential complications, but positive results in an open trial with children with ADHD and
Tourette s disorder (Jankovic, 1993) were not replicated in a controlled trial with ADHD adults (Ernst et al.,
1995).
Alpha-adrenergic Agonists. Clonidine is an alpha-noradrenergic agonist. One small study (Hunt et
al., 1985) and clinical experience suggest that clonidine may be useful in modulating mood and activity
level and improving cooperation and frustration tolerance in a subgroup of children with ADHD, especially
those who are very highly aroused, hyperactive, impulsive, defiant, and labile (Hunt et al., 1990). Although
clonidine is not effective in treating inattention per se, it may be used alone to treat behavioral symptoms of
ADHD in children with tics (Steingard et al., 1993) or those who are nonresponders or negative responders
to stimulants. Open trials suggest that it may be most useful in combination with a stimulant, when
stimulant response is only partial or stimulant dose is limited by side effects (Hunt et al., 1991). The
combination may allow a lower dose of stimulant medication (Hunt et al., 1991). Questions have been
raised about the safety of combining methylphenidate and clonidine (see section below on combinations of
medications). Clonidine often improves ability to fall asleep, whether insomnia is due to ADHD
overarousal, oppositional refusal, or stimulant effect or rebound (Wilens et al., 1994a).
Before starting a patient on clonidine, the clinician should take a thorough cardiovascular history, to include
recent clinical cardiac examination, measurement of pulse and blood pressure, and ECG. History of
syncope is a relative contraindication (Cantwell et al., submitted). Complete blood cell count with
1997 AACAP
20
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
differential is sometimes done, adding a fasting blood glucose if the personal or family history suggests
diabetes. Clonidine is initiated at a dose of 0.05 mg at bedtime. This maximizes its usefulness and
minimizes initial sedation. An alternate strategy is to begin with 0.025 mg QID. Either way, the dose is
titrated gradually over several weeks to 0.15 to 0.3 mg/day in three or four divided doses. Pulse and blood
pressure should be monitored for bradycardia or hypotension. The skin patch or transdermal form may be
useful to improve compliance and reduce variability in blood levels (Hunt, 1987). The patch lasts only five
days in children (compared to seven days in adults) (Hunt, et al., 1990). Once the daily dose is determined
with pills, an equivalent patch may be substituted (0.1, 0.2, 0.3 mg/day, which may be cut to adjust dose).
Unfortunately, allergic skin reactions are common, and the patch does not adhere well in hot, humid
weather.
Clonidine has a gradual onset of therapeutic action, in part because of the slow dose titration
needed to minimize side effects, and perhaps due to the time required for receptor down-regulation (Hunt,
et al. 1991). Significant clinical response is not seen for as long as a month, and maximal effect may be
delayed for another several months. When discontinuing clonidine, the dose should be tapered rather than
stopped suddenly, to avoid a withdrawal syndrome consisting of increased motor restlessness, headache,
agitation, elevated blood pressure and pulse rate, and possible exacerbation of tics (reported in patients
with Tourette s with ADHD symptoms) (Leckman et al., 1986). Erratic compliance with medication
increases the risk of adverse cardiovascular events. Families should be cautioned about this, and clonidine
should not be prescribed if it cannot be administered reliably.
The most common side effect is sedation, although it tends to decrease after several weeks (Hunt
et al., 1985). Dry mouth, nausea, and photophobia have been reported, with hypotension and dizziness
possible at high doses. The skin patch often causes local pruritic dermatitis, and may cause a toxic
reaction if eaten or chewed. Depression may occur, most often in patients with a history of depressive
symptoms in themselves or their families (Hunt et al., 1991). Glucose tolerance may decrease, especially
in those at risk for diabetes.
Guanfacine hydrochloride, a long-acting alpha-2 noradrenergic agonist with a longer half-life and a
more favorable side effect profile than clonidine, has recently begun to be used alone for children with
ADHD and Tourette s disorder whose tics worsen on a stimulant, or in combination with a stimulant in the
treatment of children with ADHD who cannot tolerate the sedative side effects of clonidine or in whom
clonidine has too short a duration of action, leading to rebound effects. As yet, only open trials have been
published (Chappell et al., 1995; Horrigan and Barnhill, 1995; Hunt et al., 1995).
Combinations of Medications
The most common combination used currently for ADHD is probably a stimulant and clonidine,
although there are no published trials of safety or efficacy. The combination is theoretically appealing, due
to complementary actions and non-overlapping side effect profiles. Anecdotal clinical experience supports
the usefulness of these two drugs, especially in children with severe ADHD who cannot be managed
satisfactorily on a stimulant alone. There have been four deaths reported to the FDA of children who at one
time had been taking both methylphenidate and clonidine, but the evidence linking the drugs to the deaths
is tenuous, at best (Fenichel, 1995; Popper, 1995; Swanson et al., 1995). Pending clarification, extra
caution is advised when treating children with cardiac or cardiovascular disease, when combining clonidine
with additional medications, or if dosing of medication is inconsistent (Swanson et al., 1995). An alternative
strategy might be to substitute dextroamphetamine for methylphenidate or guanfacine for clonidine.
1997 AACAP
21
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Although used safely in some contexts (Pataki et al., 1993), the combination of imipramine and
methylphenidate has been associated with a syndrome of confusion, affective lability, marked aggression
and severe agitation (Grob and Coyle, 1986). Methylphenidate may interfere with hepatic metabolism of
imipramine, resulting in a longer half-life and elevated blood levels. One study found that the combination
of desipramine and methylphenidate had more side effects than either drug alone, but they were not more
serious than with desipramine alone (Pataki et al., 1993). Carlson et al. (1995) have evaluated the use of
the combination of desipramine and methylphenidate in a blind controlled crossover study of 16
psychiatrically hospitalized children with ADHD, mood disorder, or both, and either conduct disorder or
oppositional defiant disorder. The efficacy of the combination was statistically significantly better than
either drug alone, but clinically the results were modest. In this highly controlled, carefully monitored
setting, there were no untoward side effects.
Neuroleptics
Early studies suggested some usefulness of thioridazine or other major tranquilizers in the
treatment of ADHD (Green, 1995), but they should be used only in the most unusual circumstances
because of lesser effectiveness relative to other drugs, excess sedation and potential cognitive dulling, and
risk of tardive dyskinesia or neuroleptic malignant syndrome.
Other Drugs
There are no data to support the use of fenfluramine, benzodiazepines, or lithium in ADHD (Green,
1995). Despite a recent review proposing the use of carbamazepine in ADHD (Silva et al., 1996), the
methodological limitations in the existing reports and the far from benign side effect profile make this drug
an alternative only for highly resistant cases, perhaps those with signs or symptoms of brain damage or
epilepsy.
PSYCHOSOCIAL INTERVENTIONS
Behavior Modification
Behavioral approaches are characterized by detailed assessment of problematic responses and
the environmental conditions that elicit and maintain them, the development of strategies to produce
change in the environment and therefore in the patient's behavior, and repeated assessment to evaluate
the success of interventions. In an operant approach, positive and negative environmental contingencies
that increase and decrease the frequency of behaviors are identified and then modified in an attempt to
decrease problem behaviors and increase adaptive ones. The token economy uses points, stars, or tokens
that can be earned for desirable behaviors (and lost for problem behaviors) and exchanged for back-up
reinforcers. These may be money, food, toys, privileges, or time with an adult in a pleasant activity.
Parents, teachers, and clinicians can successfully use token economies, with groups or individuals.
In the short term, behavioral interventions improve targeted behaviors, social skills, and academic
performance in specific settings (Ayllon and Rosenbaum, 1977; Dubey and Kaufman, 1983; Mash and
Dalby, 1979), but are less useful in reducing inattention, hyperactivity, or impulsivity (Abikoff and Gittelman,
1984). Hyperactive children often require both instruction to remedy deficits in social or academic skills,
and contingency management to induce them to use the skills (Pelham and Bender, 1982). The greatest
weaknesses of behavior therapy are lack of maintenance of improvement over time and failure of changes
to generalize to situations other than the ones in which training occurred. Generalization can be maximized
1997 AACAP
22
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
by conducting training in the settings in which behavior change is desired at multiple times and places,
facilitating transfer to naturally occurring reinforcers, gradually fading reinforcement on an intermittent
schedule (Stokes and Baer, 1977), and teaching parents and teachers to cue the desired behavior and
continue to provide contingencies. Lack of maintenance of gains can be addressed through the use of
periodic booster sessions (Hechtman, 1993). Unfortunately it is difficult for parents and teachers to
sustain the energy required to implement a consistent behavioral program. Maximally effective programs
benefit from home and school cooperation, focus on specific target behaviors, provide contingencies that
follow behavior quickly and consistently, and incorporate novelty to maintain interest. Both punishment
(time-out and response cost, in which reinforcers are withdrawn) and reward components are required.
Many youngsters require programs that are intensive and prolonged (months to years).
In general, behavior modification alone is less effective than medication alone. Although clinical
experience suggests otherwise, most controlled studies have been able to demonstrate little additional
benefit when behavior modification is added to medication (Klein and Abikoff, 1989). Attempts to
demonstrate that behavior modification can facilitate medication withdrawal have not been successful.
Behavioral Techniques in School Settings
Techniques for use in schools include token economies, class rules, and attention to positive
behavior, as well as time-out and response cost programs (Abramowitz, 1994; Pfiffner and Barkley, 1990).
One such program for children with attention and conduct problems was effective using only one check by
the teacher on off-task behavior with feedback to the child every 30 minutes (Pelham and Murphy, 1986).
Reinforcers may be dispensed by the teacher (positive recognition, stars on a chart, or notes to parents) or
by parents through the use of daily report cards (Kelley and McCain, 1995). The homework notebook,
reviewed and signed daily by parent and teacher(s), is often useful in improving organization of and
compliance with assignments. To be effective, the support of a contingency program is usually required.
An interesting feature of behavior modification is the possibility of positive spill-over to untreated overactive
children and perhaps even to average children in the same classroom. This has been demonstrated in at
least one school-based study (Loney et al., 1979).
Relaxation training as an adjunctive treatment to aid in anger control appears anecdotally to be
useful in adult-supervised group settings such as day treatment and schools, although there are no
systematic data. For the most part, an adult must provide the cue to use the techniques (Robin et al.,
1976).
Parent Training
Parent behavior modification training packages, based on social learning theory, have been
developed for parents of noncompliant, oppositional, and aggressive children (Barkley, 1987; Forehand and
McMahon, 1981; Patterson, 1975; Patterson and Forgatch, 1987). Parent training has been suggested as
a way to improve the social functioning of ADHD children by teaching parents to recognize the importance
of peer relationships, to use naturally occurring opportunities to teach social skills and self-evaluation, to
take an active role in organizing the child s social life, and to facilitate consistency among the adults in the
child s environment (Cousins and Weiss, 1993). Parents are taught to give clear instructions, to positively
reinforce good behavior, to ignore some behaviors, and to use punishment effectively. One frequently used
negative contingency is the time-out, so called because it puts the child in an unstimulating situation where
naturally occurring positive reinforcement is not available. Although many parents find behavior
1997 AACAP
23
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
management training more difficult to sustain than pharmacotherapy (Firestone et al., 1981), some may
prefer behavioral to medical treatment (Thurston, 1981). Some studies have demonstrated positive results
of parent training, at least in the short term (Anastopoulos et al., 1993; Barkley, 1987; 1990). The most
powerful parent training programs use a combination of written materials, verbal instruction in social
learning principles and contingency management, modeling by the clinician, and behavioral rehearsal of
specific skills. Families characterized by low socioeconomic status, parental psychopathology, marital
conflict, and lack of a social support network require maximally potent interventions, with parental problems
addressed as necessary. Other families may be able to succeed with written materials only (Long et al.,
1993) or manuals supplemented by group lectures. Parent training has not been consistently
demonstrated to add benefit to stimulant treatment (Lalongo et al., 1993). The high prevalence of ADHD
among parents of children with ADHD often makes compliance with training programs and execution of
interventions difficult.
Family Therapy
Clinical models for family therapy of ADHD have been developed (Ziegler and Holden, 1988),
although outcome data are few. Family psychotherapy may be indicated to address family dysfunction
stemming either from the difficulty of raising and managing an ADHD child or from primary parental or
marital pathology. Although there are no systematic clinical trials in ADHD, data on treatment of children
with other disruptive behavior disorders (Dadds et al., 1987) and clinical experience suggest this modality
as an adjunctive treatment or to facilitate consistent implementation of medication or behavior
management. Behavioral intervention can be done in the context of family therapy where the family
learns how to negotiate and to solve problems together. One technique is parent-child contingency
contracting, which entails a written agreement between parent and child to change behaviors in both, with
specified contingencies (Blechman, 1981).
In many cases, referral to a parent support group such as CHADD is a cost-effective intervention
that is well accepted by families.
Social Skills Training
Social skills training is a common part of multimodal treatment packages. Evaluation of the
efficacy of social skills training has been hampered by the heterogeneity of ADHD patients and the varying
etiology of social skills deficits in this group. Practical problems include the need to tailor training to each
patient s particular deficits and the failure of patients to apply the skills they have learned (Conners et al.,
1994). Clinical experience suggests that individual training is not useful, due to lack of self-observation in
ADHD patients. When training is conducted in groups, the target behaviors emerge naturally and can be
addressed through modeling, practice, feedback, and contingent reinforcement. Use of natural
environments such as the school, rather than the clinic, may enhance generalizability (Conners et al.,
1994). Student-mediated conflict resolution programs may decrease playground aggression and improve
implementation of problem-solving skills (Cameron and Dupuis, 1991).
Academic Skills Training
Academic skills training is a form of specialized individual or group tutoring that teachers patients to
follow directions, become organized, use time efficiently, check their work, take notes, and study effectively.
Although academic skills training has not been systematically tested, clinical experience suggests its use
1997 AACAP
24
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
when academic deficiencies are present. Remediation of specific learning disabilities also may be
indicated.
Individual Psychotherapy
The relative lack of insight and failure to generalize therapeutic effects that are characteristic of
ADHD mitigate against the usefulness of individual psychotherapy for the treatment of ADHD per se.
However, individual psychotherapy can be useful in actively engaging the child in a positive therapeutic
alliance, addressing low self-esteem and demoralization, and facilitating compliance with treatment.
Although there are no clinical trials, many child psychiatrists find that individual therapy is useful in treating
comorbid anxiety and depression in children and adolescents with ADHD. Episodic use of individual
psychotherapy may be a useful way to deal with compliance problems, relationship issues, and adaptations
to the difficulties created by ADHD. There may also be a role for individual psychotherapy in assisting the
adolescent make the transition to assuming responsibility for their own medication. For the patient in crisis,
the therapist can provide support until the stressor resolves or other adults are able to take on the
supportive role.
Cognitive Behavior Modification
Cognitive Behavior Modification (CBM) or Problem-Solving Therapy may be administered
individually or in a group. It combines the teaching of cognitive strategies, such as step-wise problem
solving and self-monitoring, with behavior modification techniques, such as contingent reinforcement or
self-reinforcement and modeling. CBM was developed in an attempt to improve the generalization and
durability of behavior modification techniques. It is theoretically appealing, because it directly addresses
presumed deficits in control of impulsivity and problem solving, and provides a structure for work with
children who otherwise would gain little from therapy. Although early studies of CBM with aggressive,
impulsive, and hyperactive children showed improvement on measures of cognitive impulsivity, social
behavior, and the use of coping strategies (Douglas et al., 1976; Hinshaw et al., 1984a; Horn et al., 1987),
subsequent results have been disappointing (Abikoff, 1991), and have not demonstrated that CBM
improves outcome when added to stimulant medication (Abikoff, 1985; Abikoff et al., 1988; Abikoff and
Gittelman, 1985). Major problems are the lack of generalization to situations where specific training has not
occurred and the fact that the children do not use the strategies they have learned unless prompted. It is
possible that a small minority of ADHD children or adolescents will benefit from CBM. Self-monitoring/selfevaluation training and attribution retraining focused on increasing sense of control may be useful (Kendall
and Braswell, 1993). Very young children and those with poor language skills appear to be least likely to
benefit (Abikoff and Hechtman, in press). An intensive model of problem-solving skills training has been
shown to be additive to milieu treatment and superior to individual relationship therapy in improving the
behavior of hospitalized and outpatient children with conduct problems, many of whom have ADHD along
with another disruptive behavior disorder (Kazdin et al., 1987; 1989). Kazdin s model, however, has not
been compared to stimulant treatment, or assessed for effects that might be additive to stimulants.
Therapeutic Recreation
Clinical experience suggests that developing sports skills or other recreational abilities can be an
important adjunct in the treatment of children and adolescents with ADHD who lack positive relationships
with peers or adults. A relationship with an adult such as a Big Brother or a YMCA counselor and an
1997 AACAP
25
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
opportunity to interact with normal peers under supervision may build self-esteem until the child or
adolescent is sufficiently improved to establish relationships independently. Some families have employed
a high school or college student one or more afternoons a week to teach social and play skills, develop a
relationship, and provide supervision and structured time. This also gives parents a respite and an
opportunity to spend time with their other children. Day or overnight summer camps may present
opportunities for improved social and recreational skills with resulting increased self-esteem. Some
youngsters can attend regular camp, while others need a special program for children and adolescents with
behavioral problems.
Multimodal Treatment
Although clinical wisdom and the need to address multiple problems favor multimodal treatment of
ADHD (Hechtman, 1993), there are very limited research data to support it. In part, this is due to the
expense, duration, and complexity of such studies, with the difficulty in sustaining child and family
participation in multiple interventions over time, and the need for a large number of subjects to address all
of the questions posed (Hechtman, 1993; Jensen, 1993; Richters et al., 1995).
In the clinical setting, multimodal treatments may be indicated to address comorbid conditions or
ADHD target symptoms that are not sufficiently improved by medication. For many youngsters with ADHD,
neither stimulant medication nor behavior therapy alone is sufficient to normalize behavior and academic
performance (Abikoff and Gittelman, 1984; DuPaul and Rapport, 1993; Elia et al., 1991; Pelham and
Murphy, 1986). Although normal children can detect medication-induced improvement in the behavior of
hyperactive children (Whalen et al., 1987), stimulant treatment alone rarely improves social skills or peer
ratings of popularity to the level of normal peers (Ullmann and Sleator, 1985; Whalen et al., 1989). Some
short-term studies, primarily with small numbers of subjects or using systematic single case study
methodology, have found intensive behavior modification or cognitive behavior modification to have
additive effects to methylphenidate, in many cases yielding performance indistinguishable from normal
peers (Ajibola and Clement, 1995; Chase and Clement, 1985; Gittelman et al., 1980; Hinshaw et al., 1984a;
Horn et al., 1983; Pelham and Bender, 1982; Pelham et al., 1986; Pelham and Murphy, 1986; Pelham et
al., 1980). Although a sufficiently intensive and structured behavioral program alone will nearly normalize
the classroom behavior of children with ADHD, 30% to 60% of children improve further with the addition of
low dose (0.3 mg/kg) methylphenidate (Pelham and Murphy 1986). The combination of classroom
behavior therapy (token economy, time-out, and daily report card) with a low dose of methylphenidate is
able to produce the same result as a high dose of medication alone (Carlson et al., 1992). The combination
may be more expensive than medication alone, but may be especially useful for children who cannot
tolerate a higher dose of medication. Other studies have found that cognitive behavior modification or
behavior modification adds little or no effect to stimulant medication (Hinshaw et al., 1984b; Pelham et al.,
1991). See Schroeder et al. (1983) for a detailed review of early studies. Both medication and behavior
modification have dose effects, and the outcome of the combination differs among children. For an
individual child, one treatment or the other may have strong effects, with the other adding little. For other
children, the combination is better than either alone (Abramowitz et al., 1992; Hoza et al., 1992). Individual
functional assessment may be necessary to tailor treatment for the individual child (Cooper et al., 1993;
DuPaul and Barkley, 1993).
1997 AACAP
26
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Satterfield et al. (1979; 1981) implemented a clinical protocol in which, following multidimensional
evaluation, individually designed treatment plans were implemented including some or all of: individually
titrated doses of methylphenidate, individual psychotherapy, group therapy, educational treatment,
individual or parent counseling, and family therapy, in any number and any combination. At one- and threeyear follow-up, the subjects who received medication with multimodal treatment had improved behavior at
home and school, increased academic achievement, and decreased delinquent behavior, compared with
expected course and other outcome studies. Children who received more treatment did better.
Subsequent follow-up found that the multi-modal group had significantly fewer arrests and less
institutionalization than those who received medication only (Satterfield et al., 1987). Unfortunately, there
are significant methodologic problems with this study, including lack of random assignment to various
treatments, differences at baseline in comparison groups, use of treatment dropouts as controls, and the
failure to use blinded assessment procedures.
In an ongoing four-year study of multimodal treatment conducted by Abikoff, Hechtman, and
colleagues, stimulant-responsive children aged 7 to 9 years with ADHD (but without comorbid severe
learning disabilities or DSM-III R conduct disorder) were randomly assigned to one of three groups:
methylphenidate medication management alone; intensive two-year multimodal treatment consisting of
medication, academic skills training, remedial tutoring, individual psychotherapy, social skills training,
parent training, family counseling, and a home-based daily report card reinforcement program for school
behavior; or medication management and non-specific education and non-directive support. The aims are
to determine whether intensive multimodal treatment is additive to stimulant medication in improving
functioning and whether following multimodal treatment a greater proportion of children with ADHD are able
to function adequately without medication (Abikoff, 1991; Hechtman, 1993). At the two-year evaluation,
medication has not been able to be withdrawn without clinical relapse (personal communication, Abikoff,
1995). Gains made by all groups in initial treatment have been maintained, but multiple outcome measures
in various domains of functioning have been unable to distinguish children who received medication
management alone from those in the two other groups. Longer-term differences between groups are, of
course, possible. It is essential to emphasize that this model of medication management bears little
resemblance to routinized prescription of medication with 15-minute medication checks monthly or even
less frequently. Medication only entailed: a detailed evaluation prior to treatment; individualized titration
of three times daily doses (seven days per week) using weekly feedback from parents, teachers, and the
children; and monthly 30 to 45 minute sessions to evaluate medication efficacy and side effects and to
provide clinical management, education, and support. Cognitive performance was evaluated by arithmetic
tests to avoid stimulant-related impairment, but this test was dropped because no impairment was found at
doses of methylphenidate up to 50 mg per day (Abikoff and Hechtman, in press). Also included was crisis
intervention (up to 8 sessions) if needed and regular contact with teachers for discussion and the
completion of rating scales.
Innovative intensive summer treatment programs treat children with moderate to severe ADHD and
associated behavior and learning problems in the context of a positive social and recreational experience
(Pelham and Hoza, 1987). The goals are to develop problem-solving skills, social skills, and social
awareness; to enhance academic learning skills; to improve compliance with adult requests and followthrough with tasks; to improve self-esteem by increasing competencies in interpersonal, recreational, and
academic areas; to teach parents behavior management techniques; and to rigorously assess medication
efficacy and side effects. The program includes a comprehensive and highly structured behavior
1997 AACAP
27
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
modification program using a token economy, time-out, and daily report cards; social skills training groups;
group problem-solving discussions; sports skills training; classroom experiences including academic skills,
computer learning, and art; parent training; and double-blind medication assessments with multiple
outcome measures. Parent- and staff-completed improvement ratings and parent and child acceptance
ratings of the program are consistently positive. Questions have been raised, however, regarding
generalization and maintenance of behavioral gains, and the cost to benefit ratio. The NIMH Collaborative
Multisite Multimodal Treatment Study of Children with ADHD includes a systematic evaluation of the
efficacy of an intensive summer day treatment program as part of a package of multimodal interventions.
Dietary Interventions
Since the mid 1970's, the advocates of dietary treatment of behavioral problems have been
remarkably persistent (Rimland, 1983) despite the lack of scientific evidence. A variety of food additives
and food allergens have been proposed as contributory or even causal in childhood hyperactivity. Reviews
of the methodologically adequate studies show that at most 5% of hyperactive children may show
behavioral or cognitive improvement on the additive-free Kaiser-Permanente or Feingold diets, but these
changes are not as dramatic as those induced by stimulants (Kavale and Forness, 1983; Mattes, 1983;
Wender, 1986). The only characteristic associated with greater likelihood of response is age less than six
years. A small number of children may respond negatively to tartrazine, a synthetic food dye (Rowe and
Rowe, 1994). Parents and some primary care practitioners find dietary treatment appealing because it is
more "natural" than medication, but special diets demand extra work and often additional expense from a
family already strained by a child's behavior problems. Given the minimal evidence of efficacy and the
extreme difficulty inducing children and adolescents to comply with restricted diets, dietary treatment should
not be recommended, except possible with preschool children. Families who insist on trying a diet should
be permitted to do so, provided the diet is nutritionally sound, because initial attempts to dissuade them
may disrupt the therapeutic alliance.
Controlled studies have been unable to demonstrate that ingestion of sugar has an effect on
activity or aggression in normal or hyperactive children, even those identified by their parents as sugar
responsive (Milich et al., 1986b; Wender and Solanto, 1991; Wolraich et al., 1995). Clinically insignificant
effects on attention have been demonstrated, only in young children, and only following a high
carbohydrate breakfast (Wender and Solanto, 1991).
Caffeine, in the form of coffee or soft drinks, has been both blamed for causing hyperactivity and
recommended by nonprofessionals for the treatment of hyperactivity, despite the lack of demonstrated
causality or efficacy, and side effects greater than stimulants (Harley, 1980).
Non-traditional Treatments
Megavitamin therapy, the prescription of vitamins in quantities greatly in excess of the RDA
guidelines, has been suggested as a treatment for hyperactivity and learning disabilities. Extreme claims
have been made from uncontrolled studies. Not only is scientific evidence of effectiveness lacking, but
there is a possibility of toxic effects (Harley, 1980; Haslam, 1992). Herbal remedies also have no empirical
support. For a discussion of unproven treatments such as anti-motion sickness medication, anti-candida
albicans medication, biofeedback, sensory integrative training, optometric vision training, Irlen lenses,
chiropractic manipulation, etc., see Ingersall and Goldstein (1993) and Silver (1986).
1997 AACAP
28
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
SPECIAL ASPECTS OF ADHD IN PRESCHOOL CHILDREN
Parent training in a group setting for families of preschoolers with ADHD can improve child
compliance, parental style of interaction, and parental management skills. Non-targeted child behaviors do
not respond (Pisterman et al., 1989).
Stimulants can reduce oppositional and aggressive behavior, increase on-task behavior, improve
mother-child interaction and compliance to parental commands, and improve attention and quality of play in
preschool children with ADHD (Alessandri and Schramm, 1991; Barkley, 1988; Cohen et al., 1981;
Conners, 1975; Schleifer et al., 1975). One single case experiment noted synergy between
dextroamphetamine and a contingency management program (Speltz et al., 1987). Stimulant efficacy is
more variable than in older children, however, and the rate of side effects is higher, especially sadness,
irritability, clinginess, insomnia, and anorexia. Stimulants should be used in this age group only in the more
severe cases or when parent training and placement in a highly structured, well-staffed preschool program
have been unsuccessful or are not possible.
SPECIAL ASPECTS OF ADHD IN ADOLESCENTS
The clinical picture in adolescents tends to include restlessness rather than gross hyperactivity,
although fidgeting and out-of-seat behaviors in school often are present. Impairment in adolescents
includes inattention, poor impulse control, poor organizational skills, difficulty setting and keeping priorities,
and weak problem-solving strategies, resulting in diminished school performance, low self-esteem, poor
peer relations, and erratic work record. Opportunities for dangerous impulsivity and poor judgment
increase with age, due to stronger peer influence and less adult supervision. Adolescent boys with ADHD,
compared to age-matched controls, have poorer driving practices, are more likely to have gotten a ticket,
have more tickets per person (especially for speeding), are more likely to have had an accident, have more
accidents per person, and experience more injuries per crash. Boys with comorbid ODD or conduct
disorder (CD) are most at risk (Barkley et al., 1993). Some data support a trend in adolescents with ADHD
toward increased suicides, suicide attempts, and accidental deaths (Weiss and Hechtman, 1993).
The Brown ADD Scale for Adolescents includes 40 self-report items assessing organization,
sustained attention and effort, difficulties with mood, sensitivity to criticism, and effective memory (Brown,
1996). Stimulants remain effective in the treatment of adolescents with cognitive or behavioral symptoms
of ADHD (Brown and Sexson, 1988; Evans and Pelham, 1991; Klorman et al., 1987; Klorman et al., 1990;
Varley, 1985), although the rate of positive response may be lower than for elementary school aged
children (Pelham et al., 1991). Youngsters who are positive responders as children do not require a change
in drug at puberty, and newly diagnosed adolescents may be started on a stimulant. Non-compliance with
medication is a greater problem in the treatment of adolescents due to the wish to avoid taking medication
during school hours and increased prevalence of stimulant-related dysphoria.
The risk of misuse of stimulants is increased in adolescence. Giving or selling medication to peers
is more common than abuse by the patients themselves.
Parent training models have been adapted for the different developmental needs of teenagers and
their families (Robin, 1990). In working with adolescents with ADHD and their families, Barkley et al. (1992)
have demonstrated that behavior management training, problem solving and communication training, and
1997 AACAP
29
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
structural family therapy have equivalent value, but gains are modest in all three formats. Multimodal
treatments are appealing for adolescents, but documentation of efficacy is even more limited than for
younger children (Brown et al., 1985).
ADHD IN ADULTS
In recent years, ADHD in adults has drawn considerable attention in the popular media, leading to
concerns about ove diagnosis. The scientific literature, although far less developed than for children,
supports the validity of the diagnosis of ADHD in adults (Spencer et al., 1994). Imaging (Zametkin et al.,
1990) and genetic (Faraone and Biederman, 1994) studies have focused on ADHD in the parents of
children with the disorder. Limitations in studies of clinical samples of adults with attention deficit disorders
include referral bias and retrospective diagnosis, often made only through self-report of the patient.
DIAGNOSTIC CRITERIA
Wender and his colleagues (Wood et al., 1976) were among the first to identify the presence of
attention deficit disorder in adults, at a time when the conventional wisdom was that ADD vanished with
puberty, or at least at the end of adolescence. His Utah criteria for diagnosis (Wender, 1995; Wender et
al., 1985b) have now largely been supplanted by the DSM-IV (Kane et al., 1990).
ASSESSMENT
ADHD is often missed in adults (Biederman et al., 1993c; Ratey et al., 1992), particularly if the
disorder was not identified when the patient was a child. Adults often seek evaluation and treatment after
their child has been diagnosed with ADHD and the parent recognizes the symptoms (Ratey et al., 1992).
The adult’s childhood ADHD may have been obscured by comorbid conduct or oppositional defiant
disorder, anxiety, depression, learning disability; or a chaotic home or school situation clouded the picture.
Some with previously undiagnosed ADHD avoided detection as children and adolescents because of a high
IQ, compliant behavior, and interpersonal charm. Others manage to compensate sufficiently due to
structured and tolerant home and school environments and learned coping strategies (Ratey et al., 1992).
Those with DSM-IV ADHD predominantly inattentive type might be more likely to remain undiagnosed than
those with prominent hyperactivity. A common finding in the history of a subgroup of adult ADHD patients
is educational and career success challenged by reaching a level of expectations at which native abilities
and compensation strategies are no longer sufficient (Ratey, 1992; Wilens et al., 1995d). Clinicians who
are not trained in a developmental perspective often fail to include ADHD in the differential diagnosis.
Clues include a school history of underachievement, and childhood labels of undisciplined, unmotivated,
immature, space cadet,
spacey, or daydreamer.
Assessment of ADHD in adults includes a complete psychiatric evaluation (American Psychiatric
Association, 1995), with particular attention to the core symptoms of ADHD (American Psychiatric
Association, 1994). Although ADHD may not have been diagnosed in childhood, a diagnosis of ADHD can
be made if the symptoms were present prior to the age of 7. Childhood history, therefore, is absolutely
essential. Due to the high prevalence of comorbid substance abuse, focused historical inquiry regarding
drugs and alcohol and a urine drug screen are often indicated (Kane et al., 1990; Wilens et al., 1994b). In
1997 AACAP
30
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
addition, because patients with ADHD often have limited insight into their difficulties and may be poor
reporters, obtaining information from spouse or significant other, parent, or employer is important. School
records and childhood psychiatric evaluation or treatment records can make a major contribution to the
evaluation. Supplementary data are especially useful for patients who abuse drugs or who have antisocial
personality disorder, who may have an ulterior motive for obtaining an ADHD diagnosis (Wilens et al.,
1995e). A medical history and a recent physical examination, with laboratory studies as necessary, are
indicated to rule out conditions that could be mistaken for ADHD or that is comorbid. Psychological testing
may be useful to evaluate intellectual potential and to identify learning disabilities. Neuropsychological
testing may be indicated to evaluate possible sequelae of traumatic brain injury or a degenerative process
(Stein et al., 1995). If the history suggests narcolepsy, sleep studies may be indicated.
Standardized rating scales may be useful. Wender adopted the Conners Abbreviated Teachers
Rating Scale (Conners, 1969) as the Wender Parents Rating Scale (originally called the Child
Temperament Questionnaire) (Wender et al., 1985b). This brief scale has 10 items that retrospectively
describe the patient s behavior between the ages of 6 and 10 years. It has been standardized using the
parents of normal school children as subjects, with the forms completed by the children s grandparents. A
score of 12 is reported to be at the 95th percentile (Wender, 1995; Wender et al., 1981; 1985b). The
Wender Utah Rating Scale (WURS) (previously called the Adult Questionnaire Childhood Characteristics)
is a 61-item self-report measure on which the adult patient describes him/herself as a child (Ward et al.,
1993; Wender et al., 1985b). Some normative data are available, and scores on a subset of 25 items have
been able to distinguish adult ADHD subjects from normal controls and from patients with agitated
depression (Ward et al., 1993; Wender, 1995). The Brown Attention-Deficit Disorder Scale for Adults,
another self-rating scale, focuses on cognitive attentional and organizational symptoms and common
affective impairments, rather than hyperactivity or behavioral symptoms (Brown, 1996).
CLINICAL FEATURES
Prospective controlled naturalistic longitudinal studies of hyperactive children (Barkley, 1996; Klein
and Mannuzza, 1991; Mannuzza et al., 1991a; Mannuzza et al., 1993; Weiss and Hechtman, 1993) find
that approximately 50% function well as adults, while the remainder suffer from some degree of impairment
in attention, impulse control, problem-solving strategies, school performance, self-esteem, peer relations,
academic attainment, and work record. Adults who were hyperactive as children are more similar to normal
controls as adults than they were as adolescents, but 30% to 70% report at least one core ADHD symptom
(Weiss and Hechtman, 1993), and 30% to 50% of young adults still meet criteria for ADHD (Barkley, 1996).
Prevalence decreases as adulthood progresses (Klein and Manuzza, 1991). The rate of reported
symptoms appears to be lower if only the subject, and not other informants, is interviewed.
The clinical characteristics of ADHD in adults are similar to those in childhood, with the exception
of less prominent gross motor hyperactivity. Because adults are expected to function far more
independently than children, and because they have less structure and supervision, the consequences of
inattention and impulsivity often have serious implications for functioning in higher education, at work, and
in social relationships. Marital disruption is increased. Socioeconomic status is decreased, likely due to
the compounding of reduced academic achievement and vocational instability (Biederman et al., 1993c).
Impulsivity and disorganization may impair parenting abilities (Daly and Fritsch, 1995; Evans et al., 1994).
1997 AACAP
31
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Adults with ADHD frequently suffer from demoralization, underachievement, and feeling overwhelmed
(Ratey et al., 1992).
DIFFERENTIAL DIAGNOSIS AND COMORBIDITY
The differential diagnosis of ADHD in adults includes agitated depression, hypomania, dissociative
disorders, borderline or antisocial personality disorder, alcohol and drug abuse or withdrawal, especially for
cocaine, and a variety of primary medical conditions and cognitive brain syndromes (Kane et al., 1990;
Wilens et al., 1995e).
In follow-up studies of clinically referred hyperactive children (Klein and Mannuzza, 1991;
Mannuzza et al., 1991a; Mannuzza et al., 1993; Weiss and Hechtman, 1993), antisocial behavior is found
in 18% to 45%, especially in those with early conduct problems and continuing ADHD symptoms. The rate
of antisocial personality disorder in some samples is as high as 25%. The rate of drug use is increased,
but is not related to stimulant treatment. The risk of drug abuse is higher if ADHD symptoms continue. In
these samples, mood and anxiety disorders are not more frequent than in controls.
Studies of adults presenting to ADHD clinics find high comorbidity with ADHD of substance abuse,
anxiety disorders, antisocial personality disorder, dysthymia, and cyclothymia (Biederman et al., 1993c;
1995b; Shekim et al., 1990; Wender, 1995). In one clinic, only 12% of the adults diagnosed with ADHD
had no other DSM-III-R Axis I diagnosis (Shekim et al., 1990). Studies of adults in chemical dependency
treatment settings find a high rate of ADHD (Wilens et al., 1994b). The theoretical notion of substance
abuse as possible self-medication has been proposed (Khantzian, 1985), although supporting data are
limited to anecdotal reports (Ratey et al., 1992). The finding that ADHD appears to be more prevalent in
cocaine abusers than in opiate addicts suggests attempts at self-medication (Carroll and Rounsaville,
1993).
In contrast, Buchsbaum et al. (1985) found that an inattentive group of college men identified by
relatively poor performance on a continuous performance test (CPT) had a higher incidence of symptoms
of hyperactivity both as children and currently, but had no higher incidence of other psychopathology than
the less inattentive control group.
EPIDEMIOLOGY
There are no community epidemiologic surveys of ADHD in adults. The prevalence in adults has
been estimated at 2% to 7%, extrapolated from epidemiologic and follow-up studies of children (Wender,
1995). If this is accurate, the frequency of suspected ADHD is not surprising. Clinical samples of adults
vary in the sex ratio of patients presenting for evaluation of presumed ADHD. In some, males predominate
by as much as two to one (Biederman et al., 1993c), while in others the ratio is more nearly equal
(American Psychiatric Association, 1994; Spencer et al., 1994; Wender et al., 1981).
TREATMENT
As with child and adolescent patients, education about ADHD is a core feature of the treatment
plan (Hallowell and Ratey, 1994; Wender, 1995). A variety of self-help books may be useful for adults with
1997 AACAP
32
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
ADHD and their significant others (see Appendix A), as may support groups such as CHADD. Involvement
of significant others in the patient s life may be useful in obtaining feedback about the efficacy of
treatments and in improving cooperation with treatment, since many adults with ADHD appear to lack
insight into their difficulties and fail to observe positive medication effects (Wender, 1995; Wender et al.,
1981).
PHARMACOTHERAPY
The state of the art of drug treatment for adult ADHD is far less developed than for other adult
psychiatric disorders or for the treatment of ADHD in childhood (see Wender, 1995; Wilens et al., 1995d for
reviews). It is interesting that no treatment studies have been conducted with adult subjects of the
longitudinal follow-up studies, since this is a population in which the diagnosis of ADHD is most certain.
ADHD adults appear to have more variability in drug response than do ADHD children. In the presence of
comorbid substance use disorders, at least one month of abstinence should elapse before initiating
pharmacotherapy (Wilens et al., 1995e). As with child patients, target symptoms should be identified, with
clear baselines and repeated reevaluation in order to assess progress. Structured instruments are
available for this purpose, such as the Targeted Attention-deficit Disorder Symptoms Rating Scale
(Wender, 1995).
In choosing among medications, the weighting of factors is somewhat different than for child and
adolescent patients, although drugs appear to have qualitatively the same therapeutic effects, regardless of
age. The advantages of stimulants include immediate response and ease of dose adjustment. The short
duration of action (2 to 6 hours) is a disadvantage. The risk of abuse and possibility of tolerance or drug
refractoriness is greater than in children, but still rare (Wender, 1995). Of the stimulants, pemoline has the
least abuse potential. Because adults typically are responsible for taking their own medication, the
requirement for frequent stimulant doses may be more problematic for adults than for children. Wender
(1995) recommends the use of a watch alarm or multi-dose pill container as reminders. Although abuse of
prescribed stimulant medication is uncommon in properly diagnosed and monitored ADHD, the common
comorbidity of substance abuse in adult ADHD patients may present more of a concern than for child
patients, for whom a parent or teacher administers medication. Substance abuse is not an absolute
contraindication for the use of stimulants, however (Schubiner et al., 1995; Weiss et al., 1985). Possible
developmental side effects of stimulants, such as irreversible tics and delayed growth, are not a problem for
adults.
When considering alternatives to stimulants, the potential cardiotoxic effects of tricyclic
antidepressants (TCAs) are of less concern for adults than they are for prepubescent children.
Advantages of TCAs over stimulants are: poor abuse potential, longer duration of action permitting once
daily dosing, and efficacy in the treatment of comorbid depression and anxiety. However, anticholinergic
side effects often limit acceptability of TCAs to adults. In addition, the lethality of TCAs in overdose is a
disadvantage for potentially self-destructive ADHD patients.
Stimulants
In Wender s samples (Wender et al., 1985b), 60% to 80% of patients meeting the Utah Criteria
(current attention problems, hyperactivity, and impulsivity; associated mood symptoms; and childhood
history consistent with ADHD combined type) respond to at least one of either methylphenidate,
dextroamphetamine, or pemoline. Higher scores on the parent- and self-rating scales appear to predict
1997 AACAP
33
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
better response (Wender et al., 1981). Patients who do not improve on a stimulant may respond to another
drug.
Five double-blind crossover placebo controlled studies of methylphenidate in ADHD adults have
been completed (Wilens et al., 1995b). Wender et al. (1981; 1985a), in two trials, found methylphenidate to
be superior to placebo for symptoms of nervousness, lack of concentration, hot temper, and fatigue.
Approximately 55% were positive responders. In contrast, Mattes et al.(1984) found no difference between
methylphenidate and placebo, with only 25% responding to methylphenidate or placebo. Mattes sample,
unlike Wender s, included subjects without a childhood history of ADD with hyperactivity and without
current hyperactivity. Mattes sample, also unlike Wender s, included patients with borderline personality
disorder or substance abuse. Wender s sample had higher parent ratings of childhood hyperactivity.
Finally, Mattes used only two daily doses of methylphenidate, leaving much of the day uncovered by
medication, while Wender and colleagues used more frequent divided doses. Spencer et al., (1995b),
using TID doses of methylphenidate up to 1 mg/kg/day in adults with full DSM-III-R ADHD (including
childhood history), found a 78% positive response rate, compared to a 4% rate with placebo. Response
was independent of lifetime comorbidity. In a sample of 120 adult ADHD methylphenidate-responders
followed openly for a year, nearly all continued to improve. Patients who had placebo substituted in a
double-blind protocol experienced a recurrence of the original symptoms (Wender, 1995).
Controlled trials of dextroamphetamine in adults are lacking, although anecdotal reports suggest
that it may be useful and does not produce euphoria (Wender et al., 1985b). The only parallel, betweengroups, double-blind, placebo-controlled trial of pemoline with adults (Wender et al., 1981) found positive
response, consisting of reduction in hyperactivity, attention difficulties, hot temper, impulsivity, and
intolerance of stress, but only in subjects with clear parent ratings of childhood hyperactivity. Subjects
varied almost tenfold in the dose of pemoline that was tolerated and effective.
Adults are more sensitive than are children to both the therapeutic and side effects of stimulants.
As a result, similar absolute doses are commonly used. For methylphenidate, the common range is 20 to
80 mg/day, although some adults may respond to as low as 2 mg/day. The usual starting dose is 10 mg
BID. Methylphenidate typically requires 3 or 4 doses per day, but some adults may require as many as 6
daily doses, because the duration of action of a single dose may be as short as 2 hours. The sustained
release form may be useful. Dextroamphetamine appears to have a longer duration of action than
methylphenidate. The usual dose range is 10 to 40 mg per day, in divided doses. Some adults cannot
tolerate the spansule because initial rapid absorption can result in excessive side effects, and the long
duration of action may cause insomnia (Wender et al., 1985b). Due to slower hepatic metabolism,
pemoline is given in lower mg/kg doses to adults than to children and appears to have a longer duration of
action in adults. Pemoline has a dose range of 37.5 to 150 mg/day, in a single daily dose or divided into two
doses. It is typically titrated up from 18.75 mg/day. Liver function should be assessed prior to starting
medication. Patients should be alerted to report any symptoms of nausea, vomiting, malaise, lethargy, or
jaundice so that liver function can be evaluated for possible hepatitis.
Adults and children experience similar side effects from stimulants, although adults appear to be
more sensitive than children. Hypertension is more of a concern, and as many as 2% to 3% of adults are
reported to develop abnormalities in liver enzymes from pemoline (Wender et al., 1985b).
Tricyclic Antidepressants (TCAs)
1997 AACAP
34
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
There is only one placebo-controlled study of these drugs in adults. Desipramine in doses of up to
200 mg daily was significantly more effective than placebo in ameliorating the core symptoms of ADHD
(Wilens et al., 1995a). Anecdotal reports have conflicting results. A systematic retrospective chart review
of 37 adult ADHD patients being treated with desipramine or nortriptyline (nearly 84% were also receiving
stimulants) demonstrated clinical improvement in a substantial portion (Wilens et al., 1995a). The onset of
action is more rapid than when TCAs are used to treat depression. Some patients require antidepressant
doses (Wilens et al., 1995), while others respond to doses as low as 10 to 50 mg per day (Ratey et al.,
1992). TCA serum levels do not appear to be helpful in titrating effective dose in ADHD, although they may
identify toxicity.
Other Antidepressants
The MAOI pargyline was useful in an open trial (Wender et al., 1983), but orthostatic hypotension
and interactions with other drugs and with foods are problematic. Response may not be sustained
(Wender, 1995). In one open trial of bupropion (Wender and Reimherr, 1990), 75% had moderate to
marked benefit, and 70% of those preferred bupropion to their previous stimulant or antidepressant
medication. Bupropion caused intolerable agitation in 25% of the subjects, however. Only anecdotal data
are available on fluoxetine, but some clinicians are using it alone or together with methylphenidate. Clinical
experience does not support the efficacy of SSRIs in improving core ADHD symptoms (Wilens et al.,
1995d), but there are suggestions of usefulness in the treatment of comorbid or secondary mood and
anxiety symptoms and lability (Adler et al., 1995; Reimherr et al., 1995; Wilens et al., 1994). Venlafaxine,
an SSRI, which also has noradrenergic properties, has been suggested by open trials and case reports as
potentially helpful (Findling et al., 1996; Hedges et al., 1995; Wilens et al., 1995c). In one series the rate of
unacceptable side effects appeared to be high (Reimherr et al., 1995).
Other Drugs
A single case report of an open trial suggested consideration of buspirone (Balon, 1990). One
open study of propranolol (Mattes, 1986) was promising in young adults with childhood histories consistent
with ADD and current temper outbursts, excitability, impulsivity, and poor concentration.
Polypharmacy is common in clinical practice (Wilens et al., 1995d), but there are no systematic
data regarding either safety or efficacy.
PSYCHOSOCIAL INTERVENTIONS
The data on psychosocial interventions in the treatment of adults with ADHD are entirely anecdotal.
Wender (1995) notes that psychotherapy is unlikely to be successful without pharmacotherapy, but this is
not a unanimous opinion (Hallowell and Ratey, 1994). Without appropriate medication, cognitive therapies
may be ineffective and psychodynamic psychotherapy even harmful (Ratey et al., 1992).
Ratey and colleagues (1992) have suggested a psychoeducational therapeutic model that first
identifies deficits characteristic of ADHD and how they affect the patient and his/her significant others.
Efforts are then made to reduce the patient s self-blame, to increase awareness of these deficits as they
occur, and to devise coping strategies by building on the patient s strengths and maximizing the fit
between capabilities and environmental demands. Cognitive remediation (Weinstein, 1994) includes direct
teaching and practice of techniques to enhance attention, memory, problem solving, and family
1997 AACAP
35
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
relationships. Teaching of time management and self-organizational skills and anger-control methods may
be useful (Kane et al., 1990). Coaching (Hallowell and Ratey, 1994), an adjunctive treatment, is the use
of a specifically trained person who may or may not be a clinician to provide daily encouragement and
assistance in setting, prioritizing, evaluating progress toward goals. Adults with ADHD often have
secondary deficits due to years of functioning without diagnosis or treatment. Specific deficiencies in
education, vocational skills, or social skills should be addressed. Family therapy may be helpful in
addressing the chaotic relationships that often result from ADHD.
LIMITATIONS IN RESEARCH
Although ADHD is the most studied disorder in child psychiatry, there are many questions related
to clinical practice for which there are few scientific data. The investigators in the NIMH Collaborative
Multisite Multimodal Treatment Study of Children with ADHD summarized the problem as follows: ...
There is an insufficient basis for answering the following manifold question: under what circumstances and
with what child characteristics (comorbid conditions, gender, family history, home environment, age,
nutritional/metabolic status, etc.) do which treatments or combinations of treatment (stimulants, behavior
therapy, parent training, school-based intervention) have what impacts (improvement, stasis, deterioration)
on what domains of child functioning (cognitive, academic, behavioral, neurophysiological,
neuropsychological, peer relations, family relations), for how long (short versus long term), to what extent
(effect sizes, normal versus pathological range), and why (processes underlying change)? (Richters et al.,
1995, page 987). Unlike many other diagnoses where extrapolation is from adults to children, in ADHD the
most is known about hyperactive boys aged 6 to 12 years. There are virtually no data on treatment of
DSM-IV predominantly inattentive type. Girls are under-represented in research, and remarkably few
studies focus on preschoolers, adolescents, or adults. The preponderance of the psychopharmacological
research has focused on stimulants, especially methylphenidate and dextroamphetamine, and many
studies have been only weeks or months in duration. Multimodal treatment studies are difficult and
expensive. Because ADHD is a chronic condition, long-term controlled studies are essential, but almost
impossible to conduct. It is only recently that there has been some uniformity in the reporting of subject
characteristics and in the use of reproducible diagnostic methods. There is extensive comorbidity,
especially with other disruptive behavior disorders in studies that used the Conners Teacher Report as a
selection criterion (Loney and Milich, 1982). Studies that have closely examined individual outcome find
extensive variability in response between subjects and among measures of different domains of functioning
in each subject (Rapport et al., 1986). Problems with existing outcome studies include inappropriate
control groups (e.g. use of drop-outs from treatment as controls or non-random assignment of the more
severe cases to medication treatment); short duration of treatment; premature drug discontinuation;
excessive, inadequate, or poorly timed doses of medication; questionable compliance with medication; lack
of attention to individual variation in response; insensitive outcome measures; and no treatment of
associated academic, social, or family problems (Pelham 1983). None of the existing treatment studies
have documented adequate compliance over time.
CONFLICT OF INTEREST
As a matter of policy, some of the authors to these practice parameters are in active clinical
1997 AACAP
36
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
practice and may have received income related to treatments discussed in these parameters. Some
authors may be involved primarily in research or other academic endeavors and also may have received
income related to treatments discussed in these parameters. To minimize the potential for these
parameters to contain biased recommendations due to conflict of interest, the parameters were reviewed
extensively by Work Group members, consultants, and Academy members; authors and reviewers were
asked to base their recommendations on an objective evaluation of the available evidence; and authors
and reviewers who believed that they might have a conflict of interest that would bias, or appear to bias,
their work on these parameters were asked to notify the Academy.
SCIENTIFIC DATA AND CLINICAL CONSENSUS
1997 AACAP
37
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Practice parameters are strategies for patient management, developed to assist clinicians in
psychiatric decision-making. These parameters, based on evaluation of the scientific literature and relevant
clinical consensus, describe generally accepted approaches to assess and treat specific disorders, or to
perform specific medical procedures. The validity of scientific findings was judged by design, sample
selection and size, inclusion of comparison groups, generalizability, and agreement with other studies.
Clinical consensus was obtained through extensive review by the members of the Work Group on Quality
Issues, child and adolescent psychiatry consultants with expertise in the content area, the entire Academy
membership, and the Academy Assembly and Council.
These parameters are not intended to define the standard of care; nor should they be deemed
inclusive of all proper methods of care or exclusive of other methods of care directed at obtaining the
desired results. The ultimate judgment regarding the care of a particular patient must be made by the
clinician in light of all the circumstances presented by the patient and his or her family, the diagnostic and
treatment options available, and available resources. Given inevitable changes in scientific information and
technology, these parameters will be reviewed periodically and updated when appropriate.
1997 AACAP
38
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
OUTLINE OF PRACTICE PARAMETERS FOR THE ASSESSMENT AND TREATMENT OF CHILDREN,
ADOLESCENTS, AND ADULTS
WITH ATTENTION-DEFICIT/HYPERACTIVITY DISORDER
CHILDREN AGED 6 TO 12 YEARS
1.
Initial evaluation (a complete psychiatric assessment is indicated; see Practice Parameters
for the Psychiatric Assessment of Children and Adolescents [American Academy of
Child and Adolescent Psychiatry, 1995])
1.
Interview with parents
1.
Child s history
1.
Developmental history
2.
DSM-IV symptoms of ADHD
i.
Presence or absence (may use symptom or criterion
checklist)
ii.
Development and context of symptoms and resulting
impairment, including school
(learning, academic productivity, and behavior), family,
peers
3.
DSM-IV symptoms of possible alternate or comorbid psychiatric
diagnoses
4.
History of psychiatric, psychological, pediatric, or neurological
treatment for ADHD; details of medication trials
5.
Areas of relative strength (e.g., talents and abilities)
6.
Medical history
i.
Medical or neurological primary diagnosis (e.g., fetal
alcohol syndrome, lead intoxication, thyroid disease,
seizure disorder, migraine, head trauma, genetic or
metabolic disorder, primary sleep disorder)
ii.
Medications that could cause symptoms (e.g.,
phenobarbital, antihistamines, theophylline,
sympathomimetics, steroids)
2.
2.
3.
1997 AACAP
Family history
1.
ADHD, tic disorders, substance use disorders, conduct disorder,
personality disorders, mood disorders, obsessive compulsive
disorder and other anxiety disorders, schizophrenia
2.
Developmental and learning disorders
3.
Family coping style, level of organization, and resources
4.
Past and present family stressors, crises, changes in family
constellation
5.
Abuse or neglect
Standardized rating scales completed by parents
School information from as many current and past teachers as possible
1.
Standardized rating scales
39
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
2.
3.
4.
5.
6.
7.
1997 AACAP
Verbal reports of learning, academic productivity, and behavior
Testing reports (e.g. standardized group achievement tests; individual
evaluations)
4.
Grade and attendance records
5.
Individual Educational Plan, if applicable
6.
Observations at school if feasible and if case is complex
Child diagnostic interview: history and mental status examination
1.
ADHD symptoms (note: may not be observable during interview and may
be denied by child)
2.
Oppositional behavior
3.
Aggressive behavior
4.
Mood and affect
5.
Anxiety
6.
Obsessions or compulsions
7.
Form, content, and logic of thinking and perception
8.
Fine and gross motor coordination
9.
Tics, stereotypes, or mannerisms
10.
Speech and language abilities
11.
Clinical estimate of intelligence
Family diagnostic interview
1.
Patient s behavior with parents and siblings
2.
Parental interventions and results
Physical evaluation
1.
Medical history and examination within 12 months or more recently if
clinical condition has changed
2.
Documentation of health history, immunizations, screening for lead level,
etc.
3.
Measurement of lead level (if not done already) only if history suggests
pica or environmental exposure
4.
Documentation or evaluation of visual acuity
5.
Documentation or evaluation of hearing acuity
6.
Further medical or neurological evaluation as indicated
7.
In preparation for pharmacotherapy
1.
Baseline documentation of height, weight, vital signs, abnormal
movements
2.
ECG before tricyclic antidepressant or clonidine
3.
Consider EEG before tricyclic antidepressant or bupropion, if
indicated
4.
Liver function studies before pemoline
Referral for additional evaluations if indicated
1.
Psychoeducational evaluation (individually administered)
40
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
2.
3.
4.
1.
IQ
2.
Academic achievement
3.
Learning disorders
2.
Neuropsychological testing
3.
Speech and language evaluation
4.
Occupational therapy evaluation
5.
Recreational therapy evaluation
Psychiatric differential diagnosis
1.
Oppositional defiant disorder
2.
Conduct disorder
3.
Mood disorders -- depression or mania
4.
Anxiety disorders
5.
Tic disorder (including Tourette s disorder)
6.
Pica
7.
Substance use disorder
8.
Learning disorder
9.
Pervasive developmental disorder
10.
Mental retardation or borderline intellectual functioning
Treatment planning
1.
Establish target symptoms and baseline impairment (rating scales may be useful)
2.
Consider treatment for comorbid conditions
3.
Prioritize modalities to fit target symptoms and available resources
1.
Education about ADHD
2.
Classroom placement and resources
3.
Medication
4.
Other modalities may assist with remaining target symptoms
4.
Monitor multiple domains of functioning
1.
Learning in key subjects (achievement tests, classroom tests, homework,
class work)
2.
Academic productivity (homework, class work)
3.
Emotional functioning
4.
Family interactions
5.
Peer relationships
6.
If on medication, appropriate monitoring of height, weight, vital signs,
relevant laboratory parameters
5.
Re-evaluate efficacy and need for additional interventions
6.
Maintain long-term supportive contact with patient, family, and school
1.
Assure compliance with treatment
2.
Address problems at new developmental stages or in response to family or
environmental changes
Treatment
1.
Education of parents, child, other significant adults
2.
School interventions
1997 AACAP
41
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
1.
Assure appropriate class placement and availability of needed resources
(e.g., tutoring)
2.
3.
4.
5.
6.
7.
Consult or collaborate with teachers and other school personnel
1.
Information about ADHD
2.
Educational techniques
3.
Behavior management
3.
Direct behavior modification program when possible, and if problems are
severe in school setting
Medication
1.
Stimulants
2.
Bupropion
3.
Tricyclic antidepressants
4.
Other antidepressants
5.
Clonidine or guanfacine (primarily as an adjunct to a stimulant)
6.
Neuroleptics -- risks usually exceed benefits in treatment of ADHD;
consider carefully before use
7.
Anticonvulsants -- few data support use in the absence of seizure disorder
or brain damage
Psychosocial interventions
1.
Parent behavior modification training
2.
Referral to parent support group, such as CHADD
3.
Family psychotherapy if family dysfunction is present
4.
Social skills group therapy for peer problems
5.
Individual therapy for comorbid problems, not core ADHD
6.
Summer day treatment
Ancillary treatments
1.
Speech and language therapy
2.
Occupational therapy
3.
Recreational therapy
Dietary treatment rarely useful
Other treatments are outside the realm of the usual practice of child and
adolescent psychiatry and are not recommended
CHILDREN AGED 3 TO 5 YEARS
Same protocol as above, except:
5.
Evaluation
1.
Higher index of suspicion for neglect, abuse, or other environmental factors
2.
More likely to require lead level evaluation
3.
More likely to require evaluation of
1.
Speech and language disorders
1997 AACAP
42
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
6.
2.
Cognitive development
Treatment
1.
Increased emphasis on parent training
2.
Highly structured preschool
3.
Additive-free diet may occasionally be useful
4.
If medications are used, exercise more caution, use lower doses, and monitor
more frequently
ADOLESCENTS
Same protocol as children aged 6 to 12 years, except:
7.
Higher index of suspicion for comorbidity with
1.
Conduct disorder
2.
Substance use disorder
3.
Suicidality
8.
Teacher reports less useful in middle and high school than in grammar school
9.
Patient must participate actively in treatment
10.
Increased risk of medication abuse by patient or peers
11.
Greater need for vocational evaluation, counseling, or training
12.
Evaluate patient s save driving practices
ADULTS
13.
Initial evaluation (a complete psychiatric assessment is indicated; see APA Practice
Guideline for Psychiatric Evaluation of Adults [1995])
1.
Interview with patient
1.
Developmental history
2.
Present and past DSM-IV symptoms of ADHD (may use symptom or
criterion checklist or self-report form)
3.
History of development and context of symptoms and resulting past and
present impairment
a.
school (learning, academic productivity, and behavior)
b.
work
c.
family
d.
peers
4.
History of other psychiatric disorders
5.
History of psychiatric treatment
6.
DSM-IV symptoms of possible alternate or comorbid psychiatric
diagnoses, especially
1.
Personality disorder
2.
Mood disorders -- depression or mania
3.
Anxiety disorders
4.
Dissociative disorder
5.
Tic disorder (including Tourette s disorder)
6.
Substance use disorder
1997 AACAP
43
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
14.
7.
Learning disorders
7.
Strengths (e.g., talents and abilities)
8.
Mental status examination
2.
Standardized rating scales completed by patient s parent
3.
Medical history
1.
Medical or neurological primary diagnosis (e.g., thyroid disease, seizure
disorder, migraine, head trauma)
2.
Medications that could be causing symptoms (e.g., phenobarbital,
antihistamines, theophylline, sympathomimetics, steroids)
4.
Family history
1.
ADHD, tic disorders, substance use disorders, conduct disorder,
personality disorders, mood disorders, anxiety disorders
2.
Developmental and learning disorders
3.
Family coping style, level of organization, and resources
4.
Family stressors
5.
Abuse or neglect (as victim or perpetrator)
5.
Interview with significant other or parent, if available
6.
Physical evaluation
1.
Examination within 12 months or more recently if clinical condition has
changed
2.
Further medical or neurological evaluation as indicated
7.
School information
1.
Standardized rating scales if done in childhood
2.
Narrative childhood reports regarding learning, academic productivity,
and behavior
3.
Reports of testing (e.g., standardized group achievement tests and
individual evaluations)
4.
Grades and attendance records
8.
Referral for additional evaluations if indicated
1.
Psychoeducational evaluation
1.
IQ
2.
Academic achievement
3.
Learning disorders evaluation
2.
Neuropsychological testing
3.
Vocational evaluation
Treatment planning
1.
Establish target symptoms of ADHD and baseline levels of impairment
2.
Consider treatment for comorbid conditions (monitor possible drug-seeking
behavior)
3.
Prioritize modalities to fit target symptoms and available resources
4.
1997 AACAP
Monitor multiple domains of functioning
44
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
15.
1.
Academic or vocational
2.
Daily living skills
3.
Emotional adjustment
4.
Family interactions
5.
Social relationships
6.
Medication response
5.
Re-evaluate periodically the efficacy of and need for additional interventions
6.
Maintain long-term supportive contact with patient and family to assure
compliance with treatment and to address new problems that arise
Treatment
1.
Education for patient, spouse, or other significant adults
2.
Consideration of vocational evaluation, counseling, or training
3.
Medication
1.
Stimulants
2.
Tricyclic antidepressants
3.
Other antidepressants
4.
Other drugs (buspirone, propranolol)
4.
Psychosocial interventions
1.
Individ
2.
Family psychotherapy if family dysfunction is present
3.
Referral to support group, such as CHADD
5.
Other treatments are outside the realm of the usual practice of psychiatry and are
not recommended
1997 AACAP
45
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
REFERENCES
References that are particularly recommended are marked with an asterisk (*).
Abikoff H (1981), Interaction of Ritalin and multimodal therapy in the treatment of attention deficit hyperactive behavior disorder.
In: Greenhill LL, Osman BB: Ritalin: Theory and Patient Management. New York, Mary Ann Liebert, Inc, pp 147-154
*Abikoff H (1985), Efficacy of cognitive training interventions in hyperactive children: a critical review. Clinical Psychology Review
5:479-512
Abikoff H (1991), Cognitive training in ADHD children: Less to it than meets the eye. Journal of Learn Disabil 24:205-209
Abikoff H, Courtney M, Pelham WE, Koplewicz HS (1993), Teachers ratings of disruptive behaviors: the influence of halo
effects. J Abnorm Child Psychol 21:519-533
Abikoff H, Ganeles D, Reiter G, Blum C, Foley C, Klein RG (1988), Cognitive training in academically deficient ADDH boys
receiving stimulant medication. J Abnorm Child Psychol 16:411-432
Abikoff H, Gittelman R (1984), Does behavior therapy normalize the classroom behavor of hyperactive children? Arch Gen
Psychiatry 41:449-454
Abikoff H, Gittelman R (1985a), Hyperactive children treated with stimulants: is cognitive training a useful adjunct? Arch Gen
Psychiatry 42:953-961
Abikoff H, Gittelman R (1985b), The normalizing effects of methylphenidate on the classroom behavior of ADDH children. J
Abnorm Child Psychol 13:33-44
Abikoff H, Hechtman L (in press), Multimodal therapy and stimulants in the treatment of children with ADHD. In Psychosocial
Treatment for Child and Adolescent Disorders: Empirically Based Approaches, Jensen P, Hibbs ED, eds. Washington
DC: American Psychological Association
Abikoff H, Klein RG (1992), Attention-deficit hyperactivity and conduct disorder: comorbidity and implications for treatment. J
Consult Clin Psychol 60:881-892
*Abramowitz AJ (1994), Classroom interventions for disruptive behavior disorders. Child and Adolescent Psychiatric Clinics of
North America 3:343-360
Abramowitz AJ, Eckstrand D, O Leary SG, Dulcan MK (1992), ADHD children s responses to stimulant medication and two
intensities of a behavioral intervention. Behav Modif 16:193-203
*Abramowitz AJ, O'Leary SG (1991), Behavioral interventions for the classroom: implications for students with ADHD. School
Psychology Review 20:220-234
Achenbach TM (1991a), Integrative Guide for the 1991 CBCL/4-18, YSR, and TRF Profiles. Burlington, VT: University of
Vermont Department of Psychiatry
Achenbach TM (1991b), Manual for the Teacher's Report Form and 1991 Profile. Burlington, VT: University of Vermont
Department of Psychiatry
Adler LA, Resnick S, Kunz M, Devinsky O (1995), Open-label trial of venlafaxine (Effexor) in attention deficit disorder.
Psychopharmacol Bull 31:544
Ahmann PA, Waltonen SJ, Olson KA, Theye FW, Van Erem AJ, LaPlant RJ (1993), Placebo-controlled evaluation of Ritalin side
effects. Pediatrics 91:1101-1106
Ajibola O, Clement PW (1995), Differential effects of methylphenidate and self-reinforcement on attention-deficit hyperactivity
disorder. Behav Modif 19:211-233
Alessandri SM, Schramm K (1991), Effects of dextroamphetamine on the cognitive and social play of a preschooler with ADHD.
J Am Acad Child Adolesc Psychiatry 30:768-772
Aman MG, Kern RA, McGhee DE, Arnold LE (1993a), Fenfluramine and methylphenidate in children with mental retardation and
ADHD: clinical and side effects. J Am Acad Child Adolesc Psychiatry 32:851-859
Aman MG, Kern RA, McGhee DE, Arnold LE (1993b), Fenfluramine and methylphenidate in children with mental retardation and
attention deficit hyperactivity disorder: laboratory effects. J Autism Devel Disorders 23:491-506
Aman MG, Marks RE, Turbott SH, Wilsher CP, Merry SN (1991), Clinical effects of methylphenidate and thioridazine in
intellectually subaverage children. J Am Acad Child Adolesc Psychiatry 30:246-256
Aman MG, Turbott SH (1991), Prediction of clinical response in children taking methylphenidate. J Autism Dev Disord 21:211228
1997 AACAP
46
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
American Psychiatric Association (1980), Diagnostic and Statistical Manual of Mental Disorders, 3rd Ed. Washington, DC:
American Psychiatric Association
American Psychiatric Association (1987), Diagnostic and Statistical Manual of Mental Disorders, 3rd Ed - Revised. Washington,
DC: American Psychiatric Association
American Psychiatric Association (1994), Diagnostic and Statistical Manual of Mental Disorders, 4th Ed. Washington, DC:
American Psychiatric Association
American Psychiatric Association Work Group on Psychiatric Evaluation of Adults (1995), Practice guideline for psychiatric
evaluation of adults. Am J Psychiatry 152(supplement): 63-80
Anastopoulos AD, Shelton TL, DuPaul GJ, Guevremont DC (1993), Parent training for attention-deficit hyperactivity disorder: its
impact on parent functioning. J Abnorm Child Psychol 21:581-96
Anderson JC, Williams S, McGeeR, Silva PA (1987), DSM-III disorders in preadolescent children: prevalence in a large sample
from the general population. Arch Gen Psychiatry 44:69-76
Atkins MS, Pelham WE, Licht MH (1988), The development and validation of objective classroom measures for conduct and
attention deficit disorders. In: Advances in Behavioral Assessment of Children and Families 4:3-31
Ayllon T, Rosenbaum MS (1977), The behavioral treatment of disruption and hyperactivity in school settings. In: Advances in
Clinical Child Psychology, Lahey BB, Kazdin AE, eds. New York: Plenum Press, pp 83-118
Balon R (1990), Buspirone for Attention Deficit Hyperactivity Disorder? Journal of Clin Psychopharmacol 10:77
*Barkley RA (1976), Predicting the response of hyperkinetic children to stimulant drugs: a review. J Abnorm Child Psychol
4:327-348
Barkley RA (1977), A review of stimulant drug research with hyperactive children. J Child Psychol Psychiatry 18:137-165
Barkley RA (1987), Defiant Children: A Clinician s Manual for Parent Training. New York: Guilford Press
Barkley RA (1988), The effects of methylphenidate on the interactions of preschool ADHD children with their mothers. J Am Acad
Child Adolesc Psychiatry 27:336-341
*Barkley RA (1990), Attention Deficit Hyperactivity Disorder: A Handbook for Diagnosis and Treatment. New York: Guilford
Press
Barkley RA (1991), The ecological validity of laboratory and analogue assessment methods of ADHD symptoms. J Abnorm
Child Psychol 19:149-178
Barkley RA (1994), Impaired delayed responding: a unified theory of attention-defict hyperactivity disorder. In: Disruptive
Behavior Disorders in Childhood, Routh DK, ed. New York: Plenum Press, pp 11-57
Barkley RA, Cunningham CE (1980), The parent-child interactions of hyperactive children and their modification by stimulant
drugs. In: Treatment of Hyperactive and Learning Disabled Children. Knights R, Bakker D, eds. Baltimore: University
Park Press, pp 219-236
Barkley RA, Fischer M, Edelbrock CS, Smallish L (1990a), The adolescent outcome of hyperactive children diagnosed by
research criteria: I. An 8-year prospective follow-up study. J Am Acad Child Adolesc Psychiatry 29:546-557
Barkley RA, Fischer M, Newby RF, Breen MJ (1988), Development of a multimethod clinical protocol for assessing stimulant
drug response in children with attention deficit disorder. Journal of Clinical Child Psychology 17:14-24
Barkley RA, Grodzinsky GM (1994), Are tests of frontal lobe functions useful in the diagnosis of attention deficit disorders?
Clinical Neuropsychologist 8:121-139
Barkely RA, Guevremont DC, Anastopoulos AD, DuPaul GJ, Shelton TL (1993), Driving-related risks and outcomes of attention
deficit hyperactivity disorder in adolescents and young adults: a 3- to 5- year follow-up survey. Pediatrics 92:212-218
Barkley RA, Guevremont DC, Anastopoulos AD, Fletcher KE (1992), A comparison of three family therapy programs for treating
family conflicts in adolescents with ADHD. J Consult Cin Psychol 60:450-462
Barkley RA, McMurray MB, Edelbrock CS, Robbins K (1990b), Side effects of methylphenidate in children with attention deficit
hyperactivity disorder: a systemic, placebo-controlled evaluation. Pediatrics 86:184-192
Barkley RA, McMurray MB, Edelbrock CS, Robbins K (1989), The response of aggressive and nonaggressive ADHD children to
two doses of methylphenidate. J Am Acad Child Adolesc Psychiatry 28:873-881
Barrickman L, Noyes R, Kuperman S, Schumacher E, Verda M (1991), Treatment of ADHD with fluoxetine: A preliminary trial. J
Am Acad Child Adolesc Psychiatry 30:762-767
Barrickman LL, Perry PJ, Allen AJ, Kuperman S, Arndt SV, Herrmann KJ, Schumacher E (1995), Bupropion versus
methylphenidate in the treatment of attention deficit hyperactivity disorder. J Am Acad Child Adolesc Psychiatry
35:649-657
1997 AACAP
47
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Bartels MG, Varley CK, Mitchell J, Stamm SJ (1991), Pediatric cardiovascular effects of imipramine and desipramine. J Am Acad
Child Adolesc Psychiatry 30:100-103
Baumgaertel A, Wolraich ML, Dietrich M (1995), Attention deficit disorders in a German elementary school-aged sample. J Am
Acad Child Adolesc Psychiatry 34:629-638
Bender B, Milgrom H (1992), Theophylline-induced behavior change in children: An objective evaluation of parents perceptions.
JAMA 267:2621-2624
Berkovitch M, Pope E, Phillips J, Koren G (1995), Pemoline-associated fulminant liver failure: testing the evidence for causation.
Clinical Phamacology and Therapeutics 57:696-698
Biederman J (1991), Sudden death in children treated with a tricyclic antidepressant. J Amer Acad Child Adolesc Psychiatry
30:495-498
Biederman J, Baldessarini RJ, Goldblatt A, Lapey KA, Doyle A, Hesslein PS (1993a), A naturalistic study of 24-hour
electrocardiographic recordings and echocardiographic findings in children and adolescents treated with desipramine.
J Am Acad Child Adolesc Psychiatry 32:805-813
Biederman J, Baldessarini RJ, Wright V, Knee D, Harmatz JS (1989), A double-blind placebo controlled study of desipramine in
the treatment of ADD: I. Efficacy. J Am Acad Child Adolesc Psychiatry 28:777-784
Biederman J, Faraone SV, Doyle A, Lehman BK, Kraus I, Perrin J, Tsuang MT (1993b), Convergence of the Child Behavior
Checklist with structured interview-based psychiatric diagnoses of ADHD children with and without comorbidity. J
Child Psychol Psychiatry 34:1241-1251
Biederman J, Faraone S, Mick E, Wozniak J, Chen L, Ouellette C, Marrs A, Moore P, Garcia J, Mennin D, Lelon E (1996),
Attention-deficit hyperactivity disorder and juvenile mania: an overlooked comorbidity? J Am Acad Child Adolesc
Psychiatry 35:997-1008
Biederman J, Faraone S, Milberger S, Curtis S, Chen L, Marrs A, Ouellette C, Moore P, Spencer T (1996), Predictors of
persistence and remission of ADHD into adolescence: results from a four-year prospective follow-up study. J Am Acad
Child Adolesc Psychiatry 35:343-351
*Biederman J, Faraone SV, Spencer T, Wilens T, Norman D, Lapey KA, Mick E, Lehman BK, Doyle A (1993c), Patterns of
psychiatric comorbidity, cognition, and psychosocial functioning in adults with attention deficit hyperactivity disorder.
Am J Psychiatry 150:1792-1798
Biederman J, Newcorn J, Sprich S (1991), Comorbidity of attention deficit hyperactivity disorder with conduct, depressive,
anxiety, and other disorders. Am J Psychiatry 148:564-577
Biederman J, Thisted RA, Greenhill LL, Ryan ND (1995a), Estimation of the association between desipramine and the risk for
sudden death in 5- to 14-year old children. J Clin Psychiatry 56:87-93
Biederman J, Wilens T, Mick E, Milberger S, Spencer TJ, Faraone SV (1995b), Psychoactive substance use disorders in adults
with attention deficit hyperactivity disorder (ADHD): effects of ADHD and psychiaric comorbidity. Am J Psychiatry
152:1652-1658
Birmaher B, Greenhill L, Cooper T, Fried J, Maminski J (1989), Sustained release methylphenidate: pharmacokinetic studies in
ADDH males. J Am Acad Child Adolesc Psychiatry 28:768-772
Blechman EA (1981), Toward comprehensive behavioral family intervention: an algorithm for matching families and
interventions. Behav Modif 5:221-236
Borcherding BG, Keysor CS, Cooper TB, Rapoport JL (1989), Differential effects of methylphenidate and dextroamphetamine on
the motor activity level of hyperactive children. Neuropsychopharmacology 2:255-263
Borcherding BG, Keysor CS, Rapoport JL, Elia J, Amass J (1990), Motor/vocal tics and compulsive behaviors on stimulant
drugs: is there a common vulnerability? Psychiatry Research 33:83-94
Breen MJ (1989), Cognitive and behavioral differences in ADHD boys and girls. J Child Psychol Psychiatry 30:711-716
Briant RH (1978), An introduction to clinical pharmacology. In: Pediatric Psychopharmacology: The Use of Behavior Modifying
Drugs in Children. Werry JS, ed. New York: Brunner/Mazel, pp 3-28
Brown RT, Borden KA, Clingerman SR (1985), Pharmacotherapy in ADD adolescents with special attention to multimodality
treatments. Psychopharmacol Bull 21:192-211
Brown RT, Borden KA, Wynne ME, Spunt AL, Clingerman SR (1987), Compliance with pharmacological and cognitive
treatments for attention deficit disorder. J Am Acad Child Adolesc Psychiatry 26:521-526
Brown RT, Sexson SB (1988), A controlled trial of methylphenidate in Black adolescents: attentional, behavioral, and physiologic
effects. Clin Pediatr 27:74-81
1997 AACAP
48
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Brown RT, Sexson SB (1989), Effects of methylphenidate on cardiovascular responses in attention deficit hyperactivity
disordered adolescents. J Adolesc Health Care 10:179-183
Brown T (1996), Brown Attention Deficit Disorder Scales: Manual. San Antonio, TX: Psychological Corporation
Buchsbaum MS, Haier RJ, Sosteck AJ, Weingartner H, Zahn TO, Siever LJ, Murphy DL, Brody L (1985), Attention dysfunction
and psychopathology in college men. Arch Gen Psychiatry 42:354-360
Buitelaar JK, Van der Gaag RJ, Swaab-Barneveld H, Kuiper M (1995), Prediction of clinical response to methylphenidate in
children with attention-defict hyperactivity disorder. J Am Acad Child Adolesc Psychiatry 8:1025-1032
Burd L, Kerbeshian J, Fisher W (1987), Does the use of phenobarbital as an anticonvulsant permanently exacerbate
hyperactivity? Can J Psychiatry 32:10-13
Bussing R, Levin GM (1993), Methamphetamine and fluoxetine treatment of a child with attention-deficit hyperactivity disorder
and obsessive-compulsive disorder. Journal of Child and Adolescent Psychopharmacology, 3:53-58
Cameron J, Dupuis A (1991), The introduction of school mediation to New Zealand. Journal of Research Development
Education 24:1-13
*Campbell SB (1985), Hyperactivity in preschoolers: Correlates and prognostic implications. Clinical Psychology Review 5:405428
Cantwell DP, Swanson J, Connor D, Clonidine use in children. Submitted to J Am Acad Child Adolesc Psychiatry
Carlson CL, Pelham WE, Milich R, Dixon J (1992), Single and combined effects of methylphenidate and behavior therapy on the
classroom performance of children with attention-deficit hyperactivity disorder. J Abnorm Child Psychol 20:213-232
Carlson GA, Rapport MD, Kelly KL, Pataki CS (1995), Methylphenidate and desipramine in hospitalized children with comorbid
behavior and mood disorders: separate and combined effects on behavior and mood. Journal of Child and Adolescent
Psychopharmacology 5:191-204
Carroll KM, Rounsaville BJ (1993), History and significance of childhood attention deficit disorder in treatment-seeking cocaine
abusers. Compr Psychiatry 34:75-82
Chappel PB, Riddle MA, Scahill L, Lynch KA, Schultz R, Arnsten A, Leckman JF, Clay TH, Gualtieri CT, Evans RW, Gullion CM
(1988), Clinical and neuropsychological effects of the novel antidepressant bupropion. Psychopharmacology Bull
24:143-148
Chappell PB, Riddle MA, Scahill L, Lynch KA, Schultz R, Arnsten A, Leckman JF, Cohen DJ (1995), Guanfacine treatment of
comorbid attention-deficit hyperactivity disorder and Tourette s syndrome: preliminary clinical experience. J Am Acad
Child Adolesc Psychiatry 34:1140-1146
Chase SN, Clement PW (1985), Effects of self-reinforcement and stimulants on academic performance in children with attention
deficit disorder. Journal of Clinical Child Psychology 14:323-333
Cohen ML, Kelly PC, Atkinson AW (1989), Parent, teacher, child: a trilateral approach to attention deficit disorder. Am J Dis
Child 143:1229-1233
Cohen NJ, Sullivan J, Minde K, Novak C, Helwig C (1981), Evaluation of the relative effectiveness of methylphenidate and
cognitive behavior modification in the treatment of kindergarten-aged hyperactive children. J Abnorm Child Psychol
9:43-54
Cohen P, Cohen J, Kasen S, Velez CN, Hartmark C, Hohnson J, Rojas M, Brook J, Streuning EL (1993), An epidemiological
study of disorders in late childhood and adolescence. I. Age- and gender-specific prevalence. J Child Psychol
Psychiatry 34:851-867
Conners CK (1969), A teacher rating scale for use in drug studies with children. Am J Psychiatry 126:884-888
Conners CK (1975), Controlled trial of methylphenidate in preschool children with minimal brain dysfunction. International Journal
of Mental Health 4:61-74
Conners CK (1985), The computerized continuous performance test. Psychopharmacology Bull 21:891-892
Conners CK, Casat CD, Gualtieri CT, Weller E, Reader M, Reiss A, Weller RA, Khayrallah M, Ascher J (1996), Bupropion
hydrochloride in attention deficit disorder with hyperactivity. J Am Acad Child Adolesc Psychiatry 35:1314-1321
Conners CK, Kronsberg S (1985), Measuring activity level in children. Psychopharmacol Bull 21:893-897
*Conners CK, Wells KC, Erhardt D, March JS, Schulte A, Osborne S, Riore C, Butcher AT (1994), Multimodality therapies:
methodologic issues in research and practice. Child and Adolescent Psychiatry Clinics of North America 3:361-377
Cooper LJ, Wacker DP, Millard T, Derby KM, Cruikshank BM, Rogers L (1993), Assessing environmental and medication
variables in an outpatient setting: a proposed model and preliminary results with ADHD children. Journal of
Developmental and Physical Disabilities 5:71-84
1997 AACAP
49
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Corkum PV, Siegel LS (1993), Is the continuous performance task a valuable research tool for use with children with attentiondeficit-hyperactivity disorder? J Child Psychol Psychiatry 34:1217-1239
Cousins LS, Weiss G (1993), Parent training and social skills training for children with attention-deficit hyperactivity disorder: how
can they be combined for greater effectiveness? Can J Psychiatry 38:449-457
Creer LT, Gustafson KE (1989), Psychological problems associated with drug therapy in childhood asthma. J Pediatr 115:850855
Crumrine PK, Feldman HM, Teodori J, Handen BL, Alvin RM (1987), The use of methylphenidate in children with seizures and
attention deficit disorder. Ann Neurol 22:441-442
Dadds MR, Schwartz S, Sanders MR (1987), Marital discord and treatment outcome in behavioral treatment of child conduct
disorders. J Consult Clin Psychol 55:396-403
Daly JM, Fritsch SL (1995), Case study: maternal residual attention-defict disorder associated with failure to thrive in a twomonth-old infant. J Am Acad Child Adolesc Psychiatry 34:55-57
Diamond JM, Deane FP (1990), Conners Teacher's Questionnaire: effects and implications of frequent administration. Journal of
Clinical Child Psychology 19:202-204
Donnelly M, Rapoport JL (1985), Attention deficit disorders. In: Diagnosis and Psychopharmacology of Childhood and
Adolescent Disorders JM Weiner ed. New York: Wiley, pp 178-197
Donnelly M, Zametkin AJ, Rapoport JL, Ismond DR, Weingartner H, Lane E, Oliver J, Linnoila M, Potter WZ (1986), Treatment of
childhood hyperactivity with desipramine: plasma drug concentration, cardiovascular effects, plasma and urinary
catecholamine levels, and clinical response. Clin Phamacol Ther 39:72-81
Douglas VI, Parry P, Marton P, Garson C (1976), Assessment of a cognitive training program for hyperactive children. J
Abnorm Child Psychol 4:389-410
Dubey DR, O'Leary SG, Kaufman KF (1983), Training parents of hyperactive children in child management: a comparative
outcome study. J Abnorm Child Psychol 11:229-246
DuPaul GJ, Barkley RA (1993), Behavioral contributions to pharmacotherapy: The utility of behavioral methodology in medication
treatment of children with attention deficit hyperactivity disorder. Behavior Therapy 24:47-65
DuPaul GJ, Barkley RA, McMurray MB (1994), Response of children with ADHD to methylphenidate: interaction with internalizing
symptoms. J Am Acad Child Adolesc Psychiatry 33:894-903
DuPaul GJ, Rapport MD (1993), Does methylphenidate normalize the classroom performance of children with attention deficit
disorder? J Am Acad Child Adolesc Psychiatry 32:190-198
DuPaul GJ, Rapport MD, Perriello LM (1991), Teacher ratings of academic skills: the development of the Academic Performance
Rating Scale. School Psychology Review 20:284-300.
Edelbrock C, Costello AJ, Kessler MK (1984), Empirical corroboration of attention deficit disorder. J Am Acad Child Psychiatry
23:285-290
*Edelbrock C, Rancurello MD (1985), Childhood hyperactivity: An overview of rating scales and their applications. Clinical
Psychology Review 5:429-445
Edwards MC, Schulz EG, Long N (1995), The role of the family in the assessment of attention deficit hyperactivity disorder.
Clinical Psychology Review 15:375-394
*Elia J, Borcherding BG, Rapoport JL, Keysor CS (1991), Methylphenidate and dextroamphetamine treatments of hyperactivity:
are there true nonresponders? Psychiatry Research 36:141-155
Elia J, Gulotta C, Rose SR, Marin G, Rapoport J (1994), Thyroid function and attention-deficit hyperactivity disorder. J Am Acad
Child Adolesc Psychiatry 33:169-172
Erhardt D, Hinshaw SP (1994), Initial sociometric impressions of attention-deficit hyperactivity disorder and comparison boys:
predictions from social behaviors and from nonbehavioral variables. J Consult Clin Psychol 62:833-842
Ernst M, Liebenauer LL, Jons PH, Murphy DL, Zametkin AJ (1995), L-deprenyl on behavior and plasma monoamine metabolites
in hyperactive adults. Psychopharmacol Bull 31:565
Evans SW, Pelham WE (1991), Psychostimulant effects on academic and behavioral measures for ADHD junior high school
students in a lecture format classroom. J Abnorm Child Psychol 19:537-552
Evans SW, Vallano G, Pelham W (1994), Treatment of parenting behavior with a psychostimulant: a case study of an adult with
attention-deficit hyperactivity disorder. Journal of Child and Adolescent Psychopharmacology 4:63-69
Famularo R, Fenton T (1987), The effect of methylphenidate on school grades in children with Attention Deficit Disorder without
Hyperactivity: A preliminary report. J Clin Psychiatry 48:112-114
1997 AACAP
50
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
*Faraone SV, Biederman J (1994), Genetics of attention-deficit hyperactivity disorder. Child and Adolescent Psychiatric Clinics
of North America 3:285-301
Faraone SV, Biederman J, Lehman BK, Spencer T, Norman D, Seidman LJ, Kraus I, Perrin J, Chen WJ, Tsuang MT (1993),
Intellectual performance and school failure in children with attention defict hyperactivity disorder and in their siblings. J
Abnorm Psychol 102:616-623
Farrington DP, Loeber R, van Kammen WB (1990), Long-term criminal outcomes of hyperactivity-impulsivity-attention defict and
conduct problems in childhood. In: Straight and Devious Pathways to Adulthood, Robins LN, Rutter M, eds. New
York: Cambridge University Press, pp 62-81
Fenichel RR (1995), Combining methylphenidate and clonidine: the role of post-marketing surveillance. Journal of Child and
Adolescent Psychopharmacology 5:155-156
Findling RL, Schwartz, MA, Flannery DJ, Manos MJ (1996), Venlafaxine in adults with attention-deficity
disorder: an open
clinical trial. J Clin Psychiatry 57: 184-189
Fine S, Jewesson B (1989), Active drug placebo trial of methylphenidate: a clinical service for children with an attention deficit
disorder. Can J Psychiatry 34:447-449
Fine S, Johnston C (1993), Drug and placebo side effects in methylphenidate-placebo trial for attention deficit hyperactivity
disorder. Child Psychiatry Hum Dev 24:25-30
Firestone P (1982), Factors associated with children s adherence to stimulant medication. Am J Orthopsychiatry 52:447-457
Firestone P, Kelly MJ, Goodman JT, Davey J (1981), Differential effects of parent training and stimulant medication with
hyperactives: a progress report. J Am Acad Child Psychiatry 20:135-147
*Fischer M, Barkley RA, Fletcher KE, Smallish L (1993), The adolescent outcome of hyperactive children: predictors of
psychiatric, academic, social, and emotional adjustment. J Am Acad Child Adolesc Psychiatry 32:324-332
*Fischer M, Newby RF (1991), Assessment of stimulant response in ADHD children using a refined multimethod clinical protocol.
Journal of Clinical Child Psychology 20:232-244
Fitzpatrick PA, Klorman F, Brumaghim JT, Borgstedt AD (1992), Effects of sustained-release and standard preparations of
methylphenidate on attention deficit disorder. J Am Acad Child Adolesc Psychiatry 31:226-234
Fletcher SE, Case CL, Sallee FR, Hand LD, Gillette PC (1993), Prospective study of the electrocardiographic effects of
imipramine in children. J Pediatr 122:652-654
Forehand RL, McMahon RJ (1981), Helping the Noncompliant Child: A Clinician's Guide to Parent Training. New York: The
Guilford Press
Fristad MA, Weller RA, Weller EB (1995), The Mania Rating Scale (MRS): further reliability and validity studies with children. Ann
Clin Psychiatry 7:127-132
Gadow KD (1992), Pediatric psychopharmacology: a review of recent research. J Child Psychol Psychiatry 33:153-195
Gadow KD, Nolan EE, Paolicelli LM, Sprafkin J (1991), A procedure for assessing the effects of methylphenidate on hyperactive
children in public school settings. Journal of Clinical Child Psychology 20:268-276
Gadow KD, Nolan EE, Sverd J (1992a), Methylphenidate in hyperactive boys with comorbid tic disorder: II. Short-term behavioral
effects in school settings. J Am Acad Child Adolesc Psychiatry 31:462-471
Gadow KD, Nolan EE, Sverd J, Sprafkin J, Paolicelli L (1990), Methylphenidate in aggressive-hyperactive boys: I. Effects on
peer aggression in public school settings. J Am Acad Child Adolesc Psychiatry 29:710-718
Gadow KD, Pomeroy JC, Nolan EE (1992b), A procedure for monitoring stimulant medication in hyperactive mentally retarded
school children. J of Child and Adolescent Psychopharmacology 2:131-143
Gadow KD, Sprafkin J, Nolan EE (1996), ADHD School Observation Code. Stony Brook, NY: Checkmate Plus.
Gadow KD, Swanson HL (1985), Assessing drug effects on academic performance. Psychopharmacol Bull 21:877-886
Gadow KD, Sverd J, Sprafkin J, Nolan EE, Ezor SN (1995), Efficacy of methylphenidate for attention-deficit hyperactivity disorder
in children with tic disorder. Arch Gen Psychiatry 52:444-455
Gammon GD, Brown TE (1993), Fluoxetine and methylphenidate in combination for treatment of attention deficit disorder and
comorbid depressive disorder. Journal of Child and Adolescent Psychopharmacology, 3:1-10
Gammon GD, Brown TE, Barua G (1991), Fluoxetine augmentation of methylphenidate for attention deficit and comorbid
disorders. Presented at American Academy of Child and Adolescent Psychiatry Annual Meeting, 1991
Gan J, Cantwell DP (1982), Dosage effects of methylphenidate on paired associate learning: positive/negative placebo
responders. J Am Acad Child Psychiatry 21:237-242
1997 AACAP
51
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Garfinkel BD, Wender PH, Sloman L, O Neill I (1983), Tricyclic antidepressant and methylphenidate treatment of attention
deficit disorder in children. J Am Acad Child Psychiatry 4:343-348
Gaub M, Carlson CL (in press), Gender differencs in ADHD: a meta-analysis and critical review. J Am Acad Child Adolesc
Psychiatry
Gittelman R, Abikoff H, Pollack E, Klein DF, Katz S, Mattes J (1980), A controlled trial of behavior modification and
methylphenidate in hyperactive children. In: Hyperactive Children: The Social Ecology of Identification and Treatment.
Whalen CK, Henker B, eds. New York: Academic Press, pp 221-243
Gittelman R, Mannuzza S, Shenker R, Bonagura N (1985), Hyperactive boys almost grown up: I. Psychiatric status. Arch Gen
Psychiatry 42:937-947
Golinko BE (1982), Side effects of dexedrine in hyperactive children: operationalization and quantification in a short-term trial.
Prog Neuropsychopharmacol Biol Psychiatry 6:175-183
Goyette CH, Conners CK, Ulrich RF (1978), Normative data on Revised Conners Parent and Teacher Rating Scales. J Abnorm
Child Psychol 221-236
*Green WH (1995), The treatment of attention-deficit hyperactivity disorder with nonstimulant medications. Child and Adolescent
Psychiatric Clinics of North America 4:169-195
Greenberg LM, Waldman ID (1993), Developmental normative data on the Test of Variables of Attention (TOVA). J Child
Psychol Psychiatry 34:1019-1030
Greenhill LL (1981), Stimulant-related growth inhibition in children: a review. In: Strategic Interventions for Hyperactive Children.
Gittleman M, ed. New York: ME Sharp, pp 39-63
*Greenhill LL (1995), Attention-deficit hyperactivity disorder: the stimulants. Child and Adolescent Psychiatric Clinics of North
America 4:123-168
*Greenhill LL, Osman BB (1981), Ritalin: Theory and Patient Management. New York: Mary Ann Liebert, Inc.
Grob CS, Coyle JT (1986), Suspected adverse methylphenidate-imipramine interactions in children. J Dev Behav Pediatr 7:265267
*Hallowell EM, Ratey JJ (1994), Driven To Distraction: Recognizing and Coping with Attention Deficit Disorder from Childhood
Through Adulthood. New York: Random House Pantheon Books
Halperin JM, Gittelman R, Katz S, Struve FA (1986), Relationship between stimulant effect, electroencephalogram, and clinical
neurological findings in hyperactive children. J Am Acad Child Psychiatry 25:820-825
Handen BL, Breaux AM, Gosling A, Ploof DL, Feldman H (1990), Efficacy of methylphenidate among mentally retarded children
with attention deficit hyperactivity disorder. Pediatrics 86:922-930
Handen BL, Breaux AM, Janosky J, McAuliffe S, Feldman H, Gosling A (1992), Effects and noneffects of methylphenidate in
children with mental retardation and ADHD. J Am Acad Child Adolesc Psychiatry 31:455-461
Handen BL, Feldman H, Gosling A, Breaux AM, McAuliffe S (1991), Adverse side effects of methylphenidate among mentally
retarded children with ADHD. J Am Acad Child Adolesc Psychiatry 30:241-245
Handen BL, Janosky J, McAuliffe S, Breaux AM, Feldman H (1994), Prediction of response to methylphendate among children
with ADHD and mental retardation. J Am Acad Child Adolesc Psychiatry 33:1185-1193
*Harley JP (1980), Dietary treatment of behavioral disorders. Advances in Behavioral Pediatrics 1:129-151
Haslam RH (1992), Is there a role for megavitamin therapy in the treatment of attention deficit hyperactivity disorder? Adv Neurol
58:303-310
Hauser P, Zametkin AJ, Martinez P, Vitiello B, Matochik JA, Mixson AJ, Weintraub BD (1993), Attention deficit-hyperactivity
disorder in people with generalized resistance to thyroid hormone. N Engl J Med 328:997-1001
*Hechtman L (1985), Adolescent outcome of hyperactive children treated with stimulants in childhood: a review.
Psychopharmacol Bull 21:178-191
Hechtman L (1991), Resilience and vulnerability in long term outcome of attention deficit hyperactive disorder. Can J Psychiatry
36:415-421
Hechtman L (1993), Aims and methodological problems in multimodal treatment studies. Can J Psychiatry 38:458-464
Hedges D, Reimherr FW, Rogers A, Strong R, Wender PH (1995), An open trial of venlafaxine in adult patients with attention
deficit hyperactivity disorder. Psychopharmacol Bull 31:779-783
*Herrero ME, Hechtman L, Weiss G (1994), Antisocial disorders in hyperactive subjects from childhood to adulthood: predictive
factors and characterization of subgroups. Am J Orthopsychiatry 64:510-521
1997 AACAP
52
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Herskowitz J (1987), Developmental toxicology. In: Psychiatric Pharmacosciences of Children and Adolescents, Popper C, ed.
Washington, DC: American Psychiatric Press, pp 81-123
Hinshaw SP (1991), Stimulant medication in the treatment of aggression in children with attentional deficits. Journal of Clinical
Child Psychology 12: 301-312
Hinshaw SP, Heller T, McHale JP (1992), Covert antisocial behavior in boys with attention-deficit hyperactivity disorder: external
validation and effects of methylphenidate. Journal of Consult Clin Psychol 60:274-281
Hinshaw SP, Henker B, Whalen CK (1984a), Self-control in hyperactive boys in anger-inducing situations: effects of cognitivebehavioral training and of methylphenidate. J Abnorm Child Psychol 12:55-77
Hinshaw SP, Whalen CK, Henker B (1984b), Cognitive-behavioral and pharmacologic interventions for hyperactive boys:
comparative and combined effects. J Consult Clin Psychol 52:739-749
Horn WF, Chatoor I, Conners CK (1983), Additive effects of dexedrine and self-control training: a multiple assessment. Behav
Modif 7:383-402
Horn WF, Wagner AE, Ialongo N (1989), Sex differences in school-aged children with pervasive attention deficit hyperactivity
disorder. J Abnorm Child Psychol 17:109-125
Horrigan JP, Barnhill LJ (1995), Guanfacine for treatment of attention-deficit hyperactivity disorder in boys. Journal of Child and
Adolescent Psychopharmacology 5:215-223
Hoza B, Pelham WE, Sams SE, Carlson C (1992), An examination of the dosage effects of both behavior therapy and
methylphenidate on the classroom performance of two ADHD children. Behav Modif 16:164-192
Hunt RD (1987), Treatment effects of oral and transdermal clonidine in relation to methylphenidate: an open pilot study in ADDH. Psychopharmacol Bull 23:111-114
Hunt RD, Arnsten AFT, Asbell MD (1995), An open trial of guanfacine in the treatment of attention-deficit hyperactivity disorder.
J Am Acad Child Adolesc Psychiatry 34:50-54
*Hunt RD, Capper S, O'Connell P (1990), Clonidine in child and adolescent psychiatry. Journal of Child and Adolescent
Psychopharmacology 1:87-102
Hunt RD, Lau S, Ryu J (1991), Alternative therapies for ADHD. In: Ritalin: Theory and Patient Management, Greenhill LL,
Osman BB, eds. New York: Mary Ann Liebert, Inc., pp 75-95
Hunt RD, Minderaa RB, Cohen, DJ (1985), Clonidine benefits children with attention deficit disorder and hyperactivity: Report of
a doubleblind placebo-crossover therapeutic trial. J Am Acad Child and Adolesc Psychiatry 24:617-629
Ialongo NS, Horn WF, Pascoe JM, Greenberg G, Packard T, Lopez M, Wagner A, Puttler L (1993), The effects of a multimodal
intervention with attention-deficit hyperactivity disorder children: a 9-month follow-up. J Am Acad Child Adolesc
Psychiatry 32:182-189
Ickowicz A, Tannock R, Fulford P, Purvis K, Schachar R (1992), Transient tics and compulsive behaviors following
methylphenidate: evidence from a placebo controlled double blind clinical trial. American Academy of Child and
Adolescent Psychiatry, 39th Annual Meeting, Washington, DC
*Ingersoll BD, Goldstein S (1993), Attention Deficit Disorder and Learning Disabilities: Realities, Myths, and Controversial
Treatments. New York: Doubleday
Jankovic J (1993), Deprenyl in attention deficit associated with Tourette s syndrome. Arch Neurol 50:286-288
Jensen PS (1993), Development and implementation of multimodal and combined treatment studies in children and adolescents:
NIMH perspectives. Psychopharmacol Bull 29:19-25
Johnston C, Fine S (1993), Methods of evaluating methylphenidate in children with attention deficit hyperactivity disorder:
acceptability, satisfaction, and compliance. J Pediatr Psychol 18:717-730
Johnston C, Pelham, WE, Hoza J, Sturges J (1988), Psychostimulant rebound in attention deficit disordered boys. J Am Acad
Child Adolesc Psychiatry 27:806-810
Kahn CA, Kelly PC, Walker WO (1995), Lead screening in children with attention deficit hyperactivity disorder and developmental
delay. Clin Pediatr (Phila) 34:498-501
*Kane R, Mikalac C, Benjamin S, Barkley RA (1990), Assessment and treatment of adults with ADHD. In RA Barkley, Attention
Deficit Hyperactivity Disorder: A Handbook for Diagnosis and Treatment. New York: Guilford, pp 613-654
Kauffman RE, Smith-Wright D, Reese CA, Simpson R, Jones F (1981), Medication compliance in hyperactive children. Pediat
Pharmacol 1:231-237
Kavale KA, Forness SR (1983), Hyperactivity and diet treatment: a meta-analysis of the Feingold hypothesis. J Learn Disabil
16:325-330
1997 AACAP
53
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Kazdin AE, Bass D, Siegel T, Thomas C (1989), Cognitive-behavioral therapy and relationship therapy in the treatment of
children referred for antisocial behavior. J Consult Clin Psychol 57:522-535
Kazdin AE, Esveldt-Dawson K, French NH, Unis AS (1987), Problem-solving skills training and relationship therapy in the
treatment of antisocial child behavior. J Consult Clin Psychol 55:76-85
Kelley ML, McCain AP (1995), Promoting academic performance in inattentive children: the relative efficacy of school-home
notes with and without response cost. Behav Modif 19:357-375
Kendall PC, Braswell L (1993), Cognitive-Behavioral Therapy for Impulsive Children, 2nd Ed. New York: Guilford Press
Kent JD, Blader JC, Koplewicz HS, Abikoff W, Foley CA (1995), Effects of late-afternoon methylphenidate administration on
behavior and sleep in attention-deficit hyperactivity disorder. Pediatrics 96:320-325
Khantzian EJ (1985), The self-medication hypothesis of addictive disorders: focus on heroin and cocaine dependence. Am J
Psychiatry 142:1259-1264
Klein RG, Abikoff H (1989), The role of psychostimulants and psychosocial treatments in hyperkinesis. In: Attention Deficit
Disorder: Clinical and Basic Research, Sagvolden T, Archer T, eds. Hillsdale, NJ: Lawrence Erlbaum Associates, pp
167-180
Klein RG, Abikoff H, Barkley RA, Campbell M, Leckman JF, Ryan ND, Solanto MV, Whalen CK (1994), Clinical trials in children
and adolescents. In: Clinical Evaluation of Psychotropic Drugs: Principles and Guidelines, Prien RF, Robinson DS,
eds. New York: Raven Press, Ltd, pp 501-546
Klein RG, Landa B, Mattes JA, Klein DF (1988), Methylphenidate and growth in hyperactive children. Arch Gen Psychiatry
45:1127-1130
Klein RG, Mannuzza S (1988), Hyperactive boys almost grown up: methylphenidate effects on ultimate height. Arch Gen
Psychiatry 45:1131-1134
*Klein RG, Mannuzza S (1991), Long-term outcome of hyperactive children: a review. J Am Acad Child Adolesc Psychiatry
30:383-387
Klorman R, Brumaghim JT, Fitzpatrick PA, Borgstedt AD (1990), Clinical effects of a controlled trial of methylphenidate on
adolescents with attention deficit disorder. J Am Acad Child Adolesc Psychiatry 29:702-709
Klorman R, Coons HW, Borgstedt AD (1987), Effects of methylphenidate on adolescents with a childhood history of attention
deficit disorder: I. Clinical findings. J Am Acad Child Adolesc Psychiatry 26:363-367
Kutcher SP, Reiter S, Gardner DM, Klein RG (1992), The pharmacotherapy of anxiety disorders in children and adolescents.
Psychiatr Clin North Am 15:41-67
*Lahey BB, Carlson CL (1991), Validity of the diagnostic category of attention deficit disorder without hyperactivity: a review of
the literature. J Learn Disabil 24:110-120
*Lambert NM (1988), Adolescent outcomes for hyperactive children: perspectives on general and specific patterns of childhood
risk for adolescent educational, social, and mental health problems. Am Psychol 43:786-799
Landman GB, McCrindle B (1986), Pediatric management of nonpervasively hyperactive children. Clin Pediatr (Phila)
25:600-604
Leckman JF, Ort S, Caruso KA (1986), Rebound phenomena in Tourette's Syndrome after abrupt withdrawal of clonidine. Arch
Gen Psychiatry 43:1168-1176
Leonard HL, Meyer MC, Swedo SE, Richter D, Hamburger SD, Allen AJ, Rapoport JL, Tucker E (1995), Electrocardiographic
changes during desipramine and clomipramine treatment in children and adolescents. J Am Acad Child Adolesc
Psychiatry 34:1460-1468
Levy F, Ward PB (1995), Neurometrics, dynamic brain imaging and attention defict hyperactivity disorder. J Paediatr Child
Health 31:279-283
Lynskey MT, Fergusson, DM (1995), Childhood conduct problems, attention deficit behaviors, and adolescent alcohol, tobacco,
and illicit drug use. J Abnorm Child Psychol 23:281-302
Livingston RL, Dykman RA, Ackerman PT (1992), Psychiatric comorbidity and response to two doses of methylphenidate in
children with attention deficit disorder. Journal of Child and Adolescent Psychopharmacology 2:115-122
Loney J, Kramer J, Milich R (1981) The hyperkinetic child grows up: predictors of symptoms, delinquency, and achievement at
follow-up. In: Psychosocial Aspects of Drug Treatment for Hyperactivity, Gadow K, Loney J, eds. Boulder CO:
Westview Press, pp 381-415
Loney J, Milich R (1982), Hyperactivity, inattention, and aggression in clinical practice. Advances in Developmental and
Behavioral Pediatrics 3:113-147
1997 AACAP
54
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Loney J, Weissenburger FE, Woolson RF, Lichty EC (1979), Comparing psychological and pharmacological treatments for
hyperactive boys and their classmates. J Abnorm Child Psychol 7:133-143
Long N, Rickert VI, Ashcraft EW (1993), Bibliotherapy as an adjunct to stimulant medication in the treatment of attention-deficit
hyperactivity disorder. J Pediatr Health Care 7:82-88
Lovejoy MC, Rasmussen NH (1990), The validity of vigilance tasks in differential diagnosis of children referred for attention and
learning problems. J Abnorm Child Psychol 18:671-681
*Mannuzza S, Klein RG, Addalli KA (1991a), Young adult mental status of hyperactive boys and their brothers: a prospective
follow-up study. J Am Acad Child Adolesc Psychiatry 30:743-751
*Mannuzza S, Klein RG, Bessler A, Malloy P, LaPadula M (1993), Adult outcome of hyperactive boys: educational achievement,
occupational rank, and psychiatric status. Arch Gen Psychiatry 50:565-576
Mannuzza S, Klein RG, Bonagura N, Konig PH, Shenker R (1988), Hyperactive boys almost grown up: II. Status of subjects
without a mental disorder. Arch Gen Psychiatry 45:13-18
Mannuzza S, Klein RG, Bonagura N, Malloy P, Giampino TL, Addalli KA (1991b), Hyperactive boys almost grown up: V.
replication of psychiatric status. Arch Gen Psychiatry 48:77-83
Mash EJ, Dalby JT (1979), Behavioral interventions in hyperactivity. In: Hyperactivity in Children: Etiology, Measurement and
Treatment Implications, Trites RL, ed. Baltimore: University Park Press, pp 161-216
Mattes JA (1983), The Feingold diet: a current reappraisal. J Learn Disabil 16:319-323
Mattes JA (1986), Propranolol for adults with temper outbursts and residual attention deficit disorder. J Clin Psychopharmacol
6:299-302
Mattes JA, Boswell L, Oliver H (1984), Methylphenidate effects on symptoms of attention deficit disorder in adults. Arch Gen
Psychiatry 41:1059-1063
McBride MC (1988), An individual double-blind crossover trial for assessing methylphenidate response in children with attention
deficit disorder. J Pediatr 113:137-145, 1988
McBride MC, Wang DD, Torres CF (1986), Methylphenidate in therapeutic doses does not lower seizure threshold. Ann Neurol
20:428
McGee R, Williams S, Anderson J, McKenzie-Parnell JM, Silva PA (1990), Hyperactivity and serum and hair zinc levels in 11year-old children from the general population. Biol Psychiatry 28:165-168
McGee R, Williams S, Silva PA (1987), A comparison of girls and boys with teacher-identified problems of attention. J Am Acad
Child Adol Psychiatry 26:711-717
Milich R, Pelham WE, Hinshaw SP (1986a), Issues in the diagnosis of Attention Deficit Disorder: a cautionary note on the
Gordon Diagnostic System. Psychopahrmacol Bull 22:1101-1104
Milich R, Roberts MA, Loney J, Caputo J (1980), Differentiation of practice effects and statistical regression on the Conner s
Hyperkinesis Index. J Abnorm Child Psychol 8:549-552
Milich R, Wolraich M, Lindgren S (1986b), Sugar and hyperactivity: a critical review of empirical findings. Clinical Psychology
Review 6:493-513
Miller LG, Kraft IA (1994), Application of actigraphy in the clinical setting: use in children with Attention-Deficit Hyperactivity
Disorder. Pharmacotherapy 14:219-223
Nehra A, Mullick F, Ishak KG, Zimmerman HJ (1990), Pemoline-associated hepatic injury. Gastroenterology 99:1517-1519
Newcorn JH, Halperin JM (1994), Comorbidity among disruptive behavior disorders: impact on severity, impairment, and
response to treatment. Child and Adolescent Psychiatry Clinics of North America 3:227-252
Pataki CS, Carlson GA, Kelly KL, Rapport MD, Biancaniello TM (1993), Side effects of methylphenidate and desipramine alone
and in combination in children. J Am Acad Child Adolesc Psychiatry 32:1065-1072
Patterson GR (1975), Families: Applications of Social Learning to Family Life. Champaign, IL: Research Press
Patterson GR, Forgatch M (1987), Parents and Adolescents Living Together. Eugene, OR: Castalia Publishing Co
Pelco LE, Kissel RC, Parrish JM, Miltenberger RG (1987), Behavioral management of oral medication administration difficulties
among children: A review of literature with case illustrations. Developmental and Behavioral Pediatrics 8:90-96
Pelham WE (1983), The effects of psychostimulants on academic achievement in hyperactive and learning-disabled children.
Thalamus 3:1-47
Pelham WE (1985), The effects of stimulant drugs on learning and achievement in hyperactive and learning disabled children.
In: Psychological and Educational Perspectives on Learning Disabilities. Torgesen JK, Wong B, eds. New York:
Academic Press, pp 259-295
1997 AACAP
55
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Pelham WE, Bender ME (1982), Relationships in hyperactive children: description and treatment. Advances in Learning and
Behavioral Disabilities 1:365-436
Pelham WE, Carlson C, Sams SE, Vallano G, Dixon J, Hoza B (1993), Separate and combined effects of methylphenidate and
behavior modification on boys with attention deficit-hyperactivity disorder in the classroom. J Consult Clin Psychol
61:506-515
Pelham WE, Greenslade KE, Vodde-Hamilton M, et al (1990a), Relative efficacy of long-acting stimulants on children with
attention deficit-hyperactivity disorder: a comparison of standard methylphenidate, sustained-release methylphenidate,
sustained-release dextroamphetamine, and pemoline. Pediatrics 86:226-237
Pelham WE, Hoza J (1987), Behavioral assessment of psychostimulant effects on ADD children in a summer day treatment
program. Advances in Behavioral Assessment of Children and Families 3:3-34
Pelham WE, McBurnett K, Harper GW, Milich R, Clinton J, Thiele C, Murphy DA (1990b), Methylphenidate and baseball playing
in ADHD children: who's on first? J Consult Clin Psychol 58:130-133
Pelham WE, Milich R, Murphy DA, Murphy HA (1989a), Normative data on the IOWA Conners Teacher Rating Scale. Journal of
Clinical Child Psychology 18:259-262
Pelham WE, Milich R, Walker JL (1986), Effects of continuous and partial reinforcement and methylphenidate on learning in
children with attention deficit disorder. J Abnorm Psychol 95:3l9-325
Pelham WE, Murphy HA (1986), Attention Deficit and Conduct Disorders. In: Pharmacological and Behavioral Treatment: An
Integrative Approach, Herson M, ed. New York: J Wiley & Sons, pp108-148
Pelham WE, Schnedler RW, Bologna NC, Contreras JA (1980), Behavioral and stimulant treatment of hyperactive children: A
therapy study with methylphenidate probes in a within-subject design. J Appl Behav Anal 13:221-236
Pelham WE, Sturges J, Hoza J, et al (1987), The effects of Sustained Release 20 and 10 mg Ritalin b.i.d. on cognitive and social
behavior in children with attention deficit disorder. Pediatrics 40:491-501
Pelham WE, Swanson JM, Furman MB, Schwindt H (1995), Pemoline effects on children with ADHD: a time-response by doseresponse analysis on classroom measures. J Am Acad Child Adolesc Psychiatry 34:1504-1513
Pelham WE, Vodde-Hamilton M, Murphy DA, Greenstein J, Vallano G (1991), The effects of methylphenidate on ADHD
adolescents in recreational, peer group, and classroom settings. Journal of Clinical Child Psychology 20:293-300
Pelham WE, Walker JL, Sturges J, Hoza J (1989b), Comparative effects of methylphenidate on ADD girls and ADD boys. J Am
Acad Child Adolesc Psychiatry 5:773-776
* Pfiffner LJ, Barkley RA (1990), Educational placement and classroom management. In Attention Deficit Hyperactivity Disorder:
A Handbook for Diagnosis and Treatment. Barkley RA ed. New York: Guilford Press, pp 498-539
Pisterman S, McGrath P, Firestone P, Goodman JT, Webster I, Mallory R (1989), Outcome of parent-mediated treatment of
preschoolers with attention deficit disorder with hyperactivity. J Consult Clin Psychol 57:628-635
Pliszka SR (1989), Effect of anxiety on cognition, behavior, and stimulant response in ADHD. J Am Acad Child Adolesc
Psychiatry 28:882-887
Popper CW (1995), Combining methylphenidate and clonidine: pharmacologic questions and news reports about sudden death.
Journal of Child and Adolescent Psychopharmacology 5:157-166
Popper CW, Zimnitzky B (1995), Sudden death putatively related to desipramine treatment in youth: a fifth case and a review of
speculative mechanisms. Journal of Child and Adolescent Psychopharmacology 5:283-300
Power TJ (1992), Contextual factors in vigilance testing of children with ADHD. J Abnorm Child Psychol 20:579-593
Rapoport JL, Quinn PO, Bradbard G, Riddle D, Brooks E (1974), Imipramine and methylphenidate treatments of hyperactive
boys. Arch Gen Psychiatry 30:789-793
Rapport MD (1995), Response to letter to the Editor, J Am Acad Child Adolesc Psychiatry 34:1559
Rapport MD, Denney C, DuPaul G, Gardner MJ (1994), Attention deficit disorder and methylphenidate: normalization rates,
clinical effectiveness, and response prediction in 76 children. J Am Acad Child Adolesc Psychiatry 33:882-893
Rapport MD, DuPaul GJ, Stoner G, Jones JT (1986), Comparing classroom and clinic measures of attention deficit disorder:
differential, idiosyncratic, and dose-response effects of methylphenidate. J Consult Clin Psychol 54:334-341
Rapport MD, Jones JT, DuPaul GJ, Kelly KL, Gardner MJ, Tucker SB, Shea MS (1987), Attention deficit disorder and
methylphenidate: group and single-subject analyses of dose effects on attention in clinic and classroom settings. J
Clin Child Psychol 16:329-338
1997 AACAP
56
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Rapport MD, Stoner G, DuPaul GJ, Kelly KL, Tucker SB, Schoeler T (1988), Attention deficit disorder and methylphenidate: a
multilevel analysis of dose-response effects on children s impulsivity across settings. J Am Acad Child Adolesc
Psychiatry 27:60-69
*Ratey JJ, Greenberg MS, Bemporad JR, Lindem KJ (1992), Unrecognized attention-deficit hyperactivity disorder in adults
presenting for outpatient psychotherapy. Journal of Child and Adolescent Psychopharmacology 2:267-275
Reimherr FW, Hedges DW, Strong RE, Wender PH (1995), An open trial of venlafaxine in adult patients with attention deficit
hyperactivity disorder. Psychopharmacol Bull 31:609
Richters JE, Arnold LE, Jensen PS, Abikoff H, Conners CK, Greenhill LL, Hechtman L, Hinshaw SP, Pelham WE, Swanson JM
(1995), NIMH Collaborative Multisite Multimodal Treatment Study of Children with ADHD: I. Background and rationale.
J Am Acad Child Adolesc Psychiatry 34:987-1000
Riddle MA, Geller B, Ryan N (1993), Another sudden death in a child treated with desipramine, J Am Acad Child Adolesc
Psychiatry 32:792-797
Riddle MA, Hardin MT, Cho SC, Woolston JL, Leckman JF (1988), Desipramine treatment of boys with attention-deficit
hyperactivity disorder and tics: prelimlinary clinical experience. J Am Acad Child Adolesc Psychiatry 27:811-813
Riddle MA, Lynch KA, Scahill L, de Vries A, Cohen DJ, Leckman JF (1995), Methylphenidate discontinuation and reinitiation
during long-term treatment of children with Tourette s disorder and attention-deficit hyperactivity disorder: a pilot
study. Journal of Child and Adolescent Psychopharmacology 5:205-214
Riddle MA, Nelson JC, Kleinman CS, Rasmusson A, Leckman JF, King RA, Cohen DJ (1991), Sudden death in children
receiving norpramin: a review of three reported cases and commentary. J Am Acad Child Adolesc Psychiatry 30:104108
Rimland B (1983), The Feingold diet: an assessment of the reviews by Mattes, by Kavale and Forness and others. J Learn
Disabil 16:331-333
Roberts MA (1990), A behavioral observation method for differentiating hyperactive and aggressive boys. J Abnorm Child
Psychol 18:131-142
Robin AL (1990), Training families with ADHD adolescents. In: Attention Deficit Hyperactivity Disorder: A Handbook for
Diagnosis and Treatment, RA Barkley, ed. New York: Guilford Press, pp 462-497
Robin AL, Schneider M, Dolnick J (1976), The turtle technique: an extensive case study of self-control in the classroom.
Psychology in the Schools 1:449-459
Rosse RB, Licamele WL (1984), Slow-release methylphenidate: problems when children chew tablets. J Clin Psychiatry 45:525
Rowe KS, Rowe KJ (1994), Synthetic food coloring and behavior: a dose response effect in a double-blind, placebo-controlled,
repeated-measures study. J Pediatr 125:691-698
Ryan ND (1990), Heterocyclic antidepressants in children and adolescents. Journal of Child and Adolescent
Psychopharmacology 1:21-31
Ryan ND (1992), The pharmacologic treatment of child and adolescent depression. Psychiatr Clin North Am 15:29-40
Safer DJ (1992), Relative cardiovascular safety of psychostimulants used to treat attention-deficit hyperactivity disorder. Journal
of Child and Adolescent Psychopharmacology 2:279-290
Safer DJ, Allen RP (1989), Absence of tolerance to the behavioral effects of methylphenidate in hyperactive and inattentive
children. Pediatric Pharmacology and Therapeutics 115:1003-1008
Sallee FR, Stiller RL, Perel JM (1992), Pharmacodynamics of pemoline in attention deficit disorder with hyperactivity. J Am Acad
Child Adolesc Psychiatry 31:244-251
Sallee FR, Stiller RL, Perel JM, Everett G (1989), Pemoline-induced abnormal involuntary movements. J Clin Psychopharmacol
9:125-129
Sallee F, Stiller R, Perel J, Bates T (1985), Oral pemoline kinetics in hyperactive children. Clin Pharmacol Ther 37:606-609
Sallee F, Stiller R, Perel J, Rancurello M (1986), Targeting imipramine dose in children with depression. Clin Pharmacol Ther
40:8-l3
Satterfield JH, Cantwell DP, Satterfield BT (1979), Multimodality treatment: a one-year follow-up of 84 hyperactive boys. Arch
Gen Psychiatry 36:965-974
Satterfield JH, Satterfield BT, Cantwell DP (1981), Three-year multimodality treatment study of 100 hyperactive boys. J Pediatr
98:650-655
*Satterfield JH, Satterfield BT, Schell AM (1987), Therapeutic interventions to prevent delinquency in hyperactive boys. J Am
Acad Child Adolesc Psychiatry 26:56-64
1997 AACAP
57
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Satterfield J, Swanson J, Schell A, Lee F (1994), Prediction of antisocial behavior in attention-deficit hyperactivity disorder boys
from aggression/defiance scores. J Am Acad Child Adolesc Psychiatry 33:185-190
Saul RC (1985), Nortriptyline in attention deficit disorder. Clin Neuropharmacol 8:382-384
Schachar R, Sandberg S, Rutter M (1986), Agreement between teachers ratings and observations of hyperactivity,
inattentiveness, and defiance. J Abnorm Psychol 14:331-345
*Schachar R, Tannock R (1993), Childhood hyperactivity and psychostimulants: a review of extended treatment studies. J Child
Adolesc Psychopharm 3:81-97
Schaughency EA, Lahey BB, Hynd GW, Stone PA, Picentini JC, Frick PJ (1989), Neuropsychological test performance and the
attention deficit disorders: clinical utility of the Luria-Nebraska Neuropsychological Battery-Children s Revision. J
Consult Clin Psychol 57:112-116
Schleifer M, Weiss G, Cohen N, Elman M, Cvejic H, Kruger E (1975), Hyperactivity in preschoolers and the effect of
methylphenidate. Am J Orthopsychiatry 45:38-50
Schlieper A, Alcock D, Beaudry P, et al (1991), Effect of therapeutic plasma concentrations of theophylline on behavior, cognitive
processing, and affect in children with asthma. J Pediatr 118:449-455
Schonfeld DJ (1993), New developments in pediatric lead poisoning. Curr Opin Pediatr 5:537-544
Schroeder JS, Mullin AV, Elliott GR, Steiner H, Nichols M, Gordon A, Paulos M (1989), Cardiovascular effects of desipramine in
children. J Am Acad Child Adolesc Psychiatry 28:376-379
Schroeder SR, Lewis MH, Lipton MA (1983), Interactions of pharmacotherapy and behavior therapy among children with learning
and behavioral disorders. Advances in Learning and Behavioral Disabilities 2:179-225
Schubiner H, Tzelepis A, Isaacson H, Warbasse LH, Zacharek M, Musial J (1995), The dual diagnosis of attentiondeficit/hyperactivity disorder and substance abuse: case reports and literature
review. J Clin Psychiatry 56:146-150
Shah MR, Seese LM, Abikoff H, Klein RG (1994), Pemoline for children and adolescents with conduct disorder: a pilot
investigation. Journal of Child and Adolescent Psychopharmacology 4:255-261
Shekim WO, Asarnow RF., Hess E, Zaucha K, Wheeler N (1990), A clinical and demographic profile of a sample of adults with
attention deficit hyperactivity disorder, residual state. Compr Psychiatry 31:416-425
Silva RR, Munoz DM, Alpert M (1996), Carbamazepine use in children and adolescents with features of attention-deficit
hyperactivity disorder: a meta-analysis. J Am Acad Child Adolesc Psychiatry 35:352-358
Silver L (1986), Controversial approaches to treating learning disabilities and attention deficit disorder. Am J Dis Child 140:10451052
Simeon JG, Ferguson HB, Fleet JVW (1986), Bupropion effects in attention deficit and conduct disorders. Can J Psychiatry
31:581-585
Spencer T, Biederman J, Kerman K, Steingard R, Wilens T (1993a), Desipramine treatment of children with attention-deficit
hyperactivity disorder and tic disorder or Tourette s syndrome. J Am Acad Child Adolesc Psychiatry 32:354-360
Spencer T, Biederman J, Steingard R, Wilens T (1993b), Bupropion exacerbates tics in children with attention-deficit
hyperactivity disorder and Tourette s syndrome. J Am Acad Child Adolesc Psychiatry 32:211-214
Spencer T, Biederman J, Wilens T, Faraone SV (1994), Is attention-deficit hyperactivity disorder in adults a valid disorder?
Harvard Review of Psychiatry 1:326-325
Spencer T, Biederman J, Wilens T, Guite J, Harding M (1995a), ADHD and thyroid abnormalities: a research note. J Child
Psychol Psychiatry 36:879-885
*Spencer T, Biederman J, Wilens T, Harding M, O Donnell D, Griffin S (1996), Pharmacotherapy of attention-deficit hyperactivity
disorder across the life cycle. J Am Acad Child Adolesc Psychiatry 35:409-432
Spencer T, Biederman J, Wilens T, Steingard R, Geist D (1993c), Nortriptyline treatment of children with attention-deficit
hyperactivity disorder and tic disorder or Tourette s syndrome. J Am Acad Child Adolesc Psychiatry 32:205-210
Spencer T, Wilens T, Biederman J, Faraone SV, Ablon S, Lapey K (1995b), A double-blind, crossover comparison of
methylphendiate and placebo in adults with childhood-onset attention-deficit hyperactivity disorder. Arch Gen
Psychiatry 52:434-443
Sprague RL, Sleator EK (1977), Methylphenidate in hyperkinetic children: differences in dose effects on learning and social
behavior. Science 198:1274-1276
Speltz ML, Varley CK, Peterson K, Beilke RL (1987), Effects of dextroamphetamine and contingency management on a
preschooler with ADHD and oppositional defiant disorder. J Am Acad Child Adolesc Psychiatry 27:175-178
1997 AACAP
58
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Stein MA, Blondis TA, Schnitzler ER, O Brien T, Fishkin J, Blackwell B, Szumowski E, Roizen NJ (in press), Methylphenidate
dosing: bid versus tid. Pediatrics
Stein MA, Rubinoff A, Pliskin N, Weiss RE (1995), Adult ADHD and AIDS. Am J Psychiatry 152:1100
Stein MA, Sandoval R, Szumowski E, Roizen N, Reinecke MA, Blondis TA, Klein Z (1995), Psychometric characteristics of the
Wender Utah Rating Scale (WURS): reliability and factor structure for men and women. Psychopharmacol Bull
31:425-433
Steingard R, Biederman J, Spencer T, Wilens T, Gonzalez A (1993), Comparison of clonidine response in the treatment of
attention-deficit hyperactivity disorder with and without comorbid tic disorders. J Am Acad Child Adolesc Psychiatry
32:350-353
Stine JJ (1994), Psychosocial and psychodynamic issues affecting noncompliance with psychostimulant treatment. Journal of
Child and Adolescent Psychopharmacology 4:75-86
Stokes TF, Baer DM (1977), An implicit technology of generalization. J Appl Behav Anal 10:349-367
Stoner G, Carey SP, Ikeda MJ, Shinn MR (1994), The utility of curriculum-based measurement for evaluating the effects of
methylphenidate on academic performance. J Appl Behav Anal 27:101-113
Strayhorn JM (1995), The case of the uncertain prescriber. J Am Acad Child Adolesc Psychiatry 34:253-254
Swanson JM (1985), Measures of cognitive functioning appropriate for use in pediatric psychopharmacological research studies.
Psychopharmacol Bull 21:887-890
Swanson JM, Flockhart D, Udrea D, Cantwell D, Connor D, Williams L (1995), Clonidine in the treatment of ADHD: questions
about safety and efficacy (letter to the editor). Journal of Child and Adolescent Psychopharmacology 5:301-304
*Swanson JM, McBurnett K, Wigal T, Pfiffner LJ, Lerner MA, Williams L, Christian DL, Tamm L, Willcutt E, Crowley K, Clevenger
W, Khouzam N, Woo C, Crinella FM, Fisher TD (1993), Effect of stimulant medication on children with attention deficit
disorder: a review of reviews. Excep Child 60:154-162
Swanson JM, Sandman CA, Deutsch C, Baren M (1983), Methylphenidate hydrochloride given with or before breakfast: I.
Behavioral, cognitive, and electrophysiologic effects. Pediatrics 72:49-55
Szatmari P, Offord DR, Boyle MH (1989), Ontario Child Health Study: prevalence of attention deficit disorder with hyperactivity.
J Child Psychol Psychiatry 30:219-230
Taylor E, Schachar R, Thorley G, Wieselberg HM, Everitt B, Rutter M (1987), Which boys respond to stimulant medication? A
controlled trial of methylphenidate in boys with disruptive behaviour. Psychol Med 17:121-143
Teicher MH, Ito Y, Glod CA, Barber NI (1996), Objective measurement of hyperactivity and attentional problems in ADHD. J Am
Acad Child Adolesc Psychiatry 35:334-342
Thurston LP (1981), Comparison of the effects of parent training and of Ritalin in treating hyperactive children. In: Strategic
Interventions for Hyperactice Children, Gittelman M, ed. New York: M.E. Sharpe, Inc., pp 178-185
*Trommer BL, Hoeppner JB, Lorber R, Armstrong K (1988), Pitfalls in the use of a continuous performance test as a diagnostic
tool in attention deficit disorder. J Dev Behav Pediatr 9:339-345
Tryon WW, Pinto LP (1994), Comparing activity measurements and ratings. Behav Modif 18:251-261
Tannock R, Ickowicz A, Schachar R (1995), Differential effects of methyphendiate on working memory in ADHD children with
and without comorbid anxiety. J Am Acad Child Adolesc Psychiatry 7:886-896
Ullman RK, Sleator EK, Sprague RL (1985a), Introduction to the use of ACTeRS. Psychopharmacol Bull 21:915-919
Ullmann RK, Sleator EK (1985), Attention deficit disorder children with or without hyperactivity: which behaviors are helped by
stimulants? Clin Pediatr (Phila) 24:547-551
Ullman RK, Sleator EK (1986), Responders, nonresonders, and placebo responders among children with attention defict
disorder. Clin Pediatr (Phila) 25:594-599
Ullmann RK, Sleator EK, Sprague RL (1985b), A change of mind: the Conners Abbreviated Rating Scales reconsidered. J
Abnorm Child Psychol 13:553-565
*Varley CK (1985), A review of studies of drug treatment efficacy for attention deficit disorder with hyperactivity in adolescents.
Psychopharmcol Bull 21:216-221
Varley CK, Trupin EW (1982), Double-blind administration of methylphenidate to mentally retarded children with attention deficit
disorder: a preliminary study. Am J Ment Defic 86:560-566
Varley CK, Trupin EW (1983), Double-blind assessment of stimulant medication for attention deficit disorder: a model for clinical
application. Am J Orthopsychiatry 53:542-547
Vincent J, Varley CK, Leger P (1990), Effects of methylphenidate on early adolescent growth. Am J Psychiatry 147:501-502
1997 AACAP
59
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Vitaro F, Tremblay RE, Gagnon C (1995), Teacher ratings of children s behaviors and teachers management styles: a
research note. J Child Psychol Psychiatry 36:887-898
*Ward MF, Wender PH, Reimherr FW (1993), The Wender Utah Rating Scale: an aid in the retrospective diagnosis of childhood
attention deficit disorder. Am J Psychiatry 150:885-890
Weinstein CS (1994), Cognitive remediation strategies: An adjunct to the psychotherapy of adults with attention-deficit
hyperactivity disorder. Journal of Psychotherapy Practice and Research 3:44-57
*Weiss G, Hechtman LT (1993), Hyperactive Children Grown Up: ADHD in Children, Adolescents, and Adults, 2nd Ed. Guilford:
New York
Weiss RG, Pope HG, Mirin SM (1985), Treatment of chronic cocaine abuse and attention deficit disorder, residual type, with
magnesium pemoline. Drug and Alcohol Dependence 15:69-72
Wender EH (1986), The food additive-free diet in the treatment of behavior disorders: a review. J Dev Behav Pediatr 7:35-42
Wender EH, Solanto MV (1991), Effects of sugar on aggressive and inattentive behavior in children with attention deficit disorder
with hyperactivity and normal children. Pediatrics 88:960-966, 1991
*Wender PH (1995), Attention-Deficit Hyperactivity Disorder in Adults. New York: Oxford University Press
Wender PH, Reimherr FW (1990), Bupropion treatment of attention-deficit hyperactivity disorder in adults. Am J Psychiatry
147:1018-1020
Wender PH, Reimherr FW, Wood DR (1981), Attention deficit disorder ("minimal brain dysfunction") in adults. Arch Gen
Psychiatry 38:449-456
Wender PH, Reimherr FW, Wood D, Ward M (1985a), A controlled study of methylphenidate in the treatment of attention deficit
disorder, residual type, in adults. Am J Psychiatry 142:547-552
Wender PH, Wood DR, Reimherr FE, Ward M (1983), An open trial of pargyline in the treatment of attention deficit disorder,
residual type. Psychiatry Research 9:329-336
Wender PH, Wood DR, Reimherr FW (1985b), Pharmacological treatment of attention deficit disorder, residual type (ADD, RT,
"minimal brain dysfunction", "hyperactivity) in adults. Psychopharmacol Bull 212:222-231
*Whalen CK, Henker B (1991a), Therapies for hyperactive children: comparisons, combinations, and compromises. J Consult
Clin Psychol 59:126-137
Whalen CK, Henker B (1991b), Social impact of stimulant treatment for hyperactive children. J Learn Disabil 24:231-241
Whalen CK, Henker B, Buhrmester D, Hinshaw SP, Huber A, Laski K (1989), Does stimulant medication improve the peer status
of hyperactive children? J Consult Clin Psychol 57:545-549
Whalen CK, Henker B, Castro J, Granger DA (1987), Peer perceptions of hyperactivity and medication effects. Child Dev 58:816828
Whalen CK, Henker B, Dotemoto S (1981), Teacher response to the methylphenidate (Ritalin) versus placebo status of
hyperactive boys in the classroom. Child Dev 52:1005-1014
Wilens TE, Biederman J (1992), The stimulants. Psychiatric Clin North Am 15:191-222
Wilens TE, Biederman J, Baldessarini RJ, Geller B, Schleifer D, Spencer TJ, Birmaher B, Goldblatt A (1996), Cardiovascular
effects of therapeutic doses of tricyclic antidepressants in children and adolescents. J Am Acad Child Adolesc
Psychiatry 35:1491-1501
Wilens TE, Biederman J, Geist DE, Steingard R, Spencer T (1993), Nortriptyline in the treatment of ADHD: a chart review of 58
cases. J Am Acad Child Adolesc Psychiatry 32:343-349
Wilens TE, Biederman J, Mick E, Spencer TJ (1995a), A systematic assessment of tricyclic antidepressants in the treatment of
adult attention-deficit hyperactivity disorder. J Nerv Ment Dis 183:48-50
Wilens T, Biederman J, Prince J, Spencer T, Faraone S, Schleifer D, Linehan C, Warburton R, Harding M, Geller D (1995b),
Double-blind comparison of desipramine (DMI) and placebo in adults with attention deficit hyperactivity disorder: final
results. Presented at Annual Meeting of American Academy of Child and Adolescent Psychiatry.
Wilens TE, Biederman J, Spencer T (1994a), Clonidine for sleep disturbances associated with attention-deficit hyperactivity
disorder. J Am Acad Child Adolesc Psychiatry 33:424-426
Wilens TE, Biederman J, Spencer TJ (1995c), Venlafaxine for adult ADHD. Am J Psychiatry 152:1099-1100
Wilens TE, Biederman J, Spencer TJ, Frances RJ (1994b), Comorbidity of attention-deficit hyperactivity and psychoactive
substance use disorders. Hosp Comm Psychiatry 45:421-435
*Wilens TE, Biederman J, Spencer TJ, Prince J (1995d), Pharmacotherapy of adult attention deficit/hyperactivity disorder: a
review. J Clin Psychopharmacol 15:270-278
1997 AACAP
60
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
Wilens TE, Prince JB, Biederman J, Spencer TJ, Frances RJ (1995e), Attention-deficit hyperactivity disorder and comorbid
substance use disorders in adults. Psychiatr Serv 46:761-765
Wiles CP, Hardin MT, King RA, et al. (1991), Antidepressant-induced prolongation of QTC interval on EKG in two children.
Abstracts, Annual Meeting American Academy of Child and Adolescent Psychiatry, p 70
Winsberg BG, Bialer I, Kupietz S, Tobias J (1972), Effects of imipramine and dextroamphetamine on behavior of
neuropsychiatrically impaired children. Am J Psychiatry 11:109-115
Winsberg BG, Goldstein S, Yepes LE, Perel JM (1975), Imipramine and electrocardiographic abnormalities in hyperactive
children. Am J Psychiatry 132:542-545
Winsberg BG, Perel JM, Hurwic MJ, et al (1974), Imipramine protein binding and pharmacokinetics in children. In: The
Phenothiazines and Structurally Related Drugs, Forrest IS, Carr CJ, Usdin E, eds. New York: Raven Press, pp 425431
Winsberg BG, Kupietz SS, Yepes LE (1980), Ineffectiveness of imipramine in children who fail to respond to methylphenidate. J
Autism Dev Disord 10:129-137
Wolraich ML, Hannah JN, Baumgaertel A, Pinnock TY, Law D (Submitted), J Abnormal Child Psychol, submitted.
Wolraich ML, Hannah JN, Pinnock TY, Baumgaertel A, Brown J (1996), Comparison of diagnostic criteria for attention-deficit
hyperactivity disorder in a county-wide sample. J Am Acad Child Adolesc Psychiatry 35:319-324
*Wolraich ML, Wilson DB, White JW (1995), The effect of sugar on behavior or cognition in children: a meta-analysis. JAMA
274:1617-1621
Wood DR, Reimherr FW, Wender PH, Johnson GE (1976), Diagnosis and treatment of minimal brain dysfunction in adults: a
preliminary report. Arch Gen Psychiatry 33:1453-60
Woods D (1986), The diagnosis and treatment of attention deficit disorder, residual type. Psychiatric Annals 16:23-28
Work Group on Quality Issues (1995), Practice parameters for the psychiatric assessment of children and adolescents. J Am
Acad Child Adolesc Psychiatry 34:1386-1402
Wroblewski BA, Leary JM, Phelan AM, Whyte J, Manning K (1992), Methylphenidate and seizure frequency in brain injured
patients with seizure disorders. J Clin Psychiatry 53:86-89
Young ES, Perros P, Price GW, Sadler T (1995), Acute challenge ERP as a prognostic of stimulant therapy outcome in attentiondeficit hyperactivity disorder. Biol Psychiatry 37:25-33
Zahn TP, Rapoport, JL, Thompson CL (1980), Autonomic and behavioral effects of dextroamphetamine and placebo in normal
and hyperactive prepubescent boys. J Abnorm Child Psychol 8:145-160
Zametkin AJ, Linnoila M, Karoum F, Sallee R (1986), Pemoline and urinary excretion of catecholamines and indoleamines in
children with attention deficit disorder. Am J Psychiatry 143:359-362
Zametkin AJ, Nordahl, TE, Gross M, King AC, Semple WE, Rumsey J, Hamburger S, Cohen RM (1990), Cerebral glucose
metabolism in adults with hyperactivity of childhood onset. New Engl J Med 323:1361-1366
Zametkin A, Rapoport JL, Murphy DL, Linnoila M, Ismond D (1985), Treatment of hyperactive children with monoamine oxidase
inhibitors. Arch Gen Psychiatry 42:962-966
Zeiner P (1995), Body growth and cardiovascular function after extended treatment (1.75 years) with methylphenidate in boys
with attention-deficit hyperactivity disorder. J Child Adolesc Psychopharmacol 5:129-138
Zentall SS, Zentall TR (1986), Hyperactivity ratings: statistical regression provides an insufficient explanation of practice effects.
J Pediatr Psychol 11: 393-396
Ziegler R, Holden L (1988), Family therapy for learning disabled and attention-deficit disordered children. Am J Orthopsychiatry
58:196-210
1997 AACAP
61
NOT FOR DISTRIBUTION OR CITATION
AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
APPENDIX A
READINGS FOR PARENTS, PATIENTS, AND TEACHERS
BOOKS
Barkley RA PhD (1995), Taking Charge of ADHD: The Complete, Authoritative Guide for Parents. The Guilford Press: New
York
Braswell L PhD, Bloomquist M PhD, Pederson S MA (1991), ADHD: A Guide to Understanding and Helping Children with
Attention Deficit Hyperactivity Disorder in School Settings. University of Minnesota, Department of Professional
Development and Conference Services, Continuing Education and Extension, 315 Pillsbury Drive S.E., Minneapolis,
MN 55455, (612) 625-3504
Clark L PhD (1989), The Time-out Solution: A Parent s Guide for Handling Everyday Behavior Problems. Contemporary Books:
Chicago (Lots of detail on using time-out, but also other punishments and positive ways of increasing appropriate
behavior. Includes examples, checklists, and tear-out reminder sheets.)
Fowler MC (1990), Maybe You Know My Kid: A Parent s Guide to Identifying, Understanding and Helping Your Child with
Attention Deficit Hyperactive Disorder. Carol Publishing Group: New York
Garber SW PhD, Garber MD PhD, Spizman RF (1990), If Your Child is Hyperactive, Inattentive, Impulsive, Distractible...Helping
the ADD (Attention Deficit Disorder) Hyperactive Child. Villard Books: New York (A practical program for changing
behavior with or without medication.)
Hallowell E MD, Ratey J MD (1994), Driven to Distraction: Recognizing and Coping with Attention Deficit Disorder from
Childhood Through Adulthood. Pantheon Books: NY (Written by two psychiatrists who have ADHD themselves.
Especially strong on the diagnosis and treatment of ADHD in adults.)
Hallowell EM MD, Ratey JJ MD (1994), Answers to Distraction. Pantheon Books: New York
Ingersoll B PhD (1988), Your Hyperactive Child: A Parent s Guide to Coping with Attention Deficit Disorder. Doubleday: New
York (A comprehensive book, with many examples. Includes brief guidelines for teachers and an appendix with
behavioral management programs for classroom use.)
Ingersoll B PhD, Goldstein S PhD (1993), Attention Deficit Disorder and Learning Disabilities: Realities, Myths and Controversial
Treatments. Doubleday Main Street Books: New York (An up-to-date review by two psychologists focusing on causes
and treatment. Good coverage of common myths and unfounded claims.)
Kelly K, Ramundo P (1996), You Mean I m Not Lazy, Stupid or Crazy?!. Fireside Books: New York
Nadeau KG PhD (1995), A Comprehensive Guide to Attention Deficit Disorder in Adults: Research, Diagnosis, and Treatment.
Brunner/Mazel: New York
Nadeau K PhD (1994), Survival Guide for College Students with ADD or LD. Magination Press: New York (A handy practical
guide for the ADHD adolescent or young adult student.)
NEWSLETTERS
Attention! The Magazine of Children and Adults with Attention Deficit Disorders, 449 N.W. 70th Avenue, Suite 208, Plantation, FL
33317
The ADHD Report, The Guilford Press, 72 Spring St., New York, NY 10012
Challenge: The First National Newsletter on Attention Deficit (Hyperactivity) Disorder. P.O. Box 2001, West Newbury, MA 01985
1997 AACAP
62
NOT FOR DISTRIBUTION OR CITATION
ADHD Parameters
Approved by Council February 22, 1997
Page 63
APPENDIX B
TEXTS FOR PHARMACOTHERAPY IN CHILDREN AND ADOLESCENTS
Green WH (1995), Child and Adolescent Clinical Psychopharmacology. Williams & Wilkins: Baltimore
Greenhill LL MD, Osman BB PhD (eds) (1991), Ritalin: Theory and Patient Management. Mary Ann Liebert, Inc: New York
Riddle MA (ed) (1995), Child and Adolescent Psychiatric Clinics of North America: Pediatric Psychopharmacology I & II
Rosenberg DR MD, Holttum J MD, Gershon SI MD (1994), Textbook of Pharmacotherapy for Child and Adolescent Psychiatric
Disorders. Brunner/Mazel: New York
Werry JS MD, Aman MG PhD (eds) (1993), Practitioner s Guide to Psychoactive Drugs for Children and Adolescents. Plenum
Publishing Company: New York
Wiener JM (ed) (1996), Diagnosis and Psychopharmacology of Childhood and Adolescent Disorders. Wiley and Sons, Inc: New
York
1997 AACAP
NOT FOR 63
DISTRIBUTION OR CITATION
Download