- validity of the
syndrome itself, particularly with regard to whether it constitutes the
far end of a normal spectrum versus a qualitatively different and distinct
condition;
- etiology;
- prevention;
- issues of over- vs.
under-diagnosis in "real world" settings;
- factors underpinning
differences in treated prevalence and in diagnostic and treatment
practices.
Validity of the
syndrome: Current evidence indicates that ADHD can be reliably diagnosed
under research conditions (Jensen et al., 1995; Schwab-Stone et al., 1996;
Shaffer et al., 1996). In fact, ADHD as a condition is unsurpassed among
other child psychiatric disorders, and consistently demonstrates the highest
levels of test-retest reliability coefficients. Validity coefficients are
also consistently high when done under ideal conditions (Jensen et al., in
press). When applying the classic validational criteria outlined by Robins
and Guze (1970), the weight of evidence indicates that ADHD does indeed meet
criteria as a valid behavioral syndrome that has reasonably discrete
defining characteristics and can be reliably diagnosed. As noted by the
consensus conference final statement, there is substantial evidence for the
validity of the disorder. However, like hypertension, ADHD likely has
multiple causes, and may instead reflect a final common pathway of
behavioral manifestations rather than a single disorder. As noted by the
consensus conference, further validational work on the syndrome is needed,
including determining whether the syndrome is best characterized along
dimensional lines or as a discrete category. This determination is likely to
be of great importance, since if there is indeed no natural cut-off,
additional efforts to identify subthreshold cases or prodromal presentations
would be quite important. Such efforts could yield substantial benefits,
ranging from identifying persons at risk, to identifying a
"broader" phenotype that could provide greater scientific benefits
for genetic studies, to developing preventive interventions.
Prevalence: Given
the fact that there appears indeed to be no natural cut-off or discontinuous
function that characterizes ADHD, it should not be surprising that wide
differences in prevalence have been noted. Across cultures, prevalence rates
ranging from 1 to 20% have been reported (Bird et al., 1999). These rates
vary as a function of the diagnostic criteria, the methods for establishing
the presence of symptoms, the nature of the informants, and the degree of
impairment (Bird, 1999). Within the United States, prevalence rates of 4-5%
are generally accepted. In Europe, application of ICD-10 criteria ("Hyperkinetic
Disorder") are substantially more demanding, and tend to yield
substantially lower rates, usually in the range of 1% (Swanson et al.,
1997). Most evidence to date suggests that children are not particularly
good reporters of the full syndrome. Inclusion of children’s reports tends
to raise prevalence rates by 25-33% (Jensen et al., in press). Similarly,
counting cases regardless of the presence of impairment, or without
requiring the presence of symptoms in multiple settings, can raise rates by
as much as 50%. Regardless, these variations indicate the need not only for
standard definitions (as in DSM-IV), but also for uniform measures and
methods for instantiation of the disorder.
Evidence to date
indicates a 6:1 to 9:1 ratio of males to females in clinical settings.
However, in epidemiology studies, ratios drop to 3:1. Further, by adulthood,
prevalence rates appear to be equal (Barkley, 1999; Johnston, 1999). There
is no significant or sizable body of evidence concerning possible
differences as a function of ethnicity or SES. However, minority and lower
SES families are less likely to seek out care and obtain treatment for their
children (Zito et al., 1998). Further, SES factors may complicate the
treatment of the disorder and/or increase the likelihood of poorer long-term
outcomes (MTA Cooperative Group, in press; Biederman et al., 1995).
Etiology: Current
evidence implicates multiple factors in the etiology of ADHD, yet it is
unclear how these factors interact at the level of the single case. The best
studied factor is familiality/heritability. Depending upon the nature of the
study, heritability has been estimated to be between 50-80%. Yet these
factors do not appear to be "all or none." Instead, specific
traits of ADHD appear to be heritable in a continuous function (Levy et al.,
1997).
Most recent evidence
indicates that ADHD symptoms have a central nervous system basis (as do all
normal and abnormal behaviors, thoughts, and emotions). However, such
brain-behavior correlations do not constitute proof that ADHD reflects a
disordered biologic state. Nonetheless, there now exists a range of
neuropsychologic, electrophysiologic, and neuroimaging studies that have
shown fairly consistent differences in prefrontal cortical, parietal, and
basal ganglia functioning associated with ADHD symptomatology. In addition,
there now have been a number of candidate gene studies exploring the
dopamine transporter (DAT1) or dopamine receptor (DRD4) genes, each of which
has now had several independent replications (Swanson & Castellanos,
1999). While these studies generally indicate an association with ADHD and
specific polymorphisms, effects are quite small. It is likely that a host of
other genes are involved, and that specific components or combinations of
environmental forces are necessary to switch on these genes and lead to the
expression of the full phenotype.
Other factors implicated
by correlational evidence in the onset, maintenance, and severity of ADHD
include pre- and perinatal factors (hypoxia, maternal smoking,
hyperbilirubinemia), exposure to lead, child abuse, specific genetic
mutation associated with thyroid disease, acquired forms of ADHD due to
traumatic brain injury, and early attachment difficulties. Remarkably,
however, despite intermittent leads in these areas, none has been subjected
to systematic programmatic research (Swanson & Castellanos, 1999).
Despite these few hints,
in truth, we know little concerning etiology, a conclusion also reached by
the consensus conference. As a result, we know essentially nothing about
primary or secondary prevention. More, however, is known about tertiary
prevention, in that effective treatments have been demonstrated to improve
longer-term outcomes several years post treatment (Gilberg et al., 1997; MTA
Cooperative Group, in press; Loney et al., in press; Biederman et al.,
1999). The lack of research in the prevention area is striking, even though
there is ample evidence that subthreshold and/or pre-morbid states can be
reasonably identified. In effect, the research field appears to have
unwittingly excluded this area of research from consciousness, perhaps
because of the taken-for-granted assumptions that ADHD symptoms are fully
biologic or inborn (immutable). Such assumptions cannot be correct, however,
given the number of children who, over the course of development, show
significant remission (20-40%) (e.g., Hechtman, 1992). How and why do such
significant improvements in symptoms take place? What developmental
processes are at work? Could similar factors come into play and be used to
clinical advantage early in the course of the disorder, perhaps before full
expression of symptoms, via some targeted prevention strategies?
Avenues of exploration
that appear to be understudied include the study of a) specific perinatal/prenatal
influences in interaction with susceptibility genes, b) the impact of home
and environmental factors that might modulate the development of
children’s attentional capacities, c) early learning experiences, exposure
to television or other factors that may up-regulate or shape children’s
attention styles, and d) early intervention strategies designed to remediate
attentional and executive functional capacities in children at risk.
Future studies of ADHD
risk should ideally combine assessments of some of the currently identified
candidate genes with neuropsychologic and neurophysiologic studies, coupled
with direct observations. Given the evidence that cultural factors can and
do exert important effects on defining specific behavioral characteristics
of the syndrome, the search for risk factors vis-à-vis the underlying
phenotype must not rely on behavioral descriptions alone. Methods for
discriminating signal from noise will likely depend upon multi-method and
multi-informant strategies, direct observation, the use of genetically
informative designs coupled with the examination of environmental forces,
and methods for compiling and sorting through the many characteristics of a
"case" to determine which cases indeed are true cases and which
are non-cases (e.g., best estimate methods with input from experienced
clinicians).
REFERENCES
American Psychiatric
Association. (1994). Diagnostic and statistical manual of mental disorders
(4th ed.). Washington, DC.
Biederman, J., Milberger,
S., Faraone, S., Kiely, K., Guite, J., Mick, E., Ablon, S., Warburton, R.,
& Reed, E. (1995). Family-environmental risk factors for
attention-deficit hyperactivity disorder. Archives of General Psychiatry,
52, 464-470.
Biederman, J., Wilens,
T., Mick, E., Spencer, T., Faraone, S. (1999). Pharmacotherapy of
attention-deficit/Hyperactivity disorder reduces risk for substance use
disorder. Pediatrics, 104, 20.
Gilberg, C., Melander,
H., Von Knorring, A., et. al. (1997). Long-term stimulant treatment of
children with attention-deficit hyperactivity disorder symptoms. Archives
of General Psychiatry, 54, 857-864.
Jensen, P., Martin, D.,
Cantwell, D. (1997). Comorbidity in ADHD: implications for research,
practice, and DSM-V. Journal of the American Academy of Child and
Adolescent Psychiatry, 36, 1065-79.
Jensen, P., Roper, M.,
Fisher, P., Piacentini, J., Canino, G., et al. (1995). Test-retest
reliability of the Diagnostic Interview Schedule for Children (DISC 2.1):
Parent, child, and combined algorithms. Archives of General Psychiatry,
52, 61-71.
*Jensen, P., *Rubio-Stipec,
M., Dulcan, M., Canino, G., Bird, H., Lahey, B., Richters, J., &
Schwab-Stone, M. (in press). The NIMH Methods for the Epidemiology of Child
and Adolescent Mental Disorders (MECA) study: Are both parent and child
informants always needed?. Journal of the American Academy of Child and
Adolescent Psychiatry, (* designates joint first authorship).
Jensen, P., Mrazek, D.,
Knapp, P., et al. (1997). Evolution and revolution in child psychiatry: ADHD
as a disorder of adaptation. Journal of the American Academy of Child and
Adolescent Psychiatry, 36, 1672-1679.
Jensen, P., Kettle, L.,
Roper, M., Sloan, M., Dulcan, M., Hoven, C., Bird, H., Bauermeister, J.,
& Payne, J. (1999). Are stimulants over-prescribed? Treatment of ADHD in
four U.S. communities. Journal of the American Academy of Child and
Adolescent Psychiatry, 38, 797-804.
Lahey, B., Applegate, B.,
McBurnett, K., Biederman, J., Greenhill, L., Hynd, G., Barkley, R., Newcorn, J.,
Jensen, P., Richters, J., Garfinkel, B., Kerdyk, L., Frick, P., Ollendick,
T., Perez, D., Hart, E., Waldman, I., & Shaffer, D. (1994). DSM IV field
trials for Attention Deficit/Hyperactivity Disorder in children and
adolescents. American Journal of Psychiatry, 151, 1673-1685.
Levy, F., Hay, D.,
McStephen, M., Wood, C., & Waldman, I. (1997). Attention-deficit
hyperactivity disorder: a category or a continuum? Genetic analysis of a
large-scale twin study. Journal of American Academic Child and Adolescent
Psychiatry, 36, 737-744.
MTA Cooperative Group.
(in press). 14-month randomized clinical trial of treatment strategies for
Attention Deficit Hyperactivity Disorder. Archives of General Psychiatry.
MTA Cooperative Group.
(in press). Moderator and mediator challenges to the MTA study: Effects of
comorbid anxiety disorder, family poverty, session attendance, and community
medication on treatment outcome. Archives of General Psychiatry.
National Institutes of
Health. (in press). Diagnosis and treatment of Attention Deficit
Hyperactivity Disorder: NIH consensus statement 1998 Nov 16-18; 16(2). Journal
of American Academic Child and Adolescent Psychiatry.
Rappley, M., Gardiner,
J., Jetton, J., & Houang, R. (1995). The use of methylphenidate in
Michigan. Archives of Pediatric and Adolescent Medicine, 149,
675-679.
Richters, J., Arnold, L.,
Jensen, P., Abikoff, H., Conners, C., Greenhill, L., Hechtman, L., Hinshaw,
S., Pelham, W., Swanson, J. (1995). NIMH collaborative multisite, multimodal
treatment dtudy of children with ADHD: I. background and rationale. Journal
of American Academic Child and Adolescent Psychiatry, 34,
987-1000.
Schwab-Stone, M., Dulcan,
M., Jensen, P., Canino, G., Bird, H., Lahey, B., & Rae, D. (1996). The
NIMH Methods for the Epidemiology of Child and Adolescent Mental Disorders (MECA)
study: Validity of the DISC - 2. Journal of American Academic Child and
Adolescent Psychiatry, 35, 878-888.
Shaffer, D., Fisher, P.,
Dulcan, M., Davies, M., Piacentini, J., Schwab-Stone, M., Lahey, B.,
Bourdon, K., Jensen, P., Bird, H., Canino, G., & Regier, D. (1996). The
second version of the NIMH Diagnostic Interview Schedule for Children (DISC
- 2). J. Am. Acad. Child Adol. Psychiatry, 35, 865-877.
Sloan, M., Jensen, P.,
& Kettle, L. (1999). Assessing services for children with ADHD: Gaps and
opportunities. Journal of Attention Disorders, 3, 13-29.
Swanson, J., Sergeant,
J., Taylor, E., Sonuga-Burke, E., Cantwell, D., & Jensen, P. (1998).
Attention Deficit Hyperactivity Disorder and Hyperkinetic Disorder. Lancet,
351, 429-33.
Weisz, J. & Jensen,
P. Efficacy and effectiveness of psychotherapy and pharmacotherapy with
children and adolescents. (in press). Mental Health Services.
Zito, J., Safer, D.,
Riddle, M., Johnson, R., Speedie, S., & Fox, M. (1998). Prevalence
variations in psychotropic treatment of children. Journal of American
Academic Child and Adolescent Psychiatry, 8, 99-105.
Zito, J., Safer, D.,
Dosreis, S., & Riddle, M. (1998). Racial disparity in psychotropic
medications prescribed for youths with medicaid insurance in Maryland. Journal
of American Academic Child and Adolescent Psychiatry, 37,
179-184.
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Thomas
M. Achenbach, Ph.D., University of Vermont
Having
metamorphosed from Minimal Brain Damage (MBD) through Hyperkinetic Reaction
of Childhood and Attention Deficit Disorder (ADD), what is now known as
Attention-Deficit/Hyperactivity Disorder (ADHD) is receiving enormous
publicity in the popular media, as well as in the professional literature.
Its precise nature, etiology, prevalence, developmental course, and
appropriate treatment remain subject to debate. However, existing findings
can help us focus in on what we need to learn.
What We Know
1. Criteria for
ADHD. The DSM criteria for ADHD changed in 1980 (DSM-III), 1987
(DSM-III-R), and 1994 (DSM-IV), and they differ from the ICD-10 (1992)
criteria. The different diagnostic criteria classify different groups and
proportions of children. In addition to these diagnostic criteria, there are
numerous rating scales and other procedures for assessing ADHD. Because
there is no single gold standard, data from multiple procedures must be
aggregated for both research and clinical purposes.
2. Gender and Age
Differences. Most research, clinical services, and diagnostic
criteria focus on young boys. Fewer girls and fewer older children meet DSM
criteria for ADHD, possibly owing to lower base rates for disruptive
behaviors in these groups. Adult ADHD has become widely publicized, but the
DSM does not provide criteria for adult ADHD.
3. Prevalence. Studies
suggest prevalence rates of about 2 to 6% for 7-10-year-old boys. Lower
prevalence rates for girls and other ages may reflect the differential
relevance of ADHD diagnostic criteria rather than real differences in
prevalence. Both epidemiologic data and the many referrals for clinical and
special education services indicate that large numbers of boys are
identified as having ADHD.
4. Correlates and
Comorbidity. Poor school achievement, poor peer relations, and
conduct problems are commonly reported correlates of ADHD. Reports of
comorbidity with other disorders may reflect biases (e.g., Berkson’s bias)
arising in the study of clinical samples.
5. Etiology.
Hyperactive behavior was initially viewed as reflecting brain damage but,
brain damage has not been supported as a typical cause. Indicating moderate
heritability, genetic research suggests polygenic influences on quantitative
parameters, rather than single gene causation of a disease entity.
6. Treatment.
Research has documented the efficacy of stimulant medications, but the
effects may not be specific to ADHD, because similar effects on attention
have been found with non-ADHD subjects. Parent training, behavior
modification, and special educational services are widely used, often in
conjunction with stimulant medications.
7. Long-term
Outcomes. Follow-ups of clinical samples show that children
diagnosed as ADHD subsequently manifest a variety of problems, suggesting
that ADHD leads to multiple kinds of psychopathology. However, longitudinal
studies of general population samples indicate that attention problems per
se mainly predict poor academic achievement.
8. Cross-cultural
Comparisons. Standardized ratings of children’s attention
problems vary modestly across epidemiologic samples from diverse cultures.
U.S. children do not rate exceptionally high in attentional problems.
9. Long-term
Trends. Comparisons of U.S. general population samples over a
13-year period showed significant increases in ADHD problems. However, the
increases in ADHD problems may reflect general increases found in many
behavior problems rather than in ADHD per se.
What We Need
to Learn
Epidemiologic tabulations
of cases meeting current diagnostic criteria are not likely to be helpful
until we learn more about the issues listed below.
1. How Can We
Take Account of Differences Related to Gender, Age, Assessment Procedures,
and Sources of Data? The application of the same a priori
diagnostic cutpoints to both genders, all ages, different assessment
procedures, and different sources of data may obscure differences related to
these factors. More research needs to focus on females, in general, and on
adolescents and adults of both genders. Empirically based multi-source
assessment instruments can provide more precise data on the base rates and
correlates of ADHD symptoms by gender, age, and source.
2. How Can We
Better Aggregate Diagnostic Data? Prevailing diagnostic
procedures for ADHD fail to specify how different kinds of data should be
aggregated in determining caseness. Rather than assuming that all procedures
are co-equivalent or that diagnosticians accurately combine all relevant
data, we need to compare algorithms for quantifying the probability and
severity of ADHD.
3. How Can We
Use Epidemiological Findings Based on Better Diagnostic Criteria to Improve
Research on Etiology? Norms and findings from epidemiological
research can help us refine etiological hypotheses and can improve
ascertainment of true cases for testing such hypotheses.
4. How Can We
Use Epidemiological and Etiological Findings to Improve Prevention and
Treatment? More accurate identification of true cases, better
documentation of incidence and prevalence, and better knowledge of
etiologies will lead to more precisely targeted prevention and treatment
efforts.
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