Content uploaded by Lydia Furman
All content in this area was uploaded by Lydia Furman on May 15, 2015
Content may be subject to copyright.
To Print: Click your browser's PRINT button.
To view the article with Web enhancements, go to:
What Is Attention-Deficit Hyperactivity Disorder (ADHD)?
Lydia Furman, MD
J Child Neurol. 2005;20(12):994-1003. ©2005 BC Decker, Inc.
Attention-deficit hyperactivity disorder (ADHD) is described as the most common neurobehavioral condition of
childhood. We raise the concern that ADHD is not a disease per se but rather a group of symptoms representing
a final common behavioral pathway for a gamut of emotional, psychological, and/or learning problems.
Increasing numbers of children, especially boys, are diagnosed with ADHD and treated with stimulant
medications according to a simplified approach. Methodical review of the literature, however, raised concerning
issues. "Core" ADHD symptoms of inattentiveness, hyperactivity and impulsivity are not unique to ADHD. Rates
of "comorbid" psychiatric and learning problems, including depression and anxiety, range from 12 to 60%, with
significant symptom overlap with ADHD, difficulties in diagnosis, and evidence-based treatment methods that do
not include stimulant medications. No neuropsychologic test result is pathognomic for ADHD, and structural and
functional neuroimaging studies have not identified a unique etiology for ADHD. No genetic marker has been
consistently identified, and heritability studies are confounded by familial environmental factors. The validity of
the Conners' Rating Scale-Revised has been seriously questioned, and parent and teacher "ratings" of school
children are frequently discrepant, suggesting that use of subjective informant data via scale or interview does
not form an objective basis for diagnosis of ADHD. Empiric diagnostic trials of stimulant medication that produce
a behavioral response have been shown not to distinguish between children with and without "ADHD." In
summary, the working dogma that ADHD is a disease or neurobehavioral condition does not at this time hold up
to scrutiny of evidence. Thorough evaluation of symptomatic children should be individualized, and include
assessment of educational, psychologic, psychiatric, and family needs.
Attention-deficit hyperactivity disorder (ADHD) has become a common diagnosis in the United States, with
reported rates in school-aged boys and girls of approximately 10% and 4%, respectively, and increasing
numbers of children on stimulant medications. Professional organizations, including the American Academy of
Pediatrics and the American Academy of Child and Adolescent Psychiatry, have issued consensus statements
on the evaluation and treatment of ADHD, and most physicians accept ADHD as a diagnostic entity.
teachers and parents also readily apply this label to children in their care. ADHD is described as the "most
common neurobehavioral disorder of childhood."
Before we permit ourselves to ride this "tidal wave" of
apparent agreement, it might be helpful to critically review underlying evidence and suppositions. What, really, is
ADHD? Is ADHD a collection of symptoms, or is it a disease entity? Who is qualified to diagnose, evaluate, and
treat these symptoms or this condition?
At first blush, the American Academy of Pediatrics guidelines would seem to provide a blanket of comfort to the
beleaguered primary care physician. They define the "core symptoms" of ADHD as "inattentiveness, impulsivity
and hyperactivity" and urge clinicians to use the Diagnostic and Statistical Manual of Mental Disorders-IV (DSM-
IV) criteria to make a diagnosis.
The guidelines acknowledge that there is no objective test or identified
etiology for ADHD and that diagnosis relies on subjective criteria. Pediatricians are directed to assess for
“comorbidities,' such as major affective disorders and learning problems. They should then begin treatment of
diagnosed children with "stimulant medications and/or behavioral treatment" after "negotiating target
The guidelines are concrete and appear to codify what many pediatricians think they are already
doing. However, a recent study found that only 25.8% of pediatricians "reported routine use of all 4 diagnostic
components" and only 53.1% performed follow-up visits three to four times per year, as recommended for their
patients on stimulant medications.
There must be obstacles to use of the guidelines, and it is reasonable to
examine assumptions underlying both the guidelines and the "diagnosis" of ADHD.
Seite 1 von 11What Is Attention-Deficit Hyperactivity Disorder (ADHD)?
PDF created with pdfFactory trial version www.pdffactory.com
Concern has been raised that symptoms or groups of symptoms do not constitute a diagnosis and that the core
symptoms of ADHD do not constitute a diagnostic entity.
Pediatricians are trained to evaluate signs and
symptoms to reach a differential diagnosis. Cough and fever are obvious examples of prominent symptoms that
are not diagnoses in themselves. Although codeine suppresses cough and ibuprofen suppresses fever,
treatment of symptoms is not the primary or only diagnostic and therapeutic approach. Either cough or fever can
be due to a concerning underlying condition or to a fleeting minor ailment, and evaluation will be based on the
details of the child's history and physical examination. To make a diagnosis, testing (such as a chest radiograph
or blood counts) and follow-up might be needed. Few clinicians would consider using suppressive medications
(such as codeine and ibuprofen) for longer than a brief finite period, and most would worry about missing a
treatable and/or less common underlying diagnosis, such as malignancy or pneumonia. Thus, there is no model
within primary care for basing diagnosis and treatment on symptoms alone, and the recommended approach to
ADHD runs counter to most pediatricians' formal training.
Following the "symptoms do not constitute a diagnosis" logic leads us in two immediate directions. First, several
authors have considered other hypotheses regarding the core symptoms of inattention, distractibility, and
hyperactivity, including the possibilities that this behavior represents (1) one end of a normal distribution of
school-aged behavior (especially for boys, who are overrepresented in every study), (2) an expression of
endogenous temperament, (3) differences in rates of developmental maturation, or (4) rigid or unreasonable
parental, societal, or educational expectations for school-aged children.
Since a relatively high percentage
of children are identified in cross-sectional studies as having core symptoms, it would be interesting to study
whether an equally high percentage of children could be identified as having "overattention and hypoactivity"
beyond 2 SD for age on the other end of a normal distribution of behavior for school-aged children.
Obviously, this study has not been done and is unlikely to be done because these children do not cause
disruption or behavior management problems.
Second, we need to examine the possibility that for some or many children, the core symptoms of ADHD are
neither a normal variant nor a defined disease state. These symptoms might represent expressions of
internalized conflict or unmet emotional or educational needs that differ from child to child. In this scenario, each
child should have a full medical, educational, and psychologic or psychiatric evaluation. The American Academy
of Child and Adolescent Psychiatry previously formally recommended as an initial evaluation (1) an interview
with the parents (to include the child's and the family's history); (2) use of standardized rating scales; (3) school
information, including the results of academic testing; (4) a (psychiatric) child diagnostic interview; (5) a family
diagnostic interview; (6) a complete physical examination; and (7) referral for additional testing as needed.
this approach, multiple diagnoses are actively considered, including psychiatric and affective disorders,
educational and learning disorders, and family psychopathology, ranging from stress following a divorce or
bereavement to domestic violence, abuse, and substance abuse. This comprehensive approach has been
condensed beyond recognition in the American Academy of Pediatrics guidelines, which direct the pediatrician
to obtain qualitative information from school and parents, make a diagnosis of ADHD based on DSM-IV criteria,
and "evaluate for co-existing conditions…although the pediatrician might not always be in a position to make a
precise diagnosis [of the same]."
The guidelines do not recommend referral to mental health or educational
specialists. The new American Academy of Pediatrics approach thus offers an expedited but significantly less
comprehensive approach to symptom evaluation.
One significant obstacle to acceptance of ADHD as a "neurobehavioral" disease entity is the lack of evidence of
an underlying unique genetic, neurologic, psychologic, or biologic pathology and the lack of an identified
etiology. Work showing the "heritability" of ADHD suffers from difficulty distinguishing genetic heritability, which
has not been proven, from environmental and parenting influences. No genetic marker has been consistently
identified, despite extensive study of putative genes in the dopaminergic, serotoninergic, and noradrenergic
Interpretation of twin studies is confounded by environmental influences.
A recent review
article concluded that "more work from twin and molecular genetic studies is needed to determine if the
increased familiality of persistent ADHD reflects the actions of genes or of familial environmental causes."
"Environmental influences" are associated with ADHD and include lower socioeconomic status, maternal
psychopathology, and family conflict.
In younger children (ages 3-7 years), maternal anxiety and mood
disorders, substance abuse, and other psychopathology, including parental childhood ADHD symptoms and
disruptive behavior, are each associated with the diagnosis of ADHD; others have reported similar findings in
older children diagnosed with ADHD.
A recent study examining correlates of comorbid psychopathology in
300 referred children with a "confirmed" diagnosis of ADHD (mean age 10.7 years; 83.3% boys) found a 19.3%
rate of parental antisocial or criminal behavior, defined as an arrest for other than a motor vehicle violation, and
a 30% rate of parental substance abuse.
Deficits in "executive function" have been postulated as a cause of ADHD or at least as a prominent
disturbance. Executive functioning is defined differently by different authors but broadly includes the ability to
self-monitor, stay focused in the face of interference, think flexibly, and organize oneself. Although
corresponding deficits on neuropsychologic testing "that likely require the interaction of several executive
functions for adequate performance" have been identified (in addition to specific cognitive deficits in other
Seite 2 von 11What Is Attention-Deficit Hyperactivity Disorder (ADHD)?
PDF created with pdfFactory trial version www.pdffactory.com
domains), there is no single profile that is diagnostic or pathognomonic for ADHD, and "many of the cognitive
deficits seen in ADHD also are observed in other neurodevelopmental disorders."
"Executive function" is currently thought to be located in five pathways in the frontostriatocortical circuitry that
connects the subcortical areas to the frontal lobe. Structural neuroimaging with computed tomography (CT) and
magnetic resonance imaging (MRI) has shown volumetric changes in these areas, including the cerebellum,
frontal lobe, and other cortical and subcortical regions, but the changes are inconsistent from study to study and
are not uniformly right or left sided.
Studies showing structural differences on neuroimaging scans between
"ADHD children" and controls suffer from small sample sizes, heterogeneous and noncomparable control
groups, a lack of replication, use of cross-sectional rather than longitudinal data, and a lack of distinction
between results that show an association and those that demonstrate cause and effect. A recent review of
research using electroencephalography and MRI in the study of ADHD concluded that, regarding "theories of
ADHD that focus on a fronto-striatal neurological circuitry substrate…, the specificity of this finding for ADHD,
"Structure-function" correlations have been attempted in which children with and without ADHD are tested on
two to three attentional tasks and then scanned with cranial MRI.
These studies also suffer from small
sample sizes, use of highly selected subjects, conflicting results, and a lack of replication. The author of one
study concluded that "the associations between attentional performance and MRI-based anatomical measures
of structure size are crude."
Functional neuroimaging studies using positron emission tomography and single-
photon emission computed tomography (SPECT) have also been conducted.
In addition to the problems
noted above, these studies have variably included control groups with symptoms overlapping the ADHD group,
have compared groups on an outcomes measure (
Tc-HMPAO brain SPECT) known to be normal in one
group, and, most significantly, speculate but cannot document a causal relationship between hypoperfusion of
given regions of the brain and "hypofunction" of those regions. To quote Roth and Saykin, "the specificity of [the]
structural and functional neuroimaging findings to ADHD is [also] largely unknown."
Meanwhile, longitudinal studies have shown that myelination of individual areas of the brain occurs at different
ages and different rates and that intracortical association might not mature until the midtwenties.
lobes are among the last regions to become functionally and anatomically mature, and maturation peaks at ages
10.5 years and again between ages 17 and 21 years.
The work of Bunge and colleagues, who performed
functional MRI on both child and adult subjects, suggests that the direct "lesion = symptom" hypothesis might be
grossly oversimplified. Although their studies were not longitudinal, they found that children and adults not only
performed differently (eg, children were more susceptible to interference on tasks) but also exhibited different
patterns of cortical activation.
Children showed "immature prefrontal activation that varied according to the
type of cognitive control required."
In other words, there appear to be developmental changes in both clinical
responses and in patterns of cortical activation associated with age and task. Whether different patterns of
activation are also related to chronic or situational stress, gender, or other influences is not known. Thus,
although patterns of cortical activation might be associated with patterns of behavior on testing, such
relationships are complex, confounded by age and possibly other factors, and do not identify a biologic etiology
for the symptoms of ADHD.
In summary, neither structural or functional neuroimaging, neuropsychologic testing, nor genetic testing offers
more than correlations between ADHD symptoms and test results, and most studies have not been replicated.
An underlying cause has not been defined, although several have been hypothesized.
In the absence of an identified underlying biologic mechanism or etiology for ADHD that would support a
diagnostic test, clinicians are asked to use criteria and rating scales. What rating scales are available to
clinicians? Psychiatrists and psychologists use a variety of techniques to identify pathology, including full and
structured interview and other diagnostic tools, whereas pediatricians have less familiarity with psychiatric
diagnostic assessment. The American Academy of Child and Adolescent Psychiatry lists seven "Common
Rating Scales" for assessing symptoms of ADHD in children in addition to the Conners' Parent and Teacher
The American Academy of Pediatrics list of "ADHD-specific Checklists" includes
only the familiar Conners' parent and teacher rating scales for children ages 6 to 17 years and an additional
scale for girls only (the SSQ-O-I Barkley's School Situations questionnaire).
The American Academy of
Pediatrics guidelines caution the clinician that these scales, which are described as able to "distinguish between
children with and without the diagnosis of ADHD," were tested under "ideal" conditions and "may function less
well in primary care clinicians" offices'and that "[the] questions on which these rating scales are based are
subjective and subject to bias."
This realistic assessment of the rating scales is borne out by further evaluation.
Research on the original Conners' rating scales showed high correlations (0.49-0.68) between items on the
teacher's scale, indicating that factors are not independent, and a high correlation on the parents' scale between
conduct problems and hyperactivity (0.55), suggesting the same problem.
Although the newer Conners'
Rating Scales-Revised are recommended, some clinicians continue to use the older version. A recent review by
Seite 3 von 11What Is Attention-Deficit Hyperactivity Disorder (ADHD)?
PDF created with pdfFactory trial version www.pdffactory.com
Collett and colleagues concluded that rating scales can "reliably, validly and efficiently measure DSM-IV based
ADHD symptoms in youth," but a careful review of the statistical methods used to reach this conclusion makes it
Only two of the nine measures examined were tested for validity, which is the crucial
question, that is, does the rating scale actually measure what we are trying to measure? Specifically, the same
population was used to both develop and validate the Conners' Rating Scale, which represents a profound
statistical oversight. Normative data for the Conners' Rating Scale-Revised are limited.
The only other ADHD
rating scale evaluated for validity (the ADHD-IV) "faired poorly with the specificity ranging as low as random
In a letter critiquing the analysis, Snyder et al stated:
In the use of rating scales, the act of applying a cutoff and assigning qualitative (clinical) meaning
to a score requires specific statistical tests to confirm the validity of the scale as used in common
practice. Considering the insubstantial results of the two rating scales [Conners and ADHD-IV] that
were tested for criterion validity and the lack of such testing of the other nine reviewed scales,
Collett et al lack sufficient evidence to conclude that rating scales can validly measure DSM-IV-
based ADHD symptoms.
Although this conclusion can be debated, it cannot be ignored. The Conners' Rating Scale-Revised, which
pediatricians commonly use and are directed to use for diagnosis and monitoring, has not yet been proven to
measure ADHD symptoms.
The use of the DSM-IV criteria for the diagnosis of ADHD is promoted. Why not accept ADHD as a psychiatric
diagnosis that primary care physicians can make based on listed criteria? The major difficulty is that the
diagnostic criteria are neither "normed" nor quantified. Judgment and experience are needed to appreciate what
is "usual" for a 7-year-old or a 10-year-old or a 14-year-old boy or girl. The impact of subjectivity on symptom
assessment is considerable. Revised DSM-IV
criteria for ADHD require that children suffer impairment from their
symptoms in more than one setting, and the American Academy of Pediatrics guidelines recommend obtaining
information from both the parent and the teacher.
It is well known, however, that there are frequent and
significant discrepancies between parent and teacher ratings of children being evaluated for ADHD.
noted: "The agreement between parent and teacher informants on the features of ADHD is quite low in virtually
For example, Mitsis et al examined 74 clinically referred children and found that "parent and
teacher agreement regarding the presence of individual symptoms in the school setting was rarely better than
chance" and that "agreement between parents and teachers on structured diagnostic interview regarding the
categorical diagnoses of ADHD…is relatively poor."
The American Academy of Pediatrics guidelines suggest
that these discrepancies might be due to differences between settings in "expectations, levels of structure,
behavioral management strategies, and/or environmental circumstances."
If these factors do impact behavior
and symptom expression (eg, attentiveness, level of activity), which most providers would acknowledge, it
becomes more difficult to attribute symptoms to an intrinsic disease condition. School referrals are more
frequent than parent referrals and are more likely to agree with physician diagnosis of ADHD.
In a study
from the United Kingdom regarding use of mental health services for hyperactivity, the strongest predictor of a
parent's perception that the child's hyperactivity was a problem meriting referral was the financial impact of the
child's behavior on either parent's work.
These and other data and many clinicians' anecdotal experiences
suggest that the disruptiveness of a child's behavior to school or home routine is the driving force for referrals;
thus, subjective assessment of the child's behavior is unlikely to be an objective diagnostic tool.
The issue of comorbid conditions is addressed in the American Academy of Pediatrics guidelines, although a
comprehensive plan with which to identify the conditions is not included. Study after study documents a
significant rate of comorbid psychiatric conditions in children diagnosed with ADHD.
conditions include problems with parent-child interaction, family violence, and parental psychopathology, as well
as childhood anxiety; mood disorders, including mania, bipolar disorder, and depression; learning disabilities;
conduct disorder; and oppositional defiant disorder. Estimates of the rates of these comorbid conditions range
from 35% to 60% for oppositional or conduct disorder, from 12% to 60% for learning disabilities, from 18% to
60% for mood disorders, including major depression, and from 25% to 34% for anxiety disorders.
nonreferral populations, it can be difficult to accurately ascertain the rates of comorbid conditions because most
primary care practitioners are not trained to make these assessments. The diagnosis of comorbid conditions is
critical because such psychopathology "may influence severity, daily functioning, treatment, and prognosis" and
"is associated with significant additional morbidity and [that] complicates the diagnosis, treatment, and prognosis
The difficulties in diagnosing and treating comorbid conditions are not trivial. For example, Plizka stated that
"almost all children younger than 12 years of age who meet criteria for [oppositional defiant disorder] or [conduct
disorder] will almost always meet criteria for ADHD."
Stimulants are reported to be efficacious for all three
conditions, although children with conduct disorder can have "aggressive outbursts" and require additional
intervention, particularly when there is significant family psychopathology.
Seite 4 von 11What Is Attention-Deficit Hyperactivity Disorder (ADHD)?
PDF created with pdfFactory trial version www.pdffactory.com
Regarding educational comorbidities, learning disability and ADHD are reported to be completely separate
conditions, although learning disability (and/or low cognitive ability) can lead to inattention and frustration in the
classroom and thus masquerade as ADHD. Children with reading disability and ADHD who are treated with
stimulants show improvement in reading scores, whereas those with reading disability alone do not; this finding
is used to support a strategy of treating all inattentive students who have academic failure with stimulant
An alternative diagnostic strategy would be to perform psychometric testing for children with
academic problems; several authors suggest that this would be the ideal approach because educational
interventions are the treatment of choice for learning problems. There is good evidence that stimulant
medications do not improve learning per se but rather improve performance on tasks requiring repetition and
One of the most difficult and controversial areas in pediatric mental health is making the diagnosis in children of
depression and other major affective disorders, including bipolar disorder.
A recent consensus statement
concluded that there are high rates of unmet needs for children and adolescents with depression or bipolar
disorder and that training in diagnosis and treatment is largely limited to child mental health specialists, with
general practitioners, including pediatricians, receiving little or no training.
According to national data, "more
than 70% of children and adolescents with serious mood disorders are either undiagnosed or inadequately
treated," and owing to the strong continuity of childhood mood disorders with adult mood disorders, this deficit
has broad implications.
Since the DSM-IV criteria were derived from adult studies, their applicability to
children is questioned, and diagnosis at least requires the input of both the parent and the child if the child is
under the age of 14 years. The consensus statement concluded that validated and developmentally appropriate
methods of diagnosis are needed, as well as trials of antidepressants, mood stabilizers, and psychotherapeutic
interventions in pediatric and adolescent populations. Stimulants are not a recommended treatment for major
affective disorders and can cause dysphoria or harmful mood dysregulation. Specifically with regard to bipolar
disorder, a recent consensus panel recommended "to carefully use the stimulants [in a child with 'coexisting
ADHD'] if clinically indicated and only after [my italics] the child's bipolar symptomatology has been controlled
with a mood stabilizer."
The combination of difficulties in both diagnosing and treating depression makes this
comorbidity a potential minefield for the primary provider not specifically trained in mental health care.
The comorbid symptoms of anxiety have received less attention but occur frequently. In the Multimodal
Trearment Study of ADHD (MTA) study, 34% of children with diagnosed ADHD also met full criteria for an
anxiety disorder, and Wilens et al found multiple (more than two) anxiety disorders in 127 (33%) of 381 school-
aged children with ADHD referred to their consultation clinic.
Possibly since anxiety is an "internalizing
disorder," compared with the more visible ("externalizing") symptoms of conduct disorder and inattention,
information from teachers is less likely to contribute to its identification.
Also, children and their parents
frequently do not concur in their assessments: the child feels anxious, and the adult does not perceive this, or
This does not mean that anxiety symptoms are unimportant; not only does the child with anxiety
symptoms suffer psychologically, but there is also strong evidence that symptoms of anxiety disorders predict
major depression and bipolar disorder.
Studies have evaluated the differential response to stimulant
medications of children with ADHD with and without symptoms of anxiety. Most studies, although not all, show
that significantly fewer children with anxiety compared with those without anxiety respond to stimulants (30%
compared with 80% in a double-blinded study).
In the MTA study, psychosocial treatment in addition to
medication benefited the anxious children with ADHD more than the nonanxious children with ADHD.
recent review concluded that "from an evidence-based perspective, cognitive-behavioral therapy is currently the
treatment of choice for anxiety [and depressive disorder] in children and adolescents."
Thus, the treatment of
choice for anxiety is not stimulants, and children with anxiety and the ADHD diagnosis do not respond as well to
stimulants. Unfortunately, most primary providers are not trained to assess children for anxiety and will be
unlikely to provide these children with optimal treatment.
In summary, the prominent and often complete symptom overlap of ADHD with other psychopathology and the
difficulties distinguishing ADHD from other pathology can be viewed as supporting the thesis that ADHD is not a
distinct neurologic or psychologic disease entity. Instead, the symptoms of hyperactivity, inattention, and
impulsivity might represent a final common behavioral pathway for a gamut of emotional, psychologic, and/or
learning problems. Clinical experience and case studies reveal that other problems, for example, occult mental
retardation, hypervigilance owing to fear or stress, and ongoing or past abuse, can masquerade as ADHD.
The primary care provider without a specific mental health background is not trained to identify or
diagnose most conditions considered "comorbid" with ADHD, and most do not have the time or experience to
fully evaluate educational and psychiatric concerns. Stimulant medication is neither the primary nor the
recommended treatment for each of these conditions, can actually be harmful in some (eg, major mood
disorders), and does not treat the underlying problem in others (eg, anxiety, abuse).
The use of stimulant medications in children with symptoms of hyperactivity and inattention is promoted by some
as a diagnostic trial. The working plan is that if the child looks, acts, or functions better on a stimulant
medication, then he or she should be on the medication, and a diagnosis of ADHD has been confirmed. The
choice of actual medication and dose is highly empiric because there is no current method of determining
Seite 5 von 11What Is Attention-Deficit Hyperactivity Disorder (ADHD)?
PDF created with pdfFactory trial version www.pdffactory.com
whether an amphetamine or a methylphenidate (or the nonstimulant amoxetine) will be "better" for an individual
patient. However, studies have shown that behavioral response to stimulants does not distinguish children with
diagnosed ADHD from normal children; thus, a behavioral response does not constitute either a diagnosis or a
treatment but rather an expected response to medication.
Motoric slowing and longer attention span for
repetitive tasks are predictable responses to stimulant medications.
Another crucial difficulty with
medication treatment is that although ADHD is described as a chronic illness, the effects of stimulant
medications on symptom suppression have not been shown to persist beyond the period of medication
treatment, and there is no evidence that the medications promote or cause psychologic, social, or emotional
Not all therapeutic trials "work," however, for the reasons discussed above. Children who demonstrate dysphoria
or outbursts or limited response to a medication trial are sometimes thought to need a higher dose of stimulant,
a different stimulant, or a second medication; in this concerning situation, many, but not all, primary providers
would ultimately refer the child to a mental health specialist. In addition, although the potential bodily side effects
of stimulants, including appetite suppression and sleep disturbance, are well known and usually monitored, the
mental and emotional side effects are less discussed and are not considered an indication to discontinue
medication. In its practice parameter, the American Academy of Child and Adolescent Psychiatry includes in its
list of "minor (expected, tolerable)" stimulant side effects mild anxiety, mild depression, mild irritability,
dull/tired/listless, mild picking at skin/nail biting, and fleeting tics.
Whether these side effects are tolerable to
the child is not known; studies that evaluate this question have not been performed. The point is that a
"diagnostic trial of stimulant medication" is not necessarily straightforward, diagnostic, or benign. Interestingly, in
the MTA trial, parents whose children received "behavioral therapy" were significantly more satisfied than those
whose children received medication alone or medication plus "behavioral therapy."
Trials examining the role
or efficacy of supportive psychotherapy for ADHD symptoms, compared with medications and/or behavioral
therapy, are not available, and the short- and long-term effects of such an approach would be interesting.
Finally, the question of extending the diagnosis of ADHD to children ages 3 to 7 years has been broached, and
medication trials are proceeding, specifically the Preschool ADHD Treatment Study, funded by the National
Institute of Mental Health, which has enrolled children ages 3 to 5 years.
The diagnostic uncertainties of
extending a criterion-based diagnosis for school-aged children to preschoolers have been reviewed.
American Academy of Child and Adolescent Psychiatry practice parameter states that preschoolers are "best
identified when the child is asked to do sedentary tasks requiring sustained attention in a structured classroom
setting, a situation not often experienced by preschoolers."
In fact, many 3-year-olds have not had previous
preschool experience, and the ability to behave acceptably and pay attention is influenced by many factors,
including separation reactions, the nature of the tasks, the expertise of the preschool staff, and the quality of the
preschool setting. The effect of longer hours of out-of-home care at an earlier age, including increased
expectations for children to "behave" in such settings in the absence of their parent or primary caregiver, might
be a factor in the expression of symptoms, including the ability to attend and focus in younger children. Gorski
noted that "the symptoms [of ADHD] are common characteristics of all very young children."
can appreciate that "attentive" for a 10-year-old is completely different than for a 4-year-old, but differences in
attention and expectations for attention differ fundamentally between grade-school children and preschoolers
owing to their different stages of personality development and brain maturation, and for good reasons, the DSM-
IV criteria for ADHD have not been extended per se to preschoolers.
Many teachers and child care
providers "on the front lines" suspect that what they are seeing in "diagnosed" preschoolers is not a disease but
developmentally shaped reactions to stress, instability, violence, bereavement, neglect, and other family and
In fact, the rates of parental and home psychopathology for preschoolers diagnosed
with ADHD are extraordinarily high.
Although use of stimulant medications in toddlers and preschoolers continues to rise, there are just six controlled
trials involving approximately 200 subjects total that have examined this subject. The limited data available
suggest that younger children require higher doses of medication for a behavioral response and have a
significantly higher rate of side effects than school-aged children and that these side effects can limit the
acceptability of treatment.
Many psychiatrists are reluctant to prescribe stimulants for preschoolers owing
to their unknown effect on the developing brain and personality and would intervene with traditional parent-child
relationship-based therapeutic interventions for preschoolers with extreme behavioral difficulties in whom the
question of an ADHD diagnosis is raised.
In conclusion, after careful review of the evidence available, it is not obvious that ADHD is either a disease or a
neurobehavioral condition. ADHD is a collection of symptoms, namely, inattention, impulsivity, and overactivity,
that overlaps with other major and minor mental health conditions. No diagnostic test confirms the diagnosis of
ADHD, and no investigative study has identified an etiology for ADHD. Screening tools and diagnostic criteria
are not validated. Although the American Academy of Pediatrics guidelines encourage primary care providers to
diagnose and treat this condition, few providers will be able to identify or appropriately manage the multiple and
significant comorbid disorders associated with the core symptoms called ADHD. There are extraordinary societal
and financial pressures that lead to the diagnosis of ADHD and the use of stimulant medications in school-aged
Seite 6 von 11What Is Attention-Deficit Hyperactivity Disorder (ADHD)?
PDF created with pdfFactory trial version www.pdffactory.com
children with behavioral difficulties. These include (1) inadequate availability and funding of both mental health
services and educational testing resources, (2) a change in 1991 that led to the inclusion of ADHD as a
reimbursable diagnosis for educational disability services under the Individuals with Disabilities Educational Act,
(3) a strong marketing effort by the pharmaceutical industry for use of stimulant medications (eg, the funding of
Children with Attention Deficit Disorder [CHADD], a parent support group for ADHD), and (4) economic
pressures on families for both parents to work longer hours, leaving less time for approaches that require
"talking therapy," making a "quick fix" involving medication and "med checks" more desirable.
Every child deserves to be cared for as an individual. Prudent and thoughtful evaluation of symptoms, including
educational, psychiatric, or psychologic, and family assessment begin the process of understanding the
individual child's difficulties and needs and of deciding which interventions will be most helpful to the child.
Children deserve our "best shot" even in the face of resource scarcity, not a "one size fits all" approach.
Certainly, many practitioners might disagree with this minority viewpoint, but the care of children can only
benefit, one hopes, from transparent dialogue about challenging clinical problems.
CLICK HERE for subscription information about this journal.
1. American Academy of Pediatrics, author Clinical practice guideline: Diagnosis and evaluation of the
child with attention-deficit/hyperactivity disorder. Pediatrics 2000;105:1158-1170.
2. American Academy of Pediatrics, author Clinical practice guideline: Treatment of the school-aged child
with attention-deficit/hyperactivity disorder. Pediatrics 2001;108:1033-1044.
3. Brown RT, Amler RW, Freeman WS, et al. Treatment of attention-deficit/hyperactivity disorder:
Overview of the evidence. Pediatrics 2005;115:e749-e757.
4. Practice parameter for the use of stimulant medication in the treatment of, children; adolescents; and,
adults. J Am Acad ChildAdolesc Psychiatry 2002;41(2 Suppl):26S-49S.
5. American Psychiatric Association . Diagnostic and Statistical Manual of Mental Disorders, 4th ed.
Washington, DC, American Psychiatric Association, 1994.
6. Rushton RL. Use of practice guidelines in the primary care of children with attention-deficit/hyperactivity
disorder. Pediatrics 2004;114:e23-e28.
7. Furman L, Berman BW. Rethinking the AAP attention deficit/hyperactivity disorder guidelines. Clin
8. Furman RA. Attention deficit/hyperactivity disorder: An alternative viewpoint. J Int Child Adolesc
9. Weinberg WA, Brumback WA. The myth of attention deficit-hyperactivity disorder: Symptoms resulting
from multiple causes. J Child Neurol 1992;7:431-435.
10. Carey WB. Is ADHD a valid disorder?. in Jensen PS, Cooper JR (eds): Attention Deficit Hyperactivity
Disorder: State of the Science. Best Practices. Kingston, NJ, Civic Research Institute, 2002, 3-1-3-19.
11. El-Sayed E, Larsson JO, Persson HE, et al. "Maturational lag" hypothesis of attention deficit
hyperactivity disorder: An update. Acta Paediatr 2003;92:776-784.
12. Coles G. The Learning Mystique. New York, Pantheon Books, 1987.
13. McGuiness D. "Attention deficit disorder: The emperor's clothes, animal "pharm," and other fiction," in
Fisher S, Greenburg RP (eds): The Limits of Biological Treatments for Psychological Distress. Hillsdale,
NJ, Lawrence Erlbaum Associates, 1989, 151-187.
14. Rydelius PA. Children of alcoholic parents: At risk to experience violence and to develop violent
behavior, in Chiland D, Young JG (eds): Children and Violence. Northvale, NJ, Jason Aronson, 1994,
15. El-Sayed E. May a genetically determined slow maturational rate explain AD/HD and hyperkinetic
disorders: A proposal of an alternate hypothesis and methodologic aspects, licentiate thesis. Stockholm,
Karolinska Institute, 1999.
16. Mattes JA. The role of frontal lobe dysfunction in childhood dyskinesis. Comp Psychiatry 1980;21:358-
17. Sandberg S. Hyperkinetic or attention deficit disorder. Br J Psychiatry 1996;169:10-17.
18. Taylor E. Developmental psychopathology of hyperactivity, in Sargeant J (ed): European Approaches to
Hyperkinetic Disorder. Zurich, Trumphimporteur, 1995, 173-189.
19. Satin MS, Winsberg BG, Monetti CH, et al. A central population screen for attention deficit disorder with
hyperactivity. J Child Psychol Psychiatry 1985;24:756-764.
20. Goldstein HS. Cognitive development in low attentive, hyperactive and aggressive 6 through 11 year old
children. J Am Acad Child Adolesc Psychiatry 1987;26:214-218.
21. Dulcan M. Practice parameter for the use of stimulant medication in the treatment of children,
adolescents, and adults. J Am Acad Child Adolesc Psychiatry 1997;36(10 Suppl):85S-121S.
22. Mill J. Quantitative trait locus analysis of candidate gene alleles associated with attention deficit
hyperactivity disorder (ADHD) in five genes: DRD4, DAT1, DRD5, SNAP-25, and 5HT1B. Am J Med
Seite 7 von 11What Is Attention-Deficit Hyperactivity Disorder (ADHD)?
PDF created with pdfFactory trial version www.pdffactory.com
Genet B Neuropsychiatr Genet 2005;133:68-73.
23. Faraone SV, Doyle AE, Mick E, Biederman J. Meta-analysis of the association between the 7-repeat
allele of the dopamine D(4) receptor gene and attention deficit hyperactivity disorder. Am J Psychiatry
24. Manor I, Tyano S, Eisenberg J, et al. The short DRD4 repeats confer risk to attention-
deficit/hyperactivity disorder in a family-based design and impair performance on a continuous
performance test (TOVA). Mol Psychiatry 2002;7:790-794.
25. Kent L, Doerry U, Hardy E, et al. Evidence that variation at the serotonin transporter gene influences
susceptibility to attention-deficit/hyperactivity disorder (ADHD): Analysis and pooled analysis. Mol
26. Steffenssson B, Lichenstein P, Larsson JO, et al. Genetic disposition for global maturity: An explanation
for genetic effects on parental report of AD/HD. Int J Behav Dev 1999;23:357-374.
27. Roth RM, Saykin AJ. Executive dysfunction in attention-deficit/hyperactivity disorder: Cognitive and
neuroimaging findings. Psychiatr Clin North Am 2004;27:83-96.
28. Levy F, Hay DA, McStephen M, et al. Attention deficit hyperactivity disorder. A category or a
continuum?. Genetic analysis of a large-scale twin study. J Am Acad Child Adolesc Psychiatry
29. Faraone SV. Genetics of adult attention-deficit/hyperactivity disorder. Psychiatr Clin North Am
30. Chronis AM, Lahey BB, Pelham WE, et al. Psychopathology and substance abuse in parents of young
children with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry 2003;42:1424-
31. Johnston C, Mash EJ. Families of children with attention-deficit/hyperactivity disorder: Review and
recommendations for future research. Clin Child Fam Psychol Rev 2001;4:183-207.
32. Fisher M. Parenting stress and the child with attention-deficit/hyperactivity disorder. J Clin Child Psychol
33. Connor DF, Edwards G, Fletcher KE, et al. Correlates of comorbid psychopathology in children with
ADHD. J Am Acad Child Adolesc Psychiatry 2003;42:193-200.
34. Giedd JN, Blumenthal J, Molloy E, Castellanos FX. Brain imaging of attention deficit/hyperactivity
disorder. Ann N Y Acad Sci 2001;931:33-49.
35. Mostofsky SH. Smaller prefrontal and premotor volumes in boys with attention-deficit/hyperactivity
disorder. Biol Psychiatry 2002;52:785-794.
36. Castellanos FX. Developmental trajectories of brain volume abnormalities in children and adolescents
with attention-deficit/hyperactivity disorder. JAMA 2002;288:1740-1748.
37. Max JE, Fox PT, Lancaster JL, et al. Putamen lesions and the development of attention-
deficit/hyperactivity symptomatology. J Am Acad Child Adolesc Psychiatry 2002;41:563-571.
38. Kates WR, Frederikse M, Mostofsky SH, et al. MRI parcellation of the frontal lobe in boys with attention-
deficit/hyperactivity disorder or Tourette's syndrome. Psychiatry Res Neuroimaging 2002;116:63-81.
39. Berquin PC, Giedd JN, Jacobsen LK, et al. Cerebellum in attention-deficit/hyperactivity disorder: A
morphometric MRI study. Neurology 1998;50:1087-1093.
40. Willis WG, Weiler MD. Neural substrates of attention deficit/hyperactivity disorder:
Electroencephalographic and magnetic resonance imaging evidence. Dev Neuropsychol 2005;27:135-
41. Semrud-Clikeman M, Steingard RJ, Filipek P, et al. Using MRI to examine brain-behavior relationships
in males with attention-deficit disorder with hyperactivity. J Am Acad Child Adolesc Psychiatry
42. Casey BJ. Implication of right frontostriatal circuitry in response inhibition and attention-
deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry 1997;36:374-383.
43. Lou HC, Henriksen L, Bruhn P, et al. Striatal dysfunction in attention deficit and hyperkinetic disorder.
Arch Neurol 1989;46:48-52.
44. Kim BN, Lee JS, Shin MS, et al. Regional cerebral perfusion abnormalities in attention
deficit/hyperactivity disorder: Statistical parametric mapping analysis. Eur Arch Psychiatry Clin Neurosci
45. Ornitz EM. Developmental aspects of neurophysiology, in: Lewis M (ed): Child and Adolescent
Psychiatry, A Comprehensive Textbook. Baltimore, MD, Williams and Wilkins, 1996, 324-335.
46. Huttenlocher PR. Morphometric studies of human cerebral cortex development. Neuropsychologia
47. Thatcher RW. Maturation of the human frontal lobes: Physiological evidence for staging. Dev
48. Hudspeth WJ, Pribram KH. Psychophysiological indices of cerebral maturation. Int J Psychophysiol
49. Bunge SA, Dudukovic NM, Thomason ME, et al. Immature frontal lobe contributions to cognitive control
in children: Evidence from fMRI. Neuron 2002;33:301-311.
50. Conners C. Conners' Rating Scales-Revised Technical Manual. North Tonawanda, NY, Multi-Health
51. Trites RL, Laprade K. Evidence for an independent syndrome of hyperactivity. J Chil