J R Soc Med 2004;97:531-535
doi:10.1258/jrsm.97.11.531
© 2004 Royal Society of Medicine
What happens when children with attention deficit/hyperactivity disorder grow up?
Giles Newton-Howes MB MRCPsych
Child and Adolescent Psychiatry, Ealing Hospital, London UB1 3HW,
UK
Correspondence to: 61 Carthew Road, London W6 0DU, UK
 |
INTRODUCTION
|
|---|
Attention deficit/hyperactivity
disorder
1 and the
associated
hyperkinetic
disorder,
2 hereafter
both referred to as ADHD,
are the most prevalent and best researched of all
the childhood
mental illnesses. Although not diagnostically identical, the
combined
type ADHD and ICD-10 hyperkinetic disorder have sufficient in
common
for research into the two to be considered in parallel.
They are, as we shall
see, common, disabling and probably neurobiologically
based. The received
wisdom over the years has been that ADHD
is a disorder of childhood whose
symptoms lessen over
time;
3,4
consequently
little attention was paid to the possibility that it might
continue
into adulthood. But is this old consensus correct? What does
happen
to the children who have ADHD?
The diagnosis and treatment of ADHD is a perplexing area for the child and
adolescent psychiatrist, and in the opinion of some clinicians and researchers
the check-lists of the DSM-IV and ICD-10 do little justice to the psychosocial
and behavioural aspects of hyperkinetic
activities.5
Moreover, review of the published work is hampered by the numerous changes in
diagnostic criteria over the
years.6 The notion
that ADHD phenomena reflect other disorders, rather than being core components
of a nosologically separate identity, persisted (particularly in the UK) long
after the discovery by Bradley in 1937 that stimulant medication has a calming
effect on hyperactive
children.7 However,
as the diagnostic tools have become more robust and the evidence to support
pharmacological treatment has become stronger, the doubters are now in a
minority. The attention dyscontrol–impulsivity–hyperactivity triad
is widely accepted not only as a formal mental disorder but also as one whose
diagnosis and management, both pharmacological and psychosocial, can offer
profound benefit for the child and family.
Because ADHD was diagnosed and managed principally by child and adolescent
psychiatrists, the long-term fate of the patients suffered relative neglect.
The likelihood of remission seemed to be supported by a steady reduction in
symptoms over time.8
However, the dearth of information has been substantially remedied over the
past two decades and the possibility of ADHD as an adult diagnosis is gaining
ground—opening treatment options for those affected. This paper explores
existing knowledge and potential areas for further research.
|
EPIDEMIOLOGY OF CHILD TO ADULT ADHD
|
|---|
Most of the epidemiological studies into ADHD and its longitudinal
trajectory
have been conducted in the Americas and the UK. In children,
ADHD
is known to be a common condition: the prevalence of hyperkinetic
disorder in
7-year-old boys in an inner-city British sample
was
1.5%.
9 A community
sample from Puerto Rico of children under
11 yielded a higher prevalence,
6.7%,
10 whilst that
in an American
paediatric population was
9.5%.
11 In a German
survey of elementary
school children, DSM-III criteria indicated a 9.6%
prevalence
of attention deficit disorders; however, use of DSM-IV raised
this
to 17.8%.
12
Clearly, some of the differences in reported
prevalence are due to variations
in the severity and breadth
of characteristics included. The ICD-10 diagnosis
of hyperkinetic
disorder is more restrictive than its DSM counterpart; it
compares
best with ADHD-combined type, which partly explains the lower
prevalence
in places (such as the UK) where ICD-10 is used as the diagnostic
tool.
ADHD is generally held to have a prevalence of between 2% and
8% in
school-aged children. In certain populations of children—including
those
in offender units and those with strong family histories
of ADHD—the
prevalence of ADHD is exceptionally high.
Garland
et
al.
13 looking
at a high-risk community sample in
San Diego, California, found ADHD and/or
disruptive behaviour
disorders in as many as half the children.
If ADHD were largely confined to childhood we would expect to see the
prevalence rates dropping sharply in late adolescent samples. The
epidemiological research to date does not indicate such a phenomenon. In an
American community sample of children in their final year at school (mean age
18 years) the prevalence was 1.5% overall, and 2.6% in the
males.14
Furthermore, prospective studies of ADHD children show that, although there is
a trend towards amelioration of symptoms, a substantial proportion continue to
have at least one disabling symptom in adolescence and young adulthood. A New
York cohort of children aged 6–12 with ADHD was followed up
longitudinally, and after 10 years about a quarter still met the diagnostic
criteria.15 A
similar study in Montreal gave even more striking results; two-thirds of
children with ADHD continued to be disabled by the disorder in early
adulthood.16 There
is little doubt that, for some at least of those affected in childhood, ADHD
continues into adult life.
|
AETIOLOGY
|
|---|
If ADHD is related to developmental dysfunction of the brain,
we would not
expect it simply to ‘go away’ in adulthood.
The phenotypic
manifestations might be altered by the person’s
environment but the
underlying deficit would persist. Such evidence
of neurobiological changes has
emerged from structural neuroimaging
in the brains of children, teenagers and
adults. With MRI, Hynd
et
al.
17 noted
abnormalities in the frontal lobes of patients
with ADHD, most pronounced in
the right frontal lobe. Others
report abnormalities of the caudate nucleus,
with reversal of
the normal asymmetry whereby the left basal ganglia are
larger
than the
right.
18 A decrease
in the volume of the corpus callosum
has been described, perhaps signifying
subnormal interhemispheric
connectivity.
19
These
variations from normal are in areas associated with control
of motor
activity and the proposed ‘attention centres’—exactly
the
areas where abnormalities would be expected in these patients.
These results,
however, await replication by other groups.
Other information has come from functional neuroimaging with positron
emission tomography. Zametkin et al. studied
adults20 and
children21 with
ADHD to see whether glucose metabolism in their brains differed from that in
normal controls. Both adults and children with ADHD proved to have subnormal
metabolism in the premotor and superior frontal cortex. Again this finding has
yet to be replicated.
There is also strong evidence that perinatal insults increase the
prevalence of ADHD. In a case–control study Mick and others found a
2-fold increase associated with prenatal smoking and a 2.5-fold increase
associated with inutero exposure to
alcohol.22 The same
group also found case–control evidence for a correlation between low
birthweight (<2500 g) and an up to 3-fold excess risk of
ADHD.23 Their work
built on earlier
reports24
suggesting that these three factors are all potential causes of neurological
damage leading to the phenotypic picture of ADHD.
The final biological link in the aetiological chain comes from twin
studies, with their ability to differentiate environmental from genetic
influences. In a study of monozygotic (MZ) and dizygotic (DZ) twin pairs
Goodman and
Stevenson25 showed
a MZ:DZ ratio of 51:33, and from this they extrapolated the heritability of
inattention and hyperactivity traits to be in the region of 30–50%
compared with a 0–30% influence for environmental factors.
Despite the above evidence, the neurobiological theory of ADHD is well
short of proof. As indicated, much of the work is preliminary, and replication
when attempted has not always been
successful.26 With
imaging reports readers need to bear in mind the vast amount of information
analysed and the fact that, with conventional statistical testing,
‘significant’ differences are to be expected for one of every
twenty comparisons. Zametkin et al., for example, looked at 60 areas
of the brain and found differences in only 4 (3 would be expected by chance
alone). We must also consider the possibility that such changes are the result
of the illness (with repeated insults to the brain) rather than the cause.
|
THE FEATURES OF ADHD AS CHILDREN GROW UP
|
|---|
If we accept the evidence for continuation of ADHD beyond childhood,
we
need to clarify the features of this disorder in adults and
how it affects
their ability to function in society. Diagnosis
in adults is hampered by a
lack of clear guidelines for the
clinician. For example, the DSM-IV
criteria
1 were
designed to
apply to children, and adults were not included in the field
trials.
27
Nevertheless
a systematic review suggests that ADHD can be reliably identified
and
diagnosed in the adult
population.
28
The core triad of features—inattention, impulsivity,
hyperactivity—applies to both children and adults, and they are chronic
and stable.29 A
reported reduction in symptoms with advancing age may be explained by
acquisition of cognitive strategies to ameliorate these
features.30 In
adults, inattention and impulsivity seem more stable markers of ADHD than
hyperactivity. Poor concentration at work (and during enjoyable leisure
activities), daydreaming and forgetfulness suggest inattention, whilst poor
tolerance to frustration, easy loss of temper and exceptional impatience
suggest inattention and impulsivity. Hyperactive manifestations such as
fidgeting and restlessness may also be present. These features can lead to
difficulties in interpersonal relationships, in maintaining a satisfactory
work record and in enjoying life in general. Such symptoms can, of course,
arise in anyone at some time. Prerequisites for the adult diagnosis are
temporality (i.e. the symptoms must have been present since childhood),
pervasiveness and functional impairment. Unfortunately, the instruments
developed to aid diagnosis are not totally specific and are particularly
error-prone in patients with comorbid psychiatric illness. Furthermore, the
boundary between ADHD and antisocial personality disorder is unclear; for
both, the essential criteria include presence since childhood, functional
impairment, interpersonal difficulties and intrapsychic distress. Just as in
young populations where hyperactive children may in fact have a primary
behavioural disorder, not all inattentive or impulsive adults should be
assumed to have ADHD.
To help resolve the clinical dilemmas, four rating scales have been
developed from the child criteria in DSM-IV, and each has been found
valid.31 The adult
attention deficit disorder evaluation scale (A-ADDES), developed by McCarney
and colleagues is most closely related to the child criteria whereas the Brown
Attention Deficit Disorder Scales and the Attention Deficit Scales for adults
give more emphasis to the temporal and cognitive features of the adult
presentation of ADHD. The Wender–Utah self-rating scale, which looks at
the symptoms of ADHD against an adult
background,32 can
be used to make a retrospective diagnosis of ADHD in childhood, thus
fulfilling the requirement for temporality. There is little to choose from
between these scales, however.
|
SOCIAL DIFFICULTIES FOR THE ATTENTION-DEFICIENT ADULT
|
|---|
Clearly, the cognitive and functional defects associated with
ADHD in
adults will lead to social and interpersonal difficulties.
The path of
adolescents with ADHD continues the childhood trend
of divergence from that of
their peers. They perform worse at
school and are at greater risk of
suspension or
expulsion.
33
Doubtless
in consequence, the occupational achievement of young adults
with
ADHD is poorer than that of matched
peers.
34 However,
possibly
the most disabling aspect of ADHD in adulthood is the disruption
it
causes in interpersonal relationships, with increased risk
of chronic conflict
with work peers, socially inappropriate
behaviours, disputes with partners and
spouses and trouble with
the
law.
35
Troubles at home in maintaining and sustaining family relationships are
most sharply highlighted in the prospective sample followed up by Weiss and
Hechtman.36 The
difficulties arose not only from the personal struggle to maintain
relationships but also from the problems of coping with their similarly
affected children. Moreover, adults with ADHD seem to produce more than the
average number of
offspring,37 and an
individual who personally struggles with inattention and impulsivity will have
difficulty in mustering the parenting skills to deal with an ADHD-disordered
child. Clearly there is substantial social morbidity in this group.
|
COMORBID PSYCHIATRIC SYMPTOMS IN ADOLESCENTS AND ADULTS
|
|---|
So many people with ADHD have coincident depression that some
workers
suggest that genetic risk factors for the two illnesses
may be
similar.
38 Up to
16% of adults with depression have been
reported as having
ADHD,
39 so the
pharmacological treatment
of adult ADHD with antidepressants has received
considerable
investigation. There is also some evidence that ADHD is
correlated
to recurrent brief depression—a disorder whose aetiology
may
differ somewhat differ from that of classic
depression.
40
The rate of substance misuse in the ADHD population is also said to be
raised.41 Not all
researchers, however, have confirmed this association and some have noted it
only in adults who continue to experience core symptoms of
ADHD.15 Alcohol
consumption in pregnancy is a risk factor for ADHD, so perhaps one disorder
predisposes to the other or they are intertwined. Since conduct disorder is
associated with ADHD in children it is not surprising that adolescents with
ADHD tend to show antisocial personality
traits.42 This is
reflected in the greater rates of criminal involvement in young
adulthood.43 The
correlation between ADHD and adult psychiatric comorbidity is stronger in
females then in males: girls with ADHD had a greater risk of psychiatric
admissions in adulthood and this was significantly increased if they also had
a history of conduct
problems.44
The research to date, although not conclusive, points to a link between
ADHD in adults and a broad range of other psychiatric ills—notably
affective, substance-misuse and antisocial disorders. Probably most adults
with ADHD seek advice from primary care or psychiatric services at some point
in their lives, and in a patient with alcohol dependence or personality
disorder the ADHD is easily missed. Clinically the diagnosis is important to
make in view of the prognostic and treatment implications.
|
MANAGEMENT OF ADULT ADHD
|
|---|
Since ADHD in adults adversely affects work, interpersonal relationships
and
ability to function constructively and happily within society,
effective
interventions might have a strongly positive effect
on the trajectory of an
individual’s life and benefit
society at large. As children treated with
stimulants for ADHD
approach adulthood, the usual practice (underwritten by
guidelines
from the National Institute for Clinical Excellence) is to try
them
off medication periodically to see if it is still required.
At this time the
external pressure to treat, from schools and
parents, is likely to be easing,
so that the young adult becomes
the sole decision-maker. Also most stimulants
are licensed only
for use in children, and care is transferred to teams
serving
adults. Thus, treatment usually stops. It is unsurprising, then,
that
the main focus of interest has been pharmacological treatment,
with the
emphasis on stimulant medications of the sort used
in children. So far,
however, only fifteen controlled studies
of stimulants have been reported in
adults, compared with over
a hundred in the child population. With
methylphenidate the
response rates ranged from
25%
45 to
78%
46 (compared
with about
70% in children). The weakness of these studies lies in the
absence
of widely recognized diagnostic criteria, instruments
to measure efficacy and
‘therapeutic medication range’.
In a novel approach, the possible
role of nicotine has been
investigated. Conners
et
al.
47 found
significant improvements
in the symptoms of adults with ADHD using a 7 mg/day
transdermal
patch. If confirmed effective, this strategy will offer the
additional
advantage of helping patients who smoke to stop; the general
health
benefits of smoking cessation tend to be underrated in
psychiatric
practice.
48
Non-stimulant medications have attracted more interest in adults than
children with ADHD, especially antidepressants, but no long-term randomized
trials of commonly used antidepressants have been reported. Noradrenergic
antidepressants have also been reported beneficial in early work, but not all
experts are persuaded: Wender argues that adults with ADHD are more prone to
the side effects of these compounds and that there is no overall
benefit.49
In children the possibility of using antihypertensives has been explored
and clonidine is considered a useful second-line when stimulants are
contraindicated (e.g. in severe tic disorders). Clonidine has not been
investigated in adults with ADHD. Some small studies suggest benefit from
beta-blockers against impulsive
symptoms.50 The
novel antidepressant bupropion has also been shown effective in treating the
core adult ADHD
symptoms,51 and
this is particularly noteworthy in view of the stimulant-like structure of
this drug. Clarification of the value of nonstimulant medication in this group
of patients is important since many are substance misusers in whom stimulant
therapy is undesirable.
Medication is not the only therapeutic option, though it is much more fully
researched than others. Several experts in the area of adult ADHD back the use
of psychotherapeutic interventions. Also, positive results are emerging from
cognitive approaches to the treatment of adult
ADHD.52
|
CONCLUSION
|
|---|
ADHD is a disorder whose features change over time but which
commonly
persists into adult life. Recognition of this fact
will lead to wider
diagnosis and better treatment. For adults
with ADHD the future is much
brighter than it was even ten years
ago.
|
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INTRODUCTION
EPIDEMIOLOGY OF CHILD TO...
