PJ Carpentier Ea P Asherson 2016 Sage Drug & Alcohol Studies CH 30 ADHD

See
discussions, stats, and author profiles for this publication at:

https://www.researchgate.net/publication/309715401
ADHD: Pathways into addiction, diagnosis

and pharmacotherapy
Chapter January 2017
CITATIONS
READS
41
3 authors:
Pieter J Carpentier
Philip Asherson
Reinier van Arkel Groep
King's College London
37 PUBLICATIONS 703 CITATIONS
419 PUBLICATIONS 15,299 CITATIONS
SEE PROFILE
SEE PROFILE
Ulrich Mller
University of Cambridge
166 PUBLICATIONS 5,036 CITATIONS
SEE PROFILE
Some of the authors of this publication are also working on these related projects:
Online Survey on Mind Wandering, Creativity, Education, and Occupation View project
CIAO II View project
All content following this page was uploaded by Pieter J Carpentier on 05 November 2016.
The user has requested enhancement of the downloaded file. All in-text references underlined in blue are added to the original document
and are linked to publications on ResearchGate, letting you access and read them immediately.
30
ADHD: Pathways into Addiction,
Diagnosis and Pharmacotherapy
P i e t e r - J a n C a r p e n t i e r, P h i l i p A s h e r s o n
and Ulrich Mller
Introduction
The diagnosis of ADHD in adult patients
with substance use disorders (SUDs) is a
relatively new concept. Although the first
reports of an association between ADHD and
addiction date from around 1970, only in the
last two decades has the high prevalence of
ADHD in SUDs patients been more systematically evaluated.
ADHD: general approaches to

diagnosis and treatment
Prevalence and clinical
characteristics
Although the diagnosis and treatment of
ADHD in childhood is well established, the
condition has for a variety of reasons been a
controversial diagnosis (Spencer et al, 1998).
SAGE-WOLFF_ET_AL.indb 491
In view of the high prevalence of this hitherto unrecognised disorder and the possible
lack of specificity of some of its symptoms,
a central issue has been the validity of the
diagnosis, although this has now been substantially addressed by several authors and
guideline groups (Faraone, 2005; National
Collaborating Centre for Mental Health,
2009). The first descriptions in children are
now a century old. Nevertheless, the ADHD
diagnosis in adults is still relatively new and
unknown, despite the first clear descriptions
by Wender, Wood and other authors in the
mid-1970s (Wood etal, 1976). In part this is
due to the decrease of motor hyperactivity
with age, which is one of the more overt and
eye-catching characteristics of the disorder
in childhood. In adulthood, ADHD symptoms are often less noticed, because adults
have learned to compensate and to adapt to a
certain extent. While motor hyperactivity
may have decreased or disappeared, the
bothersome inner restlessness is hardly
9/22/2016 12:01:10 PM
492
The SAGE Handbook of Drug & Alcohol Studies
visible and it is the inattentive symptoms

that tend to be most prominent in adults
(Biederman, 2011). Nevertheless, in a significant subset of cases (4060%) h yperactiveimpulsive symptoms persist and may be
most prominent in high risk populations
with antisocial behaviour or substance abuse
disorders. The current version of the US
diagnostic criteria, the DSM-5, is the first
diagnostic manual to explicitly recognise the
validity of the diagnosis in adulthood, specifying some of the ways in which the symptoms and other manifestations of the disorder
vary with age (Table 30.1).
A further controversy relates to the dimensional nature of the disorder. While the
symptoms that define the inattention and
hyperactivity-impulsivity of ADHD reliably cluster together, the difference between
ADHD patients and normal people is quantitative rather than qualitative. This is because
the symptoms are continuously distributed
throughout the population. The debate on
validity does not concern the more severe
cases of ADHD, where the problems are usually quite apparent, so much as the separation
between the less severe cases and normal variations in concentration and impulse control
(McGough & Barkley, 2004). In this respect,
it is important to emphasise that the diagnosis
is not based solely on the presence of ADHD
symptoms, but that these symptoms must
also be pervasive across time, be apparent in
different situations and cause clinically significant impairments, in order to define the
condition as a mental health disorder.
This is usually evident when investigating the influence of symptoms on life
history. Frequently, underachievement in
educational and occupational experiences is
a recurring theme (Fayyad & Kessler, 2015).
Circumstances and requirements also determine the level of dysfunction, and patients
often try knowingly or not to compensate
for these problems by, for example, reducing their work load and by functioning at a
less demanding level. Erratic and impulsive
behaviour also has an impact on personal
relationships, disturbing the building of stable relationships. ADHD patients tend to

meet with more frustrations and disappointments, which can have a negative impact
on their personal development, self-esteem
and mood (Weiss, 2015). The accumulation
of negative life events is one of the reasons
why ADHD is often associated with other
psychiatric disorders, including mood disorders, anxiety disorders, personality disorders and addiction. Other clinical features
that are often seen to accompany ADHD in
adults can also be a considerable source of
distress, including persistent restless agitation, emotional lability, ceaseless unfocused
mental activity and sleep problems (Adler
et al, 2015). Many of these characteristics
are non-specific and can occur in other psychiatric disorders as well, although it is the
characteristic early onset, persistent trait like
course and association with the core inattentive and hyperactive-impulsive symptoms
that distinguishes ADHD from other conditions. Nevertheless, many adult health professionals remain unfamiliar with the chronic
and persistent (as opposed to episodic) nature
of ADHD symptoms and impairments, this
helps to explain why many ADHD adults
remain undiagnosed or misdiagnosed as
other common mental health disorders.
The relatively high prevalence of ADHD
in children, as well as in adults, adds to the
controversy (Fayyad & Kessler, 2015)
given that it has only relatively recently been
recognised as a valid and treatable disorder
in adults. ADHD is one of the most common
psychiatric disorders among children and
adolescents, with the worldwide prevalence
estimated to be between 56% (Faraone
etal, 2003; Polanczyk etal, 2007; Willcutt,
2012). In children, the disorder is diagnosed
two to four times more often in boys than in
girls, but this gender difference in prevalence
seems to diminish in adulthood (Willcutt,
2012). The disorder tends to decrease with
age, but contrary to earlier expectations, the
majority of patients continue to suffer from
clearly troublesome symptoms in adulthood
9/22/2016 12:01:11 PM
ADHD: Pathways into Addiction, Diagnosis and Pharmacotherapy
493
Table 30.1Adult ADHD DSM-IV-TR-5 criteria (abridged version)

People with ADHD show a persistent pattern of inattention and/or hyperactivity-impulsivity that
interferes with functioning or development:
1. Inattention*:
1. Often fails to give close attention to details or makes careless mistakes in schoolwork, at work, or with other
activities.
2. Often has trouble holding attention on tasks or play activities.
3. Often does not seem to listen when spoken to directly.
4. Often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace
(e.g., loses focus, side-tracked).
5. Often has trouble organizing tasks and activities.
6. Often avoids, dislikes, or is reluctant to do tasks that require mental effort over a long period of time (such as
schoolwork or homework).
7. Often loses things necessary for tasks and activities (e.g. school materials, pencils, books, tools, wallets, keys,
paperwork, eyeglasses, mobile telephones).
8. Is often easily distracted
9. Is often forgetful in daily activities.
2. Hyperactivity and Impulsivity*:
1. Often fidgets with or taps hands or feet, or squirms in seat.
2. Often leaves seat in situations when remaining seated is expected.
3. Often runs about or climbs in situations where it is not appropriate (adolescents or adults may be limited to feeling
restless).
4. Often unable to play or take part in leisure activities quietly.
5. Is often on the go acting as if driven by a motor.
6. Often talks excessively.
7. Often blurts out an answer before a question has been completed.
8. Often has trouble waiting his/her turn.
9. Often interrupts or intrudes on others (e.g., butts into conversations or games).
In addition, the following conditions must be met:
Several inattentive or hyperactive-impulsive symptoms were present before age 12 years.
Several symptoms are present in two or more settings, (e.g., at home, school or work; with friends or relatives; in
other activities).
There is clear evidence that the symptoms interfere with, or reduce the quality of social, academic and/or
occupational functioning.
The symptoms are not better explained by another mental disorder (e.g. Psychotic Disorder, Mood Disorder, Anxiety
Disorder, Dissociative Disorder, Personality Disorder, substance intoxication or withdrawal).
Based on the types of symptoms, three kinds (presentations) of ADHD can occur:
Combined Presentation: if enough symptoms of both criteria inattention and hyperactivity-impulsivity were present
for the past 6 months
Predominantly Inattentive Presentation: if enough symptoms of inattention, but not hyperactivity-impulsivity, were
present for the past six months
Predominantly Hyperactive-Impulsive Presentation: if enough symptoms of hyperactivity-impulsivity but not
inattention were present for the past six months.
Because symptoms can change over time, the presentation may change over time as well.
* Age criterion: Six or more symptoms of inattention/hyperactivity and impulsivity for children up to age 16, or five or more
for adolescents 17 and older and adults.
Duration: symptoms have been present for at least 6 months, and are inappropriate for developmental level.
(and even in old age). The problem of underdiagnosis of ADHD in adults has long been
overlooked, and has only come to the attention of professionals and general public in
the past two decades. In adults, the worldwide prevalence has now been estimated to
be around 2.54.3% (Kessler et al, 2006;
Fayyad et al, 2007; Simon et al, 2009).
9/22/2016 12:01:11 PM
494
Higher prevalence rates are found in specific

populations, for example amongst prisoners,
psychiatric patients and patients with addiction disorders (Rosler et al, 2004; Almeida
Montes et al, 2007; Nylander et al, 2008;
Rosler et al, 2009b; Huntley et al, 2012;
van Emmerik-van Oortmerssen etal, 2012).
These studies indicate a substantial prevalence, in the order of 1030%, indicating that
many adult patients with ADHD and serious
mental health or behavioural problems are
not yet diagnosed or treated.
To a substantial degree prevalence estimates are influenced by the diagnostic
thresholds applied, particularly the degree to
which impairment is taken into account when
classifying cases of ADHD (Adler et al,
2015). Helped by good intelligence, positive personality traits, support by a partner
or family and a well-structured environment,
some individuals are able to function without
apparent difficulties. Upon further investigation more subjective complaints are often
identified in such high functioning cases of
ADHD, including problems with procrastination, chronic inner restlessness, intrusive levels of mind wandering and sleep problems.
Diagnosis of ADHD in adults

For the reasons mentioned above, the diagnosis of ADHD should be substantiated by
convincing evidence of the impairing influence of the symptomatology. Information is
therefore needed about life course functioning, preferably from multiple sources, such
as partners, family members or friends, but
also previous assessments and school reports.
In most patients, objective difficulties in
social, educational and occupational activities can be readily identified, frequently
accompanied by more subjective complaints
of persistent symptoms (Adler et al, 2015).
Often a partner provides a clearer picture of
the severity of the current problems. As many
patients have limited memories of their childhood functioning, parents or older siblings
can offer relevant details on symptomatology

in childhood. In the absence of such corroborating information, clinicians have to form a
judgment on the likelihood that the symptoms in adulthood are a continuation of the
same problems from childhood.
As it is for many other mental health
disorders, assessing psychiatric comorbidity is an integral and indispensable part of
the diagnostic procedure (Adler & Cohen,
2004). Clearly it is essential to establish that
ADHD like symptoms are not secondary to
other conditions, and the presence of comorbid disorders will determine the treatments
and order of treatments that are used. An
assessment of general cognitive ability (IQ)
can be helpful in evaluating the severity of
functional impairments. Neuropsychological
assessments can be used to establish specific
problems with working memory, inattention
or inhibitory control. However, available
tests are found to lack sufficient specificity and sensitivity for diagnostic purposes
and are thought to add little additional value
to the diagnostic assessment (Murphy &
Gordon, 2006).
Neurobiology of ADHD
ADHD is a neurodevelopmental disorder
with genetic, environmental and biological
aetiologies. Genetic influences are established with high heritability estimated to be
in the range of 7080% in children, adolescents and adults (Faraone etal, 2005; Chang
etal, 2013; Larsson etal, 2013). Until now,
molecular genetic studies have only revealed
a limited number of candidate genes associated with ADHD, each of which making no
more than a small contribution to the development of the disorder. A number of these
genes are involved in dopamine and serotonin neurotransmission (Faraone etal, 2005).
Recent genome wide-scan research has also
identified genes that are involved in neural
cell growth and metabolism (Lasky-Su etal,
2008; Poelmans etal, 2011). Presently, little
9/22/2016 12:01:11 PM
is known about how this genetic disposition

interacts with environmental factors.
Although it has been established that in most
cases ADHD is not caused by negative circumstances or traumatisation during childhood, these factors can be expected to have a
negative influence on existing vulnerabilities. This also applies to neurotoxic influences (e.g. lead poisoning) and other forms
of brain damage (e.g. low birth weight, preterm births, perinatal brain damage, traumatic brain injury) (Barkley, 2006b).
Research attempting to elucidate the
neuropathophysiology of ADHD has not
only shed light on the disorder itself, it has
simultaneously provided new insights into
the mechanisms of normal cognition and
attention (Bush, 2010). Imaging techniques
in ADHD patients have chiefly revealed
abnormalities in the frontal, prefrontal and
subcortical parts of the brain (Bush et al,
2005). Functional MRI, combining neuroimaging and neuropsychological testing, has
been used to explore three cognitive domains
of impairment and their related neural networks: attention, inhibition and reward.
Patients with ADHD appear to have consistent functional abnormalities in two distinct domain-dissociated right hemispheric
fronto-basal ganglia networks, including the
inferior frontal cortex, supplementary motor
area, and anterior cingulate cortex for inhibition and dorsolateral prefrontal cortex,
parietal, and cerebellar areas for attention
(Hart et al, 2013). Aberrant ventro-striatal
responsiveness has been correlated to attentional deficiencies and impulsivity (Plichta &
Scheres, 2014).
Currently, it is impossible to capture the
clinical entity of ADHD in a single neurocognitive model, and contemporary models
emphasise a heterogeneous set of neurobiological processes (Castellanos & Tannock,
2002; Johnson et al, 2009; Dowson &
Blackwell, 2011). A well-studied model for
ADHD focuses on disruption of the executive functions, which can be detected in many
patients. The executive functions of the brain
495
are responsible for planning and organisation of purposeful behaviour in response to

incoming stimuli. One prominent hypothesis
proposed that as a result of too little inhibition of unimportant stimuli, problems arise
in the regulation and control of planned
behaviour (Barkley, 2006a). Another theory
(sometimes referred to as delay aversion)
focuses on the difficulty ADHD patients
have with maintaining long-term goals and
postponing rewards; they are far more likely
to respond impulsively to immediate than
delayed rewards (Sonuga-Barke etal, 2008).
Other hypotheses emphasise deficient energetic state regulation during cognitive tasks
(Sergeant, 2005), inappropriate activity of
the default-mode network thought to support a pattern of generalised task-non-specific cognitions during rest that interfere with
task-specific processing (Sonuga-Barke &
Castellanos, 2007; Liddle et al, 2011), and
dysfunction of the dopamine reward pathway
associated with motivational and attention
deficits (Volkow et al, 2011). The dynamic
developmental theory of ADHD explores
the development of ADHD symptomatology
as a result of altered reinforcement of novel
behaviour and deficient extinction of inadequate behaviour (Sagvolden etal, 2005).
Treatment of adult ADHD

A correct ADHD diagnosis has an important
psychological impact, as it offers an explanation for a host of problems and frustrations patients have experienced during their
lives, and opens the door to a range of effective treatments. This is the first step in helping them to deal with the disorder. Moreover
the majority of adult patients with ADHD
benefit from treatment (Kooij et al, 2010).
For the majority of patients effective pharmacotherapy is available (Table 30.2).
Medication, primarily the psychostimulants
methylphenidate and dexamphetamine, is
often highly effective in diminishing ADHD
symptomatology, but even then significant
9/22/2016 12:01:11 PM
496
Table 30.2Medication used in adult ADHD

Order of
preference
1
Medication
Standard adult
daily dosage
Efficacy in RCTs
Methylphenidate
30 80 mg
Dexamphetamine
15 40 mg
Atomoxetine
40 100 mg
Bupropion
300 450 mg
Desipramine
(tricyclic
antidepressant)
100 200 mg
Venlafaxine
75 225 mg
(+) (Amiri etal, 2012)
Guanfacine
1 4 mg
no RCTs
Clonidine
0.1 0.4 mg
no RCTs
problems in planning and structuring and

control of impulsive behaviour remain. For
adults with ADHD, several cognitive behavioural therapy programmes have been developed that help overcome such continued
impairments (Safren et al, 2005; Solanto
etal, 2010; Emilsson etal, 2011). The ingredients of these programmes are similar and
include psychoeducation, training in planning and organising skills, time management, developing strategies to counter
distractibility and procrastination, decreasing negative thinking, and emotional issues,
including acceptance of the diagnosis and
coping with disappointments and failures.
Offering these treatments in group form enables mutual recognition and the exchange of
experiences. It is also recommended to
involve the patient's partner in the treatment
(Murphy, 2005).
+++ (21 RCTs)

(Faraone & Glatt, 2010;
Koesters etal, 2008)
+++ (8 RCTs)
(Faraone & Glatt, 2010;
Koesters etal, 2008)
++ (9 RCTs)
(Cunill, 2013
CUNILL2013 /id)
+ (5 RCT)
(Maneeton etal, 2011)
++ (1 RCT)
(Wilens etal, 1996)
Remarks
Abuse potential of short-acting
formulations
Abuse potential of short-acting
formulations
Not a stimulant, no abuse
potential, continuous
efficacy
No abuse potential
More effective for hyperactivity/
impulsivity than for
concentration problems; side
effects limit use
Positive findings in open studies
(Findling etal, 1996;
Upadhyaya etal, 2001)
Effective in children and
adolescents, not well studied
in adult ADHD
Effective in children and
adolescents, not well studied
in adult ADHD.
Side effects limit use
The association between ADHD

and addiction
Prevalence
The SUDs are among the most frequently
occurring problems in adults with ADHD.
Cigarette smoking is significantly more
common in children and adults with ADHD
compared to the general population (Kollins
& Adcock, 2014). ADHD has consistently
been found in a substantial minority of any
population of addicted patients, irrespective
of the primary substance of abuse. A recent
meta-analysis of 29 well-executed studies on
the prevalence of ADHD in various SUD
populations, comprising 6689 subjects,
yielded an overall prevalence estimate of
23.1% (van Emmerik-van Oortmerssen etal,
2012). Somewhat surprising was that the
9/22/2016 12:01:11 PM
prevalence was not influenced by subjects

age, gender, ethnicity or setting. Furthermore,
the substance of abuse appeared to influence
the prevalence rate to only a limited extent;
in cocaine addicted populations a significantly lower prevalence was found. The
latest studies, using standardised and reliable
diagnostic instruments, tend to show a somewhat lower prevalence. A large international
study showed an average prevalence around
12%, although the wide variation in prevalence between study sites (from 5.4% to
31.3%) illustrated that ADHD prevalence is
also determined by patient and treatment
centre characteristics (van de Glind et al,
2013). A smaller UK study estimated the
prevalence of undiagnosed ADHD within a
drug and alcohol detox unit around 12%
(Huntley etal, 2012).
Clinical characteristics
In the majority of addicted patients currently
identified with ADHD, the diagnosis of
ADHD has never been made previously and
they have never received treatment for the
condition as children. Contrary to what has
often been assumed, and in line with the
prevalence studies, SUD patients with ADHD
do not seem to have a selective preference for
stimulant psycho-active drugs, such as cocaine
or amphetamines; rather they tend to use sedative medications, most commonly cannabis
and alcohol and sometimes heroin (Clure etal,
1999). It is quite common to encounter polydrug abuse among addiction patients with
ADHD. Some patients report paradoxical
effects of stimulants such as amphetamines
and cocaine. They can become calm and
focused, instead of driven and agitated. Such
experiences are strongly suggestive of ADHD,
but do not form firm proof of the diagnosis.
Furthermore, not all patients with ADHD will
react positively to psychostimulants in this
way particularly if they use higher dosages
and intravenous or intranasal routes of administration. Adults with ADHD may also describe
497
cannabis as reducing some of the symptoms of

ADHD, especially mental and physical restlessness and sleep problems, an observation
that requires further investigation.
Many patients with ADHD and SUDs
have a history of serious behavioural problems in childhood: 40%93% of these
patients would have met the diagnostic criteria for oppositional-defiant disorder and/
or conduct disorder in their youth (Carroll
& Rounsaville, 1993; Schubiner etal, 2000;
Carpentier etal, 2012). In addition, as adults
many of them have developed an antisocial personality disorder, with an estimated
prevalence of 5060%, compared to 25%
in SUD patients without ADHD (Schubiner
etal, 2000; Carpentier etal, 2011). Another
characteristic of this patient population is
early initiation of substance use, most often
before the age of 20 years and not unusually before the age of 15 years (Wilens etal,
1997). There are indications that the presence
of ADHD accelerates the transitions from use
to abuse to dependence and the progression
to hard drugs (Biederman etal, 1998). Lastly,
addicted patients with ADHD tend to have a
higher incidence of comorbid psychiatric disorders, such as mood, anxiety and personality disorders (Wilens etal, 2005a; Carpentier
etal, 2011).
ADHD as a pathway into

addiction
The association between ADHD and SUDs
can be regarded as the end product of developmental interactions between ADHD symptoms (e.g. impulsivity or behavioural
dysregulation) and their consequences (e.g.
poor academic achievement). These interactions are influenced by genetic factors in several ways. ADHD seems to occur more
frequently in the families of addicted patients,
while SUDs occur more frequently in the
families of ADHD patients (Wilens, 2004;
Knopik et al, 2009; Marmorstein et al, 2009 ).
In accordance with the concept of the
9/22/2016 12:01:12 PM
498
externalising disorders spectrum (Krueger

et al, 2005), an extensive review of genetic
studies has revealed a common genetic network underlying SUDs and externalising disorders, such as ADHD (Arcos-Burgos et al,
2012). One likely section of this common
genetic basis for ADHD and addiction is probably the dopamine neurotransmission, as its
pathophysiology plays a role in both ADHD
and SUDs (Faraone et al, 2005; Kalivas &
Volkow, 2005; Volkow etal, 2009b). A pattern
of inheritance in families corresponding to a
variable expression of a common risk factor
was confirmed for the association of ADHD
and drug dependence (but surprisingly, not for
the combination of ADHD and alcohol
dependence) (Biederman etal, 2008b).
Severe (antisocial) behavioural problems
in childhood and adolescence, diagnosed
as Conduct Disorder (CD), have an even
stronger influence. In its most severe and
persisting form (in up to 40 % of adolescents with CD), this disorder is a precursor
of Antisocial Personality Disorder (ASPD)
in adulthood. A DSM-5 diagnosis of ASPD
requires a retrospective diagnosis of CD in
childhood. It has been known for some time
that CD strongly increases the risk of addiction problems in adulthood (Kim-Cohen
etal, 2003; Fergusson etal, 2007; Knop etal,
2009). ADHD and CD frequently co-occur:
the prevalence of CD in ADHD children is
estimated at around 25% (Jensen etal, 1997).
The prevalence (based on retrospective diagnosis in adulthood) is even higher (40% to
even 93%) in patients with ADHD and SUD
(Carroll & Rounsaville, 1993; Schubiner
etal, 2000). Some authors maintain that the
development of CD is the principal (if not
the only) explanation for the association of
ADHD and addiction (Lynskey & Hall, 2001;
Flory & Lynam, 2003; Tuithof et al, 2012;
Torok etal, 2012; Serra-Pinheiro etal, 2013).
Increasing evidence, however, suggests that
coexisting ADHD and CD pose the highest
risk of all for SUD (Flory etal, 2003; Marshal
& Molina, 2006; Roy, 2008; Dalsgaard etal,
2014). In practice, the combination of ADHD
and CD is most often found in addicted

patients with the more severe and complex
SUDs (e.g. opioid dependence): many of
them also have ASPD (Soderstrom et al,
2004; Carpentier etal, 2012).
Importantly, ADHD has been shown to
increase the risk for addiction independent of
CD, with the more severe forms of the disorder involving the greatest risk (Elkins et al,
2007). This is in agreement with the finding
that persistent ADHD in adulthood is more
commonly combined with addiction problems than childhood-only ADHD (Wilens &
Biederman, 2006). The risk seems to be more
closely associated with hyperactive-impulsive
symptoms than with the inattentive symptoms (Elkins etal, 2007; Chang etal, 2012)
and is therefore likely to be a more prominent
risk when the hyperactive-impulsive as well
as the inattentive symptoms persist through
adolescence and into adulthood.
A self-medication hypothesis has often
been cited in this connection (Khantzian,
1997). According to this model, patients
with a psychiatric disorder use substances
in an attempt to influence and control their
psychiatric symptoms. In practice, a lot of
ADHD patients will spontaneously mention
this kind of experience. Particularly the fact
that substances such as cannabis and alcohol induce a relaxed and calm state of mind
which they are unable to achieve themselves,
while others such as caffeine and nicotine
help them to concentrate, is given as the
reason for continued substance use. In this
way self-medication might play a prominent
role in the development of problematic substance use (Glass & Flory, 2010; Silva, Jr.
etal, 2013). In this regard, nicotine needs to
be mentioned, as studies in both adults and
adolescents have found ADHD to be associated with earlier initiation of regular cigarette
smoking and higher rates of lifetime smoking (4142% vs 26% for ADHD and nonADHD respectively) (Pomerleau etal, 1995;
Kollins & McClernon, 2015). Nicotine has
a positive effect on ADHD symptomatology, presumably because of its influence on
9/22/2016 12:01:12 PM
dopaminergic/nicotinic and acetylcholinergic

circuit dysregulation, implicated in ADHD
neuropathology (Potter & Newhouse, 2004).
Apart from cognitive, social, psychobiological and genetic factors, this mechanism of
self-medication has been proposed to explain
the alarmingly higher rates of smoking in
ADHD patients.
Secondary problems that often occur in
ADHD (such as frequent failure and demoralisation) and other comorbid disorders (such
as depression and anxiety disorders) can
increase the vulnerability towards addiction
even further (Wilens etal, 2005a).
In summary, ADHD can be considered as
a moderately serious risk factor for the development of addiction.
Prognosis
The course of an addiction seems to be more
protracted, and treatment more difficult, in
SUD patients with untreated ADHD than in
SUD patients without ADHD. Patients with
ADHD seem to derive less benefit from treatment for SUDs, show poorer treatment compliance and have greater difficulty with
achieving and maintaining abstinence
(Wilens etal, 1998; Levin etal, 2004). It is
likely that core symptoms of ADHD (e.g.
disorganisation, impulsiveness, restless agitation) and associated features (e.g. emotional instability) contribute to earlier
substance use relapse. In addition, ADHD
cannot be treated adequately until the addiction has been stabilised. Therefore, the two
disorders need to be treated together, preferably in an integrated approach.
Pathways into treatment

Diagnosis
A careful diagnostic assessment is always
recommended in ADHD patients with
499
addiction disorders (Fatseas etal, 2012). The

psychiatric comorbidity that is often seen in
these patients, can also give rise to differential diagnostic problems. Another diagnostic
issue is that ADHD symptomatology can be
masked or even mimicked by symptoms of
intoxication or withdrawal (Levin, 2007).
Although abstinence at the time of assessment is clearly preferable, it is still possible
to reliably diagnose ADHD in non-abstinent
patients. As mentioned above, the diagnosis
is not based solely on current clinical findings, but critically on anamnestic information that supports the life-long presence of
debilitating symptoms of inattention, overactive restlessness and impulsivity. A documented chronic course can help to
differentiate ADHD symptomatology from
similar (episodic) drug-induced symptoms.
Special attention must therefore be focused
on the presence of ADHD symptoms in
childhood before the initiation of drug use,
and in periods of abstinence and/or periods
of relatively stable substance use (Schubiner,
2005). ADHD symptoms should reflect a
stable and enduring pattern of symptoms and
behaviour that are present regardless of exacerbating factors such as periods of anxiety,
depression or drug and alcohol use. Bringing
in other informants (partner, parents, family)
can help to clarify the picture (Murphy &
Gordon, 2006), although further research
found good concordance in reports from
ADHD patients with addiction and their parents (Huntley et al, 2012). To accurately
judge the severity of the ADHD symptomatology (and in the case of persistent diagnostic uncertainty) it is recommended to repeat
the evaluation after stable abstinence has
been achieved (Wilens, 2004).
Treatment
Treatment planning
In adult as well as in childhood ADHD, psychiatric comorbidity can have a major impact
9/22/2016 12:01:12 PM
500
on the clinical presentation and treatment

strategy. The diagnostic workout should
therefore include an assessment of comorbid
psychopathology (mood disturbances, anxiety disorders, personality disorders) and
somatic pathology, and an evaluation of current psychosocial problems. Care should be
taken not to exclude ADHD because of the
presence of comorbid conditions as ADHD
will often be seen to accompany such disorders. This is particularly important for personality disorders which can be mimicked by
severe ADHD, particularly when accompanied by emotional instability or for more
complex cases, where ADHD symptoms
form a treatable component of a more profound behavioural disorder. Emotional instability is a common feature of ADHD and
should be expected in many cases with
ADHD and addiction disorders.
The next step is to draw up a detailed treatment plan to treat these complex problems in
a systematic and integrated manner (Magon
& Mueller, 2012). Treatment planning will
be individualised, and dictated in a large part
by the nature and severity of the SUD. In the
majority of cases treatment will start with stabilisation of the addiction: either abstinence
or maintenance (as in opioid dependence)
will be the first treatment aim. Subsequent
treatment aims at further stabilisation, usually
by means of symptomatic (mostly pharmacological) treatment of the psychiatric comorbidity. ADHD medication can be considered
at this point. When patients are sufficiently
stable, a start can be made on the more extensive (psychosocial and psychotherapeutic)
treatment of the SUD (e.g. relapse prevention) and the comorbid psychiatric disorders
(e.g. treatment of the personality disorder or
anxiety disorder). In this phase, the psychosocial treatment of ADHD can be intensified.
The importance of abstinence
In patients with serious addiction disorders,
abstinence is a necessary precondition for the
treatment of ADHD (with the exception of
patients on stable maintenance treatment
such as methadone). Persistent substance use

will have a negative effect on the medication,
either directly through interference at the
neurotransmitter level, or indirectly due to
reduced treatment compliance and irregular
medication intake. In addition, possible positive effects of the medication might be
masked by substance use (Mariani & Levin,
2007). Another problem is the risk of dangerous interactions between medication and
psychoactive drugs, although this does not
seem to be particularly detrimental in the
case of psychostimulants (Winhusen et al,
2006). If the patient is unable to remain
abstinent with outpatient support, inpatient
detoxification should be considered.
In the past, medication was rarely started
until after long-term abstinence, in order to
totally exclude interference from the psychoactive substances. The disadvantage of
this approach is that after detoxification, a
lot of patients experience more troublesome
ADHD symptoms, which makes it difficult
for them to remain abstinent and engage in
therapy. Particularly on the basis of clinical
experience, it is now advised to start ADHD
medication shortly after detoxification,
although the decision should be made on a
case-by-case basis (Wilens, 2004; Schubiner,
2005; Perez de Los Cobos etal, 2012). This
approach can also be applied to outpatient
patients with less severe addictions. In those
patients using drugs such as cannabis and
alcohol who already have some control over
their substance use and who are well motivated to curb any excessive use, a trial of
ADHD medication can be started simultaneously with further reduction in substance use.
Pharmacological treatment
There are still no widely accepted guidelines
for the appropriate pharmacological treatment of ADHD in the presence of SUDs
(Perez de Los Cobos etal, 2012). In principle, the same medication is prescribed as
that for ADHD adults without SUDs (Mariani
& Levin, 2007). Mainly for practical reasons, the lack of acute effects, the slow and
9/22/2016 12:01:12 PM
501
stable treatment response and the lack of

abuse potential (see below), atomoxetine is
easier to use in this patient population and is
often recommended as the first line drug
(Klassen etal, 2012; Upadhyaya etal, 2013).
Although positive results have been published in case reports and open studies,
convincing scientific evidence of the effectiveness of ADHD medication in this patient
group is still lacking, particularly for the
stimulant medications such as methylphenidate (Koesters et al, 2008; Perez de Los
Cobos et al, 2012). Over the years only a
limited number of placebo-controlled trials
have been conducted in comorbid ADHD
and addiction disorder groups and they were
largely unable to demonstrate any clear positive effects (Table 30.3). These negative
results are surprising, because, as highlighted before, ADHD is found to be eminently treatable, both in children and in
adults, with robust effectiveness of
pharmacotherapy in placebo-controlled trials

(Biederman & Faraone, 2005).
More research is therefore necessary to
understand the reason for these negative
results. First, there is the potential influence
of psychiatric comorbidity, particularly the
combination with a history of CD (Schubiner
et al, 2002; Levin et al, 2007). The best
results have always been achieved in patients
with a definite diagnosis of ADHD without
comorbidity, with patients with addiction
problems usually excluded from most positive controlled trials (Spencer et al, 1995;
Michelson etal, 2003). In patients with more
complex problems, diagnostic inaccuracy is
more likely to occur. The ADHD symptoms
can be caused or aggravated by other disorders (e.g. traumatic brain injury), which
might explain decreased effectiveness of the
medication.
In addition, it is quite plausible that the
long-term use of psychoactive substances
Table 30.3Randomised controlled trials of ADHD medication in adolescent (in italics) and
adult SUD patients
Study, year
Schubiner, 2002
Riggs, 2004
(adolescents)
Carpentier, 2005
Levin, 2006
Levin, 2007
Wilens, 2008
Thurstone, 2010
(adolescents)
Konstenius, 2010
McRae-Clark, 2010
Riggs etal, 2011
(adolescents)
Konstenius, 2013
Levin, 2015
Sample
size
SUD Type
Medication, maximum dose
Effect on
ADHD*
Effect on
SUD*
48
69
Cocaine
Various
Methylphenidate IR 3 30 mg
Pemolide, 75112.5 mg
+
+
0
0
25
98
Various
Opioid (MMT**)
0
0
0
++
0
0 (+)
+
0
106
80
70
Cocaine
Alcohol
Various
Methylphenidate IR, 3 15 mg
Methylphenidate SR, 2 2040 mg
Bupropion, 400 mg
Methylphenidate SR, 40 + 20 mg
Atomoxetine, 25100 mg
Atomoxetine, 25100 mg
24
38
303
Amphetamine
Cannabis
Various
Methylphenidate (OROS), 72 mg
Atomoxetine
0
+
(+)
0
0
(+)
54
126
Amphetamine
Cocaine

Amphetamine MAS, 60 or 80 mg
++
++
+
++
* Symbols used to indicate effectiveness:

0 no significant difference
+ / ++ / +++ strength of the difference (with a positive effect of active treatment)
** MMT = methadone maintenance treatment
IR = immediate release formulation, SR = slow release formulation (duration of action: 46 hours)
9/22/2016 12:01:12 PM
502
reduces the effectiveness of the medication

due to constant interaction with the same
neurotransmitter systems (Thomas et al,
2008). In outpatient trials most participants
are unable to remain abstinent (Riggs et al,
2004; Levin et al, 2006; Konstenius et al,
2010; McRae-Clark et al, 2010; Thurstone
et al, 2010; Riggs et al, 2011). The first
studies with stimulant medication were conducted with older short acting formulations
that were less reliable to deliver (Levin etal,
2006; Levin etal, 2007). Furthermore, inadequate dosages of the medication played a
role (Carpentier et al, 2005). On the basis
of case reports, there is evidence that (some)
ADHD patients with addiction need a higher
dosage as a result of their substance use. Due
to their chronic psychoactive drug use, these
patients are assumed to suffer from a more
severe dysregulation of brain dopamine neurotransmission (Volkow etal, 2009a; Volkow
et al, 2010). This hypothesis seems to be
confirmed in two recent trials in which robust
doses of methylphenidate (up to 180 mg per
day) in patients with amphetamine dependence, and mixed amphetamine salts-extended
release (60 and 80 mg per day) in cocaine
addicted patients were used (Konstenius
etal, 2014; Levin etal, 2015); both ADHD
and SUD outcomes were significantly better
with active treatment. Further work is needed
to investigate whether these positive clinical outcomes are due to improved control
of ADHD symptoms or management of the
drug problem by substitution with high dose
stimulant medication.
The type of addiction may also play a
role. For example, there is speculation that
ADHD in patients with alcohol use disorders
responds better to medication than ADHD
patients with other forms of drug addiction
(Wilens etal, 2008b). When the effectiveness
of the active drug is fairly low, even a limited placebo response will make it more difficult to demonstrate a significant difference
for active treatment (Carpentier etal, 2005).
The placebo response in ADHD medication
trials is lower than that usually observed in
drug treatment trials of mood and anxiety

disorders, and is usually limited to about
25% of the participants (Prince etal, 2006).
However, recent studies have found placebo
responders in around 40% of cases of adult
ADHD (Rosler et al, 2009a; Huss et al,
2014). Furthermore there are indications that
the placebo response is stronger in ADHD
patients with addictive disorders (Levin
etal, 2007; Perez de Los Cobos etal, 2012).
Similarly, treatment differences between the
active treatment and placebo groups can be
diminished when concurrent therapy (e.g.
cognitive behavioural treatment) also affects
treatment outcome (Riggs etal, 2011).
Psychostimulant diversion and abuse
The risk of diversion and abuse of psychostimulants forms an important consideration
in SUD patients with ADHD. Although the
psychostimulants methylphenidate and dexamphetamine have documented abuse potential, there is very little evidence that these
drugs are abused in any widespread manner.
According to the literature and clinical experience, it is comparatively rare for the psychostimulants prescribed for ADHD to lead
to clinically significant levels of abuse or
dependence (Kollins, 2008b). However, more
large-scale problems seem to be related to
the misuse and diversion of these drugs to
individuals who do not have ADHD. This
diversion is usually associated with efforts to
increase concentration and attention, often in
competitive academic environments (Teter
etal, 2006; Wilens etal, 2008a).
In animal experiments injected methylphenidate showed characteristics similar to
cocaine (Kollins, 2008a). Although methylphenidate can induce euphoria, this effect
does not occur when therapeutic dosages are
taken orally, since this requires higher dosages coming to the brain by faster absorption (via intranasal or intravenous route).
Furthermore, regular use of therapeutic
dosages does not lead to misuse or addiction (Volkow & Swanson, 2003). For example, longitudinal follow-up studies show no
9/22/2016 12:01:13 PM
increase in addiction among children treated

with stimulants for ADHD (Humphreys
etal, 2013; Molina etal, 2013). One of the
major clinical issues when treating children
with stimulants when they enter the teenage
years is poor compliance (i.e. they generally stop their medication with no adverse
effects beyond reducing control of ADHD
symptoms).
When prescribing psychostimulants, the
physician must always take into account
the risk of medication abuse by the patient
and/or third parties. However, it is possible
to contain this risk in various ways. Abuse
potential is significantly lower (and therapy
compliance is clearly better) when certain
longer-acting methylphenidate formulations
are prescribed. For example, OROS methylphenidate (Concerta) is a good option,
because it is not easy to extract methylphenidate from the capsules, whereas some other
formulations can be crushed and snorted. An
interesting alternative has recently become
available: lisdexamfetamine, a prodrug that
comprises dexamphetamine conjugated to
the amino acid lysine. After oral administration and absorption, the prodrug is activated
by splitting off lysine and releasing the active
substance dexamphetamine. Because of the
need for metabolic activation, and because
the pharmacokinetic profile cannot be altered
by the route of administration, with similar
effects whether taken orally or injected, this
product has a reduced potential for parenteral
abuse (Faraone, 2008). As effective as dexamphetamine, lisdexamfetamine has not yet
been properly studied in ADHD patients with
SUDs. A clear line should be drawn when the
risk of abuse cannot be controlled for. In such
cases, psychostimulants are not to be used
and atomoxetine, as indicated, is the first
line drug: as a non-stimulant, it lacks abuse
potential (Jasinski etal, 2008).
As other pharmacological alternatives
are often not as effective, psychostimulants
must remain a therapeutic option. Both
for reasons of diminished abuse potential and improved therapeutic compliance,
503
long-acting formulations are clearly indicated in this patient group. As these extended
release preparations or atomoxetine are not
available or reimbursed in all countries, it
may still be necessary to prescribe traditional immediate-release psychostimulants.
Efforts should be made to ensure that a
range of formulations and medications are
available to avoid this situation as far as is
possible. In the meantime, a safe strategy is
to prescribe these short-acting medications
under strict conditions only, and to discontinue prescription when these conditions are
not met. The central issue in this strategy is
a reliable working alliance with the patient.
The patient must be informed about the risks
of the medication and must agree to the conditions of its use. Continued prescription of
the medication should only take place after
a trial period demonstrating convincing
effectiveness of the medication. Especially
in the beginning medication should be dispensed in small quantities. An interesting
option is to involve a person close to the
patient, supervising the correct and regular
intake of the medication. Abstinence (or in
some cases agreed controlled maintenance)
during treatment is not only a precondition
for optimal effectiveness, but also an indication of the commitment of the patient to
the therapy. The same applies to meeting
appointments and participating in treatment.
Under these strict circumstances, psychostimulants can be used sufficiently safely
by this patient group. Moreover, the abovementioned controlled studies have demonstrated that psychostimulant use does not
lead to an increase in substance use (Wilens
etal, 2005b).
However, it is also important to be aware
of the poor therapy compliance associated
with multiple dosages per day to be taken
at fixed times (Swanson, 2003). Medication
adherence is always a concern in pharmacotherapy, but even more of an issue in this
patient group. The strict and repetitive dosage of short-acting psychostimulants is particularly difficult for people with ADHD, and
9/22/2016 12:01:13 PM
504
for some patients just impossible to maintain.

Moreover the fluctuating effects of short-acting formulations can be troublesome for some
patients. These are additional arguments why
short-acting formulations are not suited for a
large group of ADHD patients with SUDs. As
mentioned, these problems can be avoided by
using atomoxetine. It is preferable to discuss
this issue openly with the patient. In some
cases this can lead to increased motivation
and better medication adherence.
Choice of medication for addicted
ADHD patients
On the basis on the evidence listed above, the
picture so far is far from clear. The medications studied in this patient group (mostly
methylphenidate and atomoxetine) showed
until recently mixed and unimpressive results
in clinical trials. It therefore appears that for
various and partially understood reasons, as
discussed in the previous sections, pharmacotherapy is less effective in this subgroup of
ADHD patients than in ADHD adults without SUDs. This means that expectations of
pharmacotherapy in this patient group should
be more modest.
However, clinical experience, backed up
by positive case reports and recently by more
positive trials, suggests that a trial of pharmacotherapy can be worthwhile. In the more
recent Swedish study, the first to demonstrate
a clear positive effect of methylphenidate
in SUD patients (Konstenius et al, 2014),
the medication was individually titrated to
dosages higher than usual, confirming the
clinical impression that SUD patients may
need higher dosages than usual. A similar
strategy with robust dosing of amphetamine
mixed amphetamine salts was used in a
recent trial in cocaine addicted patients, with
equally impressive positive results (Levin
etal, 2015). There are some indications that
patients with more severe ADHD symptomatology will be more likely to benefit from
pharmacotherapy (Ginsberg & Lindefors,
2012; Nunes et al, 2013; Tamm et al, 2013).
The best results of pharmacotherapy will be
seen in well-motivated patients with a clear

ADHD diagnosis and little or stable comorbidity, during sustained abstinence and using
modern formulations: hardly the conditions one can expect when treating complex
patients with chronic addictions. In this heterogeneous patient population a clear benefit
can only be expected from an individualised
treatment, in which all available medications
(Table 30.2) are considered and tried if necessary (Perez de Los Cobos etal, 2012).
In line with adult ADHD patients without addiction, psychostimulants remain
the medication of first choice whenever
possible. However, atomoxetine is recommended in cases where there are concerns
about abuse potential. It should be noted
that the differences in effect size estimated
from meta-analyses of ADHD pharmacotherapy are only slightly greater for methylphenidate (d ~ 0.5) than for atomoxetine
(d ~ 0.4) (Koesters et al, 2008; Castells
etal, 2011; Cunill etal, 2013). Furthermore
some patients with addiction disorders prefer non-simulants. One of the reasons is
because the relatively short-term effects of
stimulants mean that the effects wear off
during the day; the moment symptoms of
ADHD return can be a time of high risk for
relapse. Atomoxetine when effective also
provides a stable effect without dips in the
control of symptoms (even when doses are
missed). However, atomoxetine may have
a lower overall effect size so that not all
patients will respond adequately, or some
patients may not tolerate adverse effects.
Furthermore a trial period of 6 weeks in
most patients and up to 12 weeks in some
others is required before there is a clear clinical response. So patients need to be advised
to stick to the medication during this period
even when there is no clinical response for
several weeks. Lisdexamfetamine, a drug
that has shown good effects in ADHD without addiction, would appear to be an excellent choice of stimulant for use in addicted
patients, because of the relatively sustained
release throughout the day, and because
9/22/2016 12:01:13 PM
of the limited abuse potential: injecting or

insufflation does not alter the slow release
profile. However, the effectiveness of lisdexamfetamine remains to be demonstrated
in this patient group, but it is surely a promising prospect. A common strategy therefore
would be a trial of atomoxetine initially, followed by extended release methylphenidate
and then lisdexamfetamine if this fails.
Further alternatives (with decreasing efficacy) are the tricyclic antidepressants or
venlafaxine.
The choice of medication therefore
depends on the medications available, and
the characteristics and circumstances of the
patient. To maximise the chances of a good
outcome, it is important to closely monitor the treatment, ensure good control of the
substance of abuse and compliance with the
treatment for ADHD. Medication adherence
is a particularly important and should be
actively promoted. Frequent check-ups are
necessary to strengthen the working alliance
as well as to safeguard abstinence and correct medication intake. Good integration of
the pharmacotherapy in the overall treatment
strategy will be advantageous to compliance.
Psychosocial treatment
Besides medication treatment, further psychotherapy and psychosocial support are
certainly indicated in patients with ADHD
and SUDs to preserve the prospect of stabilising the two disorders (Mariani & Levin,
2007). Appropriate treatment of the addiction, such as relapse prevention, is necessary
to maintain abstinence. In many patients,
ADHD will be diagnosed for the first time
during their addiction treatment: psychoeducation and cognitive therapy for ADHD will
help them to accept the diagnosis, improving
their adaption to their limitations (Safren
et al, 2005; Solanto et al, 2010; Emilsson
etal, 2011). The cognitive therapies have not
yet been systematically evaluated in SUD
patients (Magon & Mueller, 2012). However,
in several medication randomised controlled
trials (RCTs), concurrent treatment of the
505
SUD by means of cognitive behavioural

therapy seems to have contributed to the
decrease of ADHD symptomatology in both
active treatment and placebo groups (Riggs
etal, 2011).
The cognitive treatment and coaching of
ADHD should be tailored to the unhealthy
aspects of the patients life-style, with extensive attention to the intertwining of ADHD
symptoms and substance use. This kind of
specific psychosocial treatment for the combination of ADHD and addiction is still under
development, and is not yet widely available.
The relevance of ADHD in

addiction
The aetiological role of ADHD in the development of addiction and the high prevalence
of the disorder in addicted patients help to
create high expectations regarding the effect
of ADHD treatment for this patient group.
Principle dictates that effective treatment of
ADHD should have a positive effect on the
prognosis of the addiction: patients become
more stable and composed, improving their
engagement in treatment and their ability to
remain abstinent. A number of case reports
illustrate the impressive progress made by
some patients after effective treatment of
their ADHD (Khantzian et al, 1984;
Schubiner et al, 1995; Stovner et al, 1996;
Levin etal, 1998).
For a long time, the increased focus on
ADHD did not result in impressive therapeutic gains, but recent RCTs have bucked the
trend (Konstenius et al, 2014; Levin et al,
2015). Several factors account for this frustrating situation and have been discussed in
the previous sections. ADHD in addicted
patients has turned out to be more difficult to
treat than expected. Although research is limited and treatment of ADHD in this patient
group has not yet been systematically evaluated, the pharmacological studies clearly
point out that ADHD in combination with
SUD is less amenable to medication than
9/22/2016 12:01:13 PM
506
simple ADHD (see Table 30.3). Moreover

the direct effect of ADHD treatment on the
prognosis of the addiction seems to be limited. In as far as the RCTs addressed this
topic, until recently they hardly showed any
positive influence on the course of the addiction (Table 30.3).
A more sobering view holds that effective treatment of ADHD will be feasible in
many addicted patients, but without a direct
and substantial influence on the SUD. Such
an assumption, more in line with clinical
experience, is based on the results achieved
in addicted patients with other comorbid
psychiatric disorders (such as mood disturbances and anxiety disorders) (Schade etal,
2005; Ostacher, 2007). Active treatment
does alleviate the comorbid disorder, but
does not directly influence the SUD (Tiet
& Mausbach, 2007). For a long time, this
classic pattern in dual diagnosis treatment
seemed to apply to ADHD as well. However
the recent RCTs have demonstrated that positive results on ADHD symptomatology are
accompanied by an improvement on SUD
outcome measures (Konstenius et al, 2014;
Levin etal, 2015).
Overall there remains a potent argument
for maximising ADHD treatment efficacy
in this patient group because of the potential benefits that are gained when there is a
good clinical response. ADHD treatment in
addicted patients is particularly worthwhile
when the symptoms of ADHD are severe.
Such patients are not only more likely to
benefit more from ADHD treatment, but
the ADHD symptoms may play a more significant driving force in their addiction.
Stabilisation of ADHD symptomatology
may therefore lead to improvements in both
ADHD related impairments as well as the
addiction disorder. Increased knowledge and
expertise in pharmacological and psychosocial treatment of ADHD in this patient group
will further extend therapeutic possibilities.
Effective treatment of ADHD in a multicausal disorder such as addiction can help to
tip the balance in a positive direction.
Prevention
ADHD in children has been identified as a
risk factor for addiction in later life.
Longitudinal studies of ADHD children followed into early adulthood have clearly indicated the increased risk for SUDs in ADHD
(Molina & Pelham, Jr., 2003; Molina et al,
2007; Charach etal, 2011; Klein etal, 2012).
In all these studies, participants, identified
with ADHD in childhood and followed up
into early adulthood show higher rates of
various SUDs, compared to normal controls.
These observations make for an excellent
target for preventive efforts. The problem
(addiction) is quite relevant, the risk group
(children with ADHD) is readily identifiable,
and an effective therapy is available.
However, the question whether effective
treatment of ADHD in childhood can
decrease this risk of SUDs, can only be
answered conclusively by long-term studies
which are hard to organise and take time.
Until recently, the consensus was that
a preventive effect of ADHD treatment in
childhood on the development of addiction
remained to be demonstrated (Molina et al,
2013; Goldstein, 2013; Humphreys et al,
2013). However recent studies suggest there
may indeed be a protective effect (Chang
et al, 2014). Using Swedish national registers, the authors studied all individuals born
between 1960 and 1998 and diagnosed with
ADHD (26,249 men and 12,504 women).
Substance abuse was found to be 31% lower
among those prescribed ADHD medication 3
years previously compared to those not prescribed medication. Similar risk reductions
were suggested among children. Overall their
data suggested a long-term protective effect
on substance abuse. There are more positive
reports: for example, earlier treatment seems
to offer more protective results (Mannuzza
et al, 2008; Dalsgaard et al, 2014). A more
recent well-executed longitudinal study demonstrated a protective effect of medication in
childhood (Groenman etal, 2013). A Danish
population study on the influence of ADHD
9/22/2016 12:01:13 PM
medication use in ADHD patients has shown

that the prevalence of SUDs is higher prior to
than following the onset of psychostimulant
medication (Steinhausen & Bisgaard, 2014).
There are several potential reasons why the
earlier longitudinal follow-up studies did not
come to these same conclusions. Difficulties
in offering continuous effective ADHD treatment during the transition from childhood
through adolescence into adulthood (and difficulties in organising longitudinal research)
certainly contribute to this paradox. The
complexity of the situation is illustrated by
the results of one research group, who failed
to find any evidence for the protective effect
of psychostimulant treatment in longer-term
follow-up (Biederman etal, 1999; Biederman
et al, 2008a). However, in this naturalistic
follow-up study, after 10 years only 22% of
the original patient group were still actively
receiving treatment, which is hardly an optimal situation to demonstrate any protective
effect. These negative results can thus be considered as indirect evidence for the need for
long-term effectiveness studies of treatment.
One of the concerns expressed in the past
was that the prescribing of stimulants to children might lead to SUD, rather than protect;
and this might be one of the causes of SUD
in ADHD. Indeed there was a legitimate concern about the effects of psychostimulant use
in childhood. For example, some animal studies indicated a potentially increased risk of
psychoactive drug use after psychostimulant
exposure in childhood, possibly as a result
of sensitisation, which increases the reinforcing effects of the drug (Robbins, 2002).
Fortunately, this has not been substantiated
by longitudinal research in patient populations. It is therefore reassuring to see robust
findings from all the longitudinal studies
which all failed to demonstrate an increased
risk of psychoactive drug abuse resulting
from psychostimulant treatment in childhood
(Molina etal, 2013; Humphreys etal, 2013;
Chang etal, 2014).
These encouraging results are an added
incentive to continue preventive efforts. The
507
risk for later addiction in ADHD children is

clear, and if ADHD treatment is insufficient
to influence this risk, more intensive intervention is required, focusing not only on
the ADHD but also more specifically on the
problematic substance use (Harstad & Levy,
2014). As prevention of substance abuse
seems elusive, a mitigation of the course of
the addiction still remains feasible, for example by delaying the age of substance use
initiation. Ultimately, effective prevention
will depend on simultaneously considering
and tackling multiple risk factors (Molina &
Pelham, 2014).
Future research
For research purposes, ADHD is an interesting model for the study of the development of
problematic substance use in patients with a
pre-existing psychiatric disorder (Wilens &
Biederman, 2006). In spite of clear evidence
of the aetiological role of ADHD in the development and persistence of problematic substance use, most interventions targeted at
ADHD have not shown the expected preventive or stabilising effect. All this points to the
fact that the relation between ADHD and
addiction is more complicated than expected,
and ADHD treatment is far less straightforward than in adult patients with ADHD but
without addiction. The complexity of the
combination of a heterogeneous disorder like
ADHD and a multi-causal disorder like addiction, in the dynamic context of the developing
brain during adolescence, the period of experimenting and drug use initiation, is certainly
part of the explanation. Both from a therapeutic and a preventive point of view, additional
research is needed to improve our understanding of this complex relation and improve
the efficacy of therapeutic options.
Increased knowledge of the aetiology of
ADHD and addiction, and their common and
separate contributing factors, will help to
identify targets for preventive and therapeutic
9/22/2016 12:01:13 PM
508
intervention. More detailed longitudinal studies starting in childhood can help to identify
prognostic factors, and also determine the
influence of timing of different interventions
in the eventual outcome. For ADHD adults
with addictions, a major challenge will be
improving the efficacy of ADHD treatment in
more complex patients. In addition to RCTs,
individualised pharmacotherapy studies can
be considered, in which several medications
(in sufficient dosages) are tried, according to
a protocol, again looking for (genetic) predictive factors. As discussed a specific cognitive
therapy for this dual diagnosis needs to be
developed and tested. As pharmacotherapy
in itself is insufficiently effective to stabilise
ADHD and SUD, a naturalistic study could
look at the effects of an integrated treatment
of this complex disorder.
Conclusion
In spite of the accomplishments discussed
above, ADHD in addiction remains a domain
full of clinical and research challenges.
Uncomplicated ADHD may be quite treatable in children and adults, but these same
interventions are simply not as effective in
addicted ADHD patients. Clinicians should
not be discouraged by these sobering results,
as we get more and more indications how to
do it right: individualising the treatment and
integrating pharmacotherapy with active psychosocial interventions.
ADHD is one of many aetiological factors in the development and persistence of
addiction. ADHD in itself may have limited influence in this process, but offers the
important advantage of preventive and therapeutic possibilities. In anticipation of further
research, more attention to this disorder in
clinical practice may provide indications for
improving treatment effectiveness, leading
to a clearer determination of the relevance
of ADHD in the diagnosis and treatment of
addicted patients.
References
Adler, L. & Cohen, J. (2004) Diagnosis and
evaluation of adults with attention-deficit/
hyperactivity disorder. Psychiatr. Clin. North
Am., 27, 187201.
Adler, L.A., Shaw, D.M., Kovacs, K., & Alperin,
S. (2015) Diagnosing ADHD in children and
adults. In: Attention-Deficit Hyperactivity Disorder in Adults and Children (ed. L. A. Adler,
T. J. Spencer, & T. E. Wilens), pp. 1623.
Cambridge University Press, Cambridge.
Almeida Montes, L.G., Hernandez Garcia, A.O.,
& Ricardo-Garcell, J. (2007) ADHD prevalence in adult outpatients with nonpsychotic
psychiatric illnesses. J Atten. Disord., 11,
1506.
Arcos-Burgos, M., Velez, J.I., Solomon, B.D., &
Muenke, M. (2012) A common genetic network underlies substance use disorders and
disruptive or externalizing disorders. Hum.
Genet., 131, 91729.
Barkley, R.A. (2006a) A theory of ADHD. In:
Attention-Deficit Hyperactivity Disorder: a
handbook for diagnosis and treatment (ed.
R. A. Barkley), pp. 297336. The Guilford
Press, New York.
Barkley, R.A. (2006b) Etiologies. In: AttentionDeficit Hyperactivity Disorder: a handbook
for diagnosis and treatment (ed. R. A.
Barkley), pp. 21947. The Guilford Press,
New York.
Biederman, J. (2011) The course and persistence of ADHD throughout the life-cycle. In:
ADHD in Adults: Characterization, diagnosis
and treatment (ed. J. K. Buitelaar, C. C. Kan,
& P. Asherson), pp. 18. Cambridge University Press, Cambridge.
Biederman, J. & Faraone, S.V. (2005) Attentiondeficit hyperactivity disorder. Lancet, 366,
23748.
Biederman, J., Monuteaux, M.C., Spencer, T.,
Wilens, T.E., Macpherson, H.A., & Faraone,
S.V. (2008a) Stimulant therapy and risk for
subsequent substance use disorders in male
adults with ADHD: a naturalistic controlled
10-year follow-up study. Am. J. Psychiatry,
165, 597603.
Biederman, J., Petty, C.R., Wilens, T.E., Fraire,
M.G., Purcell, C.A., Mick, E., Monuteaux,
M.C., & Faraone, S.V. (2008b) Familial risk
analyses of attention deficit hyperactivity
9/22/2016 12:01:14 PM
disorder and substance use disorders. Am. J.

Psychiatry, 165, 10715.
Biederman, J., Wilens, T., Mick, E., Spencer, T., &
Faraone, S.V. (1999) Pharmacotherapy of
attention-deficit/hyperactivity disorder reduces
risk for substance use disorder. Pediatrics,
104, e20.
Biederman, J., Wilens, T.E., Mick, E., Faraone,
S.V., & Spencer, T. (1998) Does attentiondeficit hyperactivity disorder impact the
developmental course of drug and alcohol
abuse and dependence? Biol. Psychiatry, 44,
26973.
Bush, G. (2010) Attention-deficit/hyperactivity
disorder and attention networks. Neuropsychopharmacology, 35, 278300.
Bush, G., Valera, E.M., & Seidman, L.J. (2005)
Functional neuroimaging of attention-deficit/hyperactivity disorder: a review and suggested future directions. Biol. Psychiatry, 57,
127384.
Carpentier, P.J., de Jong, C.A., Dijkstra, B.A.,
Verbrugge, C.A., & Krabbe, P.F. (2005) A
controlled trial of methylphenidate in adults
with attention deficit/hyperactivity disorder
and substance use disorders. Addiction, 100,
186874.
Carpentier, P.J., Knapen, L.J., van Gogh, M.T.,
Buitelaar, J.K., & de Jong, C.A. (2012) Addiction in developmental perspective: influence
of conduct disorder severity, subtype, and
attention-deficit hyperactivity disorder on
problem severity and comorbidity in adults
with opioid dependence. J. Addict. Dis., 31,
4559.
Carpentier, P.J., van Gogh, M.T., Knapen, L.J.,
Buitelaar, J.K., & de Jong, C.A. (2011) Influence of attention deficit hyperactivity disorder and conduct disorder on opioid
dependence severity and psychiatric comorbidity in chronic methadone-maintained
patients. Eur. Addict Res., 17, 1020.
Carroll, K.M. & Rounsaville, B.J. (1993) History
and significance of childhood attention deficit disorder in treatment-seeking cocaine
abusers. Compr. Psychiatry, 34, 7582.
Castellanos, F.X. & Tannock, R. (2002) Neuroscience of attention-deficit/hyperactivity disorder: the search for endophenotypes. Nat.
Rev. Neurosci., 3, 61728.
Castells, X., Ramos-Quiroga, J.A., Rigau, D.,
Bosch, R., Nogueira, M., Vidal, X., & Casas, M.
509
(2011) Efficacy of methylphenidate for adults

with attention-deficit hyperactivity disorder:
a meta-regression analysis. CNS Drugs, 25,
15769.
Chang, Z., Lichtenstein, P., Asherson, P.J., &
Larsson, H. (2013) Developmental twin study
of attention problems: high heritabilities
throughout development. JAMA Psychiatry,
70, 3118.
Chang, Z., Lichtenstein, P., Halldner, L.,
D'Onofrio, B., Serlachius, E., Fazel, S., Langstrom, N., & Larsson, H. (2014) Stimulant
ADHD medication and risk for substance
abuse. J. Child Psychol. Psychiatry, 55,
87885.
Chang, Z., Lichtenstein, P., & Larsson, H. (2012)
The effects of childhood ADHD symptoms
on early-onset substance use: a Swedish
twin study. J. Abnorm. Child Psychol., 40,
42535.
Charach, A., Yeung, E., Climans, T., & Lillie, E.
(2011) Childhood attention-deficit/hyperactivity disorder and future substance use disorders: comparative meta-analyses. J. Am.
Acad. Child Adolesc. Psychiatry, 50, 921.
Clure, C., Brady, K.T., Saladin, M.E., Johnson,
D., Waid, R., & Rittenbury, M. (1999) Attention-deficit/hyperactivity disorder and substance use: symptom pattern and drug
choice. Am. J. Drug Alcohol Abuse, 25,
4418.
Cunill, R., Castells, X., Tobias, A., & Capella, D.
(2013) Atomoxetine for attention deficit
hyperactivity disorder in the adulthood: a
meta-analysis and meta-regression. Pharmacoepidemiol. Drug Saf, 22, 9619.
Dalsgaard, S., Mortensen, P.B., Frydenberg, M.,
& Thomsen, P.H. (2014) ADHD, stimulant
treatment in childhood and subsequent substance abuse in adulthood a naturalistic
long-term follow-up study. Addict. Behav.,
39, 3258.
Dowson, J.H. & Blackwell, A.D. (2011) Neurocognitive characteristics of adults with attention-deficit hyperactivity disorder. In: ADHD
in Adults: Characterization, Diagnosis and
Treatment (ed. J. K. Buitelaar, C. C. Kan, & P.
Asherson), pp. 106120. Cambridge University Press, Cambridge.
Elkins, I.J., McGue, M., & Iacono, W.G. (2007)
Prospective effects of attention-deficit/hyperactivity disorder, conduct disorder, and sex
9/22/2016 12:01:14 PM
510
on adolescent substance use and abuse.

Arch. Gen. Psychiatry, 64, 114552.
Emilsson, B., Gudjonsson, G., Sigurdsson, J.F.,
Baldursson, G., Einarsson, E., Olafsdottir, H.,
& Young, S. (2011) Cognitive behaviour
therapy in medication-treated adults with
ADHD and persistent symptoms: a randomized controlled trial. BMC Psychiatry,
11, 116.
Faraone, S.V. (2005) The scientific foundation
for understanding attention-deficit/hyperactivity disorder as a valid psychiatric disorder.
Eur. Child Adolesc. Psychiatry, 14, 110.
Faraone, S.V. (2008) Lisdexamfetamine dimesylate: the first long-acting prodrug stimulant treatment for attention deficit/
hyperactivity disorder. Expert. Opin. Pharmacother., 9, 156574.
Faraone, S.V., Perlis, R.H., Doyle, A.E., Smoller,
J.W., Goralnick, J.J., Holmgren, M.A., &
Sklar, P. (2005) Molecular genetics of attention-deficit/hyperactivity disorder. Biol. Psychiatry, 57, 131323.
Faraone, S.V., Sergeant, J., Gillberg, C., & Biederman, J. (2003) The worldwide prevalence
of ADHD: is it an American condition? World
Fatseas, M., Debrabant, R., & Auriacombe, M.
(2012) The diagnostic accuracy of attentiondeficit/hyperactivity disorder in adults with
substance use disorders. Curr. Opin. Psychiatry, 25, 21925.
Fayyad, J., De Graaf, R., Kessler, R., Alonso, J.,
Angermeyer, M., Demyttenaere, K., De,
Girolamo, G., Haro, J.M., Karam, E.G., Lara,
C., Lepine, J.P., Ormel, J., Posada-Villa, J.,
Zaslavsky, A.M., & Jin, R. (2007) Crossnational prevalence and correlates of adult
attention-deficit hyperactivity disorder. Br. J
Fayyad, J. & Kessler, R.C. (2015) The epidemiology and societal burden of ADHD. In:
Attention-Deficit Hyperactivity Disorder in
Adults and Children (ed. L. A. Adler, T. J.
Spencer, & T. E. Wilens), pp. 2441. Cambridge University Press, Cambridge.
Fergusson, D.M., Horwood, L.J., & Ridder, E.M.
(2007) Conduct and attentional problems in
childhood and adolescence and later substance use, abuse and dependence: results
of a 25year longitudinal study. Drug Alcohol Depend., 88 Suppl 1, S1426.
Flory, K. & Lynam, D.R. (2003) The relation

between attention deficit hyperactivity disorder and substance abuse: what role does
conduct disorder play? Clin. Child Fam.
Psychol Rev., 6, 116.
Flory, K., Milich, R., Lynam, D.R., Leukefeld, C.,
& Clayton, R. (2003) Relation between childhood disruptive behavior disorders and substance use and dependence symptoms in
young adulthood: individuals with symptoms
of attention-deficit/hyperactivity disorder
and conduct disorder are uniquely at risk.
Psychol Addict Behav., 17, 15158.
Ginsberg, Y. & Lindefors, N. (2012) Methylphenidate treatment of adult male prison
inmates with attention-deficit hyperactivity
disorder: randomised double-blind placebocontrolled trial with open-label extension.
Br. J. Psychiatry, 200, 6873.
Glass, K. & Flory, K. (2010) Why does ADHD
confer risk for cigarette smoking? A review
of psychosocial mechanisms. Clin. Child Fam.
Psychol. Rev., 13, 291313.
Goldstein, B.I. (2013) Do stimulants prevent
substance use and misuse among youth with
attention-deficit/hyperactivity disorder? The
answer is still maybe. J. Am. Acad. Child
Adolesc. Psychiatry, 52, 2257.
Groenman, A.P., Oosterlaan, J., Rommelse, N.,
Franke, B., Roeyers, H., Oades, R.D., Sergeant, J.A., Buitelaar, J.K., & Faraone, S.V.
(2013) Substance use disorders in adolescents with attention deficit hyperactivity disorder: a 4-year follow-up study. Addiction,
108, 150311.
Harstad, E. & Levy, S. (2014) Attention-deficit/
hyperactivity disorder and substance abuse.
Pediatrics, 134, e293301.
Hart, H., Radua, J., Nakao, T., Mataix-Cols, D.,
& Rubia, K. (2013) Meta-analysis of functional magnetic resonance imaging studies
of inhibition and attention in attention-
deficit/hyperactivity disorder: exploring taskspecific, stimulant medication, and age
effects. JAMA Psychiatry, 70, 18598.
Humphreys, K.L., Eng, T., & Lee, S.S. (2013)
Stimulant medication and substance use
outcomes: a meta-analysis. JAMA Psychiatry,
70, 7409.
Huntley, Z., Maltezos, S., Williams, C., Morinan,
A., Hammon, A., Ball, D., Marshall, E.J.,
Keaney, F., Young, S., Bolton, P., Glaser, K.,
9/22/2016 12:01:14 PM
Howe-Forbes, R., Kuntsi, J., Xenitidis, K.,

Murphy, D., & Asherson, P.J. (2012) Rates of
undiagnosed attention deficit hyperactivity
disorder in London drug and alcohol detoxification units. BMC Psychiatry, 12, 223.
Huss, M., Ginsberg, Y., Tvedten, T., Arngrim, T.,
Philipsen, A., Carter, K., Chen, C.W., &
Kumar, V. (2014) Methylphenidate hydrochloride modified-release in adults with
attention deficit hyperactivity disorder: a
randomized double-blind placebo-controlled
trial. Adv. Ther., 31, 4465.
Jasinski, D.R., Faries, D.E., Moore, R.J., Schuh,
L.M., & Allen, A.J. (2008) Abuse liability
assessment of atomoxetine in a drug-abusing population. Drug Alcohol Depend., 95,
1406.
Jensen, P.S., Martin, D., & Cantwell, D.P. (1997)
Comorbidity in ADHD: implications for
research, practice, and DSM-V. J Am Acad.
Child Adolesc. Psychiatry, 36, 106579.
Johnson, K.A., Wiersema, J.R., & Kuntsi, J.
(2009) What would Karl Popper say? Are
current psychological theories of ADHD falsifiable? Behav. Brain Funct., 5, 15.
Kalivas, P.W. & Volkow, N.D. (2005) The neural
basis of addiction: a pathology of motivation
and choice. Am J Psychiatry, 162, 140313.
Kessler, R.C., Adler, L., Barkley, R., Biederman,
J., Conners, C.K., Demler, O., Faraone, S.V.,
Greenhill, L.L., Howes, M.J., Secnik, K.,
Spencer, T., Ustun, T.B., Walters, E.E., &
Zaslavsky, A.M. (2006) The prevalence and
correlates of adult ADHD in the United
States: results from the National Comorbidity
Survey Replication. Am. J. Psychiatry, 163,
71623.
Khantzian, E.J. (1997) The self-medication
hypothesis of substance use disorders: a
reconsideration and recent applications.
Harv. Rev. Psychiatry, 4, 23144.
Khantzian, E.J., Gawin, F., Kleber, H.D., &
Riordan, C.E. (1984) Methylphenidate (Ritalin) treatment of cocaine dependence a
preliminary report. J Subst. Abuse Treat., 1,
10712.
Kim-Cohen, J., Caspi, A., Moffitt, T.E., Harrington, H., Milne, B.J., & Poulton, R. (2003)
Prior juvenile diagnoses in adults with mental
disorder: developmental follow-back of a
prospective-longitudinal cohort. Arch. Gen.
511
Klassen, L.J., Bilkey, T.S., Katzman, M.A., &

Chokka, P. (2012) Comorbid attention deficit/hyperactivity disorder and substance use
disorder: treatment considerations. Curr.
Drug Abuse Rev., 5, 1908.
Klein, R.G., Mannuzza, S., Olazagasti, M.A.,
Roizen, E., Hutchison, J.A., Lashua, E.C., &
Castellanos, F.X. (2012) Clinical and functional outcome of childhood attention-
deficit/hyperactivity disorder 33 years later.
Arch. Gen. Psychiatry, 69, 1295303.
Knop, J., Penick, E.C., Nickel, E.J., Mortensen,
E.L., Sullivan, M.A., Murtaza, S., Jensen, P.,
Manzardo, A.M., & Gabrielli, W.F., Jr. (2009)
Childhood ADHD and conduct disorder as
independent predictors of male alcohol
dependence at age 40. J Stud. Alcohol
Drugs, 70, 16977.
Knopik, V.S., Jacob, T., Haber, J.R., Swenson,
L.P., & Howell, D.N. (2009) Paternal alcoholism and offspring ADHD problems: a children of twins design. Twin. Res Hum. Genet,
12, 5362.
Koesters, M., Becker, T., Kilian, R., Fegert, J.M.,
& Weinmann, S. (2008) Limits of meta-
analysis: methylphenidate in the treatment
of adult attention-deficit hyperactivity disorder. J. Psychopharmacol, 23, 73344.
Kollins, S.H. (2008a) A qualitative review of
issues arising in the use of psycho-stimulant
medications in patients with ADHD and comorbid substance use disorders. Curr. Med
Res. Opin., 24, 134557.
Kollins, S.H. (2008b) ADHD, substance use
disorders, and psychostimulant treatment:
current literature and treatment guidelines.
J Atten. Disord., 12, 11525.
Kollins, S.H. & Adcock, R.A. (2014) ADHD,
altered dopamine neurotransmission, and
disrupted reinforcement processes: Implications for smoking and nicotine dependence.
Prog. Neuropsychopharmacol. Biol. Psychiatry., 52, 708.
Kollins, S.H. & McClernon, F.J. (2015) ADHD
and smoking. In: Attention-Deficit Hyperactivity Disorder in Adults and Children (ed. L.
A. Adler, T. J. Spencer, & T. E. Wilens),
pp. 32742. Cambridge University Press,
Cambridge.
Konstenius, M., Jayaram-Lindstrom, N., Beck,
O., & Franck, J. (2010) Sustained release
methylphenidate for the treatment of ADHD
9/22/2016 12:01:15 PM
512
in amphetamine abusers: a pilot study. Drug

Alcohol Depend., 108, 1303.
Konstenius, M., Jayaram-Lindstrom, N., Guterstam, J., Beck, O., Philips, B., & Franck, J.
(2014) Methylphenidate for attention deficit
hyperactivity disorder and drug relapse in
criminal offenders with substance dependence: a 24-week randomized placebo-
controlled trial. Addiction, 109, 4409.
Kooij, S.J., Bejerot, S., Blackwell, A., Caci, H.,
Casas-Brugue, M., Carpentier, P.J., Edvinsson, D., Fayyad, J., Foeken, K., Fitzgerald, M.,
Gaillac, V., Ginsberg, Y., Henry, C., Krause, J.,
Lensing, M.B., Manor, I., Niederhofer, H.,
Nunes-Filipe, C., Ohlmeier, M.D., Oswald, P.,
Pallanti, S., Pehlivanidis, A., Ramos-Quiroga,
J.A., Rastam, M., Ryffel-Rawak, D., Stes, S.,
& Asherson, P. (2010) European consensus
statement on diagnosis and treatment of
adult ADHD: The European Network Adult
ADHD. BMC Psychiatry, 10, 67.
Krueger, R.F., Markon, K.E., Patrick, C.J., &
Iacono, W.G. (2005) Externalizing psychopathology in adulthood: a dimensional-
spectrum conceptualization and its
implications for DSM-V. J. Abnorm. Psychol.,
114, 53750.
Larsson, H., Chang, Z., D'Onofrio, B.M., &
Lichtenstein, P. (2013) The heritability of
clinically diagnosed attention deficit hyperactivity disorder across the lifespan. Psychol.
Med., 44, 22239.
Lasky-Su, J., Neale, B.M., Franke, B., Anney,
R.J., Zhou, K., Maller, J.B., Vasquez, A.A.,
Chen, W., Asherson, P., Buitelaar, J.,
Banaschewski, T., Ebstein, R., Gill, M.,
Miranda, A., Mulas, F., Oades, R.D., Roeyers,
H., Rothenberger, A., Sergeant, J., SonugaBarke, E., Steinhausen, H.C., Taylor, E., Daly,
M., Laird, N., Lange, C., & Faraone, S.V.
(2008) Genome-wide association scan of
quantitative traits for attention deficit hyperactivity disorder identifies novel associations
and confirms candidate gene associations.
Am. J. Med. Genet. B Neuropsychiatr.
Genet., 147B, 134554.
Levin, F.R. (2007) Diagnosing attention-deficit/
hyperactivity disorder in patients with substance use disorder. J, Clin. Psychiatry, 68
Suppl 11, 914.
Levin, F.R., Evans, S.M., Brooks, D.J., & Garawi,
F. (2007) Treatment of cocaine dependent
treatment seekers with adult ADHD: doubleblind comparison of methylphenidate and

placebo. Drug Alcohol Depend., 87, 209.
Levin, F.R., Evans, S.M., Brooks, D.J., Kalbag,
A.S., Garawi, F., & Nunes, E.V. (2006) Treatment of methadone-maintained patients
with adult ADHD: double-blind comparison
of methylphenidate, bupropion and placebo.
Drug Alcohol Depend., 81, 13748.
Levin, F.R., Evans, S.M., & Kleber, H.D. (1998)
Prevalence of adult attention-deficit hyperactivity disorder among cocaine abusers seeking treatment. Drug Alcohol Depend., 52,
1525.
Levin, F.R., Evans, S.M., Vosburg, S.K., Horton,
T., Brooks, D., & Ng, J. (2004) Impact of
attention-deficit hyperactivity disorder and
other psychopathology on treatment retention among cocaine abusers in a therapeutic
community. Addict. Behav., 29, 187582.
Levin, F.R., Mariani, J.J., Specker, S., Mooney,
M., Mahony, A., Brooks, D.J., Babb, D., Bai,
Y., Eberly, L.E., Nunes, E.V., & Grabowski, J.
(2015) Extended-release mixed amphetamine salts vs placebo for comorbid adult
attention-deficit/hyperactivity disorder and
cocaine use disorder: a randomized clinical
trial. JAMA Psychiatry, 72, 593602.
Liddle, E.B., Hollis, C., Batty, M.J., Groom, M.J.,
Totman, J.J., Liotti, M., Scerif, G., & Liddle, P.F.
(2011) Task-related default mode network
modulation and inhibitory control in ADHD:
effects of motivation and methylphenidate.
J. Child Psychol. Psychiatry, 52, 76171.
Lynskey, M.T. & Hall, W. (2001) Attention deficit hyperactivity disorder and substance use
disorders: Is there a causal link? Addiction,
96, 81522.
Magon, R. & Mueller, U. (2012) ADHD with
comorbid substance use disorder: review of
treatment. APT, 18, 43646.
Mannuzza, S., Klein, R.G., Truong, N.L.,
Moulton, J.L., III, Roizen, E.R., Howell, K.H.,
& Castellanos, F.X. (2008) Age of methylphenidate treatment initiation in children with
ADHD and later substance abuse: prospective follow-up into adulthood. Am. J. Psychiatry, 165, 6049.
Mariani, J.J. & Levin, F.R. (2007) Treatment
strategies for co-occurring ADHD and substance use disorders. Am. J. Addict., 16
Suppl 1, 4554.
9/22/2016 12:01:15 PM
Marmorstein, N.R., Iacono, W.G., & McGue, M.

(2009) Alcohol and illicit drug dependence
among parents: associations with offspring
externalizing disorders. Psychol. Med., 39,
14955.
Marshal, M.P. & Molina, B.S. (2006) Antisocial
behaviors moderate the deviant peer pathway to substance use in children with ADHD.
J Clin. Child Adolesc. Psychol., 35, 21626.
McGough, J.J. & Barkley, R.A. (2004) Diagnostic controversies in adult attention deficit
hyperactivity disorder. Am. J. Psychiatry, 161,
194856.
McRae-Clark, A.L., Carter, R.E., Killeen, T.K.,
Carpenter, M.J., White, K.G., & Brady, K.T.
(2010) A placebo-controlled trial of atomoxetine in marijuana-dependent individuals
with attention deficit hyperactivity disorder.
Am. J. Addict., 19, 4819.
Michelson, D., Adler, L., Spencer, T., Reimherr,
F.W., West, S.A., Allen, A.J., Kelsey, D., Wernicke, J., Dietrich, A., & Milton, D. (2003)
Atomoxetine in adults with ADHD: two randomized, placebo-controlled studies. Biol.
Molina, B.S., Flory, K., Hinshaw, S.P., Greiner,
A.R., Arnold, L.E., Swanson, J.M., Hechtman, L., Jensen, P.S., Vitiello, B., Hoza, B.,
Pelham, W.E., Elliott, G.R., Wells, K.C.,
Abikoff, H.B., Gibbons, R.D., Marcus, S.,
Conners, C.K., Epstein, J.N., Greenhill, L.L.,
March, J.S., Newcorn, J.H., Severe, J.B., &
Wigal, T. (2007) Delinquent behavior and
emerging substance use in the MTA at 36
months: prevalence, course, and treatment
effects. J. Am. Acad. Child Adolesc. Psychiatry, 46, 102840.
Molina, B.S., Hinshaw, S.P., Eugene, A.L.,
Swanson, J.M., Pelham, W.E., Hechtman, L.,
Hoza, B., Epstein, J.N., Wigal, T., Abikoff,
H.B., Greenhill, L.L., Jensen, P.S., Wells, K.C.,
Vitiello, B., Gibbons, R.D., Howard, A.,
Houck, P.R., Hur, K., Lu, B., & Marcus, S.
(2013) Adolescent substance use in the multimodal treatment study of Attention-Deficit/
Hyperactivity Disorder (ADHD) (MTA) as a
function of childhood ADHD, random assignment to childhood treatments, and subsequent medication. J. Am. Acad. Child
Molina, B.S. & Pelham, W.E., Jr. (2003) Childhood predictors of adolescent substance use
513
in a longitudinal study of children with

ADHD. J. Abnorm. Psychol., 112, 497507.
Molina, B.S. & Pelham, W.E. (2014) Attentiondeficit/hyperactivity disorder and risk of substance use disorder: developmental
considerations, potential pathways, and
opportunities for research. Annu. Rev. Clin.
Psychol. 10, 60739.
Murphy, K. (2005) Psychosocial treatments for
ADHD in teens and adults: a practice-friendly
review. J. Clin. Psychol., 61, 60719.
Murphy, K.R. & Gordon, M. (2006) Assessment
of adults with ADHD. In: Attention-Deficit
Hyperactivity Disorder: a handbook for diagnosis and treatment (ed. R. A. Barkley),
pp. 42552. The Guilford Press, New York.
National Collaborating Centre for Mental
Health. Attention Deficit Hyperactivity Disorder. Diagnosis and management of ADHD
in children, young people and adults.
National Institute for Health and Clinical
Excellence. 72. 2009. The British Psychological Society and The Royal College of Psychiatrists. National Clinical Practice
Guideline.
Nunes, E.V., Covey, L.S., Brigham, G., Hu, M.C.,
Levin, F.R., Somoza, E.C., & Winhusen, T.M.
(2013) Treating nicotine dependence by targeting attention-deficit/ hyperactivity disorder (ADHD) with OROS methylphenidate:
the role of baseline ADHD severity and treatment response. J. Clin. Psychiatry, 74,
98390.
Nylander, L., Holmqvist, M., Gustafson, L., &
Gillberg, C. (2008) ADHD in adult psychiatry.
Minimum rates and clinical presentation in
general psychiatry outpatients. Nord. J Psychiatry, 63, 6471.
Ostacher, M.J. (2007) Comorbid alcohol and
substance abuse dependence in depression:
impact on the outcome of antidepressant
treatment. Psychiatr. Clin. North Am., 30,
6976.
Perez de Los Cobos, J., Sinol, N., Perez, V., &
Trujols, J. (2012) Pharmacological and clinical
dilemmas of prescribing in co-morbid adult
attention-deficit/hyperactivity disorder and
addiction. Br. J. Clin. Pharmacol. 77,
33756.
Plichta, M.M. & Scheres, A. (2014) Ventralstriatal responsiveness during reward anticipation in ADHD and its relation to trait
9/22/2016 12:01:15 PM
514
impulsivity in the healthy population: a

meta-analytic review of the fMRI literature.
Neurosci. Biobehav. Rev., 38, 12534.
Poelmans, G., Pauls, D.L., Buitelaar, J.K., &
Franke, B. (2011) Integrated genome-wide
association study findings: identification of a
neurodevelopmental network for attention
deficit hyperactivity disorder. Am. J. Psychiatry, 168, 36577.
Polanczyk, G., de Lima, M.S., Horta, B.L., Biederman, J., & Rohde, L.A. (2007) The worldwide prevalence of ADHD: a systematic
review and metaregression analysis. Am J
Pomerleau, O.F., Downey, K.K., Stelson, F.W., &
Pomerleau, C.S. (1995) Cigarette smoking in
adult patients diagnosed with attention deficit hyperactivity disorder. J. Subst. Abuse, 7,
3738.
Potter, A.S. & Newhouse, P.A. (2004) Effects of
acute nicotine administration on behavioral
inhibition in adolescents with attention-deficit/hyperactivity disorder. Psychopharmacology (Berl), 176, 18294.
Prince, J.B., Wilens, T.E., Spencer, T.J., & Biederman, J. (2006) Pharmacotherapy of ADHD in
adults. In: Attention-Deficit Hyperactivity Disorder: a handbook for diagnosis and treatment (ed. R. A. Barkley), pp. 70436. The
Guilford Press, New York.
Riggs, P.D., Hall, S.K., Mikulich-Gilbertson, S.K.,
Lohman, M., & Kayser, A. (2004) A randomized controlled trial of pemoline for
attention-deficit/hyperactivity disorder in
substance-abusing adolescents. J Am Acad.
Child Adolesc. Psychiatry, 43, 4209.
Riggs, P.D., Winhusen, T., Davies, R.D., Leimberger, J.D., Mikulich-Gilbertson, S., Klein,
C., Liu, D. (2011) Randomized controlled
trial of osmotic-release methylphenidate
with cognitive-behavioral therapy in adolescents with attention-deficit/hyperactivity disorder and substance use disorders. J. Am.
Acad. Child Adolesc. Psychiatry, 50,
90314.
Robbins, T.W. (2002) ADHD and addiction. Nat.
Med, 8, 245.
Rosler, M., Fischer, R., Ammer, R., Ose, C., &
Retz, W. (2009a) A randomised, placebocontrolled, 24-week, study of low-dose
extended-release methylphenidate in adults
with attention-deficit/hyperactivity disorder.
Eur. Arch. Psychiatry Clin. Neurosci., 259,

1209.
Rosler, M., Retz, W., Retz-Junginger, P., Hengesch, G., Schneider, M., Supprian, T.,
Thome, J. (2004) Prevalence of attention
deficit/hyperactivity disorder (ADHD) and
comorbid disorders in young male prison
inmates. Eur. Arch. Psychiatry Clin. Neurosci.,
254, 36571.
Rosler, M., Retz, W., Yaqoobi, K., Burg, E., &
Retz-Junginger, P. (2009b) Attention deficit/
hyperactivity disorder in female offenders:
prevalence, psychiatric comorbidity and psychosocial implications. Eur. Arch. Psychiatry
Clin. Neurosci., 259, 98105.
Roy, A. (2008) The relationships between
attention-deficit/hyperactive
disorder
(ADHD), conduct disorder (CD) and problematic drug use (PDU). Drugs: Education, Prevention and Policy, 15, 5575.
Safren, S.A., Otto, M.W., Sprich, S., Winett,
C.L., Wilens, T.E., & Biederman, J. (2005)
Cognitive-behavioral therapy for ADHD in
medication-treated adults with continued
symptoms. Behav. Res. Ther., 43, 83142.
Sagvolden, T., Johansen, E.B., Aase, H., & Russell, V.A. (2005) A dynamic developmental
theory of attention-deficit/hyperactivity disorder (ADHD) predominantly hyperactive/
impulsive and combined subtypes. Behav.
Brain Sci., 28, 397419.
Schade, A., Marquenie, L.A., van Balkom, A.J.,
Koeter, M.M., van den Brink, W., & van
Dyck, R. (2005) The effectiveness of anxiety
treatment on alcohol-dependent patients
with a comorbid phobic disorder: a randomized controlled trial. Alcohol Clin. Exp.
Res., 29, 794800.
Schubiner, H. (2005) Substance abuse in
patients with attention-deficit hyperactivity
disorder: therapeutic implications. CNS
Drugs, 19, 64355.
Schubiner, H., Saules, K.K., Arfken, C.L., Johanson, C.E., Schuster, C.R., Lockhart, N.,
Edwards, A., Donlin, J., & Pihlgren, E. (2002)
Double-blind placebo-controlled trial of
methylphenidate in the treatment of adult
ADHD patients with comorbid cocaine
dependence. Exp. Clin. Psychopharmacol.,
10, 28694.
Schubiner, H., Tzelepis, A., Isaacson, J.H., Warbasse, L.H., III, Zacharek, M., & Musial, J.
9/22/2016 12:01:15 PM
(1995) The dual diagnosis of attention-

deficit/hyperactivity disorder and substance
abuse: case reports and literature review.
J. Clin. Psychiatry, 56, 14650.
Schubiner, H., Tzelepis, A., Milberger, S., Lockhart, N., Kruger, M., Kelley, B.J., & Schoener,
E.P. (2000) Prevalence of attention-deficit/
hyperactivity disorder and conduct disorder
among substance abusers. J Clin. Psychiatry,
61, 24451.
Sergeant, J.A. (2005) Modeling attention-deficit/hyperactivity disorder: a critical appraisal
of the cognitive-energetic model. Biol. Psychiatry, 57, 124855.
Serra-Pinheiro, M.A., Coutinho, E.S., Souza,
I.S., Pinna, C., Fortes, D., Araujo, C., Szobot,
C.M., Rohde, L.A., & Mattos, P. (2013) Is
ADHD a risk factor independent of conduct
disorder for illicit substance use? A metaanalysis and metaregression investigation.
J. Atten. Disord., 17, 45969.
Silva, N., Jr., Szobot, C.M., Shih, M.C., Hoexter,
M.Q., Anselmi, C.E., Pechansky, F., Bressan,
R.A., & Rohde, L.A. (2013) Searching for a
neurobiological basis for self-medication
theory in ADHD comorbid with substance
use disorders: an in vivo study of dopamine
transporters using 99mTc-TRODAT-1 SPECT.
Clin. Nucl. Med., 9, e12934.
Simon, V., Czobor, P., Balint, S., Meszaros, A.,
& Bitter, I. (2009) Prevalence and correlates
of adult attention-deficit hyperactivity disorder: meta-analysis. Br. J. Psychiatry, 194,
20411.
Soderstrom, H., Sjodin, A.K., Carlstedt, A., &
Forsman, A. (2004) Adult psychopathic personality with childhood-onset hyperactivity
and conduct disorder: a central problem
constellation in forensic psychiatry. Psychiatry Res., 121, 27180.
Solanto, M.V., Marks, D.J., Wasserstein, J.,
Mitchell, K., Abikoff, H., Alvir, J.M., &
Kofman, M.D. (2010) Efficacy of meta-cognitive therapy for adult ADHD. Am. J. Psychiatry, 167, 95868.
Sonuga-Barke, E.J. & Castellanos, F.X. (2007)
Spontaneous attentional fluctuations in
impaired states and pathological conditions:
a neurobiological hypothesis. Neurosci.
Biobehav. Rev., 31, 97786.
Sonuga-Barke, E.J., Sergeant, J.A., Nigg, J., &
Willcutt, E. (2008) Executive dysfunction and
515
delay aversion in attention deficit hyperactivity disorder: nosologic and diagnostic implications. Child Adolesc. Psychiatr. Clin. N. Am,
17, 36784, ix.
Spencer, T., Biederman, J., Wilens, T.E., & Faraone, S.V. (1998) Adults with attention-
deficit/hyperactivity disorder: a controversial
diagnosis. J. Clin. Psychiatry, 59 Suppl 7,
5968.
Spencer, T., Wilens, T., Biederman, J., Faraone,
S.V., Ablon, J.S., & Lapey, K. (1995) A double-blind, crossover comparison of methylphenidate and placebo in adults with
childhood-onset attention-deficit hyperactivity disorder. Arch. Gen. Psychiatry, 52,
43443.
Steinhausen, H.C. & Bisgaard, C. (2014) Substance use disorders in association with
attention-deficit/hyperactivity disorder, comorbid mental disorders, and medication in
a nationwide sample. Eur. Neuropsychopharmacol., 24, 23241.
Stovner, A.M., Wyller, T.B., Skulberg, A., Os, L.,
& Korsmo, G. (1996) [Treatment of hyperactivity and attention deficit with amphetamine. Experience with five adult prisoners].
Tidsskr. Nor Laegeforen., 116, 20025.
Swanson, J. (2003) Compliance with stimulants
for attention-deficit/hyperactivity disorder:
issues and approaches for improvement.
CNS Drugs, 17, 11731.
Tamm, L., Trello-Rishel, K., Riggs, P., Nakonezny, P.A., Acosta, M., Bailey, G., & Winhusen, T. (2013) Predictors of treatment
response in adolescents with comorbid substance use disorder and attention-deficit/
hyperactivity disorder. J. Subst. Abuse Treat.,
44, 22430.
Teter, C.J., McCabe, S.E., LaGrange, K., Cranford, J.A., & Boyd, C.J. (2006) Illicit use of
specific prescription stimulants among college students: prevalence, motives, and
routes of administration. Pharmacotherapy,
26, 150110.
Thomas, M.J., Kalivas, P.W., & Shaham, Y.
(2008) Neuroplasticity in the mesolimbic
dopamine system and cocaine addiction. Br.
J. Pharmacol., 154, 32742.
Thurstone, C., Riggs, P.D., Salomonsen-Sautel,
S., & Mikulich-Gilbertson, S.K. (2010) Randomized, controlled trial of atomoxetine for
attention-deficit/hyperactivity disorder in
9/22/2016 12:01:15 PM
516
adolescents with substance use disorder. J.

Am. Acad. Child Adolesc. Psychiatry, 49,
57382.
Tiet, Q.Q. & Mausbach, B. (2007) Treatments
for patients with dual diagnosis: a review.
Alcohol Clin. Exp. Res., 31, 51336.
Torok, M., Darke, S., & Kaye, S. (2012) Attention deficit hyperactivity disorder and severity
of substance use: the role of comorbid psychopathology. Psychol. Addict. Behav., 26,
9749.
Tuithof, M., Ten, H.M., van den, B.W., Vollebergh, W., & de, G.R. (2012) The role of
conduct disorder in the association between
ADHD and alcohol use (disorder). Results
from the Netherlands Mental Health Survey
and Incidence Study-2. Drug Alcohol
Depend., 123, 11521.
Upadhyaya, H.P., Desaiah, D., Schuh, K.J.,
Bymaster, F.P., Kallman, M.J., Clarke, D.O.,
Allen, A.J. (2013) A review of the abuse
potential assessment of atomoxetine: a nonstimulant medication for attention-deficit/
hyperactivity disorder. Psychopharmacology
(Berl), 226, 189200.
van de Glind, G., Konstenius, M., Koeter,
M.W., van Emmerik-van Oortmerssen, K.,
Carpentier, P.J., Kaye, Svan den Brick, W.
(2013) Variability in the prevalence of adult
ADHD in treatment seeking substance use
disorder patients: Results from an international multi-center study exploring DSM-IV
and DSM-5 criteria. Drug Alcohol Depend.
134, 15866.
van Emmerik-van Oortmerssen, K., van de
Glind, G., van den Brink, W., Smit, F., Crunelle, C.L., Swets, M., & Schoevers, R.A.
(2012) Prevalence of attention-deficit hyperactivity disorder in substance use disorder
patients: a meta-analysis and meta-regression
analysis. Drug Alcohol Depend., 122,
1119.
Volkow, N.D., Fowler, J.S., Wang, G.J., Baler, R.,
& Telang, F. (2009a) Imaging dopamine's role
in drug abuse and addiction. Neuropharmacology, 56 Suppl 1, 38.
Volkow, N.D. & Swanson, J.M. (2003) Variables
that affect the clinical use and abuse of
methylphenidate in the treatment of ADHD.
Am. J. Psychiatry, 160, 190918.
Volkow, N.D., Wang, G.J., Fowler, J.S., Tomasi,
D., Telang, F., & Baler, R. (2010) Addiction:
decreased reward sensitivity and increased

expectation sensitivity conspire to overwhelm the brain's control circuit. Bioessays,
32, 74855.
Volkow, N.D., Wang, G.J., Kollins, S.H., Wigal,
T.L., Newcorn, J.H., Telang, F., Swanson,
J.M. (2009b) Evaluating dopamine reward
pathway in ADHD: clinical implications.
JAMA, 302, 108491.
Volkow, N.D., Wang, G.J., Newcorn, J.H., Kollins, S.H., Wigal, T.L., Telang, F., Swanson,
J.M. (2011) Motivation deficit in ADHD is
associated with dysfunction of the dopamine
reward pathway. Mol. Psychiatry, 16,
114754.
Weiss, M. (2015) Functional impairment in
ADHD. In: Attention-Deficit Hyperactivity Disorder in Adults and Children (ed. L. A. Adler,
T. J. Spencer, & T. E. Wilens), pp. 4252.
Cambridge University Press, Cambridge.
Wilens, T.E. (2004) Attention-deficit/hyperactivity disorder and the substance use disorders: the nature of the relationship, subtypes
at risk, and treatment issues. Psychiatr. Clin.
North Am, 27, 283301.
Wilens, T.E., Adler, L.A., Adams, J., Sgambati,
S., Rotrosen, J., Sawtelle, R., Utzinger, L., &
Fusillo, S. (2008a) Misuse and diversion of
stimulants prescribed for ADHD: a systematic
review of the literature. J. Am. Acad. Child
Wilens, T.E., Adler, L.A., Weiss, M.D., Michelson,
D., Ramsey, J.L., Moore, Levine, L.R.
(2008b) Atomoxetine treatment of adults
with ADHD and comorbid alcohol use disorders. Drug Alcohol Depend., 96, 14554.
Wilens, T.E. & Biederman, J. (2006) Alcohol,
drugs, and attention-deficit/ hyperactivity
disorder: a model for the study of addictions
in youth. J. Psychopharmacol., 20, 5808.
Wilens, T.E., Biederman, J., & Mick, E. (1998)
Does ADHD affect the course of substance
abuse? Findings from a sample of adults
with and without ADHD. Am J Addict., 7,
15663.
Wilens, T.E., Biederman, J., Mick, E., Faraone,
S.V., & Spencer, T. (1997) Attention deficit
hyperactivity disorder (ADHD) is associated
with early onset substance use disorders. J
Nerv. Ment. Dis., 185, 47582.
Wilens, T.E., Kwon, A., Tanguay, S., Chase, R.,
Moore, H., Faraone, S.V., & Biederman, J.
9/22/2016 12:01:15 PM
(2005a) Characteristics of adults with attention deficit hyperactivity disorder plus substance use disorder: the role of psychiatric
comorbidity. Am. J. Addict., 14, 31927.
Wilens, T.E., Monuteaux, M.C., Snyder, L.E.,
Moore, H., Whitley, J., & Gignac, M. (2005b)
The clinical dilemma of using medications in
substance-abusing adolescents and adults
with attention-deficit/hyperactivity disorder:
what does the literature tell us? J. Child Adolesc. Psychopharmacol., 15, 78798.
Willcutt, E.G. (2012) The prevalence of DSM-IV
attention-deficit/hyperactivity disorder: a
517
meta-analytic review. Neurotherapeutics., 9,

4909.
Winhusen, T., Somoza, E., Singal, B.M., Harrer,
J., Apparaju, S., Mezinskis, J., Desai, P.,
Elkashef, A., Chiang, C.N., & Horn, P. (2006)
Methylphenidate and cocaine: a placebocontrolled drug interaction study. Pharmacol.
Biochem. Behav., 85, 2938.
Wood, D.R., Reimherr, F.W., Wender, P.H., &
Johnson, G.E. (1976) Diagnosis and treatment of minimal brain dysfunction in adults:
a preliminary report. Arch. Gen. Psychiatry,
33, 145360.
9/22/2016 12:01:15 PM

PJ Carpentier Ea P Asherson 2016 Sage Drug & Alcohol Studies CH 30 ADHD

Caricato da

Informazioni sul documento

Titolo originale

Copyright

Formati disponibili

Condividi questo documento

Condividi o incorpora il documento

Opzioni di condivisione

Hai trovato utile questo documento?

Questo contenuto è inappropriato?

Copyright:

Formati disponibili

PJ Carpentier Ea P Asherson 2016 Sage Drug & Alcohol Studies CH 30 ADHD

Caricato da

Copyright:

Formati disponibili

See

discussions, stats, and author profiles for this publication at:

ADHD: Pathways into addiction, diagnosis

Reinier van Arkel Groep

King's College London

37 PUBLICATIONS 703 CITATIONS

419 PUBLICATIONS 15,299 CITATIONS

CIAO II View project

ADHD: general approaches to

The SAGE Handbook of Drug & Alcohol Studies

visible and it is the inattentive symptoms

relationships, disturbing the building of stable relationships. ADHD patients tend to

ADHD: Pathways into Addiction, Diagnosis and Pharmacotherapy

Table 30.1Adult ADHD DSM-IV-TR-5 criteria (abridged version)

The SAGE Handbook of Drug & Alcohol Studies

Higher prevalence rates are found in specific

Diagnosis of ADHD in adults

can offer relevant details on symptomatology

ADHD: Pathways into Addiction, Diagnosis and Pharmacotherapy

is known about how this genetic disposition

are responsible for planning and organisation of purposeful behaviour in response to

Treatment of adult ADHD

The SAGE Handbook of Drug & Alcohol Studies

Table 30.2Medication used in adult ADHD

(+) (Amiri etal, 2012)

problems in planning and structuring and

+++ (21 RCTs)

The association between ADHD

ADHD: Pathways into Addiction, Diagnosis and Pharmacotherapy

prevalence was not influenced by subjects

cannabis as reducing some of the symptoms of

ADHD as a pathway into

The SAGE Handbook of Drug & Alcohol Studies

externalising disorders spectrum (Krueger

and CD is most often found in addicted

ADHD: Pathways into Addiction, Diagnosis and Pharmacotherapy

dopaminergic/nicotinic and acetylcholinergic

Pathways into treatment

addiction disorders (Fatseas etal, 2012). The

The SAGE Handbook of Drug & Alcohol Studies

on the clinical presentation and treatment

such as methadone). Persistent substance use

ADHD: Pathways into Addiction, Diagnosis and Pharmacotherapy

stable treatment response and the lack of

pharmacotherapy in placebo-controlled trials

Medication, maximum dose

Methylphenidate (OROS), 180 mg

* Symbols used to indicate effectiveness:

The SAGE Handbook of Drug & Alcohol Studies

reduces the effectiveness of the medication

drug treatment trials of mood and anxiety

ADHD: Pathways into Addiction, Diagnosis and Pharmacotherapy

increase in addiction among children treated

The SAGE Handbook of Drug & Alcohol Studies

for some patients just impossible to maintain.

seen in well-motivated patients with a clear

ADHD: Pathways into Addiction, Diagnosis and Pharmacotherapy

of the limited abuse potential: injecting or

SUD by means of cognitive behavioural

The relevance of ADHD in

The SAGE Handbook of Drug & Alcohol Studies

simple ADHD (see Table 30.3). Moreover

ADHD: Pathways into Addiction, Diagnosis and Pharmacotherapy