Hindawi Publishing CorporationISRN AddictionVolume 2013, Article ID 815096, 10 pageshttp://dx.doi.org/10.1155/2013/815096

Review Article�a�e Ado�escent �ubstance �se Disorder and Attention�De�citHyperactivity Disorder: A Review of the Literature

Robert Eme

Illinois School of Professional Psychology, Argosy University, Schaumburg Campus, 999 Plaza Drive, Schaumburg, IL 60173, USA

Correspondence should be addressed to Robert Eme; reme@argosy.edu

Received 7 September 2012; Accepted 16 October 2012

Academic Editors: H. Krampe, M. Naassila, and J. F. Rodriguez-Orengo

Copyright © 2013 Robert Eme.is is an open access article distributed under the Creative Commons Attribution License, whichpermits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Approximately, one-third of male adolescents in treatment for a substance use disorder (SUD) also have an Attention-De�citHyperactivity Disorder (ADHD). is strongly suggests that ADHD is a major risk factor for the development of SUD whichpractitioners must address if they are to provide adequate treatment for adolescents with SUD/ADHD.is paper supports a causalrole for ADHD in the development of SUD and examines the developmental mechanisms whereby ADHD increases risk for SUD.esemechanisms include increased risk for conduct disorder, academic failure, deviant peer affiliation, engaging in risk behaviors,and self-medication. Assessment and treatment recommendations for those comorbid for SUD/ADHD are provided.

1. Introduction

Substance use, which includes smoking, drinking alcohol,or using other addictive substances, exists on a continuumranging from no use on one end, to use that does notinvolve negative consequences, to risky use, to a substanceuse disorder (SUD) [1]. SUD is characterized by inabilityto consistently abstain, impairment of behavioral control,craving, and signi�cant problems in behavior and interper-sonal relationships [1]. SUDs are a worldwide major publichealth problem [2]. In theUnited States, adolescent substanceuse is arguably, if not incontestably, the number one publichealth problem for several reasons [3]. Addictive substanceuse is widespread as almost half of high school students(46.1 percent) are current users (used in the past 30 days) ofcigarettes, alcohol, marijuana, or cocaine; one in eight (11.9percent) meet clinical criteria for a substance use disorder(SUD) [3]. Adolescence is the critical period for the initiationof substance use and its consequences as nine out of 10Americanswho suffer froma SUD started smoking, drinking,or using other drugs before age 18 [3]. e �nancial andhuman consequences are staggering. Financially, the cost isestimated as an astonishing $1500 per year for every personin the United States [3].e human costs include, in addition

to heightened risk of addiction, reduced academic perfor-mance and educational achievement; criminal involvement;unintended pregnancies; accidents and injuries which makeit among the leading causes of death among youth under 21[3, 4].

Despite being the most important public health problem,only 15.4% of adolescents with SUD receive treatment [5],and this treatment is generally suboptimal [3]. Indeed, thereis such a profound disconnect between evidence and practicethat “…the vast majority of people in need of addiction treat-ment do not receive anything that approximates evidence-based care” [1, page 1]. Hence it is not surprising that morethan 50% of adults and adolescents who begin treatmentdrop out or terminate with unsatisfactory progress [1, 4].For example, in the largest psychosocial treatment study todate of adolescents with SUD (𝑛𝑛 = 600), the Cannabis YouthTreatment Study (CYT), only 25% were in recovery at a 1-year followup, de�ned as no substance use or dependenceproblems and living in the community [6, 7]. Similarly, the�ndings aremixed for the effectiveness of juvenile drug courts[8] and brief interventions with adolescents in acute settingswho present with risky alcohol use [9]. An important reasonfor treatment typically being suboptimal with the resultantbleak outcomes is the failure to treat mental health disorders

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that co-occur in two-thirds of people seeking treatment forSUDs [1]. A prime example is the failure to identify andproperly treat adolescents with SUD who are comorbid forAttention De�cit Hyperactivity Disorder (ADHD) [10]. Asthe review will document, at least one-third of adolescentsin treatment for SUD are comorbid for ADHD and thiscomorbidity is associated with an earlier onset of SUD,more severe and longer duration of SUD, more difficultyremaining in treatment, and a greater likelihood of relapseaer treatment [11–13].

Despite this high rate of comorbidity, ADHD oen goesuntreated in adolescents with SUDs [14]. Hence it is criticallyimportant that practitioners understand the relationshipbetween SUD and ADHD in adolescents since cooccuringdisorders present serious challenges to traditional mentalhealth and substance abuse treatments systems for adoles-cents [11]. e purpose of this paper is to provide such anunderstanding for male adolescents as data for females isjust emerging [15]. It will do so by �rst establishing thatadolescents in treatment for SUD are frequently comorbid forADHD. Second, it will discuss the mechanisms that explainthis comorbidity. ird, it will provide recommendations forassessment and treatment. Fourth, it should be noted thatgiven the vastness of the literature on SUD and ADHD andgiven that the goal of the review is to be broadly synthetic, thepaper will draw on �ndings of authoritative critical reviewsand meta-analyses as well as individual studies. Lastly, sinceit is clearly beyond the scope of this paper to address thenumerous other risk factors involved in SUD, the readerdesiring such a discussion should consult these two current,comprehensive, and authoritative sources [1, 3].

2. Prevalence of ADHD in Adolescents inTreatment for SUD

ADHD is the most common neurodevelopmental disorderin juveniles [16] with a prevalence estimate for juveniles inthe United States aged 4–17 based upon parental report ofever having been diagnosed with ADHD of 9.5% (13.2%male, 5.6% female) [17]. However, its prevalence amongadolescents with SUD is much greater. Aggregate data fromstudies in the United States yield prevalence rates rangingfrom 38% to 50% [6, 18]. In the largest sample to date of 7,435cases in treatment for SUD, most of whom were male andunder 18, Conrad and colleagues [19] reported an ADHDprevalence rate of 43% based on DSM-IV criteria assessedat intake. Van-Emmerik-van Oortmerssen and colleagues[2] conducted a meta-analysis of all methodologically soundstudies (as of January, 2010) of ADHD prevalence amongadolescents in treatment for SUD. e analysis identi�ed14 studies involving 4054 patients conducted in 6 countries.Studies were only included if ADHDwas diagnosed bymeansof a (semi) structured diagnostic instrument or a systematicDSM-based clinical interview using DSM III or DSM IVcriteria. Overall 24.2% (CI. 19.0–30.4%) of the patients metDSM-criteria for comorbid ADHD. Furthermore, since thetiming of the evaluation for ADHD is crucial as symptomsof substance intoxication or withdrawal can be mistaken

for ADHD symptoms, an analysis was conducted on the14 studies which explicitly stated that they had assessed forADHD aer a period of at least 4 days abstinence. e�ndings were the same.

Lastly, as van-Emmerik-van Oortmerssen and colleagues[2], as well as others have noted, because information fromfamily members is typically not part of the assessmentprocedure for ADHD, the sole reliance upon the self-reportof troubled adolescents probably resulted in an underestimateof the true prevalence of ADHD. us, in the largest studyof juveniles in detention facilities in the United States,Teplin et al. [20, page 1135] remarked that “Attention-de�cithyperactivity disorder (ADHD) is difficult to assess via self-report and is evenmore challenging to diagnose amongdelin-quents.” For example, Schwaab-Stone et al. [21] in examiningthe criterion validity of the Diagnostic Interview Schedulefor Children Version 2.3. found little more than chanceagreement (Kappa correlation of .10) between youth (aged9–18) report of ADHD symptoms and clinical assessment.Because of this limitation, the most recent authoritativeclinical practice guidelines for the diagnosis of ADHD forjuveniles (4–18) specify that information should be obtainedprimarily from reports from “parents or guardians, teachers,and other school and mental health clinicians involved in thechild’s care” [16, page 1]. Failure to obtain information fromparents, teachers (or in the case of adults, a signi�cant other)can be expected to result in substantial under diagnosis notonly in juveniles [22, 23], but also adults [24].

e best evidence that sole reliance on self-report resultsin a substantial underestimate of ADHD comes from thefollow-up study into young adulthood (age 21) of 147 maleswho had previously been diagnosed with ADHD in a child-hood [23]. Using a developmentally referenced criteria fordiagnosing ADHD in adults resulted in a huge discrepancywhen the criteria were assessed by self-report (12%) versusparental report (66%). e correlation between self- andparent-reported levels of ADHD symptoms was just .21.Because parent-reported symptoms were found to have a fargreater association with various measure of impairment atage 21 than self-reported symptoms, the study concludedthat parent reports provided a more accurate description ofcurrent ADHD symptoms and impairments than self-report.Similarly, Young and colleagues [25] conducted a study todetermine the most reliable source of information of ADHDsymptoms by comparing rating scales scored by 54 maledelinquents who were detained in a high risk care home andby their teachers with psychiatric diagnosis of ADHD madeby a professional clinical assessment. Sensitivity rates were33% for delinquent self-report compared to 67% for teacherreport.

In summary, ADHD prevalence rates for adolescents intreatment with an SUD range from 25% to 50%. Moreover,because assessment for ADHD in most studies failed toobtain information from parents and teachers, most studiesprobably underestimated the true prevalence rate of ADHD.Given this wide range and the high probability of underdiag-nosis, Molina [15], one of the foremost experts on the linkagebetween ADHD and SUD, has estimated that approximately

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a third of adolescents in treatment for SUD are comorbid forADHD.e paper will adopt this conservative estimate.

Among the various conceptualizations that have beensuggested to explain this comorbidity, two have the mostresearch support: the secondary substance abuse disordermodel and the common factor model [11]. e secondarysubstance abuse disorder model explains comorbidity bypositing that disorders such as ADHD increase risk for thedevelopment of SUD. e common factor model posits thathigh rates of comorbidity are the result of shared risk factors.

3. Secondary Substance Abuse Disorder Model

ere is a robust consensus, including two recent meta-analytic reviews, that ADHD is a major risk factor for thedevelopment of SUD [12, 13, 26, 27]. For example, in theirmeta-analytic review, Lee et al. [27] concluded that childrenwith ADHD were at least 1.5 times more likely to developSUD across diverse forms of substances, including nearly 3times higher for nicotine dependence.

Four distinct risk mechanisms, discussed in order ofimportance, are operative in this model. e �rst is acascading sequence in which ADHD increases risk for thedevelopment of the disruptive behavior disorders of opposi-tional de�ant disorder (ODD) and conduct disorder (CD),thereby increasing the risk for the development of SUD, inpart through association with deviant peers. e second isincreased risk for school failure caused by ADHD leading toassociationwith deviant peers.e third is that the behavioraland emotional impulsivity of ADHD, independent of comor-bid CD, increases risk for SUD. e fourth is the use of legaland illegal substances to self-medicate ADHD symptoms.

4. ADHD as a Risk Factor for CD

It is widely acknowledged that the deviance proneness ofchildren with CD increases risk for the development of SUD[15]. Although there has been a great debate over the bestway to integrate the multitude of factors that place a childat risk for developing CD into comprehensive causal models,recently a consensus has emerged for three developmentalpathways which have substantial research support [28]. Adevelopmental pathway is the “…orderly behavioral develop-ment between more than two problems behaviors with indi-viduals differing in their propensity to progress along the suc-cessive problem behavior represented by the pathway duringdevelopment” [29, page 34]. Note that the conceptualizationof a developmental pathway for CD is not deterministic, butrefers to a propensity, a probability that CD will develop [29].One developmental pathway that leads to CD begins withhigh levels of emotional and behavioral dysregulation thatresult in problems in the executive control of behavior [28].is is essentially a description of ADHD predominantlypresenting with hyperactive-impulsive symptoms [22, 30–32]. In this model, ADHD behaviors emerge �rst, followedbyODD behaviors re�ecting a pattern of negativistic, de�ant,disobedient, and hostile behavior towards authority �guresfollowed by more severe conduct problem behaviors (CD)

re�ecting a repetitive and persistent pattern of behavior inwhich the basic rights of others or major age-appropriatesocietal rules or norms are violated [33–36].

4.1. ADHD Increases Risk forODD. It is widely acknowledgedthat behavioral impulsivity is a core impairment in ADHD[32]. However, it is only recently that emotional impulsiv-ity/dysregulation has also been recognized as a core ADHDimpairment [31, 37]. ese twin impairments commonlyresult in symptoms such as irritability, impatience, anger,low frustration threshold, and reactive aggression [31, 38]which greatly increase the risk for coercive, oppositionalinterchanges [22, 39–41]. Indeed, it is estimated that a typicalchild with ADHD has an astonishing half a million ofthese negative interchanges each year [42]. ese negativeinterchanges result in a formal diagnosis of ODD for 52% ofjuveniles who have been diagnosed with ADHD in combinedcommunity and clinical settings [32]. Furthermore, Barkley[31] has observed that having ADHD virtually creates aborderline case of ODD in children.

Perhaps the most persuasive evidence that, becauseADHD is a disorder of impaired executive functioning, thatis, impaired self-control/self-regulation [31], it increases therisk for ODD and thereby increases the risk for CD (whichwill be subsequently discussed), comes from the most recent�ndings of the landmark Dunedin Multidisciplinary Healthand Development study [43]. is longitudinal study, whichfollowed a complete birth cohort of 1,037 children from birthto age 32, found that self-control assessed during the �rstdecade of life predicted increased risk of criminal offendingat age 32 aer controlling for IQ and social class origins.When the sample was segmented into the highest and lowest�hs on self-control, the lowest �h had much higher crimeconviction rates than the highest �h: 43% versus 13%.Since themeasures used to assess self-control were essentiallymeasures of the core features of the behavioral and emotionalimpulsivity that characterize ADHD (hyperactivity, impul-sivity, inattention, lack of persistence, impulsive aggression,and low frustration tolerance) in effect what the study foundwas that children with many symptoms of ADHD (althoughthey were not formally diagnosed as such in the study)were at high risk for criminality compared to those withgood self-control. us impressive support has been addedto the consensus that “self-control theory is one of themost thoroughly researched and cited theories of deviance,delinquency, and crime” [44, page 245] and that impulsivityis the most crucial variable that predicts antisocial behavior[45].

4.2. ADHD/ODD Increases Risk for CD. e role of ODD asa developmental precursor to CD has been well documented[46–48]. Moreover, it is now understood that far from beingsimply a benign, milder form of CD, ODD plays a keyrole in the development of CD and is one of the strongestpredictors of the onset of CD and of the course of CDsymptoms over time [35]. And, although the majority ofchildren with ODD do not go on to develop CD [35], ifchildhood onset CD develops, it is almost always preceded

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developmentally by ODD [49]. is development is likely tooccur when social contexts increase rather than decrease theantisocial propensity of ADHD/ODD [40, 50–52]. Amongthe various social contexts which increase the antisocialpropensity, association with deviant peers is perhaps themost important, as deviant peer affiliation is one of thebest predictors of adolescent substance use [53, 54]. us,there is substantial evidence from numerous studies thatantisocial youth selectively affiliate with deviant peers, andthis association in turn increases the antisocial propensity byproviding new opportunities to engage in behaviors such asthe use and abuse of various substances [55].

In addition, there is emerging evidence that there aresubdimensions of ODD symptomatology that are not equallyassociatedwith the risk of developingCD [37].e symptomsthat index a negative affect dimension predict internalizingproblems whereas oppositional symptoms such as oenar�ues with adults� oen activel� de�es or refuses to co��l�with adult’s requests or rules, which index a “headstrong”dimension, predict CD [37]. e “headstrong” dimensionof ODD has been found to be associated with ADHD [56]and thus provides even more support for a developmentalpathway to CD which begins with ADHD.

As a consequence of this pathway, 22% of those withADHD develop CD based upon combining data from com-munity and clinical samples [32]. Furthermore, in clinicstudies of child onset CD, the vast majority of males withCD have been found to be comorbid for ADHD [15, 47, 57–60]. As Molina [15, page 193] concluded in her literaturereview of the relationship between ADHD and delinquency,“the difficulty of identifying children with conduct problemswithout symptoms of ADHD, or traits akin to ADHDsuch as impulsivity and distractibility, has strengthened theargument that inattention, hyperactivity, and particularlyimpulsivity, contribute to the development of serious conductproblems for a substantial portion of delinquent youth.”

4.3. ADHD Increases Risk for School Failure and Associationwith Deviant Peers. School failure has long been recognizedas a risk factor for SUD [15]. Academic functioning is adomain of tremendous difficulty for youth with ADHD suchthat approximately 30% repeat a grade, 30–40% may beplaced in special education, 45% may be suspended fromschool, and 10–35%may drop out [22].

ADHD increases risk for academic failure in the followingways. First, the severe impairments in selective attention,working memory, and sustaining attention that characterizeADHD adversely affect academic performance [22]. Sec-ondly, the development of ODD in 52% of youth withADHD further exacerbates these severe academic difficulties[22]. irdly, the combination of ADHD/CD plus academicfailure leads to a loss of self-esteem, frustration and peerrejection. Consequently they are less likely to be socializedinto academic pursuits that direct them away from negativesocial in�uences and more likely to associate with deviantpeers who in turn are more likely to be substance-using andsubstance-tolerant [15, 54, 61].

4.4. SUD as Self-Medication for ADHD. Although theincreased risk that ADHD poses for the development of CDis the most important pathway that leads SUD, it is clear thatADHD can increase risk for SUD independent of increasingrisk for CD [15, 62–65] through the mechanism of self-medication. ere is signi�cant evidence that a subgroupof adolescents with ADHD may be using licit and illicitsubstances for the purpose of self-medication (though notnecessarily consciously so) which can be de�ned as the use ofsubstances for reasons other than their euphoric properties,such as ameliorating ADHD symptoms of inattention [12, 15,66].

e biological basis of this self-medication can beexplained by the linkage of ADHD and substances to theneurotransmitter dopamine. ere is consistent researchsupport that links ADHD to a de�ciency in dopamine [67,68]. Also, all substances of abuse (both legal and illegal)exert their rewarding effects by increasing dopamine [69–71], although the speci�c pathways used by the differentdrugs to increase dopamine vary among the drug classes[71]. us there is solid scienti�c evidence that drugs ofabuse can function as a form of self-medication because,like stimulant medication, they acutely but temporarily raisethe concentration of dopamine in the brain and hencecan temporarily improve ADHD symptoms [72]. Unlikestimulant medication, however, drugs of abuse can also causeeuphoric effects by triggering a massive dopamine surgefollowed by rapid clearance [73].

Lastly, perhaps the most impressive evidence that someSUD has it origins as self-medication comes from researchon nicotine (tobacco, cigarette smoking) and ADHD. Sincecigarette smoking has been shown more to be more con-sistently associated with childhood ADHD than any othersubstance and less likely than other substances of abuse tohave this association explained by CD or antisocial comor-bidity, it suggests that the ADHD-tobacco associationmay beexplained by a vulnerability speci�c to nicotine rather thanaccess to drugs of abuse in deviant peer groups [15]. epossibility of a speci�c vulnerability is strongly supported byfact that research is being conducted using nicotinic agentsto treat ADHD [13]. us, while initial exposure in adoles-cence to cigarette smoking is most likely to be affected bynumerous factors such as parental smoking and deviant peerassociation, the progression to habitual use and addictionmay be due to the positively reinforcing, self-medicatingeffects of nicotine [15]. Support for this theory comes fromstudies demonstrating that nicotine administration enhancesattention in smoking and nonsmoking adults with ADHDto a degree comparable to methylphenidate [74]. Moreover,evidence that nicotine can prime the brain, making it moresusceptible to developing addiction to illegal substances [1],provides support for the theory that cigarette use oenprovides a “gateway” to other drugs such as marijuana [15,18] which may also serve a self-medicating function. Forexample, the following interview excerpt (from the author’sprivate practice) of a male adolescent who smokedmarijuanaseveral times a day for years and was known at school as the“Weed God” illustrates this possibility.

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Interviewer: What is it like when you go to schoolhigh?

Client: I can sit there and it helps me concentrate.It’s like medicine.

Interviewer: How does it help you concentrate?

Client: I do not know, it just does. I can concen-trate.

Interviewer: Do you have concentration problemsotherwise?

Client: Yeah.

Interviewer: Can you explain those to me?

Client: I do not know, like I get distracted easilybut when on weed I focus more.

Interviewer: Will you tell me more about beingdistracted?

Client: I do not know. I do not, like…pay atten-tion. I’m �dgety. I cannot, like, when I do notsmoke weed all I do is like shake my leg or some-thing. I cannot calm down. I use it more—I thinkI use it more as a medicine than I do to have fun.

5. Common Factor Model

e common factor model posits that high rates of comor-bidity are the result of shared risk factors [11]. With regard toADHD and SUD, both of which can be aptly characterized asdisorders of impaired control [75], two of themost importantshared risk factors which impair control are the neurobe-havioral traits of impulsivity and sensation-seeking [75–78].ese traits characterize ADHD [22, 31, 67, 79, 80], markedlyincrease risk for SUD, [81], and, as will subsequently bediscussed, are mediated by neuronal brain circuits that aresimilarly impaired in ADHD and SUD [76, 80].

6. Impaired Control/Impulsivity

Impulsivity refers to the difficulty in withholding a prepotentresponse (i.e., impaired response inhibition which might belabeled “cannot stop”) [77]. With regard to ADHD, thereis a substantial literature which links impaired frontostri-atal connectivity to impaired response inhibition [82]. Asimilar impairment has been found in SUD [83], but untilvery recently there has been the question of whether theimpairment was due to the SUD or predated drug-taking,rendering individuals vulnerable for the development of anSUD.e study by Ersche and colleagues [83] provides strongsupport for this impairment predating drug-taking. eyindenti�ed abnormalities in frontostriatal connectivity notonly in addicted individuals but also in their nonaddictedsiblings as compared to control group of healthy nonaddictedunrelated individuals. Despite having the same vulnerability,

it is not clear why one sibling became addicted and theother did not. Volkow and Baler [75] suggested the possibilityof different environmental exposures, different resiliencefactors, or additional neurobiological vulnerabilities.

7. Impaired Control/Sensation-Seeking

Sensation-seeking can be de�ned as the seeking of varied,novel, complex, and intense sensations and experiences andthe willingness to take physical, social, legal, and �nancialrisks for the sake of such experience [84]. AswithADHD/CD,this trait increases risk for SUD primarily by increasing riskfor affiliation with deviant peers in that juveniles high insensation-seeking will tend to seek out peers who can provideopportunities for novel, nonnormative stimulation such assubstance use [53].

Sensation-seeking is thought to result from an impair-ment in the dopamine reward system that characterizesADHD and SUD [10, 67, 68, 70, 77, 85]. In ADHD, thisde�ciency, in turn, results in a blunted response to typicalrewards, an accentuated response to novelty [67], and thuscreates a “craving” for more intense, exciting experiences. Forexample, as Hallowell and Ratey noted [79, page 25], “manyof us with ADHD crave high-stimulus situations. In my case,I love casinos and horse races. Obviously a craving for highstimulation can get a person into trouble.” In SUD, drugs canbe used to compensate for this de�ciency (reward de�ciencyhypothesis) [70, 77].

8. Recommendations for Assessment andTreatment of Adolescents with SUD/ADHD

Unfortunately adolescents with comorbid disorders oen failto receive effective treatment, if any at all [11]. If this dismalrecord is to be recti�ed with regard to adolescents comorbidfor SUD/ADHD, the essential �rst step of treatment isobviously premised on the identi�cation of such individuals.

9. Assessment of ADHD

Assessment for ADHD should be integrated into a compre-hensive psychiatric, addictive, social, cognitive, educational,and family evaluation [86]. Failure to do so, with sole relianceon prior clinical records for diagnosis, can be expectedto result in a vast underestimate of ADHD. For example,McAweeney and colleagues [87] found a huge differencewhen the prevalence of ADHD was solely determined bya prior diagnosis in the clinical record (3%) and aer athorough clinical assessment (44%).is assessment shouldbe conducted in accordance with the following guidelines.

First, all of the adolescent’s existing documentationshould be examined for a prior diagnosis of ADHD inchildhood. If it does contain a prior diagnosis, a referral fora more comprehensive con�rmatory evaluation is warrantedsince most children diagnosed with ADHD continue to havethe disorder into adolescence [22, 88].

Second, since acute intoxication or withdrawal symptomsmay mimic ADHD symptoms, such as impulsive behaviors,

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concentration difficulties or restlessness [89], at least 1monthof abstinence is essential before an evaluation can accu-rately and reliably assess for ADHD symptoms based uponadolescent self-report or observation [86]. However, muchmore importantly, since adolescents with ADHD providenotoriously inaccurate self-reports of symptoms and relatedimpairments [88, 90], it is essential that information also beobtained from the adolescent’s parent or caretaker and ideallyalso a core academic teacher [16, 88].

ird, if the prior screening suggests the possibility ofADHD, the adolescent should be referred to an expert for acon�rmatory evaluation.

10. Treatment of SUD/ADHD

If a diagnosis of ADHD is made, it is essential to treat thisdisorder along with the SUD in an simultaneous, integratedapproach,with SUD treated �rst [10, 11, 86].ekey questionis how. Although there is a substantial literature on evidence-based treatments for either SUD [1, 3, 4, 91] or ADHD[16, 42, 92], there are no evidence based guidelines for howthese treatments should be integrated for both disorders [11,18]. Furthermore, clinicians may be reluctant to incorporatestimulants (the �rst line of treatment for ADHD in juveniles,APA [93]) into treatment for ADHD in adolescents with SUDbecause of concerns regarding safety and misuse [14]. isissue and the issue of treatment efficacy follows.

11. Concerns Regarding Safety andMisuse

First, some concerns can be laid to rest. e concern ofwhether the widespread use of stimulant medications to treatchildren with ADHD increases risk for SUD later in life hasbeen decisively answered. A substantial body of literature hasfound that stimulant treatment begun in childhood or earlyadolescence does not increase susceptibility to SUD [15, 18,86, 94]. ese �ndings may be explained in part by evidencethat stimulants act somewhat differently with respect to abusepotential in patients with ADHD [73]. However, the �ndingsare mixed with regard to whether or not stimulant treatmentreduces liability to developing SUD [15]. For example inthe landmark Multimodal Treatment Study of children withADHD (MTA), although 14 months of state-of-art treatmentcombining an optimal medication regimen with intensivebehavior therapy was highly successful in that 68% achievednormal functioning at the end of treatment [95], 36 monthsaer treatment began, this group (at ages 11–13) had higherrates of substance use (17.4%), mostly tobacco and alcohol,than an local normative comparison group (7.8%) [96].(e MTA study is the largest and most comprehensivestudy of both stimulant medication and behavior therapyof children with ADHD that has ever been conducted. Itwas a randomized clinical trial that lasted for 14 monthsof four treatment strategies for 576 children aged 7–9 withADHD: medication management, behavioral treatment, acombination of these two, and an active control conditionbased on usual treatment available in the community.)Additional concerns regarding adolescents using drugs and

alcohol while taking stimulant medication may also notbe warranted, as there does not appear to be an increasein severe drug reactions between stimulants and drugs oralcohol [14, 97]. Also, Winhusen and colleagues [98] foundthat adolescents with SUD/ADHD who were treated withstimulant medication (osmotic-released methylphenidate)OROS-MPH compared to placebo controls did not misusethe medication, nor experience differences in cravings fortheir medication or other substances

Second, legitimate concerns regarding safety and misuseshould be addressed by a careful monitoring for signs ofpossible abuse or diversion such as missed appointments,repeated requests for higher doses and a pattern of “lost”prescriptions [73]. Problems of potential abuse of stimulantmedication can be reduced in two ways. First, a prodrug orlong-acting formulations can be used, as they are less easilymanipulated than immediate release formulations to enableabuse by intranasal or intravenous methods to produce aneuphoric effect [73]. (A prodrug is a medication that isinitially inactive when �rst administered and is convertedinto an active form in the body by the normal metabolicprocesses involved in digestion.) Second, recently developednovel delivery systems such as the crush resistant shell ofConcerta (methylphenidate) or amethylphenidate skin patchcan be used [99].

12. Treatment Efficacy

ere have been only a few studies to date which havecombined medication and psychological treatment (threeopen, 𝑛𝑛 = 42 subjects and �ve controlled, 𝑛𝑛 = 557 subjects)[18, 94] with the most important comprehensive study beingthe National Institute of Health multisite study of outpatienttreatment of 303 adolescents (aged 13–18 years) comorbid forSUD/ADHD [14, 98, 100]. Almost all subjects met criteriafor cannabis abuse or dependence (96%), following by lowerrates for alcohol abuse or dependence (56%), and muchlower rates (<10%) for other substances such as cocaineand amphetamines. In this 16-week randomized, placebo-controlled study, the adolescents received two treatments:OROS-MPH plus weekly cognitive behavior therapy (CBT)versus placebo plus weekly cognitive behavioral therapy.e primary substance outcome measure was the numberof days of past-28-day of adolescent reported nontobaccodrug/alcohol use, assessed using a timeline followback pro-cedure (TLFB). (is procedure involved asking adolescentsto retrospectively estimate their nontobacco drug/alcohol useat 28-day intervals over the 16-week treatment time period.)OROS-MPH plus cognitive behavior therapy did not showgreater efficacy than placebo plus CBT for ADHD or reduc-tion in substance use. Furthermore, despite a modest declinein non-tobacco substance use from the beginning to the endof study, most adolescents in both groups were nonabstinentin the �nal 28 days of treatment interval, averaging 8–10 daysof nontobacco drug/alcohol use. A subsequent secondaryanalysis was conducted to investigate potential predictors oftreatment outcomes with the major outcome measure beingwhether or not the subject was an “SUD responder” de�ned

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as achieving a 50% reduction in substance use days frombaseline to week 16 based on self-report on the TLFB. emajor �nding was an interaction effect which showed thatOROS-MPH improved SUD outcomes in adolescents withcomorbid CD compared to placebo with 42% of the OROS-MPH group being classi�ed as responders versus 18% ofthe placebo group. e authors concluded that while this�nding is only preliminary, it does suggest that OROS-MPH“may be a useful and effective approach when combinedwith cognitive behavioral therapy for reducing drug andalcohol abuse in these adolescents” [100, page 5]. eyalso speculated that more intensive treatments involving daytreatment or residential care may produce better results. Insummary, integrated treatment of SUD/ADHD having justbegun, much work needs to be done to develop and evaluateefficacious strategies [18, 94].

13. Conclusion

e literature provides robust support for the extensive agree-ment that ADHD is a major risk factor for the developmentof SUD. is risk results in approximately one-third of maleadolescents in treatment for SUDbeing comorbid for ADHD.e developmental mechanisms whereby ADHD increasesrisk for SUD include increasing the risk for conduct disorder,academic failure, deviant peer affiliation, engaging in riskybehaviors, and self-medication.is widespread comorbidityindicates that assessment for ADHD should be integratedinto a comprehensive psychiatric, addictive, social, cognitive,educational, and family evaluation which should be providedfor all males with SUD. If a diagnosis of ADHD is made, itis essential to treat this disorder along with the SUD in ansimultaneous, integrated approach. Integrated treatment ofSUD/ADHDhas just begun, andmuchwork needs to be doneto develop and evaluate efficacious strategies.

References

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