Stimulants and noradrenergic agonists are ADHD psychotropic treatments approved by the US Food and Drug Administration for use in adolescents [also see (Barkley, 2004a) for a general review]. Stimulants include methylphenidate (e.g., Ritalin, Concerta, Metadate ER) and amphetamine compounds (e.g., Adderall, Dexedrine, and DextroStat), and have a long-standing history in the treatment of ADHD (Conners, 2002). Both classes of stimulants have slightly differing mechanisms of action. Whereas both block the reuptake of dopamine and norepinephrine into the presynaptic neuron and thereby increase neurotransmitter concentrations, amphetamine compounds also increase the release of dopamine from presynaptic cytoplasmic storage vesicles (Connor, 2006). Stimulants are effective in approximately 70 % of adolescents with ADHD (Biederman, Spencer, & Wilens, 2004; Evans et al., 2001; Wilens & Spencer, 2000). At least seven randomized controlled trials have been conducted among adolescents with ADHD—all but one support the efficacy of stimulants [reviewed in (Connor, 2006)]. Consistent with findings that there is diagnostic continuity of ADHD from childhood to adolescence (Faraone, Biederman, & Monuteaux, 2002), the efficacy of stimulants (specifically, methylphenidate) is largely equal from childhood to adolescence (Smith, Pelham, Gnagy, & Yudell, 1998). In a meta-analysis of children and adolescents comparing the comparative efficacy of the two broad class of stimulants (i.e., methylphenidate and amphetamine compounds), amphetamine compounds had a small yet statistically significant advantage over a standard-release form of methylphenidate for parent and clinician ratings of ADHD symptoms and global ratings (but not for teacher ratings) (Faraone, Biederman, & Roe, 2002). Although stimulants such as methylphenidate are efficacious in acutely reducing ADHD symptoms, medication side effects (e.g., decreased appetite) are common and have prompted consideration of other pharmacological interventions (Schachter, Pham, King, Langford, & Moher, 2001).

Noradrenergic agonists approved for use in ADHD children and adolescents by the US Food and Drug Administration include guanfacine extended release (Intuniv) and clonidine modified release [see (Bidwell, Dew, & Kollins, 2010) for a review]. Though the precise mechanism of action for treating ADHD is unclear, these medications likely facilitate dopamine and noradrenaline neurotransmission thought to play a role in the pathophysiology of ADHD (Arnsten, 2009; Bidwell et al., 2010). In 2009, guanfacine extended release was the first α-2 agent to be approved by the US Food and Drug Administration for use in treatment of ADHD in children and adolescents. According to one randomized controlled trial in children and adolescents with ADHD, guanfacine performed better than a placebo in reducing teacher-rated ADHD symptoms, but not parent-rated ADHD symptoms (Scahill et al., 2001). In three double-blind, placebo-controlled trials involving child and adolescent participants, guanfacine extended release performed significantly better than placebo in reducing symptoms (Biederman, Melmed, Patel, McBurnett, Konow, et al., 2008; Kollins, Spencer, Findling, et al., 2009; Sallee et al., 2009). A 2-year, open-label, follow-up study of guanfacine extended release in children and adolescents, with or without coadministration of stimulants, demonstrated continued efficacy as that seen in short-term randomized controlled trials (Sallee, Lyne, Wigal, & McGough, 2009). Such findings emerged in a similar study (Biederman, Melmed, Patel, McBurnett, Donahue, et al., 2008), although the attrition rate in both studies was greater than 75 % and therefore limits generalizability. Two randomized, double-blind, placebo-controlled studies evaluating the efficacy of clonidine modified release in children and adolescents with ADHD have been conducted. One assessed clonidine modified release as a monotherapy, while another studied it as an add-on agent in patients on a nonoptimal stimulant drug regimen. In both trials, clonidine modified release significantly reduced ADHD symptoms from baseline and was well tolerated (Jain, Kollins, Baily, et al., 2008; Kollins, Findling, Wigal, et al., 2009).

Atomoxetine (Strattera) is another noradrenergic agonist approved for use in adolescents with ADHD [see (Cheng, Chen, Ko, & Ng, 2007; Thomason & Michelson, 2004; Wilens, Newcorn, et al., 2006) for reviews and meta-analyses] and has comparable efficacy with methylphenidate in reducing core ADHD symptoms in children and adolescents (Hazell et al., 2011). In one randomized, placebo-controlled, dose–response study of atomoxetine in children and adolescents with ADHD, atomoxetine was consistently associated with a significant reduction of ADHD symptoms (Michelson et al., 2001). Social and family functioning also improved among those taking atomoxetine with statistically significant improvements in measures of ability to meet psychosocial role expectations and parental impact. In a randomized, placebo-controlled study of atomoxetine among children and adolescents with ADHD, atomoxetine-treated participant reductions in ADHD symptoms were superior to those of the placebo treatment group as assessed by investigator, parent, and teacher ratings (Michelson et al., 2002). Additional trials have demonstrated the efficacy and tolerability of this medication in children and adolescents with ADHD (Buitelaar et al., 2004; Kratochvil et al., 2007; Michelson et al., 2007; Newcorn, Spencer, Biederman, Milton, & Michelson, 2005; Prasad et al., 2007; Wehmeier et al., 2008). Although these studies included children and adolescents, acute atomoxetine treatment appears to be equally effective and tolerated in children and adolescents (Wilens, Kratochvil, Newcorn, & Gao, 2006). Such findings suggest that pharmacological differences in tolerability or ADHD symptom response are negligible between children and adolescents.

When considering pharmacotherapy, one issue relevant to adolescents with ADHD involves treatment discontinuation. The prevalence of prescribing by general practitioners to patients with ADHD drops significantly in adolescence (Charach, Ickowicz, & Schachar, 2004). Further, this decrease is greater than the reported age-related decrease in symptoms, indicating that treatment is prematurely discontinued in many cases where symptoms persist (McCarthy et al., 2009). In one longitudinal study, 48 % of children between the ages of 9 and 15 had discontinued ADHD medication. Age was a significant moderator of medication adherence such that adolescents were less likely to continue their medication (Thiruchelvam, Charach, & Schachar, 2001). Thus, in addition to a need for continued research devoted to efficacious treatments for adolescents with ADHD (Smith et al., 2000), unique barriers to treatment such as premature discontinuation needs to be addressed.

In terms of psychosocial treatments for adolescents with ADHD, the empirical literature is sparse in comparison to pharmacotherapy options. In addition, due to the many developmental and environmental changes that occur during transition into adolescence, childhood treatments are not easily translated for this age group (Chronis, Jones, & Raggi, 2006). Among the developmental changes that have implications for treatment, adolescents have a greater cognitive capacity for abstraction, behavioral self-awareness, identity formation and need for independence, peer influence, variability in daily school routines, and physiological changes (e.g., development of secondary sex characteristics) (Smith et al., 2000). Thus, treatments are recommended to include increased involvement of the teenager, behavioral contingencies that involve more opportunities to socialize with peers and exert independence, collaboration with multiple teachers, homework issues (particularly time management and organizational skills), and self-monitoring strategies (Chronis et al., 2006). Among studies that have considered psychosocial treatments for adolescents with ADHD, family-based and school-based approaches are the most promising (Chronis et al., 2006; Pelham & Fabiano, 2008).

Three studies have involved family-based interventions. One study randomized 12–18-year-olds to 8–10 sessions of behavior management training, problem-solving and communication training, or structural family therapy (Barkley, Guevremont, Anastopoulos, & Fletcher, 1992). All conditions resulted in significant improvement in negative communication, conflict, anger during conflicts, school adjustment, internalizing and externalizing symptoms, and maternal depressive symptoms at posttreatment and were largely maintained for a 3-month follow-up. However, only 5–20 % in each condition demonstrated clinically significant reliable change following treatment. Another study compared parent behavior management training to parent behavior management training/problem-solving and communication therapy (Barkley, Edwards, Laneri, Fletcher, & Metevia, 2001). Both treatments demonstrated significant improvement in parent–teen conflicts, but were not statistically different from one another. Although such group-level analysis and normalization rates supported the efficacy of these treatments, reliable change indices were similar to Barkley et al. (1992). Another study evaluated a behavior management, problem-solving, and education group for parents of adolescents with ADHD (McCleary & Ridley, 1999). Pre- and posttreatment comparisons indicated statistically significant decreases in the frequency and intensity of self-reported parent–adolescent conflict and in parent-reported problem behavior, and positive effects on parent skills and confidence. Although these studies are promising, they did not produce much clinically significant reliable change or are limited by methodological design (i.e., lack of a control or alternative treatment group). In terms of clinical implications, multimodal, long-term treatment may be useful to assist parents in their interactions with their teens to manage parental and family distress (Robin, 2006), as opposed to simply reducing ADHD symptom severity.

Academic functioning is one of the most common concerns of parents of adolescents with ADHD (Robin, 2006). Interventions targeting academic impairment in adolescents with ADHD are promising (Raggi & Chronis, 2006). One school-based intervention involving directed note taking through group-based didactic and modeling yielded statistically significant improvement in on-task behavior, material comprehension, and daily assignment scores in an adolescent ADHD sample (Evans, Pelham, & Grudberg, 1995). A more comprehensive treatment, called the Challenging Horizons Program (Evans, Axelrod, & Langberg, 2004), involving (a) after-school academic training incorporating behavioral strategies in a group and individual setting and (b) monthly group parent training has yielded moderate to large effect sizes on parent and teacher-rated academic functioning and classroom disturbance in comparison to a community care group among middle school students with ADHD (Evans, Langberg, Raggi, Allen, & Buvinger, 2005). Although effect sizes were less promising for social functioning and methodological designs limited the generalizability of these findings (e.g., quasi-experimental design, small sample size), a 3-year treatment outcome study of this program indicated cumulative long-term benefits for the treatment group in comparison to a community care control group for parent ratings of ADHD symptoms and social functioning (Evans, Serpell, Schultz, & Pastor, 2007). However, this latter study did not indicate any academic benefits of the treatment. Single-subject design studies also indicate the beneficial impact of behavioral techniques (e.g., self-monitoring and functional analysis) in improving goal-oriented behavior in the classroom while decreasing disruptive behavior among adolescents with ADHD (Ervin, DuPaul, Kern, & Friman, 1998; Stewart & McLaughlin, 1992), which deserves additional consideration in future research.

A variant of the interventions discussed above targeting academic behavior in adolescents with ADHD is also emerging. That is, the Homework Intervention Program is a behaviorally based parent training program targeting homework in middle school students. In a pilot study of a small sample of middle school students diagnosed with ADHD (n  =  11), multiple-baseline design analyses indicated an improvement in parent-reported homework problems and ADHD symptoms, overall grade point average, and teacher-reported productivity (Raggi, Chronis-Tuscano, Fishbein, & Groomes, 2009).

Overall, comprehensive school-based interventions are promising and, similar to family-based interventions, warrant future research. Psychosocial treatment development for adolescents with ADHD is a small, yet developing field of research. Current treatments need to be more thoroughly assessed. For example, social impairment continues into adolescence (Bagwell, Molina, Pelham, & Hoza, 2001) and needs to be assessed more thoroughly. Further, social impairment with ADHD increases the risk for substance use and related problems (Greene et al., 1999), which demonstrates the need to also target social functioning in adolescent ADHD interventions. Treatments need to also consider ADHD adolescents and how to individualize treatment for the various comorbidities that can be presented. In addition, treatments that complement existing psychosocial treatment approaches should also be considered to target the multidimensional challenges that adolescents with ADHD face (Smith et al., 2000). Some potentially complimentary treatments have yielded promising results. For example, attention training in cognitive training programs (Epstein & Tsal, 2010), mindfulness meditation (Zylowska et al., 2008), and physical exercise to reduce disruptive behaviors (Allison, Faith, & Franklin, 1995) have potential, although more methodologically rigorous trials are required.

Although stimulant medications are efficacious in targeting ADHD symptoms, there are several controversial topics that are common about this particular type of pharmacotherapy. One concern involves the non-prescribed use of stimulants. One study assessing poison control center calls among 13–19-year-olds indicates that the rates of stimulant medication abuse in adolescents are rising (Setlik, Bond, & Ho, 2009). In one longitudinal sample, 11 % of an ADHD group reported selling their medications in comparison to no subjects in a control group taking other medications (Wilens, Gignac, Swezey, Monuteaux, & Biederman, 2006). Also, significantly more participants with ADHD reported misusing their stimulant medications (22 %). Those with comorbid CD or a substance use disorder accounted for this trend, which further demonstrates the necessity to understand and consider the role of comorbidity in clinical settings. In another study among junior and senior high school students who were prescribed stimulants, 7 % had sold their medications (Michelson et al., 2001). In a sample of college students taking ADHD medications, 31 % had misused their medication by taking larger or more frequent doses than prescribed or by using someone else’s medication (Rabiner et al., 2009). In addition, 8 % engaged in intranasal use and 26 % had diverted their medications to peers. Although nonacademic reasons for misuse were reported, enhancing ability to study outside of class was the primary motive for misuse. These findings indicate the need to monitor medication use in adolescents with ADHD, particularly those with comorbid CD or substance use disorders, and to consider treatments that have a lower likelihood of misuse or diversion (Wilens, Gignac, et al., 2006). In cases in which the primary motive of misuse is to assist in studying and other academic behavior, concerns about inadequate dosing and the need to improve communication between adolescents and their prescribing physicians need to be addressed.

Another issue regarding stimulant medication use involves its suppressive impact on physical growth. Reviews indicate that treatment with stimulant medication does lead to subsequent delays in height (approximately amounted to 1 cm/year during the first 3 years) and weight (Faraone, Biederman, Morley, & Spencer, 2008; Ptacek, Kuzelova, & Paclt, 2009). These reviews also indicate that the effect of stimulants on growth suppression reduces over time, growth deficits may be dose dependent, growth suppression effects may not differ between methylphenidate and amphetamine, stimulant discontinuation may lead to growth normalization, and ADHD may itself be associated with dysregulated growth. In one longitudinal study, methylphenidate treatment was associated with small yet significant delays in height, weight, and body mass index (Faraone & Giefer, 2007). Within the ADHD sample, those who had not received prior stimulant therapy and those who entered the study with an above average height, weight, and body mass index were most likely to experience growth deficits while taking stimulants. Further, the impact on all growth indices was most apparent during the first year of treatment and attenuated over time. In another longitudinal study evaluating the effect of stimulant medication on physical growth, a newly medicated group exhibited decreases in size after 3 years of treatment relative to a non-medicated group—the newly medicated group was 2.0 cm shorter and weighed 2.7 kg less (Swanson et al., 2007).

Other studies have considered non-stimulant ADHD medications as well and have reported a relationship with growth suppression. In one study, for example, lisdexamfetamine dimesylate treatment lead to statistically significant reductions in expected height, weight, and body mass index (Faraone, Spencer, Kollins, & Glatt, 2010). These findings indicate that in clinical settings, the potential benefits in symptom reduction and daily functioning need to be contrasted with the small but significant effects of pharmacotherapy (particularly stimulants) on growth. In most cases, growth suppression effects do not appear to be a clinical concern for most children treated with stimulants (Faraone et al., 2008). Although future studies are required to clarify the effects of continuous pharmacotherapy into adulthood to attain a better perspective of the long-term impact on growth, these findings suggest that growth rate should be monitored during treatment for ADHD.

Another controversial issue regarding the use of stimulants is whether they increase risk for substance use later in life. While some studies have reported that nicotine and cocaine abuse were associated with previous stimulant treatment in children with ADHD (Lambert, 1998, 2002; Lambert & Hartsough, 1998; Lambert, McLeod, & Schenk, 2006), others have found that stimulant treatment does not increase risk for substance use disorders (Barkley, Fischer, Smallish, & Fletcher, 2003; Biederman, Monuteaux, et al., 2008; Faraone, Biederman, Wilens, & Adamson, 2007; Katusic et al., 2005; Mannuzza, Klein, & Moulton, 2003; Paternite, Loney, Salisbury, & Whaley, 1999). Further, some studies have reported that stimulant pharmacotherapy may have a protective effect against later substance use disorders (Biederman, Wilens, Mick, Spencer, & Faraone, 1999; Whalen, Jamner, Henker, Gehricke, & King, 2003).

In a meta-analysis of six studies assessing the relationship between stimulant pharmacotherapy and later substance use disorder, a 1.9-fold reduction in risk for a substance use disorder was reported for youths treated with stimulants (Wilens, Faraone, Biederman, & Gunawardene, 2003). This protective effect was particularly strong in adolescence. Stimulant therapy was also reported to reduce risk for substance use disorders by 50 %, which reduced risk for this comorbidity in ADHD individuals to normal population risk levels (Faraone & Wilens, 2003). Given the contradictory findings assessing the relationship between stimulant and subsequent substance use, future studies need to assess methodological issues that limit these findings. In particular, future studies should further consider the developmental period assessed that confers differing risk for substance use (e.g., adolescence, young adulthood), comorbidity that also predicts substance use (particularly CD), sample composition that limits generalizability (e.g., gender, race, ADHD diagnostic criteria), different substances of abuse and substance use outcomes (e.g., substance use vs. substance use disorder), and naturalistic designs using retrospective reporting of stimulant treatment (including dose and medication adherence) and substance use.

Consistent with findings that adolescents with ADHD appear more emotionally immature relative to non-diagnosed peers (Hoy, Weiss, Minde, & Cohen, 1978), recent reviews argue that emotion dysregulation is an additional feature of ADHD (in addition to the core symptoms of inattention and hyperactivity–impulsivity) that should be incorporated into theoretical conceptualizations and DSM-V diagnostic criteria (Barkley, 2010; Martel, 2009; Skirrow, McLoughlin, Kuntsi, & Asherson, 2009).

Despite that there is no consistently agreed upon definition of emotion dysregulation (Putnam & Silk, 2005), most accounts describe it as a multidimensional construct (Gratz & Roemer, 2004) that includes (a) the inhibition of behavior associated with strong negative or positive emotion and (b) subsequent engagement in self-regulatory actions, including self-soothing, refocusing attention, moderating the initial emotion, and organizing for coordinated action in the service of goal-directed behavior (Barkley, 2010; Gottman & Katz, 1989; Hinshaw, 2003; Martel, 2009; Melnick & Hinshaw, 2000). According to one account of emotion dysregulation in ADHD (Barkley, 2010), those with the disorder are less likely to inhibit their emotions, particularly those pertaining to frustration, impatience, and anger, as a result of deficient cognitive control. The outcome of this poor inhibitory process is emotional impulsivity, which “refers to the quickness or speed with which and the greater likelihood that an individual with ADHD will react with negative emotions in response to events relative to others of the same developmental level or age without ADHD” [p. 5, (Barkley, 2010)]. In other words, deficient emotion regulation involves a failure to inhibit negative emotions that leads to negative affectively driven impulsive behavior in ADHD. Much like other emotion dysregulation definitions, this is not the same as emotional intensity or reactivity (Gratz & Roemer, 2004); rather emotions are less moderated by top-down, effortful executive control (Barkley, 2010).

Empirical support for the inclusion of emotion dysregulation as a feature of the disorder comes from several sources. First, neuroanatomical networks associated with ADHD also underlie emotional functioning [see (Barkley, 2010) for a review]. For example, the anterior cingulated cortex and the lateral prefrontal cortex are identified in studies of ADHD (Bush, Valera, & Seidman, 2005; Paloyelis, Mehta, Kuntsi, & Asherson, 2007; Valera, Faraone, Murray, & Seidman, 2007) and emotion regulation (Ochsner & Gross, 2005). Emotion dysregulation may emerge in ADHD because of structural and functional deficits in top-down emotion regulation in these regions that support goal-directed (Bush, Luu, & Posner, 2000).

Second, several studies involving behavioral observations, rating scales, and clinician ratings have supported overlap between the construct of emotion dysregulation and ADHD among children and adults (Anastopoulos et al., 2011; Barkley & Fischer, 2010; Barkley & Murphy, 2010; Maedgen & Carlson, 2000; Melnick & Hinshaw, 2000; Mitchell, Robertson, Anastopolous, Nelson-Gray, & Kollins, 2012; Reimherr et al., 2005, 2010; Walcott & Landau, 2004). For instance, a recent study reported that emotion dysregulation is higher in children with ADHD and that it plays an important role in determining functional impairment and comorbidity outcomes (Anastopoulos et al., 2011). Another study in adults with ADHD found that symptoms of emotional impulsivity thought to be involved in ADHD (a) were higher in a group of adults with ADHD than in clinical and community control groups and (b) added explanatory and predictive power to various forms of impairment (e.g., occupational, educational, criminal history, driving outcomes, marital satisfaction) above and beyond core inattentive and hyperactive–impulsive symptoms (Barkley & Murphy, 2010). In a longitudinal sample of hyperactive children followed into adulthood, these findings were replicated in similar domains of impairment among those meeting ADHD criteria into adulthood (Barkley & Fischer, 2010). In addition, clinician-rated emotion dysregulation symptoms of ADHD (i.e., items assessing emotional overreactivity, temper, and affective lability) were higher among adults with ADHD than non-diagnosed individuals (Reimherr et al., 2005, 2010). These emotion dysregulation symptoms were responsive to both stimulant and non-stimulant ADHD pharmacological treatments. Finally, evidence from studies indicating that ADHD is associated with other emotion-related abilities (Miller, Hanford, Fassbender, Duke, & Schweitzer, 2011) and emotion-related constructs (Martel, Nigg, & von Eye, 2009; Mitchell & Nelson-Gray, 2006; Nigg et al., 2002) indirectly suggest a relationship between ADHD and emotion dysregulation.

It is noteworthy that emotion dysregulation is functionally impairing above and beyond the hallmark symptoms of ADHD (Barkley & Fischer, 2010; Barkley & Murphy, 2010). Similar findings may emerge among adolescent samples, although such studies have yet to be conducted. Delineating the role of emotion dysregulation may be crucial as it has also been linked to various forms of substance use (Bonn-Miller, Vujanovic, & Zvolensky, 2008; Weinstein, Mermelstein, Shiffman, & Flay, 2008) and may be a contributory factor in the highly comorbid relationship between ADHD and substance use. Further, emotion dysregulation in adolescents with ADHD may be an additional symptom set that should be targeted in treatment.

Although this chapter has focused on ADHD during adolescence, which is an important period of development in which many unique challenges emerge, it is important to consider adolescence as both an outcome (as we have in this chapter) and an antecedent to another relevant developmental period: young adulthood. Continuation of ADHD into adulthood is a highly relevant issue for anyone studying adolescent ADHD as most who carry the diagnosis into adolescence will meet criteria for ADHD in adulthood (Barkley et al., 2008). Various domains are negatively impacted among those who continue to meet diagnostic criteria into adulthood, including driving, financial, occupational, educational, criminal, and relational (Barkley et al., 2008; Biederman et al., 2006; Mannuzza et al., 1993, 1998; Weiss & Hechtman, 1993). Similar to adolescence, comorbidity in adults with ADHD is common (Miller et al., 2007). Continued empirically guided treatment to target such domains is crucial for adaptive developmental outcome. Although empirically supported treatments including pharmacotherapy and cognitive-behavioral therapy are available (Price, Wilens, Spencer, & Biederman, 2006; Safren et al., 2010; Solanto et al., 2010), they may not necessarily be disseminated or utilized. In particular, health care coverage may pose a barrier to young adults with ADHD seeking treatment. The percentage of those without health insurance coverage increases from 12 % among those under age 18 to approximately 32 % among those 18–24 years of age (White, 2002). Consistent with this trend, young adults aged 18–24 years are more likely than any other age group to be uninsured (Newacheck, Park, Brindis, Biehl, & Irwin, 2004). For someone with ADHD, health care coverage is important as the median costs of health care for those with ADHD are twice that of non-ADHD peers (Leibson, Katusic, Barbaresi, Ransom, & O’Brien, 2001). Given the importance of continued treatment to manage ADHD symptoms, health coverage is a particularly relevant topic for adolescents as they enter into adulthood. This area deserves attention in future research.