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ADHD and Addiction: Diagnosis and Management

ADHD and Addiction: Diagnosis and Management. Outline. ADHD diagnosis and complications of diagnosis ADHD epidemiology and comorbid conditions ADHD and substance use disorder (SUD) epidemiology Association between ADHD and SUDs: determining causality and functional impact

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ADHD and Addiction: Diagnosis and Management

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  1. ADHD and Addiction: Diagnosis and Management

  2. Outline • ADHD diagnosis and complications of diagnosis • ADHD epidemiology and comorbid conditions • ADHD and substance use disorder (SUD) epidemiology • Association between ADHD and SUDs: determining causality and functional impact • Potential explanations for the ADHD/SUD association • Stimulant treatment and the risk for SUDs • Diversion and misuse of stimulant medications • Treatment recommendations

  3. Making the ADHD diagnosis:DSM criteria

  4. Inattention symptoms Six (or more) of the following symptoms of inattention have persisted for at least 6 months … • fails to give close attention to details or makes careless mistakes • difficulty sustaining attention • does not seem to listen when spoken to directly • does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace • has difficulty organizing tasks and activities • avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort (such as schoolwork or homework) • loses things necessary for tasks or activities • often easily distracted by extraneous stimuli • often forgetful in daily activities

  5. Hyperactivity/Impulsivity Symptoms Six (or more) of the following symptoms of hyperactivity/impulsivity have persisted for at least 6 months … • Hyperactivity • fidgets or squirms in seat • leaves seat • Often runs about or climbs excessively (in adolescents or adults, may be limited to subjective feelings of restlessness) • has difficulty playing or engaging in leisure activities quietly • "on the go" or often acts as if "driven by a motor" • talks excessively • Impulsivity • blurts out answers before questions have been completed • has difficulty awaiting turn • interrupts or intrudes on others

  6. DSM-IV Diagnosis • Symptoms that caused impairment were present before age 7 years. • Evidence of clinically significant impairment in social, academic, or occupational functioning. • Impairment present in two or more settings (e.g., at school [or work] and at home). • The symptoms do not occur exclusively during the course of a Pervasive Developmental Disorder, Schizophrenia, or other Psychotic Disorder and are not better accounted for by another mental disorder (e.g., Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder). • Subtypes – Primarily Inattentive (6), Hyperactive/Impulsive (6), or Combined Type (6+6)

  7. Making the ADHD diagnosis(general points) • ADHD is a disorder of both childhood and adulthood • ADHD is highly comorbid with substance use disorders • Follow the general rule of evaluating sxs during periods of sobriety • Collateral hx can be crucial as the sxs should have been present prior to age 7 • The diagnosis is a CLINICAL one – ie. neuropsych can be a helpful adjunct but is insufficient alone to make the dx. • ADHD may be better described as a dimensional rather than categorical diagnosis

  8. Making the ADHD diagnosis(clinical reality!) Sxs in adults can present differently1 • Hyperactive sxs may “resolve”, or may be adapted to with life changes • Impulsivity can present functionally (ending relationships, quitting jobs, arrests, driving violations) – and may be better elicited as such • Adult ADHD may actually be better dx’d with either different or perhaps less stringent criteria Adults frequently can not recall sxs prior to age 7 – particularly in chaotic households! • Again, collateral data wherever possible, including report cards/testing results • Concept of “late-onset” ADHD challenges stringent age criteria, as research shows this population to be similar to “full” ADHD2

  9. Making the ADHD diagnosis(clinical reality!) Comorbidities may complicate diagnosis… • Depression: • attention/concentration are shared sxs • chronic suggests ADHD, guilt/worthlessness, suicidality all suggest depression • Bipolar Disorder: • hyperactivity, inattention, talkativeness, impulsivity are shared • Grandiosity, expansive mood and a cyclical pattern vs chronicity suggest Bipolar Disorder • Pay attention to family history

  10. Epidemiology of ADHD • Attention-Deficit Hyperactivity Disorder (ADHD) prevalence is approx. 3-7% in school age children3 • 75% of children continue to have sxs into adolescence, approximately 50% into adulthood4 • Adult prevalence is estimated to be 3-5%5 • ADHD is over-represented in substance abusing populations and SUDs similarly in adults with ADHD

  11. Epidemiology of ADHD (continued) There are also high rates of other Axis I disorders among adult ADHD populations (NCS-R)5 • 38% 12-month prevalence for any mood disorder • 19% for MDD, 19% for Bipolar Disorder • 47% 12-month prevalence for any anxiety disorder Conduct disorder is also highly comorbid with ADHD – reportedly 30-50% in adolescents6

  12. ADHD and SUD comorbidity • NCS-R data5: • Among adults with ADHD, 12-month prevalence for any SUD is 15% vs 5% in non-ADHD responders • Among those w/SUDs, ADHD prevalence is 11% vs 4% • In clinical samples, percentages are higher!7 • 17-45% ADHD adults have h/o EtOH abuse or dependence • 9-30% ADHD adults have h/o drug abuse/dependence • Opioid dependent pts: 5-22% with ADHD8 • Cocaine dependent pts: 10-35%8 • EtOH dependent pts: 33-71%8

  13. Potential impact of ADHD on SUDs Given the bidirectional preponderance, early work reported associations, but also assumed causality. Early work reported that individuals with co-occurring ADHD had: • Earlier onset of substance use • More severe course of SUD • Poorer treatment adherence • More difficulty achieving treatment goals Examples: Carroll & Rounsaville (cocaine)9, Wise et al. (adolescents seeking residential treatment)10 Criticisms: • Retrospective studies prone to possible recall bias • Often failed to account for comorbidies – ie Conduct Disoder! • Fail to look at individual drugs, gender and dimensional ADHD sxs or subtypes

  14. Rethinking old data, and new research • The role of conduct d/o • ADHD symptom dimensions vs categorical diagnosis • Specific substances of abuse/dependence

  15. Conduct Disorder: A complicating factor? Given that Conduct Disorder is so highly comorbid with ADHD and also with SUDs, could this account for the association? • Flory and Lynam’s 2003 review suggests that ADHD alone (controlling for Conduct D/O) is not associated with a significant risk for SUDs, although ADHD + CD may afford higher risk then either alone11 • 2 subsequent prospective studies support this trend: • August et al. (2006)12 – ADHD+CD group at higher risk for SUD, but risk disappears when CD controlled for • Barkley et al. (2004)13 – also ADHD+CD with increased risk, and not ADHD alone, although ADHD severity independently linked to “drug related antisocial activity”

  16. Conduct Disorder: A complicating factor?(continued) To the contrary… • Even within the body of data reviewed by Flory and Lynam11 , multiple studies show that ADHD predicts earlier tobacco use and dependence, independent of CD • More recent studies: • Molina & Pelham (2003)14 prospectively study 142 subjects: • Inattentive sxs predict ealier use of drugs, frequency of EtOH/MJ use and heavier tobacco use even controlling for CD. • CD+ADHD = more use and problems.

  17. Conduct Disorder: A complicating factor?(continued) More recent studies (cont): • Elkins et al. (2007)15 use Minnesota twin data to examine dimensional aspects of ADHD/CD (760F, 752M) • Initiation of use: Hyperactive/imp sxs significantly predict use of tobacco/EtOH/illicit drugs, as does CD, inattentive sxs only EtOH and ADHD dx tobacco/illicit drugs only • SUDs: HI sxs predict tobacco/MJ, inattentive predict no SUDs, CD predict tobacco/MJ/EtOH, ADHD dx predicts none • Hyperactive/impulsive sxs emerge as important • Arias et al. (2008) – retrospective analysis of 2047 individuals ascertained in siblings pairs from community sample (although only 92 pts dx’d with ADHD) • ADHD associated with earlier age of substance use, more SUD dxs, more psych dxs, more suicide attempts/hospitalizations • ADHD/SUD pts may represent a more severe phenotype of addicted patients

  18. What to make of all this?!? • Conduct D/O independently and significantly predicts risk of SUDs • ADHD may independently predict SUDs, in particular nicotine use/dependence • Investigation of IN/HI sxs subsets is clearly important, and recent data suggests hyperactivity/impulsivity as significant risks for SUDs • ADHD in combination with CD likely predicts a risk of SUDs/outcomes greater than ADHD or CD alone

  19. Why the relationship between SUD and ADHD? Self medication? • Anecdotal theories: pts use nicotine/MJ/cocaine to increase focus/attention, EtOH/MJ/opioids to calm internal sense of restlessness, or that impulsivity predisposes to use • Some supporting data: Wilens et al. (2007)16 find on self-report scales that 36% of ADHD pts cited “self-medication” as a motivation to use vs. 25% to “get high” Familial link? • Recent work by Biederman et al. (2008)17 suggests a variable expressivity model for ADHD and drug dependence (shared risk factors), but independent transmission for EtOH dependence • This work suggests shared risks but does not necessarily imply genetic links – ie environment can not be ruled out

  20. ADHD and Substance Abuse: Potential biological pathways Dopamine (DA) pathways: • ADHD is almost certainly a polygenic disorder (multiple different genes interacting with environmental stressors) • Genes implicated include DA transporter and receptor genes, enzymes involved in metabolism, although also serotonin receptor/transporter genes • However, DA is particularly interesting given the DA dysfxn associated with addictive disorders • Specifically, DA dysfunction in prefrontal regions, subcortical structures (dorsal/ventral striatum) and connecting circuits may provide a common pathway between ADHD and addictive disorders

  21. ADHD and Substance Abuse: Potential biological pathways Preliminary research: • Adults with ADHD have been found to have decreased DA synthesis/metabolism in prefrontal cortex18 in addition to decreased DA release in the caudate and decreased DA receptor availability (D2/D3)19 • Decreased DA release in caudate correlates with inattentive sxs AND “drug liking” responses to IV methylphenidate (Ritalin)19 • Decreased DA in these regions (or decreased receptor availability) may modulate reinforcing effect of substances of abuse • Both alcohol and cocaine dependence are associated with decreased dopamine receptor availability (D2/D3) and decreased DA release in the ventral striatum (NAc) and putamen21,22

  22. Relationship between stimulant treatment and SUDs • Does stimulant tx decrease, increase or have no effect on the risk of developing a SUD?

  23. Relationship between stimulant treatment and SUDs • Concern stems from “sensitization hypothesis” – that early exposure to stimulants alters DA system, increasing reinforcing effects of substances • In some rat models, adolescent animals exposed to methylphidate are more likely to self administer cocaine as adults22 • However, even in rat models, data is at times contradictory! • Route of administration is likely important (IM vs oral) • Length of exposure also likely important, as is age of exposure • Dose/pharmacokinetics are hard to match up with humans • Thanos et al. (2007) find that 2 mo oral treatment in adolescent rats lead to increased cocaine self-administration, while 8 mo of treatment actually decreased cocaine SA23

  24. Relationship between stimulant treatment and SUDs Studies in humans… • Through 80s and 90s conflicting data emerged, showing increased risk/no risk/decreased risk of SUD associated with prior stimulant tx • 2003: Wilens et al. perform meta-analysis revealing small protective effect of stimulant tx on later SUDs24 • Only 6 studies included • Protective effect much greater on adolescent use than adult use… Why? • Adolescents more closely monitored by parents? • Adolescents hadn’t passed through “full risk period”?

  25. Relationship between stimulant treatment and SUDs More recent studies… • Faraone et al. (2007)25 – retrospective data in adults with ADHD (n=206), separated by exposure to stimulant tx • No differences in prevalence of nicotine/EtOH/drug use/abuse/dep • Also no protective effect • Biederman et al. (2008)26 – 10 year f/u data from prospective study of boys with ADHD • At f/u subjects were in early 20s • No evidence of increased SUDs but also no protective effect • 4 year f/u data actually showed protective effect, again suggesting that stimulant tx may delay onset of substance use

  26. Relationship between stimulant treatment and SUDs More recent studies… • Wilens et al. (2008)27 – 5 year f/u data from prospective study of girls with ADHD (mean age 16) • Stimulant tx associated with decreased risk of SUDs • Mannuzza et al (2008)28 – f/u data of boys ascertained in 1970s, evaluated in late adolescence and adulthood (20s) • Risk of SUD was associated with age of stimulant tx – ie kids treated later had a significantly higher risk • Development of antisocial personality disorder largely accounted for the increased risk – ie kids who were treated were less likely to develop ASPD and then SUDs Conclusions: At this time there is no convincing evidence that stimulant treatment increases the risk for SUDs, but also no conclusive evidence of a decreased risk.

  27. Concerns about diversion/misuse of stimulants • Among middle school and HS students, 23% of those prescribed stimulants were asked for their meds, 4.5% of total sample reported misuse/diversion29 • Among college students lifetime prevalence of stimulant misuse between 6-16%30, 31, 32 • More likely to be white, male, fraternities/sororities and lower grades • In Biederman’s 10-year prospective study of boys with ADHD, 22% admitted misusing their medications, 11% diverting33 • All of misuse attributed to conduct disorders or substance use disorders and occurred with immediate release meds • Little clinical data available about risks in pts with SUDs and ADHD

  28. Treatment Recommendations • Careful thoughtful diagnosis with collateral data • Include loved ones/family members in tx plans, w/close f/u/monitoring • Unfortunately, relatively few DB, placebo controlled trials available for adults with ADHD/SUDs, and data is underwhelming.34 • Avoid stimulant rx if pt actively using, consider non-stimulant tx in those in recent recovery (Wellbutrin, Strattera) • Extended release preparations are preferred among stimulants (Concerta, Adderall XR, Vyvanse) • Clinical data and imaging/binding studies suggest rate of administration correlates with “likability” of stimulants • ER vs IR have slower onset curves and are less “likable” • ER formulations much harder to crush and then sniff/inject

  29. Summary • ADHD persists into adulthood and is associated with significant (-) functional impairments • ADHD can be difficult to diagnose in adults – but careful dx is essential, with caveat that sxs often present differently • ADHD and substance use disorders are each overrepresented in samples of the other • In the ADHD/SUD samples, pts have more severe SUDs which are much harder to treat • The ADHD/SUD relationship is complex – conduct disorder clearly accounts for some of the overlap, but those with ADHD+CD may represent a more severe phenotype of ADHD/SUD pts

  30. Summary • The reasons for the ADHD/SUD are not clear although self-medication and/or common biological pathways are leading hypotheses • At this time there is no convincing evidence that stimulant treatment increases the risk for SUDs, but also no conclusive evidence of a decreased risk. • Stimulant medications are abused/diverted at a fairly high rate, and misuse among those prescribed may be as high as 25%. However, 75% do NOT abuse their meds! • Treatment recommendations focus on careful diagnosis, close follow up and careful choice of medication to minimize risks.

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