Tag Archives: ADHD

Comorbidity: Substance Abuse Disorders (SUDs)

Comorbid, or comorbidity, is literally defined as “recurring together.”  (Shiel, Jr. & Stoppler, 2008, p. 94)  For our purposes, comorbidity will refer to cases where two or more psychiatric conditions coexist, and where one of the conditions is a substance abuse disorder (SUD).  “There are 11 groups of substances specifically discussed in the DSM-IV: alcohol; amphetamines and related sympathomimetics; caffeine; cannabis; cocaine; hallucinogens; inhalants; nicotine; opiates; phencyclidine and related drugs (PCP); and sedatives, hypnotics, and anxiolytics.”  (Colman, 2009, p. 741)  Any one of the above substances, or combination of the above substances, can contribute to and be related this discussion of comorbidity with SUDs.

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Although this list is by no means exhaustive, “long-term substance use is related to psychiatric conditions such as suicide and depression, affective disorders, eating disorders (ED), and personality disorders (PD).”  (Netherton, Holmes, & Walker, 1999, p. 248)  Increased risk of mood disorders has been documented across all substance categories and across all mood related diagnoses.  (Blaney & Millon, 2009, p. 287)  Substance-Related Disorders are commonly comorbid with many mental disorders, including Conduct Disorder in adolescents; Antisocial and Borderline Personality Disorders, Schizophrenia, Bipolar Disorder.  (American Psychiatric Association, Diagnostic and statistical manual of mental disorders, 2000, p. 204)   Schneier et al. (2010) also concluded that alcohol use disorders and social anxiety disorder (SAD) is a prevalent dual diagnosis, associated with substantial rates of additional co-morbidity.

ADHD represents a risk factor for substance abuse.  ADHD patients with a high degree of nicotine consumption may be consuming large quantities as a form of self-medication.  Nicotine and alcohol, when combined, pose a markedly greater risk for the development of other addictions.  (Ohlmeier et al., 2007, p. 542)  There is “high comorbidity between heavy drinking and heavy smoking.”  (Blaney & Millon, 2009, p. 266)  These admissions seem to support the premise that alcohol and nicotine continue to serve as “gateway drugs” for people whom suffer from ADHD.

“In terms of clinical presentation, a concurrent Personality Disorder (PD) diagnosis is associated with an earlier age of onset of alcohol-related problems, increased addiction severity, more secondary drug use, more psychological distress, and greater impairment in social functioning.  As for course in addiction treatment, a concurrent PD diagnosis has been associated with premature discontinuation of treatment, earlier relapse, poorer treatment response, and worse long-term outcome.”  (Zikos, Gill, & Charney, 2010, p. 66)  Cluster B (Antisocial, Borderline, Histrionic, and Narcissistic) Personality Disorders (PDs) appear to be particularly prevalent, perhaps because the link between substance dependency and antisocial behavior can be found genetically.  (Blaney & Millon, 2009, p. 263)

“Among individuals with schizophrenia, between 40% and 50% also meet criteria for one or more substance use disorders.”  (Blaney & Millon, 2009, p. 288)  Comorbid substance use complicates adherence to sometimes complex schizophrenia treatment regimens.  Poor adherence to treatment results in worsening of schizophrenia symptoms, relapse, worsening of overall condition, increased utilization of health care facilities, re-hospitalization, reduced quality of life, social alienation, increased substance abuse, unemployment, violence, high rates of victimization, incarceration, and death.  (Hardeman, Harding, & Narasimhan, 2010, p. 405-406)  The compounding effect of substance abuse on the quality of life for individuals with schizophrenia can’t be understated.  Substance abuse is particularly common and also worsens the course of schizophrenia.  (Buckley, Miller, Lehrer, & Castle, 2009, p. 396)

Differential diagnosis and treatment can sometimes be a troublesome proposition.  Comorbidity complicates the diagnosis, treatment, and clinical course of Substance Abuse Disorders (SUDs).  (Blaney & Millon, 2009, p. 287)  “If symptoms precede the onset of substance use or persist during extended periods of abstinence from the substance, it is likely that the symptoms are not substance induced.”  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 210)  Carbaugh and Sias (2010) concluded that successful outcomes can be increased through proper diagnosis and early intervention, at least in the case of comorbid Bulimia Nervosa and substance abuse.  Prevention of substance use disorders can help alleviate or decrease much impairment in psychiatric patients in particular.  (Powers, 2007, p. 357)  Furthermore, a review of treatments for patients with severe mental illness and comorbid substance use disorders concluded that mental health treatment combined with substance abuse treatment is more effective than treatment occurring alone for either disorder or occurring concurrently without articulation between treatments.  (Hoblyn, Balt, Woodard, & Brooks, 2009, p. 54)

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American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC: Author.

Blaney, P. H., & Millon, T. (2009). Oxford textbook of psychopathology (2nd ed.). New York, New York: Oxford University Press.

Buckley, P. F., Miller, B. J., Lehrer, D. S., & Castle, D. J. (2009, Mar). Psychiatric comorbidities and schizophrenia. Schizophrenia Bulletin, 35(2), 383-402. doi: 10.1093/schbul/sbn135

Carbaugh, R. J., & Sias, S. M. (2010, Apr). Comorbidity of bulimia nervosa and substance abuse: Etiologies, treatment issues, and treatment approaches. Journal of Mental Health Counseling, 32(2), 125-138. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=2026599321&sid=2&Fmt=3&clientId=4683&RQT=309&VName=PQD

Colman, A. M. (2009). Oxford dictionary of psychology (3rd ed.). Oxford, NY: Oxford University Press.

Hardeman, S. M., Harding, R. K., & Narasimhan, M. (2010, Apr). Simplifying adherence in schizophrenia. Psychiatric Services, 61(4), 405-408. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=2006767471&sid=3&Fmt=3&clientId=4683&RQT=309&VName=PQD

Hoblyn, J. C., Balt, S. L., Woodard, S. A., & Brooks, J. O. (2009, Jan). Substance use disorders as risk factors for psychiatric hospitalization in bipolar disorder. Psychiatric Services, 60(1), 50-55. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1654365811&sid=6&Fmt=3&clientId=4683&RQT=309&VName=PQD

Netherton, S. D., Holmes, D., & Walker, C. E. (1999). Child and adolescent psychological disorders: A comprehensive textbook. Oxford, NY: Oxford University Press.

Ohlmeier, M. D., Peters, K., Kordon, A., Seifert, J., Wildt, B. T., Weise, B., … Schneider, U. (2007, Aug). Nicotine and alcohol dependence in patients with comorbid attention-deficit/hyperactivity disorder (ADHD). Alcohol and Alcoholism : International Journal of the Medical Council on Alcoholism, 42(6), 539-543. doi: 10.1093/alcalc/agm069

Powers, R. A. (2007, May). Alcohol and drug abuse prevention. Psychiatric Annals, 37(5), 349-358. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1275282831&sid=5&Fmt=3&clientId=4683&RQT=309&VName=PQD

Schneier, F. R., Foose, T. E., Hasin, D. S., & Heimberg, R. G. (2010, Jun). Social anxiety disorder and alcohol use disorder co-morbidity in the National Epidemiologic Survey on Alcohol and Related Conditions. Psychological Medicine, 40(6), 977-988. doi: 10.1017/S0033291709991231

Shiel, W. C., Jr., & Stoppler, M. C. (Eds.). (2008). Webster’s new world  medical dictionary (3rd ed.). Hoboken, NJ: Wiley Publishing.

Zikos, E., Gill, K. J., & Charney, D. A. (2010, Feb). Personality disorders among alcoholic outpatients: Prevalence and course in treatment. Canadian Journal of Psychiatry, 55(2), 65-73. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1986429431&sid=1&Fmt=3&clientId=4683&RQT=309&VName=PQD


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With the increased prevalence of ADHD in the Western world, there is an immediate and pressing need to justify and explain the underlying cause of explosive growth in the ADHD population.  This justification comes with high stakes, since critics of the pharmaceutical industry and psychiatry in general have implicated greed on the part of North American mental health providers.

At stake is ADHD’s identity as a bona fide mental disorder (as opposed to a social construction).  When initial reports of ADHD prevalence emerged, higher prevalence in North American than European samples was remarked upon. This observation spawned a 10-year debate, exemplified by articles with titles such as “Is Childhood Hyperactivity the Product of Western Culture?” and, more recently, “ADHD Is Best Understood as a Cultural Construct?”  Having an explanation for inconsistencies in the cross-national prevalence of ADHD is important because such inconsistencies fuel assertions that ADHD is a fraud propagated by the “profit-dependent pharmaceutical industry and a high-status profession [psychiatry] looking for new roles.”  (Moffitt & Melchior, 2007)

Later, in the same article, it is suggested that prevalence in North America is elevated primarily because of differences in the definition of ADHD.  Specifically, the DSM-IV-TR is more lenient in its definition of ADHD when compared to the ICD-10.

The ICD-10 strictly requires that a child must show symptoms in all three dimensions (inattention, hyperactivity, and impulsivity) and must meet all criteria at home and at school. The ICD-10 also excludes children with co-occurring disorders. DSM-IV is more lenient. It is possible to diagnose a child who shows symptoms in only one dimension (inattention). Some impairing symptoms – but not all- must be shown at home and at school. DSM-IV allows diagnosing ADHD alongside co-occurring disorders.  (Moffitt & Melchior, 2007)

Although differences in clinical definition can have an impact over space (geography), can they also have an impact over time?  Leon Eisenberg, M.D. would assert that the continued refinement of the definition has contributed to a broader interpretation of what constitutes ADHD.  Hyperkinetic reaction of childhood appeared as a category in DSM II in 1968.  It was not, however, until DSM III (1980) that attention-deficit/hyperactivity disorder (ADHD) entered the official lexicon.  (Eisenberg, 2007)  The end result is a shift from diagnosing the presenting features of ADHD as symptoms of other classified disorders, to a new and entirely separate diagnosis.  And so, ADHD was “staking a claim” to the prominent clinical features it encompassed, thus differentiating itself as a clinically valid diagnosis and not a sub-type of an underlying behavior disorder.  ADHD has morphed from a relatively un-common condition 40 years ago to one whose current prevalence is estimated to be just under 8% of U.S. children 4–17 years of age.  (Eisenberg, 2007, p. 283)

Societal expectations and parental influences continue to play a significant role in the search for the etiological roots of all pathologies, including ADHD.  We as a culture have a long history of implicating parental inadequacies in child psychopathology.  The continued search for biological causes serves to reinforce our convictions that we are indeed good parents.

In many public school jurisdictions, the diagnosis led to additional services for such children because of the implication that their problems were organic or endogenous, as opposed to psychological or psychogenic. For this very reason, parents welcomed it. Furthermore, the term proved they were not responsible for their child’s problems (no small victory at a time when parent blaming was widespread in child psychiatry and education).   (Eisenberg, 2007)

Parental pressures, when taken in conjunction with recent advances in brain imaging and the relative effectiveness of pharmacological interventions, have contributed to a “consensus that neurochemical imbalances play a central role in the etiology of ADHD.”    (Netherton, Holmes, & Walker, 1999, p. 103)  This biological model is further supported by evidence that, in a limited number of cases, “it can be acquired after birth, via head injury, neurological illness, elevated lead levels, and other biological complications.”  (Netherton et al., 1999, p. 103)

Recent technological advances in brain imaging have served as catalysts to futher underscore attempts to localize the etiology of ADHD in the brain.  In a recent morphological study of ADHD, researchers incorporated the novel measures of local shape, complexity, volume, and thickness and align structural MRI with other imaging modalities, such as the delineation of white matter tracts by diffusion tensor imaging and maps of brain activation generated by functional MRI.  The study’s most striking finding was marked volume loss in the region of the pulvinar nuclei bilaterally in the ADHD group.  (Shaw, 2010, p. 363)

Despite mounting evidence that ADHD can be attributed to biological factors, there remains a contingent of dedicated psychological practitioners who would assert that familial deficiencies do serve to exacerbate the biological predispositions of ADHD.  (Netherton et al., 1999, p. 104)  If we aim to address the etiological causes of ADHD, we have to do so with a conscious widening of our world view.  We need to take the entirety of geographic, historical, societal, technological, and pharmacological information into consideration before passing judgment on the etiology of Attention-Deficit/Hyperactivity Disorder (ADHD).  Although it is not within the scope of this article to drill down on any one specific aspect, it should serve as a baseline by which we can all being to explore the complexities of the etiology of ADHD.

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Eisenberg, L. (2007, Jun). Commentary with a historical perspective by a child psychiatrist: When “ADHD” was the “brain-damaged dhild”. Journal of Child and Adolescent Psychopharmacology, 17(3), 279–283. doi: 10.1089/cap.2006.0139

Moffitt, T. E., & Melchior, M. (2007, Jun). Why does the worldwide prevalence of childhood attention deficit hyperactivity disorder matter?. The American Journal of Psychiatry, 164(6), 856-859. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1288245351&sid=3&Fmt=3&clientId=4683&RQT=309&VName=PQD

Netherton, S. D., Holmes, D., & Walker, C. E. (1999). Child and adolescent psychological disorders: A comprehensive textbook. Oxford, NY: Oxford University Press.

Shaw, P. (2010, April). The shape of things to come in attention deficit hyperactivity disorder. The American Journal of Psychiatry, 167(4), 363-366. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1996846691&sid=2&Fmt=3&clientId=4683&RQT=309&VName=PQD

Disruptive Behavior: ODD/CD ADHD

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Oppositional Defiant Disorder (ODD) and Conduct Disorder (CD), along with the comorbid Attention-Deficit/Hyperactivity Disorders (ADHD), are among the most prevalent and the most treated pathologies globally. Children who exhibit overactive, noncompliant, oppositional, and aggressive behaviors are among the most commonly referred for professional help. (Netherton, Holmes, & Walker, 1999, p. 118) As clinicians, the question isn’t if we will run into it, it’s more of a question of when… and so I consider ODD and CD, along with ADHD, to be among the most important and clinically significant studies we will likely undertake.

Complaints about ODD/CD children include annoying or aversive interpersonal behaviors (e.g., recurrent yelling, temper tantrums, impulsivity, excessive motor activity, lying, stealing), noncompliance with authority figures, defiance of social norms, and physically aggressive behaviors (e.g., hitting, fighting). (Netherton et al., 1999, p. 118) They are more aggressive, less empathetic, and more deficient in social-problem-skills, and they tend to misperceive the social environment. (Netherton et al., 1999, p. 119) In my experience, all of the above apply, and more. I have witnessed or seen presentations that coexist with ADHD, major depression, low self-esteem, and alcohol/substance abuse. Although my experience in a clinical setting is limited, I have rarely met individuals who exhibit ODD/CD traits that do not also exhibit symptoms of other pathologies. I believe the interplay of these comorbid pathologies has a compounding effect, intensifying the behaviors, thereby making them more difficult to diagnose and even more difficult to treat.

I was particularly drawn to the developmental course of the pathology, and I was wholly unaware that behaviors could begin to develop as early as infancy. Pre-reading, I was prone to implicate family interaction and environmental stress variables before genetic or temperamental. However, I think I will defer that judgment, as it would appear that heredity and temperamental inconsistencies (I almost used defects here, but it seemed too condemning?) play a significant role in the etiology. I was not at all surprised that the typical developmental course gets progressively more severe with age, especially as the kids being to identify with an oppositional and delinquent peer group. (Netherton et al., 1999, p. 121)

Am I the only one to notice that males always seem to have a higher prevalence of pathology? Aside from Rett’s Disorder, which is exclusively dedicated to females, males are almost always more likely to exhibit pathological behavior. I think it’s a conspiracy.

I understood, appreciated, and agreed with the statement that “the assessment process should strive to accurately understand the child’s behavioral and emotional functioning across time and multiple settings, as well as the contexts in which the child normally functions.” (Netherton et al., 1999, p. 124) I especially appreciate the last part of the statement, and I think it is important to recognize and appreciate situations where the child does accelerate. I think that’s a key part of the assessment that was under addressed in the text, as it gives us the opportunity to demonstrate the child (during the course of the interview) that they do, indeed, “have it in them.”

Custodial parents may harbor some psychopathology (e.g., anti-social behavior, alcohol abuse, depression) that might help to maintain the child’s problems and impede treatment efforts if not also addressed. (Netherton et al., 1999, p. 125) It would suffice to say that is pretty consistent with my experience. Matter of fact, “might” implies it happens less frequently than we are probably aware. Parent Management Training (PMT) looks like an ingenious intervention if the parents are willing, I wasn’t aware there was such a thing. I wouldn’t rule out individual or group therapy as a possible outlet as well, depending on the situation.

“Treatment professionals recognize the chronic nature of the difficulties which these children experience and follow the child and the family over the long run, similar to medical follow-up of an individual with a chronic illness.” (Netherton et al., 1999, p. 133) Simply because we are able to mitigate and subsequently resolve the immediate and pressing issues surrounding the precipitating event, doesn’t necessarily mean that we have really solved the problem. Inevitably there will be underlying systemic issues in the family structure, or adjunct issues that we can continue to address that will help prevent recurrence of disruptive behaviors. I really like this proactive approach, and I think it’s imperative that we continue to impress on families that we should attempt to “get ahead” and proactively address potential issues.

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Netherton, S. D., Holmes, D., & Walker, C. E. (1999). Child and adolescent psychological disorders: A comprehensive textbook. Oxford, NY: Oxford University Press.

Attention Deficit Hyperactivity Disorder (ADHD)

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Attention-deficit/hyperactivity disorder (ADHD) is characterized by chronic, pervasive, and developmentally inappropriate patters of inattention, impulsivity, and/or hyperactivity.  (Netherton, Holmes, & Walker, 1999, p. 98)

I wasn’t surprised at all that ADHD was mockingly referred to as “the latest fad in psychiatry” or “the disorder of the 90s.”  I graduated from high school in 1995, and I remember hearing about it as early as 8th grade.  It was probably the first “formal” pathology I was ever exposed to, and the first disorder I was able to have a conversation about with my school peers.  Obviously this was driven by the media to some degree, but at some point it became part of our collective conscious as high school students.  Even as kids, we could drop ADHD in a conversation and everyone would have some general idea what you were talking about.  I was barely 14 the first time I saw someone trade Ritalin for enough cash to get a soda and a candy bar.

We all grew up with people that “didn’t listen to instructions” or “became bored easily.”  We’ve all ran into the kid who “makes indiscreet remarks without regard for social consequences,” I like to call them the class-clowns.  What confuses me, is that the ambiguous nature of the criteria for diagnosis could probably apply to most kids in one way, shape, or another.

This is the first DSM-IV-TR I have experienced that requires sub-typing.  I was previously unaware of ADHD Combined Type, ADHD Predominantly Inattentive Type, ADHD Predominantly Hyperactive-Impulsive Type, ADHD in Partial Remission, or ADHD NOS.  (Netherton et al., 1999, p. 101)  The separation of the diagnostic criteria in the DSM-IV-TR and the ICD-10 seems to make logical sense to me.

I, too, was under the impression that most people outgrow their ADHD problems as they reach adolescence.  (Netherton et al., 1999, p. 103)  I still know a few adults that would describe themselves as ADHD, despite the fact that research suggests that the vast majority of people learn to compensate for these problems and therefore make a satisfactory adult adjustment.  Perhaps the few self-described adults I know are more the exception than the rule.  It leaves me to wonder about prevalence, and how many “normal” adults I know that were previously diagnosed with ADHD.

ADHD is best diagnosed outside the clinical environment since symptoms are much more likely to occur in situations that are highly repetitive, boring, or familiar.  (Netherton et al., 1999, p. 104)  Because of the nature of the pathology, we are increasingly dependent on the accounts that are reproduced by parents, teachers, and other engaged caretakers.  I totally agree with Netherton and associates that it can provide “a basis for determining how likely it is that parents and other caretakers will implement recommended treatment strategies on behalf of their child or adolescent,” (Netherton et al., 1999, p. 106) but I question the consistency of the reporting as a measure of diagnosis.  While I can’t totally discount second hand accounts, I would be inclined to go observe personally so that I can draw my own conclusions.  Is it considered acceptable for a clinician to go observe a kid in the classroom?

I have never heard of “drug-free holidays,” nor have I know my associates who were diagnosed with ADHD to discontinue the use of pharmacotherapy on the weekends… but I would be inclined to recommend it just we can get a measure of exactly what effects the medication is having.  I think the concept is especially useful where combined interventions have been implemented.


Netherton, S. D., Holmes, D., & Walker, C. E. (1999). Child and adolescent psychological disorders: A comprehensive textbook. Oxford, NY: Oxford University Press.

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