Daily Archives: August 23, 2010

Oppositional Defiant Disorder (ODD) | Conduct Disorder (CD) | Disruptive Behavior Disorders


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While Oppositional Defiant Disorder (ODD) and Conduct Disorder (CD) are both categorized under the general heading of “Disruptive Behavior Disorders,” there are specific features that allow us to compare and contrast them during diagnosis.  Primary features of ODD include a pattern of negativistic, defiant, noncompliant, and uncooperative behaviors.  Primary features of CD include a pattern of behavior in which the basic rights of others and/or major age-appropriate norms or rules are violated.  The primary feature that distinguishes ODD from CD is the emphasis in CD on the recurrent violation of the rights of others and/or societal norms and rules.   (Netherton, Holmes, & Walker, 1999, p. 118)  The diagnosis (of ODD) is not made if the disturbance in behavior occurs exclusively during the course of a Psychotic or Mood Disorder; or if the criteria are met for Conduct Disorder of Antisocial Personality Disorder (in an individual over age 18 years).  (American Psychiatric Association, Diagnostic and statistical manual of mental disorders, 2000, p. 100)

Despite our ability to differentiate the diagnoses, current etiological evidence suggests that they do follow a common developmental course.  Genetic, temperamental, family interaction and environmental stress variables have all been implicated in the development of ODD/CD.  (Netherton et al., 1999, p. 122)  In a comprehensive study of gender and its relationship to genetic influence of ODD/ADHD, Derks and associates (2007) concluded that the size of the genetic influences does not depend on the child’s sex, but partly different genes are expressed in boys and girls.  They also found that parent and teacher ratings may be inconsistent because qualitative description depending on the context in which they are observed.  Compensating for that inconsistency, there is no quantitative evidence indicating that ODD/CD is more common in boys than girls.  (Derks, Dolan, Hudziak, Neale, & Boomsma, 2007)

These children often exhibit deficits in social skills, including difficulties developing and maintaining peer relationships.  They are more aggressive, less empathetic, and more deficient in the social-problem-solving skills, and they tend to misperceive the social environment, often incorrectly attributing hostile intentions to others.  (Netherton et al., 1999, p. 119)  Considering these deficiencies are displayed in childhood, I would posit the question; how do they fare as adults?  A recent study utilized data from a 20-year community follow-up study to investigate the extent to which youth irritability (one of the DSM-IV criteria for ODD) is a risk for adult psychiatric disorders.  The results measured irritability in children and found that they could reliably predict depressive disorders and generalized anxiety disorder in same subject adults.  (Stringaris, Cohen, Pine, & Leibenluft, 2009)

A recent study performed by Glantz and associates (2009) focused on early onset mental disorders and their ability predict substance dependence into adulthood.  The study chose to focus on dependence rather than abuse because mental disorders are known to predict the dependence more strongly than abuse.  Glantz and associates inquired about the efficacy mounting mental health treatments in childhood to produce results in substance dependence among adults.  Although the study concluded that “treatment of prior mental disorders would not be a cost-effective way to prevent substance dependence,” they did acknowledge that “prevention of substance dependence might be considered an important secondary outcome of interventions for early-onset mental disorders.”  (Glantz, Anthony, Berglund, & Degenhardt, 2009)  This study serves to emphasize the lifelong benefits we can provide children as our efforts continue to yield dividends into their adult lives.

Ramchand and associates raised the stakes and underscored the possible outcomes of we fail to address ODD/CD in childhood.  They examined outcomes for adolescent offenders, and gave them the opportunity to express how they were faring in young adulthood.  Seven years after court referral to long-term residential group-home care, 12 of our sample of 449 youths were dead before turning 25, almost one third were in prison or jail, close to one half did not have a high-school diploma, two thirds reported ongoing criminal activity, and almost two thirds reported illegal drug use in the previous year (and more than half of those acknowledged the use of hard drugs).  Nine of the 11 known causes of death involved gunshot wounds or murder, highlighting the dangerous conditions to which many delinquents are exposed even after long-term rehabilitative care.  Supplemental analyses provided further evidence of this danger: 60% of the 383 surveyed respondents reported having been shot at with a gun, and 19% reported having suffered a gunshot wound.  (Ramchand, Morral, & Becker, 2009)

Despite our challenges in determining a specific etiology, and subsequently diagnosing ODD/CD, it is clear that there is an unprecedented demand for work within the context of these two pathologies.  Aside from the fact that they are among the most commonly referred for professional help, the stakes couldn’t be higher to resolve these mental health issues in childhood so as to prevent future problems for our clients in the future.  Although current research provides a baseline for analysis, further research is needed to determine the specific effects mental health treatment in children as it relates to the punitive effects it can have leading into adulthood.

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References

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

Derks, E., Dolan, C., Hudziak, J., Neale, M., & Boomsma, D. (2007, Jul). Assessment and etiology of attention deficit hyperactivity disorder and oppositional defiant disorder in boys and girls. Behavior Genetics, 37(4), 559-566. doi: 10.1007/s10519-007-9153-4

Glantz, M. D., Anthony, J. C., Berglund, P. A., & Degenhardt, L. (2009, Aug). Mental disorders as risk factors for later substance dependence: estimates of optimal prevention and treatment benefits. Psychological Medicine, 39(8), 1365-1378. doi: 10.1017/S0033291708004510

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

Ramchand, R., Morral, A. R., & Becker, K. (2009, May). Seven-year life outcomes of adolescent offenders in los angeles. American Journal of Public Health, 99(5), 863-871. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1683162651&sid=2&Fmt=3&clientId=4683&RQT=309&VName=PQD

Stringaris, A., Cohen, P., Pine,  . S., & Leibenluft, E. (2009, Sep). Adult outcomes of youth irritability: A 20-year prospective community-based study. The American Journal of Psychiatry, 166(9), 1048-1055. doi: 10.1176/appi.ajp.2009.08121849

ADHD


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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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References

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

Feeding Disorders of Infancy and Early Childhood


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Herein lies a brief overview of the epidemiology, theoretical models, assessment techniques, and intervention methods as it relates to Pica (307.52), Rumination Disorder (307.53), and Feeding Disorder of Infancy and Early Childhood (307.59).

Pica is the persistent ingestion of nonnutritive substances including paint, plaster, hair, cloths, toys, feces, sand, and bugs.  (Netherton, Holmes, & Walker, 1999, p. 139)  The term pica comes from the Latin for “magpie,” a bird known for voraciously eating food and nonfood items alike.  (Stiegler, 2005, expression Abstract)  Exploration of objects by mouthing and tasting is part of normal, healthy development and is not considered pathological pica behavior. Pica is suspected only when (a) nonfood items are consumed repeatedly over the course of a month or longer, despite efforts to curtail the behavior; (b) the behavior is considered inappropriate for the individual’s developmental age (i.e., beyond the 18-month level); (c) it is not a cultural practice; and (d) the behavior is a symptom of another mental disorder and is of sufficient concern to warrant medical attention.  (American Psychiatric Association, Diagnostic and statistical manual of mental disorders, 2000, p. 103)  On the whole, what surprised me most, what the distinct lack of aversion to food.  I would have expected that kids subject to pica would abstain or otherwise have trouble eating “real food,” but that is not the case with pica.  I was also surprised and that behavioral interventions included punishment, which is a first in my research.  It’s not that I particularly enjoy disciplining kids, but I do marvel at the novelty of having a psychologist tell me it’s perfectly acceptable… here I thought it was a lost art?

Rumination is the practice of voluntarily bringing previously ingested food back into the oral cavity and then either ejecting it or re-chewing and swallowing.  (Netherton et al., 1999, p. 140)  My first reaction was “gross!”  Evidently I wasn’t the only one since “social interactions with the infant or individual with mental retardation can be adversely affected by the unpleasant nature of this behavior.”  (Netherton et al., 1999, p. 141)  I was suitably surprised that researchers found willing parents that would subject their children to electric shock therapy.  It seems a bit extreme, but the cases were described as “life-threatening” and it proved to work.  (Netherton et al., 1999, p. 141)

The list of MR comorbid pathologies with is growing; we can add feeding disorders to the list of possible comorbid pathologies among the developmentally disabled population.  (Netherton et al., 1999, p. 143)  Aside from the specific exclusions, it would appear that MR is comorbid with just about everything?

Finally, the most intriguing aspect for me the research performed that implicated paternal influences in feeding disorders.  This is the first disorder I have experienced that would suggest “global family functioning and parental interactions may have both direct and indirect effects” on the pathological development of a disorder.  Drotar and Sturm (1987) suggested that (1) conflictual relationships between the parents, (2) inconsistent paternal support for the mother, (3) paternal psychopathology (e.g., substance abuse, domestic violence), (4) poor paternal nutritional standards, and (5) the fathers infantilization of the child may all act to interfere with the maternal-child feeding dyad.  (Netherton et al., 1999, p. 145)  As a guy, I thought it was refreshing that psychology professionals give us some credit for the development of the kids, even if it is in the negative context.  If we have potential to do harm, I hope later in the text they acknowledge our ability to nurture?

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References

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

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

Stiegler, L. N. (2005, Spring). Understanding pica behavior: A review for clinical and education professionals. Focus on Autism and Other Developmental Disabilities, 20(1), 27-39. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=809692351&sid=1&Fmt=4&clientId=4683&RQT=309&VName=PQD