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.
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