Although scientists and clinicians continue to make new discoveries as well as refine existing practices over how to diagnose and treat ADHD— the FDA’s recent approval of the use of EEG or brainwave recording technology to aid in the diagnosis of ADHD in children (Food and Drug Administration, 2013) is one such example—there is no debate among well-informed healthcare professionals that ADHD is a real condition and causes significant impairments. The American Academy of Child and Adolescent Psychiatry acknowledges as such in its most recent Practice Parameters for the Assessment and Treatment of Children and Adolescents with Attention-Deficit/Hyperactivity Disorder, naming it “a valid neurobiological condition” (2007). This refers to our current understanding of ADHD as caused by the combination of many inherited genes, some childhood experiences, and early medical history and these in turn cause a change in how the brain distributes certain chemical receptors and molecular pumps to its cells, changing how it uses signaling chemicals, in particular, one called dopamine. The genes involved are diverse, and environmental factors can include such things as birth weight, head trauma, and alcohol/nicotine exposure.
ADHD is not an American invention. Over the years, the ADHD is reported at fairly consistent rates across diverse geographic, racial, and socioeconomic conditions (Wood, Elia, Ambrosini, & Rapoport, 1991). Although different countries and cultures have tended to reported different rates, this difference has been shown as result of different definitions used (Faraone, Sergeant, Gillberg, & Biederman, 2003)—criteria more narrowly focused on hyperactive behaviors had evolved over the years to include ‘subtypes’ which also capture impulsiveness and inattention, leading to more diagnosis. Neither is ADHD medication over-prescribed. A US national survey conducted to obtain reports from parents of 79,264 children between the ages of 4 and 17 found that although 7.8% were diagnosed with ADHD, only a little over half were currently taking medication for the disorder (Visser, Lesesne, & Perou, 2007). Certainly one good reason not to avoid treating ADHD is the finding that the brains of children show closer-to-normal growth in the number of brain cells and nerve fibers after long-term treatment, when compared to those whom had just been diagnosed and had not yet received treatment (Castellanos, et al., 2002).
Given our understanding of how ADHD is caused by genetic and developmental factors which influence the neurology of children around the world and across many cultures, we should therefore not expect many of these children to just “grow out of it”. A review on the diagnosis of adult ADHD (Primich & Iennaco, 2012) notes that although 4.4% of the adult population is estimated to have ADHD, only 10.9% of those are in treatment. Because the inattentive and distractible symptoms of ADHD can easily coexist or even cause the symptoms seen in other disorders such as anxiety and depression, clinicians must take special care to uncover the nuances of the impairments of an adult seeking help—they may be experiencing a variety of difficulties across many different settings of daily life stretching far back into earlier stages of life.
We can see that even though our understanding of ADHD has gone through definitional changes over the years, the core symptoms of this neurobiological syndrome has always been defined on the basis of behavioral characteristics. For example the authors of a 1976 preliminary report titled “Diagnosis and Treatment of Minimal Brain Dysfunction in Adults” (Wood, Reimherr, Wender, & Johnson) had identified a group of adult patients with the diagnostic labels (in use at that time) of sociopathy, explosive personality, hysterical character and labile personality that were difficult to treat but responded to low doses of stimulants and an antidepressant. They concluded with a set hypothesis that is striking in how similar it is to our current understanding of ADHD and how it can persist into adulthood with accompanying or related psychiatric disorders, including: MDB (minimal brain dysfunction) is a “genetically transmitted abnormality…in arousal that produces increased activity and an inability to focus attention, concentrate, or inhibit irrelevant responses”; untreated adults can produce a “heterogeneous and perhaps incomprehensible group of symptoms”; adults with MDB develop “abortive compensatory mechanisms” due to many impairments in all spheres of life leading to further diagnoses etc.
With so much clinical data gathered over the years on the effectiveness of medications and other strategies in improving the symptoms of ADHD, it seems hard to imagine how recent discoveries in neurophysiology can bring new insights into its diagnosis and treatment. Indeed the AACAP quotes the American Medical Association’s Council on Scientific Affairs review of the literature (Goldman, Genel, Bezman, & Slanetz, 1998) in its Practice Parameter, saying “Overall, ADHD is one of the best-researched disorders in medicine, and the overall data on its validity are far more compelling than for many medical conditions”. A lack of clarity in our understanding of what we mean when we say “attention” may be behind our odd feelings as clinicians that both know too much and too little about ADHD at the same time. That is, continuing basic research into how certain parts or circuits of the brain contribute to our cognition and behavior may be causing the commonly used mentalist or psychological labels that we refer to (in the negative) when we describe the impairments of ADHD, such as “executive control”, “impulse inhibition”, “working memory”, etc. to fall apart. It is interesting to note that the public is already being made aware of how drawing conclusions from the parallel presentation of measures in the brain (neurophysiological data) and subjective reporting (behavioral observation) without adequate interpretation can be confusing if not disturbing. For example, this article from the magazine Science gives a good explanation by contrasting the difference between good fMRI imaging research on the recognition of faces using powerful pattern recognition techniques, and results published by the New York Times claiming that one or two differences in scanned brains could indicate which candidate a person would vote for in the 2008 presidential elections (Miller, 2008).
Therefore the EEG (brainwave) scanning device developed by Neba Health© to aid in the diagnosis of ADHD in children previously mentioned to be approved by the FDA for marketing deserves scrutiny. The Neba device compares the amount of beta and theta waves measured and uses that to determine if a child is likely to have ADHD, and whether the child will need further testing for another condition that is not ADHD. According to the study data released by the company (Neba Health, 2013), a triple-blinded study was conducted at 13 clinical sites on 275 children and adolescents who were seeking help for attentional and behavioral concerns and the device was found to reduce the rate at which a clinician working alone misdiagnosed ADHD—that is, when another factor could better account for the problematic behavior of the child —from 34% of the time down to 3%. The strength of this study may be supported by the multidisciplinary team used to eventually evaluate all these children, and whose diagnoses were used as the “benchmark”—this team included a child and adolescent psychiatrist, a clinical psychologist, and a neurodevelopmental pediatrician, and they tested for a variety of conditions which could indicate that a child’s problematic behaviors were not due to ADHD, such as hearing and vision problems, having tried medications with no improvement, and acting out mostly due to anger.
Although the study data provided is not extensive perhaps due to propriety concerns, the potential for this device to be used to improve practice especially in settings where an extensive multidisciplinary screening for a child may not be readily available is clear. More importantly, the materializing idea that “biomarkers” derived directly from neurophysiology such as the “standardized theta/beta ratio” that this device measures can lead to direct applications in clinical practice and decision-making, points to the possibility of an increasingly less “dualist” approach to ADHD and other neurodevelopmental disorders to come.
American Academy of Child and Adolescent Psychiatry. (2007). Practice Parameter for the Assessment and Treatment. Journal of the American Academy of Child and Adolescent Psychiatry, 894-920.
Castellanos, F., Lee, P., Sharp, W., Jeffries, N., Greenstein, D., Clasen, L., . . . Rapoport, J. (2002). Developmental Trajectories of Brain Volume Abnormalities in Children and Adolescents With Attention-Deficit/Hyperactivity Disorder. The Journal of the American Medical Association, 288(14), 1740-1748.
Faraone, S., Sergeant, J., Gillberg, C., & Biederman, J. (2003). The worldwide prevalence of ADHD: is it an American condition? World Psychiatry, 2(2), 104-113.
Food and Drug Administration. (2013, July 15). Press Announcements > FDA permits marketing of first brain wave test to help assess children and teens for ADHD. Retrieved from US Food and Drug Administration Home Page: http://www.fda.gov/newsevents/newsroom/pressannouncements/ucm360811.htm
Goldman, L., Genel, M., Bezman, R., & Slanetz, P. (1998). Diagnosis and Treatment of Attention-Deficit/Hyperactivity Disorder in Children and Adolescents. The Journal of the American Medical Association, 279(14), 1100-1107.
Miller, G. (2008). Growing Pains for fMRI. Science, 320, 1412-1414.
Neba Health. (2013, July 22). Summary of Neba Clinical Investigation – Key Results. Retrieved October 20, 2013, from http://www.nebahealth.com/PR0779_neba_press_release-20130722_Cr.pdf
Primich, C., & Iennaco, J. (2012). Diagnosing adult attention-deficit hyperactivity disorder:. Journal of Psychiatric and Mental Health Nursing, 19, 362-373.
Visser, S., Lesesne, C., & Perou, R. (2007). National Estimates and Factors Associated With Medication Treatment for Childhood Attention-Deficit/Hyperactivity Disorder. Pediatrics, 119(1), 99-106.
Wood, A., Elia, J., Ambrosini, P., & Rapoport, J. (1991). Treatment of Attention-Deficit-Hyperactivity Disorder. The New England Journal of Medicine, 340(10), 780-788.
Wood, D., Reimherr, F., Wender, P., & Johnson, G. (1976). Diagnosis and Treatment of Minimal Brain Dysfunction in Adults. Archives of General Psychiatry, 33, 1453-1460.