MEMBER PORTAL

JOIN  ATTEND   SPONSOR   DONATE

A Brief History of ADHD

Jan 29, 2020 | Research Updates, Stephen Faraone, Ph.D.

A Brief History of ADHD

I have too often seen on the Internet or media the statement that ADHD is a recent invention of psychiatrists and/or pharmaceutical companies. Such statements ignore the long history of ADHD that my colleague and I reviewed in our “Primer” about ADHD, http://rdcu.be/gYyV. As you can see from The Figure, ADHD has a long history. The first ADHD syndrome was described in a German medical textbook by Weikard in 1775. That’s not a typo. The ADHD syndrome had been identified before the birth of the USA. Dr. Weikard did not use the term ADD or ADHD, yet he described a syndrome of hyperactivity and inattention that corresponds to what we call ADHD today. As you can see from the Figure, ADHD-like syndromes were described in Scotland in 1798 and in France in the late 19th century. The first description of an ADHD-like syndrome in a medical journal was by Dr. George Still in 1901 who described what he called a ‘defect of moral control” in The Lancet. The discovery that stimulant drugs are effective in treating ADHD occurred in 1937 when Dr. Charles Bradley discovered that Benzedrine (an amphetamine compound) improved the behavior of children diagnosed with behavioral disorders. In subsequent years, several terms were used to describe children with ADHD symptoms. Examples are Kramer-Pollnow syndrome, minimal brain damage, minimal brain dysfunction and hyperkinetic reaction. It was not until the 1980s that the term Attention Deficit Disorder (ADD) came into widespread use with the publication of the American Psychiatric Association’s Diagnostic and Statistical Manual (DSM). During the ensuing decades, several changes were made to the diagnostic criteria and the term ADD was replaced with ADHD so as not to overemphasize either inattention of hyperactivity when diagnosing the disorder. And, as the graphic below describes, these new and better diagnostic criteria led to many breakthroughs in our understanding of the nature of the disorder and the efficacy of treatments. So, if you think that ADHD is an invention of contemporary society, think again. It has been with us for quite some time.

REFERENCE
Faraone, S. V. et al. (2015) Attention-deficit/hyperactivity disorder Nat. Rev. Dis. Primers doi:10.1038/nrdp.2015.20 ; http://rdcu.be/gYyV

Adult Onset ADHD:  Does it Exist?  Is it Distinct from Youth Onset ADHD?

Jan 27, 2020 | Research Updates

Adult Onset ADHD:  Does it Exist?  Is it Distinct from Youth Onset ADHD?

There is a growing interest (and controversy) about ‘adult’ onset ADHD.    No current diagnostic system allows for the diagnosis of ADHD in adulthood, yet clinicians sometimes face adults who meet all criteria for ADHD, except for age at onset.    Although many of these clinically referred adult onset cases may reflect poor recall, several recent longitudinal population studies have claimed to detect cases of adult onset ADHD that showed no signs of ADHD as youth (Agnew-Blais, Polanczyk et al. 2016, Caye, Rocha et al. 2016).  They conclude, not only that ADHD can onset in adulthood, but that childhood onset and adult onset ADHD may be distinct syndromes (Moffitt, Houts et al. 2015).

In each study, the prevalence of adult onset ADHD was much larger than the prevalence of childhood-onset adult ADHD).   These estimates should be viewed with caution.  The adults in two of the studies were 18-19 years old.  That is too small a slice of adulthood to draw firm conclusions.    As discussed elsewhere (Faraone and Biederman 2016), the claims for adult onset ADHD are all based on population as opposed to clinical studies.  Population studies are plagued b the “false positive paradox”, which states that, even when false positive rates are low, many or even most diagnoses in a population study can be false.

Another problem is that the false positive rate is sensitive to the method of diagnosis.  The child diagnoses in the studies claiming the existence of adult onset ADHD used reports from parents and/or teachers but the adult diagnoses were based on self-report.  Self-reports of ADHD in adults are less reliable than informant reports, which raises concerns about measurement error.   Another longitudinal study found that current symptoms of ADHD were under-reported by adults who had had ADHD in childhood and over-reported by adults who did not have ADHD in childhood (Sibley, Pelham et al. 2012).   These issues strongly suggest that the studies claiming the existence of adult onset ADHD underestimated the prevalence of persistent ADHD and overestimated the prevalence of adult onset ADHD.  Thus, we cannot yet accept the conclusion that most adults referred to clinicians with ADHD symptoms will not have a history of ADHD in youth.

The new papers conclude that child and adult ADHD are “distinct syndromes”, “that adult ADHD is more complex than a straightforward continuation of the childhood disorder” and that that adult ADHD is “not a neurodevelopmental disorder”.   These conclusions are provocative, suggesting a paradigm shift in how we view adulthood and childhood ADHD.   Yet they seem premature.   In these studies, people were categorized as adult onset ADHD if full-threshold ADHD had not been diagnosed in childhood.  Yet, in all of these population studies there was substantial evidence that the adult onset cases were not neurotypical in adulthood (Faraone and Biederman 2016).  Notably, in a study of referred cases, one-third of late adolescent and adult onset cases had childhood histories of ODD, CD and school failure (Chandra, Biederman et al. 2016).   Thus, many of the “adult onsets” of ADHD appear to have had neurodevelopmental roots.

Looking through a more parsimonious lens, Faraone and Biederman (2016)proposed that the putative cases of adult onset ADHD reflect the existence of subthreshold childhood ADHD that emerges with full threshold diagnostic criteria in adulthood.   Other work shows that subthreshold ADHD in childhood predicts onsets of the full-threshold ADHD in adolescence (Lecendreux, Konofal et al. 2015).   Why is onset delayed in subthreshold cases? One possibility is that intellectual and social supports help subthreshold ADHD youth compensate in early life, with decompensation occurring when supports are removed in adulthood or the challenges of life increase.  A related possibility is that the subthreshold cases are at the lower end of a dimensional liability spectrum that indexes risk for onset of ADHD symptoms and impairments.  This is consistent with the idea that ADHD is an extreme form of a dimensional trait, which is supported by twin and molecular genetic studies (Larsson, Anckarsater et al. 2012, Lee, Ripke et al. 2013).  These data suggest that disorders emerge when risk factors accumulate over time to exceed a threshold.  Those with lower levels of risk at birth will take longer to accumulate sufficient risk factors and longer to onset.

In conclusion, it is premature to accept the idea that there exists an adult onset form of ADHD that does not have its roots in neurodevelopment and is not expressed in childhood.   It is, however, the right time to carefully study apparent cases of adult onset ADHD to test the idea that they are late manifestations of a subthreshold childhood condition.

REFERENCES

Agnew-Blais, J. C., G. V. Polanczyk, A. Danese, J. Wertz, T. E. Moffitt and L. Arseneault (2016). “Persistence, Remission and Emergence of ADHD in Young Adulthood:Results from a Longitudinal, Prospective Population-Based Cohort.” JAMA.

Caye, A., T. B.-M. Rocha, L. Luciana Anselmi, J. Murray, A. M. B. Menezes, F. C. Barros, H. Gonçalves, F. Wehrmeister, C. M. Jensen, H.-C. Steinhausen, J. M. Swanson, C. Kieling and L. A. Rohde (2016). “ADHD does not always begin in childhood: E 1 vidence from a large birth cohort.” JAMA.

Chandra, S., J. Biederman and S. V. Faraone (2016). “Assessing the Validity of  the Age at Onset Criterion for Diagnosing ADHD in DSM-5.” J Atten Disord.

Faraone, S. V. and J. Biederman (2016). “Can Attention-Deficit/Hyperactivity Disorder Onset Occur in Adulthood?” JAMA Psychiatry.

Larsson, H., H. Anckarsater, M. Rastam, Z. Chang and P. Lichtenstein (2012). “Childhood attention-deficit hyperactivity disorder as an extreme of a continuous trait: a quantitative genetic study of 8,500 twin pairs.” J Child Psychol Psychiatry 53(1): 73-80.

Lecendreux, M., E. Konofal, S. Cortese and S. V. Faraone (2015). “A 4-year follow-up of attention-deficit/hyperactivity disorder in a population sample.” J Clin Psychiatry 76(6): 712-719.

Lee, S. H., S. Ripke, B. M. Neale, S. V. Faraone, S. M. Purcell, R. H. Perlis, B. J. Mowry, A. Thapar, M. E. Goddard, J. S. Witte, D. Absher, I. Agartz, H. Akil, F. Amin, O. A. Andreassen, A. Anjorin, R. Anney, V. Anttila, D. E. Arking, P. Asherson, M. H. Azevedo, L. Backlund, J. A. Badner, A. J. Bailey, T. Banaschewski, J. D. Barchas, M. R. Barnes, T. B. Barrett, N. Bass, A. Battaglia, M. Bauer, M. Bayes, F. Bellivier, S. E. Bergen, W. Berrettini, C. Betancur, T. Bettecken, J. Biederman, E. B. Binder, D. W. Black, D. H. Blackwood, C. S. Bloss, M. Boehnke, D. I. Boomsma, G. Breen, R. Breuer, R. Bruggeman, P. Cormican, N. G. Buccola, J. K. Buitelaar, W. E. Bunney, J. D. Buxbaum, W. F. Byerley, E. M. Byrne, S. Caesar, W. Cahn, R. M. Cantor, M. Casas, A. Chakravarti, K. Chambert, K. Choudhury, S. Cichon, C. R. Cloninger, D. A. Collier, E. H. Cook, H. Coon, B. Cormand, A. Corvin, W. H. Coryell, D. W. Craig, I. W. Craig, J. Crosbie, M. L. Cuccaro, D. Curtis, D. Czamara, S. Datta, G. Dawson, R. Day, E. J. De Geus, F. Degenhardt, S. Djurovic, G. J. Donohoe, A. E. Doyle, J. Duan, F. Dudbridge, E. Duketis, R. P. Ebstein, H. J. Edenberg, J. Elia, S. Ennis, B. Etain, A. Fanous, A. E. Farmer, I. N. Ferrier, M. Flickinger, E. Fombonne, T. Foroud, J. Frank, B. Franke, C. Fraser, R. Freedman, N. B. Freimer, C. M. Freitag, M. Friedl, L. Frisen, L. Gallagher, P. V. Gejman, L. Georgieva, E. S. Gershon, D. H. Geschwind, I. Giegling, M. Gill, S. D. Gordon, K. Gordon-Smith, E. K. Green, T. A. Greenwood, D. E. Grice, M. Gross, D. Grozeva, W. Guan, H. Gurling, L. De Haan, J. L. Haines, H. Hakonarson, J. Hallmayer, S. P. Hamilton, M. L. Hamshere, T. F. Hansen, A. M. Hartmann, M. Hautzinger, A. C. Heath, A. K. Henders, S. Herms, I. B. Hickie, M. Hipolito, S. Hoefels, P. A. Holmans, F. Holsboer, W. J. Hoogendijk, J. J. Hottenga, C. M. Hultman, V. Hus, A. Ingason, M. Ising, S. Jamain, E. G. Jones, I. Jones, L. Jones, J. Y. Tzeng, A. K. Kahler, R. S. Kahn, R. Kandaswamy, M. C. Keller, J. L. Kennedy, E. Kenny, L. Kent, Y. Kim, G. K. Kirov, S. M. Klauck, L. Klei, J. A. Knowles, M. A. Kohli, D. L. Koller, B. Konte, A. Korszun, L. Krabbendam, R. Krasucki, J. Kuntsi, P. Kwan, M. Landen, N. Langstrom, M. Lathrop, J. Lawrence, W. B. Lawson, M. Leboyer, D. H. Ledbetter, P. H. Lee, T. Lencz, K. P. Lesch, D. F. Levinson, C. M. Lewis, J. Li, P. Lichtenstein, J. A. Lieberman, D. Y. Lin, D. H. Linszen, C. Liu, F. W. Lohoff, S. K. Loo, C. Lord, J. K. Lowe, S. Lucae, D. J. MacIntyre, P. A. Madden, E. Maestrini, P. K. Magnusson, P. B. Mahon, W. Maier, A. K. Malhotra, S. M. Mane, C. L. Martin, N. G. Martin, M. Mattheisen, K. Matthews, M. Mattingsdal, S. A. McCarroll, K. A. McGhee, J. J. McGough, P. J. McGrath, P. McGuffin, M. G. McInnis, A. McIntosh, R. McKinney, A. W. McLean, F. J. McMahon, W. M. McMahon, A. McQuillin, H. Medeiros, S. E. Medland, S. Meier, I. Melle, F. Meng, J. Meyer, C. M. Middeldorp, L. Middleton, V. Milanova, A. Miranda, A. P. Monaco, G. W. Montgomery, J. L. Moran, D. Moreno-De-Luca, G. Morken, D. W. Morris, E. M. Morrow, V. Moskvina, P. Muglia, T. W. Muhleisen, W. J. Muir, B. Muller-Myhsok, M. Murtha, R. M. Myers, I. Myin-Germeys, M. C. Neale, S. F. Nelson, C. M. Nievergelt, I. Nikolov, V. Nimgaonkar, W. A. Nolen, M. M. Nothen, J. I. Nurnberger, E. A. Nwulia, D. R. Nyholt, C. O’Dushlaine, R. D. Oades, A. Olincy, G. Oliveira, L. Olsen, R. A. Ophoff, U. Osby, M. J. Owen, A. Palotie, J. R. Parr, A. D. Paterson, C. N. Pato, M. T. Pato, B. W. Penninx, M. L. Pergadia, M. A. Pericak-Vance, B. S. Pickard, J. Pimm, J. Piven, D. Posthuma, J. B. Potash, F. Poustka, P. Propping, V. Puri, D. J. Quested, E. M. Quinn, J. A. Ramos-Quiroga, H. B. Rasmussen, S. Raychaudhuri, K. Rehnstrom, A. Reif, M. Ribases, J. P. Rice, M. Rietschel, K. Roeder, H. Roeyers, L. Rossin, A. Rothenberger, G. Rouleau, D. Ruderfer, D. Rujescu, A. R. Sanders, S. J. Sanders, S. L. Santangelo, J. A. Sergeant, R. Schachar, M. Schalling, A. F. Schatzberg, W. A. Scheftner, G. D. Schellenberg, S. W. Scherer, N. J. Schork, T. G. Schulze, J. Schumacher, M. Schwarz, E. Scolnick, L. J. Scott, J. Shi, P. D. Shilling, S. I. Shyn, J. M. Silverman, S. L. Slager, S. L. Smalley, J. H. Smit, E. N. Smith, E. J. Sonuga-Barke, D. St Clair, M. State, M. Steffens, H. C. Steinhausen, J. S. Strauss, J. Strohmaier, T. S. Stroup, J. S. Sutcliffe, P. Szatmari, S. Szelinger, S. Thirumalai, R. C. Thompson, A. A. Todorov, F. Tozzi, J. Treutlein, M. Uhr, E. J. van den Oord, G. Van Grootheest, J. Van Os, A. M. Vicente, V. J. Vieland, J. B. Vincent, P. M. Visscher, C. A. Walsh, T. H. Wassink, S. J. Watson, M. M. Weissman, T. Werge, T. F. Wienker, E. M. Wijsman, G. Willemsen, N. Williams, A. J. Willsey, S. H. Witt, W. Xu, A. H. Young, T. W. Yu, S. Zammit, P. P. Zandi, P. Zhang, F. G. Zitman, S. Zollner, B. Devlin, J. R. Kelsoe, P. Sklar, M. J. Daly, M. C. O’Donovan, N. Craddock, P. F. Sullivan, J. W. Smoller, K. S. Kendler and N. R. Wray (2013). “Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs.” Nat Genet 45(9): 984-994.

Moffitt, T. E., R. Houts, P. Asherson, D. W. Belsky, D. L. Corcoran, M. Hammerle, H. Harrington, S. Hogan, M. H. Meier, G. V. Polanczyk, R. Poulton, S. Ramrakha, K. Sugden, B. Williams, L. A. Rohde and A. Caspi (2015). “Is Adult ADHD a Childhood-Onset Neurodevelopmental Disorder? Evidence From a Four-Decade Longitudinal Cohort Study.” Am J Psychiatry: appiajp201514101266.

Sibley, M. H., W. E. Pelham, B. S. Molina, E. M. Gnagy, J. G. Waxmonsky, D. A. Waschbusch, K. J. Derefinko, B. T. Wymbs, A. C. Garefino, D. E. Babinski and A. B. Kuriyan (2012). “When diagnosing ADHD in young adults emphasize informant reports, DSM items, and impairment.” J Consult Clin Psychol 80(6): 1052-1061.

 

 

ADHD Symptoms Manifest in Automatic and Controlled Processing

Jan 23, 2020 | Research Updates

ADHD Symptoms Manifest in Automatic and Controlled Processing

Jennifer Lee, Doctoral Candidate

Beth Krone, PhD

Long Island University Post Campus

Investigating and understanding the underlying nature of attention processes in ADHD can help drive improvements in treatment. In a new study, Caprì, Santoddi, and Fabio (2020)1 examined whether children with ADHD exhibited deficits in automatic and controlled attentional processes, compared to typically developing (TD) children. They administered the Multi-Source Interference Task (MSIT2,3) to characterize automatic and controlled attention among 60 youth: ADHD-Inattentive presentation: boys = 17, girls = 3; M = 8.50 years, SD = 4.52; ADHD-Combined presentation: boys = 16, girls = 4; M = 8.50 years, SD = 4.51; and typically developing controls: boys = 33, girls = 7; M = 8.50 years, SD = 4.53. The MSIT measures responses to task with incongruent (associated with controlled processing) and congruent (associated with automatic processing) stimulus conditions over the course of 3 hours.

On congruent trials characterizing automatic processing, despite some variability between the ADHD-I and ADHD-C group’s performance, the team found no significant differences between clinical groups and controls in accuracy of responses. The ADHD-I group responded significantly more slowly to these task prompts, indicating difficulty with processing speed. On congruent trials characterizing controlled processing, the ADHD-I group’s accuracy was lower than the TD group. Further, both ADHD groups scored significantly lower than the TD group for attentional processing overall, indicating more difficulty with attentional processes in the clinical groups.

The authors suggested that differences in performance across groups for congruent and incongruent trials indicate that automatic and controlled processing are linked entities, in support of findings from a prior study from their lab4. Findings such as these support the literature surrounding executive control problems among individuals with ADHD, and add to the body of evidence supporting the neuropsychological hierarchy of attentional processes.

All clinicians, and particularly clinicians-in-training, benefit from a strong understanding of the underlying mechanisms driving attention and performance in ADHD. We may not currently, as a field, have the tools to elucidate all mechanisms of ADHD. We do, however, have well-validated and reliable tools that allow us to objectively characterize certain aspects of cognitive processing that transfer to behaviors. These behaviors translate to symptom profiles, although not always neatly or uniformly for all individuals. By characterizing what we can, we find targets for intervention and begin to personalize treatments. Where bottom-up (automatic) and top-down (controlled) deficits may not precisely model performance measured within or across all ADHD presentations, future work should continue to examine the factors that differ between ADHD presentations and with co-occurring disorders, and across developmental stages. Youth who exhibit deficits in these cognitive functions may benefit from high quality assessment and clinical treatment planning targeting their needs.

References

  1. Caprì, T., Santoddi, E., & Fabio, R. A. (2020). Multi-Source Interference Task paradigm to enhance automatic and controlled processes in ADHD. Research in Developmental Disabilities, 97, 103542.
  2. Bush, G., & Shin, L. M. (2006). The Multi-Source Interference Task: an fMRI task that reliably activates the cingulo-frontal-parietal cognitive/attention network. Nature protocols, 1(1), 308.
  3. Bush, G., Shin, L. M., Holmes, J., Rosen, B. R., & Vogt, B. A. (2003). The Multi-Source Interference Task: validation study with fMRI in individual subjects. Molecular psychiatry, 8(1), 60.
  4. Fabio, R. A., & Caprì, T. (2019). Automatic and controlled attentional capture by threatening stimuli. Heliyon, 5(5), e01752.

 

 

 

Bullying, Aggression and ADHD

Jan 13, 2020 | Annual Conference, Conference Blog, Research Updates

Conference Posters: Don’t miss the poster sessions at the 2020 Annual Meeting of APSARD. Hear new voices and see new research!

Bullying, Aggression and ADHD

Jessica Simmons, M.A.

Kevin Antshel, Ph.D.

Department of Psychology

ADHD Lifespan Treatment, Education and Research (ALTER) program

Syracuse University

 

Bullying is a repetitive aggressive behavior that occurs in an unequal power dynamic between a bully and victim. Bullying is associated with significant negative mental health outcomes for both victims and perpetrators. Youth who both bully others and are bullied by others (“bully-victims”) have the worst outcomes. Not surprisingly, within the past decade, youth bullying was labeled a public health problem by the Centers for Disease Control (CDC). ADHD represents a diathesis for bullying involvement, both as a perpetrator and a victim. In fact, multiple studies have suggested that youth with ADHD are up to 50% more likely to be involved in bullying, both perpetration and victimization, than their typically developing peers.

The links to victimization are clear in ADHD; bullying victims (not specific to ADHD) exhibit poor social behaviors, including hyperactivity and impulsivity, which irritate or annoy others and/or cause them stand out from their same-age peers. Violating social expectations (i.e., acting or saying things that are immature), missing social cues, and disregarding personal space are other reasons why children may be victimized by their peers.

The links to bully perpetration and being a “bully-victim”, however, require additional consideration. Certainly, youth with ADHD can act aggressively toward their peers. For example, youth with ADHD may respond aggressively if bullied. Indeed, aggression is one of the primary reasons that youth with ADHD are socially rejected. Nonetheless, not all aggression is bullying.

Aggression in ADHD appears to be linked to frustration, unsatisfied anticipation of reward, and difficulties controlling impulses. Aggression in ADHD seems to be more reactive and be an impulsive emotional response to environmental stimuli. Proactive aggression is an intentional response viewed as an acceptable way to achieve a goal. Proactive aggression is less common in ADHD and most likely to occur in those with comorbid oppositional defiant disorder (ODD) and/or conduct disorder (CD).

Distinguishing whether aggression is reactive and/or proactive is clinically important to better understand trajectories of behavior and plan interventions. Understanding whether aggression is reactive and/or proactive is also important for understanding the extant bullying literature. Insufficient operationalization of “bullying” has been an ongoing problem in the literature, leading researchers to question whether youth and adults have a similar idea of the behaviors that meet the standards of “bullying”.

A study by Murray and colleagues1 examined this important distinction and longitudinally considered whether proactive or reactive aggression has a stronger association with symptoms of ADHD. Data on ADHD symptoms and reactive and proactive aggressive behaviors were annually collected from teachers of 1,571 students in Zurich, Switzerland over eight years, beginning when the children were 7 years old and ending at age 15. Growth curve models were used to assess how symptoms of ADHD were related to reactive and proactive aggressive behaviors over the eight data collection points. Results indicated that the average growth curves for reactive and proactive aggression declined from ages 7 to 15 years of age. However, ADHD symptoms showed stronger and more significant developmental relations with reactive aggression than proactive aggression. Notably, the declines in reactive aggression were strongly and significantly correlated with declines in hyperactivity / impulsivity more so than inattention symptoms.

The results of the Murray et al. study are important for understanding bullying behaviors in ADHD. Despite being aggressive, reactive aggression often does not meet the standards of bullying. Murray and colleagues’ data should encourage us as a field to clearly operationalize bullying in our research and to question the data suggesting youth with ADHD (without comorbid ODD/CD) are more likely to be bully perpetrators than their peers. This distinction is more than semantic; important clinical, research and public policy implications depend upon correctly identifying the aggressive behavior.

If you too share my passion and interest for understanding bullying in ADHD, please visit my poster at the upcoming APSARD conference. I would love to continue this dialogue!

1 Murray, A. L., Obsuth, I., Zirk-Sadowski, J., Ribeaud, D., & Eisner, M. (2016). Developmental relations between ADHD symptoms and reactive versus proactive aggression across childhood and adolescence. Journal of Attention Disorders, 1-10. doi: 10.1177/1087054716666323.

Emotion Dysregulation: A Major Problem For Adolescents With ADHD   

Jan 9, 2020 | Editorial, Research Updates

EMOTION DYSREGULATION: A MAJOR PROBLEM FOR ADOLESCENTS WITH ADHD   

By: Joel Young

The consequences of emotion dysregulation (ED) is a major problem for adolescents with ADHD, whether the behavior is shrieking at a teacher who confiscates a cell phone not allowed during class or punching another student who crashed into the teen, maybe not on purpose. But does it matter which subtype of ADHD the adolescent carries, whether the child is male or female, or if the adolescent also has oppositional defiant disorder (ODD)? Researcher Nora Bunford and colleagues studied 180 adolescents with ADHD, ages 12-16 years old to evaluate aspects of emotion dysregulation affecting adolescents with ADHD.

In this study, the adolescent subjects were previously diagnosed with ADHD with either the inattentive subtype of ADHD or the ADHD combined type. Some subjects were comorbid for  ODD. The subjects were recruited by flyers sent to middle schools in Ohio. All children had a minimum intelligence quotient of 80 on the Wechsler Abbreviated Scale of Intelligence. The study occurred over 1 academic year and six months.

The researchers found three key aspects of emotion dysregulation were predictive for both parent-reported and child-reported social impairment, regardless of the ADHD subtype, gender, or presence or absence of ODD. These factors were the following:

  • A low threshold for emotional excitability/impatience
  • Behavioral dyscontrol accompanying strong emotions
  • Inflexibility/slow return to baseline

The researchers explained ED is comprised of two main deficits. “These are an inhibitory deficit, which manifests in socially inappropriate behavioral responses to strong emotion, and a self-regulatory deficit, which manifests in an inability to (a) self-soothe physiological arousal that strong emotion induces, (b) refocus attention, and (c) organize the self for coordinated action in the service of an external goal.”

Many different scales were used to evaluate the adolescents, such as the Difficulties in Emotion Regulation Scale (DERS), the Emotion Regulation Index for Children and Adolescents (ERICA), the Social Skills Improvement System-Rating Scales (SSIS-RS), and others. The researchers also compared the teens with ADHD to those from a community sample of youth without ADHD.

There were no significant differences between subtypes of ADHD in the subjects in terms of social impairment and emotion dysregulation, nor was it significant if the adolescent had ODD.

The researchers did discover that, compared to females in the community, females with ADHD and emotion dysregulation exhibited a lack of awareness and inattention to emotional responses. They also experienced difficulties in controlling their behavior in the face of negative em0tions and lacked confidence in their ability to control their emotions. Among the males with ADHD experiencing ED, compared to a community sample of males without ADHD, the ADHD males were significantly more emotionally inflexible with a slower return to emotional baseline. They had difficulty with socially appropriate emotional responses, lacked awareness and were inattentive emotional responses. In addition, the ADHD males struggled to control their behavior while experiencing negative emotions and lacked knowledge and clarity about the emotions they were experiencing.

The researchers noted psychosocial interventions with adolescents resembling the subjects in the study may fail because such an intervention could miss the importance of emotion dysregulation. The researchers recommended mindfulness mediation or dialectical behavior therapy as possible therapeutic techniques for these subjects.

It is unknown if the adolescents in this study were medicated, but it seems likely at least some were receiving ADHD medications. A further study on subjects taking ADHD medications and considering their levels of ED would be useful to determine if ADHD medications may help affected subjects improve their emotion dysregulation. In addition, including a group of teens with  the predominantly hyperactive-impulsive subtype as a comparison basis with the other subtypes could provide useful information. One wonders if hyperactive and impulsive teens might be more emotionally labile than adolescents who are inattentive or have the mixed subtype of ADHD.

The researchers provided important food for thought in this unique study.

Nora Bunford, Steven W. Evans, and Joshua M. Langberg, “Emotion Dysregulation Is Associated with Social Impairment Among Young Adolescents with ADHD,” Journal of Attention Disorders 32, n. 1 (2018):66-82.

 

 

Web Portal That Helps Providers Implement the New ADHD Guideline Offered Free to Providers Across the U.S.

Jan 7, 2020 | Research Updates

Web Portal That Helps Providers Implement the New ADHD Guideline Offered Free to Providers Across the U.S.

A web-based technology that helps pediatric providers, parents and educators improve the quality of care for Attention-Deficit/Hyperactivity Disorder (ADHD), is being offered for free to pediatric practices nationwide by Cincinnati Children’s Hospital Medical Center. This technology has the potential to help providers implement the American Academy of Pediatrics’ (AAP) recently released and updated ADHD clinical practice guideline.

NIMH awarded Cincinnati Children’s a four-year $2.8 million grant to support the initiative, which focuses on accelerating improved patient outcomes at community-based and other practices where delivery of evidence-based ADHD care can be challenging, according to Jeff Epstein, PhD, a pediatric psychologist and director of the Center for ADHD at Cincinnati Children’s.

Research shows that many pediatric practices carry heavy caseloads, and staff members struggle to coordinate care for complex behavioral conditions like ADHD.  At the same time, the number of diagnosed cases of ADHD continues to increase, further straining practice resources.

Epstein is part of the team of pediatric providers, behavioral specialists and computer technology experts that developed the technology platform called “mehealth for ADHD.”  A 2016 study published in the journal Pediatrics reported when tested at 50 community based pediatrics practices involving 199 physicians and 577 children with ADHD, the mehealth for ADHD technology resulted in improved ADHD medication care and significantly better behavioral improvement in patients.  Since that study was published, the mehealth system has been expanded and improved by adding functions allowing parents and teachers to develop and implement behavioral treatments.

During the grant and technology rollout’s first year, Epstein and his colleagues will be working with participating practices and an advisory committee of parents, educators and caregivers to find ways to enhance the portal’s financial sustainability, as well as its effectiveness. Through the current NIH grant, the team is able to offer the mehealth technology to pediatric providers free of charge until 2021.  The ultimate goal, Epstein said, is to offer the ADHD care portal at no cost to pediatric providers or families in perpetuity.

Cincinnati Children’s Hospital Medical Center encourages pediatric providers to sign up to use the mehealth for ADHD web portal at www.mehealth.com.