What is Sluggish Cognitive Tempo and is it Relevant to ADHD?

What is Sluggish Cognitive Tempo and is it Relevant to ADHD?

By Stephen V. Faraone, PhD

Over the past few decades, a consensus has emerged among psychopathologists that some patients exhibit a well-defined syndrome referred to as sluggish cognitive tempo or SCT.   There are no diagnostic criteria for SCT because it has not yet been accepted as a separate disorder by the American Psychiatric Association.  People with SCT are slow-moving, indolent and mentally muddled.  They often appear to be lost in thoughts, daydreaming, drowsy or listless.  In reviewing these symptoms and the literature, Barkley suggested that SCT be referred to as Concentration Deficit Disorder (CDD).  This term is less pejorative but is not yet commonly used.  Becker and colleagues recently evaluated the internal and external validity of SCT via a meta-analysis of 73 studies.  Internal validity addresses the consistency of SCT symptoms as measure of an underlying construct.  Based on factor analytic studies using more than 19,000 participants, the authors concluded that the items purported to measure SCT are sufficiently correlated with one another to justify the idea that they measure the same underlying construct.  Further support for internal validity was found in studies reporting high test-retest and interrater reliability.    As regards ADHD, the authors found that SCT correlated significantly with both inattentive (r = 0.72) and hyperactive-impulsive (r = 0.46) symptoms in adults.  The greater correlation with inattentive symptoms makes sense given the nature of SCT symptoms.  So these data confirm two key points about SCT: 1) it is definitely associated with ADHD symptoms and 2) it is a meaningful construct in its own right.  Very little is known about the implications of SCT for the treatment of ADHD.   In a naturalistic study of 88 children and adolescents with ADHD, Ludwig and colleagues examined the effect of SCT on the response of ADHD symptoms to methylphenidate. They found no significant differences in treatment response between subjects with and without SCT. McBurnett and colleagues tested the effects of atomoxetine on SCT in children with ADHD and dyslexia (ADHD+D) or dyslexia only. Atomoxetine treatment led to significant reductions in both ADHD symptoms and SCT outcomes.  Because controlling for changes in ADHD symptoms did not predict changes in SCT outcomes, the authors concluded that change in SCT in response to atomoxetine is mostly independent of change in ADHD.  Although these data are preliminary and in need of replication, they do provide some guidance for clinicians dealing with ADHD patients who also have SCT.

REFERENCE

Becker, S. P., Leopold, D. R., Burns, G. L., Jarrett, M. A., Langberg, J. M., Marshall, S. A., McBurnett, K., Waschbusch, D. A. & Willcutt, E. G. (2016). The Internal, External, and Diagnostic Validity of Sluggish Cognitive Tempo: A Meta-Analysis and Critical Review. J Am Acad Child Adolesc Psychiatry 55, 163-78.

 

Ludwig, H. T., Matte, B., Katz, B. & Rohde, L. A. (2009). Do sluggish cognitive tempo symptoms predict response to methylphenidate in patients with attention-deficit/hyperactivity disorder-inattentive type? J Child Adolesc Psychopharmacol 19, 461-5.

 

McBurnett, K., Clemow, D., Williams, D., Villodas, M., Wietecha, L. & Barkley, R. (2016). Atomoxetine-Related Change in Sluggish Cognitive Tempo Is Partially Independent of Change in Attention-Deficit/Hyperactivity Disorder Inattentive Symptoms. J Child Adolesc Psychopharmacol.

 

Barkley, R. A. (2014). Sluggish cognitive tempo (concentration deficit disorder?): current status, future directions, and a plea to change the name. J Abnorm Child Psychol 42, 117-25.

A Brief History of ADHD

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?

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

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.

 

 

 

APSARD 2020 Mentorship Initiative

The annual meeting of APSARD is an opportunity to bring experts together to share knowledge and build collaborative relationships for improving research and clinical practice. This year, the leadership of APSARD joined together to provide an unprecedented mentoring opportunity for young clinical investigators in the first APSARD Mentorship Awards Day. Ten outstanding junior clinician-researchers were selected to attend a full day session hosted by APSARD’s past, present, and future presidents, all of whom are icons in the field of ADHD clinician research. This year’s Mentor Awardees were:

Atilla Ceranoglu, MD, of Massachusetts General Hospital, who presented his findings from a pilot study of a novel, non-medication intervention for ADHD, and presented his plans for integrating these treatments into a telemedicine framework.

Beth Krone, PhD, of the Icahn School of Medicine at Mount Sinai, in New York City, who presented her research on objective measures of sluggish cognitive tempo within ADHD, and presented a novel framework for studying biomarkers of SCT as a neuroinflammatory disorder comorbid with ADHD

Carrie Vaudreuil, MD, of Massachusetts General Hospital, who is active in research on pediatric psychopharmacology and functional outcomes

Cindy Ola, PhD, of the Seattle Children’s Hospital, who presented her research on Latinx parenting perspectives, and engaging Latinx families in behavioral parent training for ADHD.

Mariely Hernandez, Doctoral Candidate, of the City University of New York, who presented her research on substance misuse among college-aged youth with ADHD.

Mei Uchida, MD, of Massachusetts General Hospital, who is active in research on pediatric psychopharmacology and functional outcomes, and presented her ideas for using fMRI to map developmental trajectories for preschoolers at risk for ADHD.

Michael Meinzer, PhD, of the University of Illinois at Chicago who discussed his research on functional outcomes among adolescents and college aged youth who are making transitions to independence.

Robert Jaffe, MD, of the Icahn School of Medicine at Mount Sinai in New York City, whose clinical work in Tics, Tourette’s and OCD has led to his research on comorbidities within ADHD, and a focus on access to services within the hospital healthcare system.

Victoria Lishak, PhD of the Hospital for Sick Children in Toronto, Canada, who presented her novel computer mediated interventions for cognitive remediation of executive functioning disorders in ADHD, and introduced her next steps in developing virtual reality systems for cognitive training.

William Pelham, PhD , of the Seattle Children’s Hospital, who presented outcomes research examining predictors for growth suppression in response to pharmacological treatment with stimulant drugs.