Kevin Antshel, PhD, ADHD in AdultsNot every child with ADHD will matriculate to a four-year college, although the numbers are increasing. For example, a follow-up survey on post-secondary trajectoires of high school students with ADHD histories (N = 364) showed that 30% of the ADHD sample were currently in pursuit of a four-year degree; this figure was 9% higher than previously reported data from a comparable sample in 20061. Thus, more children with ADHD are becoming college students with ADHD. College students seeking on-campus ADHD evaluations and ADHD treatment and are also increasing in prevalence. The most recent data from the Association of University and College Counseling Center Directors (AUCCCD) annual survey, completed by 518 college counseling center directors, suggests that approximately 9% of the students seen during the 2014-2015 academic year presented at their counseling centers with concerns specifically related to ADHD2. To put this in perspective, this means that depending upon the size of the college, college counseling centers are seeing anywhere from 1 to 775 students per year with concerns specifically related to ADHD2. It is not possible to know which students the college counseling centers are not seeing and certainly there are plenty of students not seeking counseling centers for ADHD related concerns. Thus, the AUCCCD data likely represents an underestimate of the number of college students with concerns specifically related to ADHD.

College students with ADHD face significant difficulties in the college academic environment and are at greatly increased risk of poor academic achievement and failure. Clinical recommendations for working with college students with ADHD include (a) a combined approach of pharmacotherapy and psychosocial interventions, typically CBT; (b) meeting with the college student more than once per week, generally by having both group CBT and individual CBT interventions operating concurrently, (c) integrate clinical services with other providers on campus (e.g., Office of Disability Services, Counseling Center, etc.) in an attempt to improve and integrate service provision; (d) specifically target treatment adherence, including a discussion of how to handle stimulant diversion requests; (e) incorporate a discussion of emerging adulthood themes such as identity exploration, feeling-in-between adolescence and adulthood, setting realistic and optimistic life goals, and becoming independent from parents; and (f) consider adopting more of a “chronic” model for treating ADHD in college students (e.g., following students over their entire four year experience rather than treating for one semester)3.

In addition to treating college students with ADHD on campus, another issue that is present on college campuses is the college students that may be motivated to over report ADHD symptoms and malinger ADHD. College students have several incentives to over-report ADHD symptoms. A substantial number of students seek stimulant medication, most often with the intent to enhance academic performance4. Prevalence rates for stimulant misuse are the highest in college students (17%) compared to all other populations5. In addition to obtaining stimulant medication, some college students seek an ADHD diagnosis for the accompanying academic accommodations (e.g., extended time for examinations, etc.), also in the hope of improving grades6. Still others may seek an ADHD diagnosis as an external attribution for perceived academic failures7. Given these incentives, it is not surprising that elevated rates of ADHD malingering exist in college students8. Despite this, no existing strategies to detect ADHD malingering in college students have adequate sensitivity and specificity9. Given concerns about students feigning symptoms in order to acquire medication and/or academic accommodations along with the great difficulty in detecting ADHD malingering, it is not surprising that the vast majority of university health professionals are not comfortable diagnosing ADHD, with over 90% referring students off campus for ADHD evaluations10.

Our knowledge of ADHD in the college student population is nascent and we know far less about ADHD in this population compared to ADHD in children and adolescents. Increasing numbers of college students have ADHD diagnoses and are seeking on campus treatment services. Similarly, college students have several clear incentives to malinger ADHD symptoms. Given the difficulties in detecting ADHD malingering, the overwhelming majority of university health professionals refer students off campus. Researchers and clinicians should continue to develop more effective ADHD treatment options, including those designed to reduce stimulant diversion/misuse. Likewise, better understanding how to accurately detect ADHD malingering in this population is important for reducing public health costs for unwarranted assessments, backlogging an already significantly limited psychological resource on college campuses2 and creating an unfair advantage (e.g., receipt of inappropriate academic accommodations).
 

References
1. Kuriyan AB, Pelham WE, Jr., Molina BS, et al. Young adult educational and vocational outcomes of children diagnosed with ADHD. Journal of abnormal child psychology. 2013;41(1):27-41.
2. Association for University and College Counseling Center Directors. The Association for University and College Counseling Center Directors Annual Survey. Indianapolis, IN: AUCCCD; 2015.
3. He A, Antshel KM. Cognitive Behavioral Therapy for Attention Deficit / Hyperactivity Disorder (ADHD) in College Students: A Review of the Literature. Cogn. Behav. Pract. In press.
4. DeSantis AD, Webb EM, Noar SM. Illicit use of prescription ADHD medications on a college campus: a multimethodological approach. Journal of American college health : J of ACH. 2008;57(3):315-324.
5. Benson K, Flory K, Humphreys KL, Lee SS. Misuse of stimulant medication among college students: a comprehensive review and meta-analysis. Clinical child and family psychology review. 2015;18(1):50-76.
6. Williamson KD, Combs HL, Berry DT, Harp JP, Mason LH, Edmundson M. Discriminating among ADHD alone, ADHD with a comorbid psychological disorder, and feigned ADHD in a college sample. The Clinical neuropsychologist. 2014;28(7):1182-1196.
7. Suhr J, Wei C. Symptoms as an Excuse: Attention Deficit/Hyperactivity Disorder Symptom Reporting as an Excuse for Cognitive Test Performance in the Context of Evaluative Threat. Journal of Social and Clinical Psychology. 2013;32(7):753-769.
8. Suhr J, Hammers D, Dobbins-Buckland K, Zimak E, Hughes C. The relationship of malingering test failure to self-reported symptoms and neuropsychological findings in adults referred for ADHD evaluation. Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists. 2008;23(5):521-530.
9. Musso MW, Gouvier WD. “Why is this so hard?” A review of detection of malingered ADHD in college students. Journal of attention disorders. 2014;18(3):186-201.
10. Thomas M, Rostain A, Corso R, Babcock T, Madhoo M. ADHD in the College Setting: Current Perceptions and Future Vision. Journal of attention disorders. 2015;19(8):643-654.

Lenard Adler, MD ADHD in AdultsE. J. Semeijn, N. C. M. Korten, H. C. Comijs, M. Michielsen, D. J. H. Deeg, A. T. F. Beekman and J. J. S. Kooij. No lower cognitive functioning in older adults with attention-deficit/hyperactivity disorder. International Psychogeriatrics: International Psychogeriatric Association 2015 doi:10.1017/S1041610215000010.

The largest percentage growth in stimulant prescriptions in the last year is in adults over the age of 50 years of age (Adler LA. ADHD in Older Adults. Paper Presentation at the Annual Meeting of the American Psychiatric Association, New York , New York, May 2014). Even though stimulant prescriptions may be increasing in older adults with ADHD, the number of studies which have examined older adults with ADHD is relatively small. One concern in studying adults with ADHD is the potential confound of cognitive decline that may occur with aging in assessing ADHD symptoms. This study examined the cognitive function of older adults without ADHD vs. those with ADHD (n=231) in the Longitudinal Study Amsterdam (LASA). Cognitive function was assessed via neuropsychological measures of functioning, information processing speed, memory, and attention/working memory. The authors only found a negative association of ADHD symptom severity and attention/working memory domain; however, when depressive symptoms were controlled for, this association was no longer significant. Neuropsychological impairments in attention and working memory have also been shown in younger adults with ADHD. This study highlights the need for further investigations of cognitive functioning in older adults with ADHD and the importance of screening for depression in these individuals.

David_Goodman_MD_ADHD_in_AdultsAttention Deficit Hyperactivity Disorder is the most common childhood psychiatric disorder and the second most prevalent adult psychiatric disorder second to Major Depression. Yet, until recently, ADHD in adults over age 50 was not identified. As we have come to understand, ADHD symptoms with impairments persist into adulthood for 60% of ADHD children.

For those adults with ADHD, how many will have symptoms that persist for the rest of their lives? How do these symptoms and impairments present? How do we discern ADHD symptoms from other factors contributing to cognitive change with age? How do we obtain clinical history in those patients who can’t remember childhood or adolescent symptoms? Would objective tests differentiate diagnoses? What treatments work well for this age group? What medical considerations are necessary for prescribing ADHD treatments to those with medical illness and multiple medications? What safety parameters need to be considered in this age group when prescribing ADHD medications? What are the drug-drug interactions that may be clinically relevant?

For clinicians and researchers, these questions represent opportunities to expand our fund of knowledge to better serve the needs of ADHD patients in all age categories.

The population of persons older than 65 years of age in the U.S. will grow from 43.1 million to 88.5 million between 2012 and 2050. A recent review of the literature on ADHD in older adults reports a prevalence rate of 2.8% in the Netherlands, 3.5% in Sweden, and 3.5% in Germany. A meta-analysis of ADHD prevalence in studies utilizing different age ranges spanning 18-78 years suggests that prevalence may decline with age. However, given that these studies used DSM-IV criteria with a symptom age threshold of 7 and the absence of a validated ADHD symptom profile for older adults, these cited prevalences may underestimate the ADHD population.

Reliance on childhood ADHD diagnosis to substantiate ADHD in older adults is often not useful because in the National Comorbidity Survey Replication in the U.S., 75% of ADHD adults ages 18-44 had not been diagnosed as children and no ADHD adults ages 60-77 were diagnosed as children. Remember that these people grew up in the 1950s and 1960s when ADHD was rarely identified and then only in the most hyperactive/impulsive and disruptive males.

I believe that ADHD in older adults will become the next clinical frontier. While there is some research beginning to accumulate to support identifying and treating this population, the relative absence of trained ADHD clinicians for this population means many unidentified older adults will be diagnosed inaccurately with age related cognitive disorders. To exemplify this likelihood, a U.S. study canvassing memory clinics demonstrated that only 1 in 5 clinics currently screen for ADHD. Therefore, older adults with ADHD are not identified and offered effective ADHD medication and treatment. The result may be ineffective treatment, unnecessary increased medical costs, and the decline in quality of life.

For those of you reading this blog, I would encourage you to consider ADHD in older adults whose cognitive complaints have been long-standing, whose negative consequences and impairments echo an ADHD life course, and in whom a first degree relative has ADHD.

A Brief Interview with Dr. David Goodman

http://medicalwritingtraining.com/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.

Joseph Biederman MD ADHD in Adults

Is ADHD Always a Childhood Onset Disorder?

by Joseph Biederman, MD – August 4, 2016

Recent population based studies raise the intriguing question as to whether adult ADHD is always preceded by childhood onset of symptoms or can develop anew in adult life. From Brazil, one group argues that child and adult ADHD are “distinct syndromes”; from the United Kingdom (UK), another group states that adult ADHD is “more complex than a straightforward continuation of the childhood disorder” and from New Zealand (NZ), a third group claimed that adult ADHD is “not a neurodevelopmental disorder”.

In each study, adult onset ADHD refers to cases in which full-threshold ADHD had not been diagnosed by the investigators at prior assessments. In the NZ study, compared with controls, the adult onset ADHD group had more teacher-rated symptoms of ADHD, more conduct disorder (CD) in childhood and were more likely to have had a combined parent/teacher report of ADHD symptom onset prior to age 12. (DSMV recognizes onset of ADHD until the age of 12.) Likewise, the adult onsets in the UK study had high rates of ADHD symptoms, CD and oppositional defiant disorder (ODD) in childhood. Thus, many “adult onsets” of ADHD cases appear to have neurodevelopmental roots.

DSM V Guide to ADHD Diagnosis downloadBecause population studies use non-referred samples, those being diagnosed may not be self-aware of their symptoms, which increases the risk of false negatives. In population studies the ability of the subject to report on his or her own symptoms is critical since it requires insight and self awareness. It has been well documented that youth with ADHD are very poor reporters of their own symptoms. Such difficulties can certainly extend to adult years. Consistent with this idea, 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.4 Thus, the UK, Brazilian and NZ studies may have underestimated the persistence of ADHD and overestimated the prevalence of adult onsets. In contrast, self awareness is not an issue for subjects referring themselves to clinical care since, by definition, it is their self awareness that brings them to the clinic.

These reports do very little to help clarify whether these “adults” do not recall childhood symptoms, are unable to report on them, or are unable to distinguish onset of symptoms form onset of symptoms-associated impairments that may account for the different ages of onset. In these cases, the onset of symptoms and impairment could be separated by many years, particularly among those with strong intellectual abilities and those living in supportive, well-structured childhood environments. Such intellectual and social scaffolding would help ADHD youth to compensate in early life, only to decompensate into a full ADHD syndrome when the scaffolding is removed.

Such an interpretation would suggest that the etiology of ADHD leads to a wide variability in age at onset of initial symptoms, symptoms exceeding diagnostic threshold and impairment arising from those symptoms. Such variability is accepted for many other medical disorders. It is also consistent with the idea that ADHD is the extreme and impairing tail of a continuum. This view of posits that ADHD symptoms and ADHD impairment emerge due to the accumulation of environmental and genetic risk factors. Those with lower levels of risk at birth will take longer to accumulate sufficient risk factors and longer to onset with symptoms and impairment. Yet, because these effects are multifactorial, there is no clean separation of etiologic factors in people above and below a certain age.

In this context it is important to remember that the age of onset of ADHD of 12 years proposed in DSM-V, while an improvement from the previous age of onset of 7 years, is still completely arbitrary, creating the immediate dilemma on how to diagnose patients who have an onset of symptoms after 12 years of age. Such a scenario may suggest that ADHD may be a disorder with a continuum of ages of onset, with some subjects starting their symptoms earlier while others later.

These concerns do not argue against the existence of adult onset ADHD or the idea that it is a clinically relevant syndrome. In fact, as a group, the adult onset cases showed significant functional impairments. Moreover, some of the studies ruled out the idea that adult onset ADHD is a misdiagnosis of another disorder. Further support for the validity of adult onset ADHD comes from a study of referred adults who retrospectively reported childhood symptoms 5. Based on clinical features and familial transmission, that study concluded that onsets of ADHD in late adolescence and early adulthood were valid.5

See: http://archpsyc.jamanetwork.com/article.aspx?articleID=2522743

ADHD Consensus Statement download

 

 

 

REFERENCES
1. Faraone S, Biederman J, Mick E. The Age Dependent Decline Of Attention-Deficit/Hyperactivity Disorder: A Meta-Analysis Of Follow-Up Studies. Psychological Medicine. 2006;36(2):159-165.
2. Moffitt TE, Houts R, Asherson P, et al. Is Adult ADHD a Childhood-Onset Neurodevelopmental Disorder? Evidence From a Four-Decade Longitudinal Cohort Study. Am J Psychiatry. 2015:appiajp201514101266.
3. Fayyad J, De Graaf R, Kessler R, et al. Cross-national prevalence and correlates of adult attention-deficit hyperactivity disorder. Br J Psychiatry. 2007;190:402-409.
4. Sibley MH, Pelham WE, Molina BS, et al. When diagnosing ADHD in young adults emphasize informant reports, DSM items, and impairment. J Consult Clin Psychol. 2012;80(6):1052-1061.
5. Chandra S, Biederman J, Faraone S. Assessing the Validity of the Age at Onset Criterion for Diagnosing ADHD in DSM-5. Journal of attention disorders. In Press.
6. Lecendreux M, Konofal E, Cortese S, Faraone SV. A 4-year follow-up of attention-deficit/hyperactivity disorder in a population sample. J Clin Psychiatry. 2015;76(6):712-719.
7. Asherson P, Trzaskowski M. Attention-deficit/hyperactivity disorder is the extreme and impairing tail of a continuum. J Am Acad Child Adolesc Psychiatry. 2015;54(4):249-250.

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

by Stephen V. Faraone, PhD – August 4, 2016

Stephen V Faraone, PhD, ADHD in AdultsThere 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.

ASRS Professional Screener DownloadThe 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.

221d4c00-f834-473c-ad77-48137e574e2c.png.jpg

 

 
 
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.

Anthony_Rostain_AIA_15_e1U3xu
Clin Psychiatry. 2015; 76(3):279-283.
“Cultural Background and Barriers to Mental Health Care for African American Adults”
Rostain, A.L., Ramsay, J.R., Waite, R.

This article delineates key patient and provider cultural biases that interfere with access to care for African American Adults with ADHD. It provides an important framework for understanding how these biases come about and what clinicians can do to address them. A brief review of the relationship between psychiatry and African Americans points out that beginning with slavery and continuing through the Tuskegee experiment, there is a legacy of racism in American medicine that influences the way patients view health care providers (and vice versa).

For instance, drapetomania was a clinical diagnosis given to slaves who demonstrated resistance to the institution by running away, refusing to follow rules, destroying property and fighting the plantation slave owners. In this fashion, psychiatry played an important role in supporting racism and racist beliefs. Similar analogies can be made to the ways that psychiatry classified homosexuality as a mental illness.

CTA_Professional_Screeners_Bo2BO7

The point of this historical review is to underscore the longstanding mistrust that exists within the African American community toward medicine in general and psychiatry in particular. Add to this, the stigma associated with mental illness and substance abuse, it becomes easier to understand why many African American adults fail to seek treatment for disorders like ADHD.

The article goes on to discuss barriers to obtaining mental health treatment including patient factors (e.g. low income, lack of health insurance, fear and other negative attitudes) and health care system factors (e.g. limited access to culturally and technically competent providers and provider biases). Without question, higher rates of poverty and of lack of insurance among the minority population leads to markedly reduced access to care. The article points out that whereas rates of adequate mental health treatment among whites is 33%, the figure drops to 12% for African Americans. Moreover. white 
children are twice as likely to receive ADHD medication as African American children. Cultural biases among providers may lead them to be insufficiently attuned to the presence of ADHD in adult patients, ascribing the symptoms of ADHD, such as inattention, restlessness and disorganization either to personal failing (e.g. lack of self-discipline) or to environmental factors (e.g. low SES, lack of education) rather than to the influence of ADHD.

The paper concludes with practical recommendations for clinicians to address these barriers including providing accurate science based information, listening and being sensitive to stigmatizing experiences that African American patients may have encountered, and recognizing the deleterious effects of conscious and unconscious biases among well-meaning providers.

 

 

Lenard A Adler, MDGray et al. (2014), The Adult ADHD Self-Report Scale (ASRS): utility in college students with attention- deficit/hyperactivity disorder. PeerJ 2:e324; DOI 10.7717/peerj.324

There has been ongoing interest in the identification of ADHD in college students; many transitional adults will present with ADHD related symptoms and problems with the transition to post-secondary education and the related demands on attention and executive function. This investigation examined the utility of the World Health Organization (WHO) Adult ADHD Self-Report Scale (ASRS) in identifying college students at risk for ADHD.

135 college students (mean age 24 years) who were enrolled in disability service programs at their respective institutions were surveyed; all students had received a prior diagnosis of ADHD and were asked to complete all scales as if they were not on ADHD medication (59% of the students were on medication at the time of the evaluation). Students first completed the six item ASRS screener by telephone and then, several weeks later, the completed a paper version of the 18 item ASRS symptom checklist. A collateral version “other-report” of the 18 item ASRS symptom checklist, and a self-report measure of executive function (BDEFS), were also collected.

There was a modest correlation of the other-report and self-report of ASRS symptoms (r(59) = .46, p < .001) and other-report scores were significantly lower than self-report scores (F(1,57) = 8.92, p = .004). There was a moderately high correlation of student self-report of symptoms on the ASRS Screener (telephonic) and the identical six items when completed on the 18 item ASRS Symptom Checklist several weeks later (r (131) = .66, p < .001), indicating some stability of self-report of ADHD symptoms. There were moderate correlations between the total score on the ASRS screener and total executive function (BDEFS summary) scores (r (129) = .40, p < .001); correlations between total scores on 18 item ASRS symptom checklist and summary score on BDEFs were higher than seen with the screener (r (131) = .62, p < .001), indicating that a total symptom inventory of ADHD symptoms better correlates with executive function than the screening subset (which is not surprising). This study has several limitations including: 1) the subjects being asked to complete scales in the hypothetical sense of when they were not on medication (and with 3/5 students being treated for ADHD), creating the possibility of reporter bias, and 2) the study utilized a non-validated version of the other report version of the ASRS symptom checklist which was not sanctioned by WHO.

The study does highlight the utility of the ASRS symptom checklist as a self-report measure in college students; this instrument carries the advantages of being easy to use and being in the public domain. It also indicates that gathering collateral information can be helpful, but as seen in other reports, collateral reports of symptoms are often lower than self and clinician symptom scores as the informant only sees the patient for a portion of their day (home vs. work vs. social).

Lenard Adler, MD ADHD in AdultsGray et al. (2014), The Adult ADHD Self-Report Scale (ASRS): utility in college students with attention- deficit/hyperactivity disorder. PeerJ 2:e324; DOI 10.7717/peerj.324

There has been ongoing interest in the identification of ADHD in college students; many transitional adults will present with ADHD related symptoms and problems with the transition to post-secondary education and the related demands on attention and executive function. This investigation examined the utility of the World Health Organization (WHO) Adult ADHD Self-Report Scale (ASRS) in identifying college students at risk for ADHD. 135 college students (mean age 24 years) who were enrolled in disability service programs at their respective institutions were surveyed; all students had received a prior diagnosis of ADHD and were asked to complete all scales as if they were not on medication (59% of the students were on medication at the time of the evaluation). Students first completed the six item ASRS screener by telephone and then, several weeks later, the completed a paper version of the 18 item ASRS symptom checklist. A collateral version “other-report” of the 18 item ASRS symptom checklist, and a self-report measure of executive function (BDEFS), were also collected.

There was a modest correlation of the other-report and self-report of ASRS symptoms (r(59) = .46, p < .001) and other-report scores were significantly lower than self-report scores (F(1,57) = 8.92, p = .004). There was a moderately high correlation of student self-report of symptoms on the ASRS Screener (telephonic) and the identical six items when completed on the 18 item ASRS Symptom Checklist several weeks later (r (131) = .66, p < .001), indicating some stability of self-report of ADHD symptoms. There were moderate correlations between the total score on the ASRS screener and total executive function (BDEFS summary) scores (r (129) = .40, p < .001); correlations between total scores on 18 item ASRS symptom checklist and summary score on BDEFs were higher than seen with the screener (r (131) = .62, p < .001), indicating that a total symptom inventory of ADHD symptoms better correlates with executive function than the screening subset (which is not surprising). This study has several limitations including: 1) the subjects being asked to complete scales in the hypothetical sense of when they were not on medication (and with 3/5 students being treated for ADHD), creating the possibility of reporter bias, and 2) the study utilized a non-validated version of the other report version of the ASRS symptom checklist which was not sanctioned by WHO.

The study does highlight the utility of the ASRS symptom checklist as a self-report measure in college students; this instrument carries the advantages of being easy to use and being in the public domain. It also indicates that gathering collateral information can be helpful, but as seen in other reports, collateral reports of symptoms are often lower than self and clinician symptom scores as the informant only sees the patient for a portion of their day (home vs. work vs. social).

Lenard Adler, MD ADHD in AdultsCheung CH, Rijdijk F, McLoughlin G, Faraone SV, Asherson P, Kuntsi J. Childhood predictors of adolescent and young adult outcome in ADHD.   J Psychiatr Res. 2015 Jan 29. pii: S0022-3956(15)00022-9. doi: 10.1016/j.jpsychires.2015.01.011. [Epub ahead of print]

This investigation examined predictors, including a variety of cognitive measures, demographics and ADHD symptoms and impairments in 116 adolescents followed for an average of 6.6 years into early adulthood.  This study is important as it addresses the critical issue of identifying risk factors for persistence of ADHD into adulthood, which would allow in the future, targeted interventions to potentially improve remission rates.  Remission was defined if individuals no longer met DSM-IV symptom (via DIVA) or impairment (via BFIS) criteria from parental and subject interviews. Symptoms and impairments were established from periods off medication.  62% of the sample was treated with medication.  21% of the sample was found to have remitted.  A number of risk factors were identified as increasing the risk of persistence of ADHD, including higher parental reports of ADHD symptoms, lower IQ and lower socio-economic status (SES).  Medication status did not significantly influence whether a subject was classified as having remitted or persistent ADHD.  These findings of significant associations of low SES and IQ and high ADHD symptoms with persistence of ADHD into young adulthood reinforce similar findings from prior studies and should be included as some of the foci of other longitudinal studies in ADHD.