Journal of Attention Disorders 1 –7 DOI: 10.1177/1087054718763736 journals.sagepub.com/home/jad

Benjamin J. Lovett and Alexander H. Jordan

Lenard Adler MD - ADHD in Adults FacultyRates of ADHD in college students have been increasing somewhat in recent years, as has use of screening tools to help identify individuals at risk for disorders such as ADHD. These investigators designed a trial to examine whether screening for adult ADHD, in essence creating some positive expectation bias of having the disorder in leading to increased reporting of ADHD symptoms and altered performance on cognitive tests. One group was screened for ADHD using the ASRS v.1.1 Screener and received feedback if they screened positive for the disorder and then completed a self ADHD symptom checklist (CAARS: S Long version) and a batter of psychological tests (three subtests on the Woodcock– Johnson IV Tests of Cognitive Abilities (WJ-IV) (processing speed), a mathematical test and Letter-Pattern Matching (LPM)/Number-Pattern Matching (NPM), and Pair Cancelation (PC) for general cognitive efficiency. The control group received the same interventions except were not screened for ADHD. There were no significant differences in the two groups in terms of ADHD symptoms or neuropsychological measures. The authors note that while there was concern that screening positive for ADHD might result in increased expectation of having more ADHD symptoms, these effects were limited and did not significantly affect reporting ADHD symptoms. Several limitations of the trial include the constraint of the sample to only college students which limits the generalizability of the results, the absence of a comparison intervention (ie. Mock screening) in the control group and the use of DSM-IV version of the adult ADHD screener, instead of the most recently validated DSM-5 version. The important take-home point for clinicians seeing college students is the lack of increased reporting of ADHD symptoms and absence of effects on neuropsychological tests introduced by the process of screening for ADHD.

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.

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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.

Lenard A. Adler, MD, ADHD in Adults
Ettinger AB1, Ottman R, Lipton RB, Cramer JA, Fanning KM, Reed ML. Attention-deficit/hyperactivity Len_Adler_AIAdisorder symptoms in adults with self-reported epilepsy: Results from a national epidemiologic survey of epilepsy. Epilepsia. 2015 Jan 15. doi: 10.1111/epi.12897. [Epub ahead of print]

The purpose of this study was to examine symptoms of ADHD and resulting functional consequences in a large community cohort of individuals with epilepsy. There is a somewhat higher rate of ADHD observed in pediatric samples of ADHD, but little data exists in terms of the comparative rates of ADHD, co-morbidity and quality of life in adults with epilepsy.

This study is important because it extends the observation of higher rates of ADHD seen in studies of pediatric ADHD to adult ADHD; the observed prevalence rate of ADHD (using a proxy of being screen positive on the ASRS v1.1) was nearly three times in this population of adults with epilepsy as compared to the general population, with substantial functional consequences in these individuals. The study also highlights the need to examine adults with epilepsy for the possibility of co-morbid ADHD.

ASRS Professional Screener Download

This study examined through telephone survey as part of The Epilepsy Comorbidities and Health Study (EPIC), 1361 respondents who had been told they had epilepsy and were receiving anti-epileptic drugs (AEDs). The group was divided into a likelihood of having ADHD via the ASRS v1.1 Screener, if they had a total score on these six items > 14 (ASRS v1.1 Screen positive and ASRS v1.1 Screen negative). Measures of co-morbidity included depression: the Physicians Health Questionnaire (PHQ-9), and generalized anxiety disorder: the Generalized Anxiety Disorder Assessment 7 (GAD-7).

Quality of life and disability were assessed with the Quality of Life in Epilepsy Inventory 10 (QOLIE-10), Quality of Life and Satisfaction Questionnaire (Q-LES-Q) and the Sheehan Disability Scale (SDS). 251 of the 1361 (18.4%) respondents were found to be at risk for having adult ADHD (ADHD+). ASRS v1.1 Screener positive vs. negative cases were significantly more likely to have seizures and AED use, along with significantly higher depression and anxiety symptom scores. The ASRS v1.1 Screen positive cohort (controlling for covariates) had lower QoL and social functioning (Q-LES-Q) and increased family and occupational disability (SDS).

Potential confounds in the data include: 1) that a formal diagnosis of adult ADHD was not obtained (just individuals at risk for the disorder, but prior trials have found that a substantial proportion of screen positive individuals when assessed, actually have adult ADHD) and 2) the possible presentation of ADHD-like symptoms from epilepsy or treatment with AEDs.