Are ADHD Screeners Safe to Use?

Lenard A. Adler, on November 8, 2018

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

Benjamin J. Lovett and Alexander H. Jordan

Rates 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.

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

Stephen V. Faraone, PhD on August 4, 2016

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.

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ADHD and Epilepsy

Lenard A. Adler, on April 16, 2015

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.


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.