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April 27, 2021
ADHD is a serious disorder that requires treatment to prevent many adverse outcomes. But, because the diagnosis of ADHD is based on how the patient responds to questions, people can pretend that they have ADHD when they do not. If you Google "fake ADHD" you'll get many pages of links, including a Psychology Today article on the topic and bloggers describing how they were able to fool doctors into giving them ADHD medications. Is fake ADHD a serious problem? Not really. The Internetseems to be faking an epidemic of fake ADHD.I say that because we have decades of research that show many objective measures of abnormality and impairment in people who say they have ADHD. These include traffic accidents, abnormalities in brain imaging, and molecular genetic differences. Some studies even suggest that ADHD adults downplay their ADHD symptoms. For example, one study diagnosed ADHD in children and then contacted them many years later when they were young adults.When they were interviewed as young adults, their responses to questions about ADHD suggested that they did not have the disorder. But when the same questions about the patient were asked to someone who lived with the patient as a young adult, it was clear that they still had ADHD. So rather than faking ADHD, many ADHD adults do not recognize that they have symptoms of the disorder. That said, we also know from research studies that, when asked to pretend that they have ADHD, adults can fake the disorder. That means that they can learn about the symptoms of the disorder and makeup examples of how they have had them when they have not. The research discussed above suggests that this is not common, but we do know that some people have motives for faking ADHD.For example, some college students seek special accommodations for taking tests; others may want stimulants for abuse, misuse, or diversion. Fortunately, doctors can detect fake ADHD in several ways. If an adult itself-referred for ADHD and asks specifically for stimulant medication, that raises the possibility of fake ADHD and drug-seeking. Because the issue of stimulant misuse has been mostly a concern on college campuses, many doctors treating college students will require independent verification of the patient's ADHD symptoms by speaking with a parent, even over the phone if an in-person visit is not possible. Using ADHD rating scales will not detect fake ADHD, and it is easy to fake poor performance on tests of reading or math ability. Neuropsychological tests can sometimes be used to detect malingering, but require referral to a specialist. Researchers are developing methods to detect faking ADHD symptoms. These have shown some utility in studies of young adults, but are not ready for clinical practice. So, currently, doctors concerned about fake ADHD should look for objective indicators of impairment (e.g., documented traffic accidents; academic performance below expectation) and speak to a parent of the patient to document that impairing symptoms of the disorder were present before the age of twelve. Because the issue of fake ADHD is of most concern on college campuses, it can also be helpful to speak with a teacher who has had frequent contact with the patient. In an era of large lecture halls and broadcast lectures, that may be difficult. And don't be fooled by the Internet. We don't want to deny treatment to ADHD patients out of undocumented reports of an epidemic of fake ADHD.
Harrison, A. G., Edwards, M. J. & Parker, K. C. (2007).Identifying students faking ADHD: Preliminary findings and strategies fordetection. Arch Clin Neuropsychol 22, 577-88.
Sansone, R. A. & Sansone, L. A. (2011). Faking attentiondeficit hyperactivity disorder. Innov Clin Neurosci 8, 10-3
Loughan, A., Perna, R., Le, J. & Hertza, J. (2014). C-88Abbreviatingthe Test of Memory Malingering: TOMM Trial 1 in Children with ADHD. Arch ClinNeuropsychol 29, 605-6.
Loughan, A. R. & Perna, R. (2014). Performance andspecificity rates in the Test of Memory Malingering: an investigation intopediatric clinical populations. Appl Neuropsychol Child 3, 26-30.
Quinn, C. A. (2003). Detection of malingering in the assessmentof adult ADHD. Arch Clin Neuropsychol 18, 379-95.
Suhr, J., Hammers, D., Dobbins-Buckland, K., Zimak, E. &Hughes, C. (2008). The relationship of malingering test failure toself-reported symptoms and neuropsychological findings in adults referred forADHD evaluation. Arch Clin Neuropsychol 23, 521-30.
Greve, K. W. & Bianchini, K. J. (2002). Using theWisconsin card sorting test to detect malingering: an analysis of thespecificity of two methods in non malingering normal and patient samples. J ClinExp Neuropsychol 24, 48-54.
Killgore, W. D. & Della Pietra, L. (2000). Using theWMS-III to detect malingering: empirical validation of the rarely missed index(RMI). J Clin Exp Neuropsychol 22, 761-71.
Ord, J. S., Greve, K. W. & Bianchini, K. J. (2008).Using the Wechsler Memory Scale-III to detect malingering in mild traumaticbrain injury. Clin Neuropsychol 22, 689-704.
Wisdom, N. M., Callahan, J. L. & Shaw, T. G.(2010). Diagnostic utility of the structured inventory of malingeredsymptomatology to detect malingering in a forensic sample. Arch ClinNeuropsychol 25, 118-25.
Antidepressants are the primary drug treatment for depressive disorders, which affect 15–20% of pregnant women. They are among the most widely prescribed medications worldwide, and their use has increased in recent decades. Understanding their reproductive safety is critical to support informed, evidence-based prescribing during pregnancy.
A new meta-analysis sheds important light on one of the most debated concerns: whether children born to mothers who took antidepressants during pregnancy face a higher risk of ADHD.
The Study:
Pooling 14 studies covering more than 14 million participants, the analysis found that prenatal antidepressant exposure was associated with a 35% higher rate of ADHD in offspring compared to no exposure. A separate look at SSRIs (the most widely prescribed class of antidepressants, including Prozac and Zoloft) across 11 studies and over four million pregnancies found an even higher apparent risk (44%) after correcting for publication bias. On the surface, these are striking numbers.
Both associations came with an important caveat: enormous variation between individual studies, a statistical red flag suggesting the results may not reflect a true underlying effect. More tellingly, the apparent risk evaporated entirely when researchers applied a more rigorous method — comparing siblings within the same family, where one child was exposed to antidepressants in the womb, and another was not.
This sibling-comparison design is particularly powerful because it automatically controls for factors that run in families: shared genes, household environment, parenting, and socioeconomic conditions. When those influences are held constant, the link between antidepressant exposure and ADHD disappears. The same pattern held for SSRIs specifically.
Two other antidepressant classes, SNRIs (serotonin norepinephrine reuptake inhibitors) and tricyclics, showed no significant association in any analysis.
“Confounding by Indication”:
The probable driver of the initial association is what researchers call confounding by indication. The very condition being treated (depression) is itself a risk factor for ADHD in offspring, independently of any medication. Mothers with more severe depression are also more likely to be prescribed antidepressants, meaning the drug and the underlying illness are difficult to disentangle in standard analyses. Sibling studies cut through this problem cleanly.
The Take-Away:
The authors concluded that the association between antidepressants and ADHD risk was non-significant across all analyses designed to account for these confounding factors. This doesn’t mean antidepressants are without any reproductive considerations, but it does suggest that ADHD risk, at least, is driven by heritable and family-level factors rather than medication exposure itself.
For clinicians and patients weighing the risks of treating or not treating depression during pregnancy, this distinction matters considerably.
Executive functions are the mental processes that allow us to plan, adapt, and follow through. This encompasses working memory, inhibitory control, cognitive flexibility, goal-directed planning, and problem-solving. In people with ADHD, weaknesses in these areas compound the disorder's core symptoms, making it substantially harder to manage complex, real-world demands.
Background:
Medication remains the frontline clinical response. Stimulant medications can meaningfully reduce both executive function deficits and ADHD symptoms, and are often combined with behavioral or psychological therapies for better overall outcomes.
Medication, however, is not entirely without risk of side effects. These risks have spurred interest in new, non-pharmacological alternatives that target the same neural pathways. One of these new therapies is Computerized Cognitive Remediation Therapy (CCRT). This therapy uses digital programs delivered via computer, tablet, or smartphone that train attention, memory, and inhibitory control through structured cognitive exercises. A key feature of many CCRT platforms is adaptive difficulty: tasks adjust in real time to match the child’s current ability, keeping training both challenging and engaging.
The Study:
Despite this promise, the evidence base in younger populations has been limited. This meta-analysis pooled results from randomized controlled trials enrolling participants under 18 who either carried an ADHD diagnosis or scored above the threshold on a validated rating scale. Comparators included no treatment (waitlist), placebo (pharmacological or psychological), or treatment as usual. The primary outcomes (overall executive function and clinical symptom severity) were assessed via questionnaires and neuropsychological testing. Studies including participants with comorbid autism, tic disorders, epilepsy, or other psychiatric conditions were excluded.
The findings were informative, but overall results were mixed. CCRT produced a small but statistically meaningful reduction in inattention symptoms across 13 studies (885 participants), with consistent results across individual trials and no evidence of publication bias. However, it had no detectable effect on hyperactivity and impulsivity (12 studies, 833 participants) or on total ADHD symptom burden (10 studies, 731 participants).
The picture was more encouraging for executive function. Nine studies (500 participants) showed small overall improvements, with specific gains in working memory (454 participants), inhibitory control (428 participants), and planning (6 studies, 335 participants). Emotional control showed no significant change (5 studies, 265 participants), nor did cognitive flexibility (4 studies, 189 participants).
The Take-Away:
Taken together, these results are modest rather than transformative, but context matters. CCRT is low-cost, digitally scalable, and carries negligible side effects. For a population where medication often comes with a significant burden of adverse reactions, even small, reliable improvements in executive function represent a meaningful clinical option.
The evidence positions CCRT not as a replacement for established treatments, but as a practical and well-tolerated addition to the therapeutic toolkit for children and adolescents with ADHD.
Methylphenidate is an effective treatment for ADHD in adults who also have bipolar disorder (BD), but it carries a potential risk of triggering manic episodes. Current guidelines therefore recommend using it only alongside mood-stabilizing medication. A new study using French nationwide claims data sought to test and extend those recommendations with greater statistical power than previous research.
The study built on findings by Viktorin et al. (2017), who observed that adults with BD not taking mood stabilizers had more than a sixfold higher risk of manic events (defined as hospitalization for mania or a new antimanic prescription) within six months of starting methylphenidate. Patients on mood-stabilizing treatment, by contrast, showed nearly half the baseline risk in the first three months. Those findings were limited, however, by small event counts (fewer than 61 manic episodes) and an effect that did not persist beyond the initial three-month window.
To build on this, researchers drew on the French National Health Data System (which is a claims database covering more than 60 million people) spanning 2008 to 2024. The final sample included 6,022 adults with BD (56% women) who had started methylphenidate. Using a self-controlled design, the study compared each patient's rate of manic events in the six months before their first methylphenidate prescription with the rate in the six months after, effectively eliminating stable individual differences as a confound.
Patients were classified as receiving continuous mood-stabilizing treatment if they had been dispensed at least two courses of specific antipsychotics (aripiprazole, olanzapine, or quetiapine) or mood stabilizers (lithium or valproate) in the nine months before starting methylphenidate, including at least one dispensation in the final six months of that window.
The results largely confirmed the earlier findings. Among the 2,745 patients not on mood stabilizers, the rate of inpatient mania diagnosis was 5.1 times higher in the first three months after starting methylphenidate, though this elevation fell to a non-significant level over the subsequent three months. Patients receiving continuous mood-stabilizing treatment showed no statistically significant change in mania risk across the full six-month post-initiation period. A formulation-specific pattern also emerged: patients without mood-stabilizing treatment had a 2.5-fold higher risk associated with extended-release methylphenidate, while no significant risk increase was seen with the immediate-release formulation or in treated patients regardless of formulation.
The authors conclude that methylphenidate at doses below 30 mg does not appear to elevate manic relapse risk when prescribed alongside mood stabilizers. The elevated risk seen in untreated patients, particularly with extended-release formulations, must be interpreted cautiously, given limited statistical power and the likelihood that it partly reflects the natural fluctuation of manic relapse over time. The authors flag this as an inherent limitation of self-controlled survival analyses when studying drug-induced mania, where temporal trends in the underlying condition can be difficult to disentangle from treatment effects.
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