The Effects of Stimulant Medications on the Sleepiness Curve of Young Men with Attention-Deficit Hyperactivity Disorder (ADHD)

The Effects of Stimulant Medications on the Sleepiness Curve of Young Men with Attention-Deficit Hyperactivity Disorder (ADHD) | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article The Effects of Stimulant Medications on the Sleepiness Curve of Young Men with Attention-Deficit Hyperactivity Disorder (ADHD) Iris Haimov, Ori Dan, Shahar Eisenstein, Kfir Asraf, Ami Cohen This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7921122/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 24 Mar, 2026 Read the published version in BMC Psychiatry → Version 1 posted 10 You are reading this latest preprint version Abstract Background The present study aimed at investigating the effects of sleep deprivation and stimulant medication (methylphenidate and amphetamine) on subjective sleepiness in young adults with ADHD, compared to individuals without ADHD. Methods Fifty-nine young men (age 18–35) of whom 39 were diagnosed with ADHD combined type (ADHD-C) and 20 without ADHD. The participants’ sleep was monitored for 5 days via actigraphy. Subsequently, the participants were kept continuously awake in a controlled environment for 25 hours (8amtill 9am the next day). Among the ADHD group, 17 participants were medicated with their regular doses of methylphenidate (n = 13) or amphetamine (n = 4) at the start of the experiment (08:00 AM) and again at midnight (00:00), while 22 were unmedicated throughout the study. The sleepiness of the participants was assessed every hour by the Karolinska Sleepiness Scale (KSS) in order to obtain the sleepiness curve of both study groups. Results Unmedicated ADHD participants reported significantly higher sleepiness throughout the protocol, especially during nighttime and early morning hours. At the end of the 25-hour wakefulness period, their KSS scores were significantly higher than both the control and medicated ADHD groups. No significant difference was found between the medicated ADHD group and controls. Additionally, 88.2% of unmedicated ADHD participants scored above 7 on the KSS (indicating extreme sleepiness), compared to 55% in controls and 36.9% in the medicated ADHD group. Conclusions Young adults with ADHD exhibit heightened vulnerability to sleep deprivation, reflected in elevated subjective sleepiness. Stimulant medications effectively attenuate sleepiness in ADHD participants, aligning their alertness levels with those of neurotypical controls. These findings support models of ADHD involving arousal dysregulation and highlight the dual therapeutic role of stimulants in managing both attentional deficits and sleep-related impairments ADHD sleepiness KSS Stimulant Medications sleep deprivation Figures Figure 1 Figure 2 Background Attention-Deficit/Hyperactivity Disorder (ADHD) is a highly prevalent, chronic neurodevelopmental disorder characterized by persistent, impairing patterns of inattention and/or hyperactivity-impulsivity, affecting an estimated 7.2% of children globally 1 , 2 . The disorder is formally recognized by three distinct clinical presentations (subtypes): Predominantly Inattentive Presentation (ADHD-PI), often associated with challenges in executive functions and organizational skills; Predominantly Hyperactive-Impulsive Presentation (ADHD-HI); and the Combined Presentation (ADHD-C), which represents the most common form 3 , 4 . The etiology of ADHD is fundamentally multifactorial, underpinned by a highly polygenic architecture; recent large-scale genome-wide association studies (GWAS) have identified 27 independent risk loci, firmly establishing genetics as the primary risk factor 5 , 6 . This genetic vulnerability impacts core brain regions, such as the prefrontal cortex, basal ganglia, and cerebellum, and is strongly linked to dopaminergic and noradrenergic system dysfunction, which supports the long-standing dopamine hypothesis 7 , 8 . Sleep disturbance is a pervasive comorbidity in Attention-Deficit/Hyperactivity Disorder (ADHD), often contributing to a more severe clinical presentation across the lifespan. Both children and adolescents with ADHD exhibit notable sleep discontinuity, characterized by increased sleep-onset latency and greater nocturnal movements compared to neurotypical peers 9 , 10 . This association extends into adulthood, with numerous systematic reviews confirming that adults with ADHD report significantly poorer sleep quality and greater sleep-onset latency across both subjective and objective (actigraphic) measures 11 , 12 . Crucially, these nocturnal deficits translate into impaired daytime functioning, manifesting as excessive daytime sleepiness (EDS) or a state of hypoarousal, which is considered by some to be a core physiological feature, particularly in children 13 . Among adults, this daytime sleepiness significantly mediates the relationship between ADHD symptom severity and deficits in cognitive performance, suggesting that sleep-related impairment acts as a key contributing factor to executive dysfunction and overall functional outcomes 14 . The Karolinska Sleepiness Scale (KSS) is a widely utilized, single-item, nine-point ordinal rating scale designed to provide a rapid, subjective assessment of an individual’s immediate sleepiness level. Originally developed and introduced by Åkerstedt and Gillberg 15 , the scale ranges from 1 ("extremely alert") to 9 ("very sleepy, fighting sleep"). The KSS is particularly valued for its high temporal resolution, reflecting moment-to-moment fluctuations in alertness, making it highly effective for measuring sleepiness during sleep deprivation protocols and shift-work simulations 15 . Furthermore, the scale has undergone rigorous validation, demonstrating a robust correlation with objective measures of central nervous system alertness, including electroencephalography (EEG) indicators (e.g., theta/alpha power) and impaired performance on vigilance tasks 16 . Its validity, simplicity, and sensitivity to acute changes in wakefulness have cemented its status as a standard tool in both clinical sleep research and occupational health studies. In our previous study, we investigated the "sleepiness curve" of young adult males (aged 18–30) with combined-type Attention-Deficit/Hyperactivity Disorder (ADHD-C) during 25 hours of continuous wakefulness, aiming to determine their vulnerability to fatigue compared to neurotypical controls 17 . Although objective baseline sleep measures via actigraphy did not reveal significant differences in total sleep time or efficiency between the groups, the hourly assessments using the Karolinska Sleepiness Scale (KSS) demonstrated a significantly elevated subjective sleepiness curve in the ADHD group throughout the sleep deprivation protocol. Crucially, this difference was most pronounced during the night and early morning hours, specifically between 1:00 a.m. and 9:00 a.m., the period associated with maximal homeostatic sleep drive and circadian misalignment. These findings suggest that young adults with ADHD-C exhibit a lower threshold for subjective fatigue when facing extended wakefulness, lending empirical support to the hypoarousal model by indicating a fundamental difference in central nervous system alertness regulation 17 . Pharmacological treatments are a foundational component of ADHD management across childhood, adolescence, and adulthood, demonstrating both efficacy and tolerability. Stimulant medications, primarily methylphenidate and amphetamines, remain the most effective and commonly prescribed agents, showing robust symptom reduction across age groups 11 , 18 . These medications often exert their benefits by enhancing dopaminergic and noradrenergic activity in the brain, mechanisms closely tied to increased wakefulness and alertness throughout the day. For individuals who are unresponsive to or cannot tolerate stimulants, non-stimulant medications such as atomoxetine and guanfacine provide alternative options, albeit with somewhat lower efficacy profiles 11 , 18 . In adolescents, pharmacotherapy has been shown to improve not only core symptoms but also broader quality-of-life domains when treatment adherence is maintained 19 , 20 . Importantly, medication effects on quality of life appear to vary by age and subtype, with early and individualized intervention showing the greatest benefits. These findings underscore the importance of tailoring pharmacological strategies to developmental stage and patient-specific needs. The present study aims to examine whether pharmacological treatment for ADHD modulates alertness levels across an extended period of wakefulness. Specifically, the research compares three groups: individuals with ADHD receiving medication, individuals with ADHD not receiving medication, and neurotypical controls without ADHD. Participants in all groups were monitored for 25 consecutive hours of wakefulness under controlled conditions, with repeated assessments of subjective alertness. We hypothesized that the medicated ADHD group would exhibit alertness levels comparable to the control group and significantly higher than the unmedicated ADHD group. Methods Participants The present study included 59 male participants aged 18–35 years (Mean: 25.46, SD: 4.37). Thirty-nine participants were diagnosed with ADHD-C, and 20 served as controls without ADHD. Among the ADHD group, 17 participants were medicated with their regular doses of methylphenidate (n = 13) or amphetamine (n = 4) at the start of the experiment (08:00 AM) and again at midnight (00:00), while 22 were unmedicated throughout the study. The sample size calculation was based on a small-to-medium effect size (η² = 0.04), with α = 0.05 and a power of 0.95 to detect an effect if present. For a design involving three groups and 25 repeated measures, the minimum required sample size was N = 48, meaning at least 16 participants per group Inclusion in the ADHD groups required: (a) a formal clinical diagnosis of ADHD made by a licensed neurologist or psychiatrist; (b) endorsement of at least six inattention and six hyperactivity–impulsivity symptoms on the ADHD Rating Scale-IV 21 ; and (c) fulfillment of DSM-IV diagnostic criteria for ADHD in the adapted Diagnostic Interview Schedule for Children (DISC-IV) 22 . Participants in the control group met the following criteria: (a) no prior ADHD diagnosis, (b) fewer than four symptoms in either the inattention or hyperactivity–impulsivity subscales, and (c) non-fulfillment of DSM-IV criteria for ADHD based on the clinical interview. Exclusion criteria for all groups included: (a) presence of any psychopathology according to the Symptom Checklist-90 (SCL-90; Derogatis., 1994) as assessed by a licensed clinical psychologist; (b) employment involving night shifts; or (c) use of medications affecting the central nervous system other than ADHD medication. All participants were male to minimize potential variability associated with menstrual cycle effects on sleep quality 23 . Participants were recruited through snowball sampling via advertisements on social media and received a monetary voucher equivalent to approximately $ 125 for their participation. Written informed consent was obtained from all participants. The Max Stern Yezreel Valley College Institutional Ethics Review Board approved the complete study protocol (approval number: EMEK YVC 2019-23). Measures Demographic Questionnaire Collected data on age, occupation and health, as well as tobacco smoking status (Yes/No), alcohol use (Yes/No) and medication use. ADHD Rating Scale–IV 21 is an 18-item questionnaire for the assessment of ADHD. The items are based on the symptoms listed in the DSM–IV for ADHD diagnosis, including 9 items assessing attentiveness and 9 items assessing hyperactivity and impulsivity. In the version used in the current study 24 , participants were asked to choose whether each described symptom was correct or incorrect with respect to them. The internal consistency (Cronbach’s α) of the attentiveness section and the hyperactivity-impulsivity section of the scale in the current study were 0.82 and 0.87, respectively. Structured Clinical Interview A modified version of the ADHD module from the DISC 22 was administered in order to determine suitability to the ADHD classification. The modified interview is similar to other interviews that assess ADHD in adulthood 25 , and it yields clinician-assessed symptom counts for inattentive and hyperactive-impulsive ADHD symptoms. Internal consistency (Cronbach’s α = 0.86–0.94) was consistent with prior studies. The Symptom Checklist–90–Revised (SCL-90-R 26 ): A 90-item self-report inventory assessing psychological symptoms across nine domains. Items were rated on a 0–4 Likert scale, with higher scores indicating greater distress. The internal consistency (Cronbach’s α) of the Hebrew translation of the SCL-90-R was found to be within the range of .71–.85 27 . An expert clinical psychologist examined the responses of each participant on the SCL-90-R to rule out any psychological disorder. Pittsburgh Sleep Quality Index (PSQI 28 ): A 18-item self-report questionnaire assessing seven components of sleep quality (Subjective Sleep Quality, Sleep Latency, Sleep Duration, Sleep Efficiency, Sleep Disturbance, Hypnotic Medication Use, Daytime Dysfunction) over the past month. The seven component scores are then totaled to provide a global PSQI score. The internal consistency (Cronbach’s α) of the Hebrew translation of the PSQI in the current study was .73. Karolinska Sleepiness Scale (KSS 15 ): A scale measuring subjective sleepiness at a given time. The participant is required to rate his level of sleepiness over the last 10 min on a 9-point Likert scale ranging from 1 (“extremely alert”) to 9 (“extremely sleepy, fighting sleep”). Actigraphy : The actigraph (Mini Motionlogger, Ambulatory Monitoring Inc., New York) is a wrist-worn ambulatory, noninvasive device designed for studies in naturalistic settings with minimal distortions. The actigraph measures wrist movements utilizing a piezoelectric element and translates them into 1-minlong epochs of sleep and wake. To that end, wrist activity levels were sampled at 10-s intervals and summed across 1-min intervals. Actigraphic raw data were translated to sleep measures using the Actigraphic Scoring Analysis program for an IBM-compatible personal computer (W2 scoring algorithm) provided by the manufacturer. Four measures of sleep were obtained: total sleep time (minutes of sleep from intended bedtime to final wake time), sleep onset latency (minutes to fall asleep from bedtime), sleep efficiency (percentage of total sleep time between falling asleep and final awakening), and wake time after sleep onset (WASO; total number of wake minutes after sleep onset). The daily actigraphy data of each subject were averaged over the five days of actigraph use in order to obtain aggregated measures that reliably characterize individuals. The participants were instructed to press a button on the actigraph when they began trying to fall asleep and when they woke up the following morning. The first button-press was used to determine bedtime and the second was used to determine wake time. For the purpose of precise analysis of the actigraph data, over the course of actigraphic recording participants were instructed to complete the Consensus Sleep Diary that included intended bedtime, initial and final wake times, number of awakenings, and lengths of awakenings. Procedure Eligible participants were provided with an actigraph device five days prior to the laboratory session and instructed to wear it continuously for five nights while completing daily evening/morning sleep diaries. They were asked to sleep at least seven hours per night to avoid prior sleep deprivation. On the experimental day, participants were collected from their homes at 07:00 AM and transported to the laboratory, where the experiment began at 08:00 AM. Actigraphy data from the previous five nights were verified to ensure compliance with sleep requirements. Participants who had slept less than seven hours per night were excluded. After completing baseline questionnaires on demographics and sleep quality (PSQI), participants remained awake for approximately 25 consecutive hours under constant supervision to prevent unintended sleep. Among the ADHD group, 17 participants were medicated with their regular doses of methylphenidate (n = 13) or amphetamine (n = 4) at the start of the experiment (08:00 AM) and again at midnight (00:00), while 22 were unmedicated throughout the study. Subjective sleepiness was recorded hourly using the KSS. Food and non-caffeinated beverages were provided ad libitum. Upon completion of the 25-hour sleep deprivation protocol, participants were thanked, debriefed, and transported home. Data Analysis Data were analyzed using Jamovi version 2.5.6. Age and PSQI scores (subjective sleep quality) were compared across groups using one-way Analysis of Variance, (ANOVA). The proportion of alcohol users and smokers were compared across groups using χ2 test. Actigraphy-derived sleep variables (e.g., total sleep time, sleep latency, WASO, sleep efficiency) were compared across groups using the non-parametric Kruskal–Wallis test due to non-normal data distribution. When significant differences emerged, beta regression analyses were conducted to identify predictors of sleep efficiency. Subjective sleepiness (KSS) was analyzed using a linear mixed-effects model, with group (control/ADHD unmedicated/ADHD medicated) and time (25 hours) as fixed effects, and participant as a random effect. Additionally, a logistic regression analysis examined the probability of reporting a KSS score > 7 at the end of the deprivation period as a function of group membership, to assess the impact of ADHD medication on subjective sleepiness under sleep deprivation conditions. Results The study groups did not differ in age or the proportion of tobacco smokers and alcohol users (Table 1 ). Group differences in sleep variables measured via the PSQI (global scores) and actigraphy were examined (Table 2 ). No significant differences were found among the three groups in the PSQI scores (subjective sleep quality). In relation to actigraphy-measures sleep variables, no significant differences were found between the groups in total sleep duration [χ 2 (2) = 0.39, p = .822, [ sleep onset latency [χ 2 (2) = 2.98, p = .224], or WASO [χ 2 (2) = 3.95, p = .138]. However, a significant difference was found in sleep efficiency [χ 2 (2) = 7.77, p = .020]. Post-hoc analyses revealed that the control group had significantly higher sleep efficiency (M = 0.95, SD = 0.01) compared to both the ADHD group without medication (M = 0.91, SD = 0.01; Z = 2.28, p = .044) and the ADHD group with medication (M = 0.90, SD = 0.01; Z = 2.69, p = .020). No significant difference was found between the two ADHD groups (Z = 0.43, p = .662). Pearson correlations between the average sleep efficiency, as measured during the week preceding the experimental trial and the level of subjective sleepiness as measured by the KSS at the beginning of the trial ( r = -0.05, p = .71) and at its end (e.g., following sleep deprivation; r = -0.05, p = .697) were not significant. Thus, sleep efficiency was not controlled for in subsequent sleepiness analyses. Table 1 Demographic Data by Group Measure Control ADHD ADHD + Medication Test Statistic Age Mean = 26.62 SD = 4.17 Mean = 24.67 SD = 5.22 Mean = 25.05 SD = 3.39 F (2,53) = 1.17 p = .315 % Of Smokers 19.05 31.58 5.26 χ 2 (2) = 4.34 p = .114 % Of Alcohol Users 42.86 47.37 73.68 χ 2 (2) = 4.35 p = .114 Table 2 Subjective Sleep (PSQI scores) and Actigraphy-Based Sleep Measures by Group Measure Control ADHD ADHD + Medication Test Statistic PSQI Mean = 3.90 SD = 2.90 Mean = 5.58 SD = 3.02 Mean = 5.0 SD = 2.55 F (2,53) = 1.76 p = .182 Sleep Duration (min) Med = 417 IQR = 409 ,474 Med = 424 IQR = 372 ,457 Med = 433 IQR = 372 ,459 χ 2 (2) = 0.39 p = .822 Sleep Latency (min) Med = 9 IQR = 7.5 ,30 Med = 13.75 IQR = 5.8 ,35.2 Med = 7.5 IQR = 5.4 ,12.5 χ 2 (2) = 2.98 p = .224 WASO (min) Med = 15 IQR = 5 ,20 Med = 20.4 IQR = 14.2 ,42.6 Med = 17.8 IQR = 9.7 ,28.5 χ 2 (2) = 3.95 p = .138 Sleep Efficiency M = 0.95 SD = 0.01 M = 0.91 SD = 0.01 M = 0.90 SD = 0.01 χ 2 (2) = 7.77 p = .020 Note: WASO: Wake After Sleep Onset; PSQI: Pittsburgh Sleep Quality Index (subjective sleep quality) Subjective Sleepiness (KSS) Over Time A linear mixed model was used to test the hypothesis that group and time interact to affect subjective sleepiness (KSS) over the 25-hour study period, and particularly following sleep deprivation. Time and group served as independent variables while participants were treated as a random variable. The random variable (σ 2 Intercept = 1.84, 95% C.I.= 1.13,1.65, ICC = 0.48) was significant (LRT = 760.70, p < .001). The model explained 66.29% of the variance (R 2 Conditional ), with the independent variables accounting for 35.18% (R 2 Marginal ). A significant interaction between time and group was found [F (48,1392.08) = 2.14, p < .001] (see Fig. 1 ). Post-hoc comparisons on the KSS scores at the end point of the study (i.e., following 25 hours of sustained wakefulness) demonstrated that while there was no difference [ t (225.45) = -0.77, p = .437] between the control group ( M = 6.70, SE = 0.43) and the ADHD + medication group ( M = 6.21, SE = 0.45), the ADHD group ( M = 8.42, SE = 0.45) reported significantly higher sleepiness than both the control group ( t (245.48) = − 2.70, p = .007) and the ADHD + medication group ( t (244.96) = − 3.43, p < .001). A second linear mixed model tested the hypothesis that from 1:00 AM onward, the ADHD group would report higher sleepiness than the control and the ADHD + medication group, with no difference between the latter two groups. Group was the independent variable, and the participants were the random variable. The random variable (σ 2 Intercept = 2.65, 95% C.I.= 1.34,2.00, ICC = 0.54) was significant (LRT = 221.7, p < .001). The model explained 57.83% of the variance (R 2 Conditional ), with Group accounting for 8.25% (R 2 Marginal ). A significant group effect was found [ (2,58.95) = 4.49, p = .015]. Post-hoc comparisons demonstrated that while there was no difference [ t (58.60) = 0.81, p = .419] between the control group ( M = 6.01, SE = 0.38) and the ADHD + medication group ( M = 5.57, SE = 0.39), the ADHD group ( M = 7.16, SE = 0.38) reported significantly higher sleepiness than both the control group ( t (59.14) = − 2.11, p = .039) and the ADHD + medication group ( t (59.12) = 2.89, p = .005). As KSS scores greater than 7 indicate extreme sleepiness with substantial difficulty remaining awake, A logistic regression tested group differences in the proportion of participants with KSS > 7 at the end of the study. The model was significant [ χ 2 (2) = 10.98, p = .004, R 2 McFadden = .0145]. It has been revealed that while the proportion of participants with KSS > 7 at the end of the study was 55.0% in the control group, it reached 88.2% in the ADHD group (see Fig. 2 ), a difference that was statistically significant ( Z = -2.07, p = .038). In the ADHD + medication group the proportion was 36.9%, significantly lower than ADHD without medication ( Z = 2.86, p = .004), and not significantly different from control ( Z = 1.13, p = .258). Discussion This study investigated the effects of sleep deprivation and stimulant medication (methylphenidate and amphetamine) on subjective sleepiness in young adults with ADHD, compared to individuals without ADHD. Subjective sleepiness was assessed hourly over a 25-hour experimental session using the Karolinska Sleepiness Scale (KSS). The findings support the study’s hypotheses: participants with ADHD exhibited significantly higher levels of sleepiness throughout the experiment, particularly following 25 hours of sleep deprivation. Notably, medicated ADHD participants and control participants did not differ significantly in their sleepiness levels. The observation that unmedicated individuals with ADHD experienced elevated sleepiness during sustained wakefulness, especially overnight and into the following morning, replicates our previous findings 17 and aligns with studies reporting excessive daytime sleepiness in both children and adults with ADHD 29 – 32 . However, our studies are among the first to systematically compare sleepiness levels throughout the day between individuals with ADHD and the general population. The sleepiness trajectory observed in the control group mirrored patterns reported in prior KSS-based studies 33 , 34 , with relatively stable levels from morning to evening followed by a gradual increase along the night. In contrast, participants with ADHD showed a significantly steeper rise in sleepiness during the night and subsequent morning. This was further reflected in the proportion of participants scoring above 7 on the KSS the morning after sleep deprivation, 88.2% in the ADHD group versus 55% in the control group, indicating heightened vulnerability to sleep deprivation among individuals with ADHD. The differences in sleepiness in the current study between the control participants and the non-medicated ADHD participants cannot be attributed to psychiatric comorbidities that are commonly associated with ADHD 35 as individuals suffering from such psychopathologies were excluded from the study. They also cannot be explained by the tendency of ADHD patients to exhibit lower sleep quantity and quality 36 – 39 . First, the study included only individuals without diagnosed sleep disorders and the participants were instructed to maintain a minimum of seven hours of sleep for nights prior to the experimental trial. Second, actigraphy data collected along these nights revealed that the study groups did not differ in total sleep duration or sleep onset latency. Although sleep efficiency was higher in the control group compared to the unmedicated ADHD group this difference likely did not account for the differences in subjective sleepiness as there were no significant correlation between sleep efficiency and the KSS scores at either the beginning of the experimental trial or its end. These findings are consistent with prior research suggesting that increased sleepiness in ADHD is not solely due to sleep disturbances 29 , 40 . Taken together, these findings support the notion that sleep deprivation exacerbates sleepiness in individuals with ADHD, indicating increased vulnerability to fatigue in this population. Stimulant medications, particularly methylphenidate and amphetamines, are the first-line treatment for ADHD 41 . The current findings demonstrate that these medications not only improve attention and reduce hyperactivity but also normalize subjective sleepiness levels in individuals with ADHD, making them comparable to those of non-ADHD participants. This is consistent with previous research indicating that stimulants can reduce daytime sleepiness 42 , 43 . The findings underscore the importance of considering sleep-related factors in both the theoretical understanding and clinical management of ADHD. From a theoretical perspective, these findings support to models that conceptualize ADHD as involving dysregulation in arousal and sleep systems, in addition to cognitive and behavioral symptoms. Pharmacologically, methylphenidate and amphetamine enhance central dopamine and norepinephrine activity by inhibiting their respective transporters 44 . Given their dual efficacy in reducing ADHD symptoms 45 , 46 and sleepiness, it is plausible that dysregulation in these neurotransmitter systems underlies both domains 38 . Although the impact of stimulants on sleepiness may be independent of their cognitive effects, prior research has shown a positive correlation between daytime sleepiness and inattentiveness in ADHD 47 , suggesting that improvements in attention may be partially mediated by reductions in sleepiness. However, this intriguing hypothesis warrants further empirical investigation. Clinically, the study highlights the dual role of stimulant medications - not only in improving attention and reducing hyperactivity but also in alleviating daytime sleepiness, particularly under conditions of sleep deprivation. However, it is important to note that the impact of stimulant medication on sleep is complex 48 , 49 . Some studies report adverse effects when stimulants are taken late in the day, including increased sleep latency and reduced sleep efficiency 49 – 52 . Therefore, clinicians should monitor sleep patterns and adjust medication timing and dosage to optimize therapeutic outcomes while minimizing sleep-related side effects. Interpretation of the present findings should be viewed in light of a few limitations. First, due to constraints imposed by the experimental design, the study sample was limited to young adult males (ages 18–30) in order to minimize variability and enhance statistical power 23 . Consequently, the generalizability of the findings to females and other age groups remains limited and warrants further investigation in future research. Second, since all ADHD participants in the current study were of the combined subtype (ADHD-C) and did not present with any psychiatric comorbidities, the applicability of these findings to individuals with other ADHD subtypes or those with co-occurring psychiatric conditions remains uncertain. Third, the experiment was conducted in a controlled laboratory setting, which may not reflect real-world conditions where environmental factors vary widely. Finally, the extreme sleep deprivation protocol (25 hours) represents an atypical scenario that may elicit exaggerated behavioral and cognitive responses. Conclusions This study provides empirical support for the heightened vulnerability of individuals with ADHD to the effects of sleep deprivation on sleepiness. The stimulant medications methylphenidate and amphetamine were shown to effectively attenuate sleepiness in ADHD participants, aligning their wakefulness levels with those of non-ADHD controls. These findings highlight the dual therapeutic role of stimulants in managing both attentional deficits and sleep-related vulnerabilities in ADHD. Abbreviations ADHD Attention-Deficit Hyperactivity Disorder ADHD - C Combined Type Attention-Deficit Hyperactivity Disorder ADHD - PI Predominantly Inattentive Attention-Deficit Hyperactivity Disorder ADHD - HI Predominantly Hyperactive-Impulsive Attention-Deficit Hyperactivity Disorder DISC Diagnostic Interview Schedule for Children DSM-IV Diagnostic and Statistical Manual of Mental Disorders, 4th Edition EEG Electroencephalography EDS Excessive Daytime Sleepiness KSS Karolinska Sleepiness Scale PSQI Pittsburgh Sleep Quality Index SCL-90 Symptom Checklist-90 WASO Wake After Sleep Onset Declarations Ethics approval and consent to participate The study was approved by the Max Stern Yezreel Valley College Institutional Ethics Review Board (Reference: EMEK YVC 2019-23). All participants provided informed consent to participate in the study. Clinical trial number not applicable Competing interests The authors declare that they have no competing interests Consent for publication Not applicable Funding This work was supported by the Max Stern Yezreel Valley College, Emek Yezreel, Israel. The funder had no role in the conceptualization, design, data collection, analysis, decision to publish, or preparation of the manuscript Author Contribution IH conceived of the study, participated in its design, data interpretation and writing the original draft; AC conceived of the study, participated in its design and data analysis, and led write-up of the manuscript; OD conceived and supervised statistical analyses and revised the original draft of the manuscript; SE conceived of the study, participated in its design, supervised data collection and participated in writing the original draft. KA performed statistical analysis, supervised data collection and participated in data curation and coordination. 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Epstein JN, Johnson D, Conners CK. Conners’s Adult ADHD Diagnostic Interview for DSM–IV. North Tonawanda, NY: Multi-Health Systems; 2000. Derogatis LR. Symptom Checklist-90-R: Administration, scoring & procedure manual for the revised version of the SCL-90. Minneapolis, MN: National Computer Systems; 1994. Ben Arzi N, Solomon Z, Dekel R. Secondary traumatization among wives of PTSD and post-concussion casualties: distress, caregiver burden and psychological separation. Brain Inj. 2000;14(8):725–36. 10.1080/026990500413759 . Buysse DJ, Reynolds CF 3rd, Monk TH, Berman SR, Kupfer DJ. The Pittsburgh Sleep Quality Index: a new instrument for psychiatric practice and research. Psychiatry Res. 1989;28(2):193–213. 10.1016/0165-1781(89)90047-4 . Golan N, Shahar E, Ravid S, Pillar G. Sleep disorders and daytime sleepiness in children with attention-deficit/hyperactive disorder. Sleep. 2004;27(2):261–6. 10.1093/sleep/27.2.261 . LeBourgeois MK, Avis K, Mixon M, Olmi J, Harsh J. Snoring, sleep quality, and sleepiness across attention-deficit/hyperactivity disorder subtypes. Sleep. 2004;27(3):520–5. Philip P, Micoulaud-Franchi JA, Lagarde E et al. Attention Deficit Hyperactivity Disorder Symptoms, Sleepiness and Accidental Risk in 36140 Regularly Registered Highway Drivers. PLoS One . 2015;10(9):e0138004. Published 2015 Sep 16. 10.1371/journal.pone.0138004 Surman CB, Adamson JJ, Petty C, et al. Association between attention-deficit/hyperactivity disorder and sleep impairment in adulthood: evidence from a large controlled study. J Clin Psychiatry. 2009;70(11):1523–9. 10.4088/JCP.08m04514 . Akerstedt T, Anund A, Axelsson J, Kecklund G. Subjective sleepiness is a sensitive indicator of insufficient sleep and impaired waking function. J Sleep Res. 2014;23(3):240–52. 10.1111/jsr.12158 . Kaida K, Åkerstedt T, Takahashi M, Vestergren P, Gillberg M, Lowden A, Kecklund G, Portin C. Performance prediction by sleepiness-related subjective symptoms during 26-hour sleep deprivation. Sleep Biol Rhythms. 2008;6(4):234–41. 10.1111/j.1479-8425.2008.00367.x . Kessler RC, Adler L, Barkley R, et al. The prevalence and correlates of adult ADHD in the United States: results from the National Comorbidity Survey Replication. Am J Psychiatry. 2006;163(4):716–23. 10.1176/ajp.2006.163.4.716 . Bartholomew K, Owens J. Sleep and ADHD: a review. Med Health R I. 2006;89(3):91–3. Hysing M, Lundervold AJ, Posserud MB, Sivertsen B. Association Between Sleep Problems and Symptoms of Attention Deficit Hyperactivity Disorder in Adolescence: Results From a Large Population-Based Study. Behav Sleep Med. 2016;14(5):550–64. 10.1080/15402002.2015.1048448 . Owens J, Gruber R, Brown T, et al. Future research directions in sleep and ADHD: report of a consensus working group. J Atten Disord. 2013;17(7):550–64. 10.1177/1087054712457992 . Zak R, Fisher B, Couvadelli BV, Moss NM, Walters AS. Preliminary study of the prevalence of restless legs syndrome in adults with attention deficit hyperactivity disorder. Percept Mot Skills. 2009;108(3):759–63. 10.2466/PMS.108.3.759-763 . Mayes SD, Calhoun SL, Bixler EO, et al. ADHD subtypes and comorbid anxiety, depression, and oppositional-defiant disorder: differences in sleep problems. J Pediatr Psychol. 2009;34(3):328–37. 10.1093/jpepsy/jsn083 . Silczuk A, Lewandowska A, Filip M, et al. Current insights into the safety and adverse effects of methylphenidate in children, adolescents, and adults - narrative review. Pharmacol Rep. 2025;77(5):1247–59. 10.1007/s43440-025-00763-0 . Banerjee D, Vitiello MV, Grunstein RR. Pharmacotherapy for excessive daytime sleepiness. Sleep Med Rev. 2004;8(5):339–54. 10.1016/j.smrv.2004.03.002 . Dodd S, Ospina-Pinillos L, Markowitz JS. Central nervous system stimulants in recreational and medical use. CNS Spectr. 2025;30(1):e52. 10.1017/S1092852925100357 . Published 2025 Jul 14. Faraone SV. The pharmacology of amphetamine and methylphenidate: Relevance to the neurobiology of attention-deficit/hyperactivity disorder and other psychiatric comorbidities. Neurosci Biobehav Rev. 2018;87:255–70. 10.1016/j.neubiorev.2018.02.00 . Morgenthaler TI, Kapur VK, Brown T, et al. Practice parameters for the treatment of narcolepsy and other hypersomnias of central origin. Sleep. 2007;30(12):1705–11. 10.1093/sleep/30.12.1705 . Spencer TJ, Adler LA, McGough JJ, et al. Efficacy and safety of dexmethylphenidate extended-release capsules in adults with attention-deficit/hyperactivity disorder. Biol Psychiatry. 2007;61(12):1380–7. 10.1016/j.biopsych.2006.07.032 . Lecendreux M, Konofal E, Bouvard M, Falissard B, Mouren-Siméoni MC. Sleep and alertness in children with ADHD. J Child Psychol Psychiatry. 2000;41(6):803–12. Snitselaar MA, Smits MG, van der Heijden KB, Spijker J. Sleep and Circadian Rhythmicity in Adult ADHD and the Effect of Stimulants. J Atten Disord. 2017;21(1):14–26. 10.1177/1087054713479663 . Zhu F, Liu B, Kuang D, et al. The association between physical activity and sleep in adult ADHD patients with stimulant medication use. Front Psychiatry. 2023;14:1236636. 10.3389/fpsyt.2023.1236636 . Published 2023 Nov 20. Fredriksen M, Halmøy A, Faraone SV, Haavik J. Long-term efficacy and safety of treatment with stimulants and atomoxetine in adult ADHD: a review of controlled and naturalistic studies. Eur Neuropsychopharmacol. 2013;23(6):508–27. 10.1016/j.euroneuro.2012.07.016 . Mattingly GW, Childress AC, Cutler AJ, Estrada J, Corliss M. Serdexmethylphenidate/dexmethylphenidate effects on sleep in children with attention-deficit/hyperactivity disorder. Front Psychiatry. 2023;14:1193455. 10.3389/fpsyt.2023.1193455 . Published 2023 Jun 23. Rao R, Tripathi R. Stimulants and sleep. In Sleep and neuropsychiatric disorders 2022 Feb 1 (pp. 811–33). Singapore: Springer Nature Singapore. 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1","display":"","copyAsset":false,"role":"figure","size":364370,"visible":true,"origin":"","legend":"\u003cp\u003eSleepiness scores as measured by the Karlinska Sleepiness Scale (KSS) each hour during 25 hr of the experimental session.\u003c/p\u003e","description":"","filename":"floatimage1.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-7921122/v1/57c7aee49d0659aa53a47b10.jpeg"},{"id":96051173,"identity":"e61e51c5-b5c1-419c-8fca-ec6bafb3838e","added_by":"auto","created_at":"2025-11-17 06:39:50","extension":"jpeg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":131283,"visible":true,"origin":"","legend":"\u003cp\u003ePercentage of participants reporting KSS above 7. *P \u0026lt; .05 in comparison to the control group.\u003c/p\u003e","description":"","filename":"floatimage2.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-7921122/v1/8bfb522bfea6f41f9bb575ed.jpeg"},{"id":105755942,"identity":"c3a302b1-1ab2-4844-a49e-8c8ceda0ed48","added_by":"auto","created_at":"2026-03-30 16:33:19","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1252340,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-7921122/v1/6657689f-9653-4328-b8b5-4576027c9b04.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"The Effects of Stimulant Medications on the Sleepiness Curve of Young Men with Attention-Deficit Hyperactivity Disorder (ADHD)","fulltext":[{"header":"Background","content":"\u003cp\u003eAttention-Deficit/Hyperactivity Disorder (ADHD) is a highly prevalent, chronic neurodevelopmental disorder characterized by persistent, impairing patterns of inattention and/or hyperactivity-impulsivity, affecting an estimated 7.2% of children globally\u003csup\u003e\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e,\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e. The disorder is formally recognized by three distinct clinical presentations (subtypes): Predominantly Inattentive Presentation (ADHD-PI), often associated with challenges in executive functions and organizational skills; Predominantly Hyperactive-Impulsive Presentation (ADHD-HI); and the Combined Presentation (ADHD-C), which represents the most common form\u003csup\u003e\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e,\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e\u003c/sup\u003e. The etiology of ADHD is fundamentally multifactorial, underpinned by a highly polygenic architecture; recent large-scale genome-wide association studies (GWAS) have identified 27 independent risk loci, firmly establishing genetics as the primary risk factor\u003csup\u003e\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e,\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e\u003c/sup\u003e. This genetic vulnerability impacts core brain regions, such as the prefrontal cortex, basal ganglia, and cerebellum, and is strongly linked to dopaminergic and noradrenergic system dysfunction, which supports the long-standing dopamine hypothesis\u003csup\u003e\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e,\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003eSleep disturbance is a pervasive comorbidity in Attention-Deficit/Hyperactivity Disorder (ADHD), often contributing to a more severe clinical presentation across the lifespan. Both children and adolescents with ADHD exhibit notable sleep discontinuity, characterized by increased sleep-onset latency and greater nocturnal movements compared to neurotypical peers\u003csup\u003e\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e,\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e\u003c/sup\u003e. This association extends into adulthood, with numerous systematic reviews confirming that adults with ADHD report significantly poorer sleep quality and greater sleep-onset latency across both subjective and objective (actigraphic) measures\u003csup\u003e\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e,\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e\u003c/sup\u003e. Crucially, these nocturnal deficits translate into impaired daytime functioning, manifesting as excessive daytime sleepiness (EDS) or a state of hypoarousal, which is considered by some to be a core physiological feature, particularly in children\u003csup\u003e\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e\u003c/sup\u003e. Among adults, this daytime sleepiness significantly mediates the relationship between ADHD symptom severity and deficits in cognitive performance, suggesting that sleep-related impairment acts as a key contributing factor to executive dysfunction and overall functional outcomes\u003csup\u003e\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003eThe Karolinska Sleepiness Scale (KSS) is a widely utilized, single-item, nine-point ordinal rating scale designed to provide a rapid, subjective assessment of an individual\u0026rsquo;s immediate sleepiness level. Originally developed and introduced by \u0026Aring;kerstedt and Gillberg\u003csup\u003e\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e\u003c/sup\u003e, the scale ranges from 1 (\"extremely alert\") to 9 (\"very sleepy, fighting sleep\"). The KSS is particularly valued for its high temporal resolution, reflecting moment-to-moment fluctuations in alertness, making it highly effective for measuring sleepiness during sleep deprivation protocols and shift-work simulations\u003csup\u003e\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e\u003c/sup\u003e. Furthermore, the scale has undergone rigorous validation, demonstrating a robust correlation with objective measures of central nervous system alertness, including electroencephalography (EEG) indicators (e.g., theta/alpha power) and impaired performance on vigilance tasks\u003csup\u003e\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e\u003c/sup\u003e. Its validity, simplicity, and sensitivity to acute changes in wakefulness have cemented its status as a standard tool in both clinical sleep research and occupational health studies.\u003c/p\u003e\u003cp\u003eIn our previous study, we investigated the \"sleepiness curve\" of young adult males (aged 18\u0026ndash;30) with combined-type Attention-Deficit/Hyperactivity Disorder (ADHD-C) during 25 hours of continuous wakefulness, aiming to determine their vulnerability to fatigue compared to neurotypical controls\u003csup\u003e\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e\u003c/sup\u003e. Although objective baseline sleep measures via actigraphy did not reveal significant differences in total sleep time or efficiency between the groups, the hourly assessments using the Karolinska Sleepiness Scale (KSS) demonstrated a significantly elevated subjective sleepiness curve in the ADHD group throughout the sleep deprivation protocol. Crucially, this difference was most pronounced during the night and early morning hours, specifically between 1:00 a.m. and 9:00 a.m., the period associated with maximal homeostatic sleep drive and circadian misalignment. These findings suggest that young adults with ADHD-C exhibit a lower threshold for subjective fatigue when facing extended wakefulness, lending empirical support to the hypoarousal model by indicating a fundamental difference in central nervous system alertness regulation\u003csup\u003e\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003ePharmacological treatments are a foundational component of ADHD management across childhood, adolescence, and adulthood, demonstrating both efficacy and tolerability. Stimulant medications, primarily methylphenidate and amphetamines, remain the most effective and commonly prescribed agents, showing robust symptom reduction across age groups\u003csup\u003e\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e,\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e\u003c/sup\u003e. These medications often exert their benefits by enhancing dopaminergic and noradrenergic activity in the brain, mechanisms closely tied to increased wakefulness and alertness throughout the day. For individuals who are unresponsive to or cannot tolerate stimulants, non-stimulant medications such as atomoxetine and guanfacine provide alternative options, albeit with somewhat lower efficacy profiles\u003csup\u003e\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e\u003c/sup\u003e. In adolescents, pharmacotherapy has been shown to improve not only core symptoms but also broader quality-of-life domains when treatment adherence is maintained\u003csup\u003e\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e,\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e\u003c/sup\u003e. Importantly, medication effects on quality of life appear to vary by age and subtype, with early and individualized intervention showing the greatest benefits. These findings underscore the importance of tailoring pharmacological strategies to developmental stage and patient-specific needs.\u003c/p\u003e\u003cp\u003eThe present study aims to examine whether pharmacological treatment for ADHD modulates alertness levels across an extended period of wakefulness. Specifically, the research compares three groups: individuals with ADHD receiving medication, individuals with ADHD not receiving medication, and neurotypical controls without ADHD. Participants in all groups were monitored for 25 consecutive hours of wakefulness under controlled conditions, with repeated assessments of subjective alertness. We hypothesized that the medicated ADHD group would exhibit alertness levels comparable to the control group and significantly higher than the unmedicated ADHD group.\u003c/p\u003e"},{"header":"Methods","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e\u003ch2\u003eParticipants\u003c/h2\u003e\u003cp\u003eThe present study included 59 male participants aged 18\u0026ndash;35 years (Mean: 25.46, SD: 4.37). Thirty-nine participants were diagnosed with ADHD-C, and 20 served as controls without ADHD. Among the ADHD group, 17 participants were medicated with their regular doses of methylphenidate (n\u0026thinsp;=\u0026thinsp;13) or amphetamine (n\u0026thinsp;=\u0026thinsp;4) at the start of the experiment (08:00 AM) and again at midnight (00:00), while 22 were unmedicated throughout the study.\u003c/p\u003e\u003cp\u003eThe sample size calculation was based on a small-to-medium effect size (η\u0026sup2; = 0.04), with α\u0026thinsp;=\u0026thinsp;0.05 and a power of 0.95 to detect an effect if present. For a design involving three groups and 25 repeated measures, the minimum required sample size was N\u0026thinsp;=\u0026thinsp;48, meaning at least 16 participants per group\u003c/p\u003e\u003cp\u003eInclusion in the ADHD groups required: (a) a formal clinical diagnosis of ADHD made by a licensed neurologist or psychiatrist; (b) endorsement of at least six inattention and six hyperactivity\u0026ndash;impulsivity symptoms on the ADHD Rating Scale-IV\u003csup\u003e21\u003c/sup\u003e; and (c) fulfillment of DSM-IV diagnostic criteria for ADHD in the adapted Diagnostic Interview Schedule for Children (DISC-IV)\u003csup\u003e\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e\u003c/sup\u003e. Participants in the control group met the following criteria: (a) no prior ADHD diagnosis, (b) fewer than four symptoms in either the inattention or hyperactivity\u0026ndash;impulsivity subscales, and (c) non-fulfillment of DSM-IV criteria for ADHD based on the clinical interview.\u003c/p\u003e\u003cp\u003eExclusion criteria for all groups included: (a) presence of any psychopathology according to the Symptom Checklist-90 (SCL-90; Derogatis., 1994) as assessed by a licensed clinical psychologist; (b) employment involving night shifts; or (c) use of medications affecting the central nervous system other than ADHD medication.\u003c/p\u003e\u003cp\u003eAll participants were male to minimize potential variability associated with menstrual cycle effects on sleep quality\u003csup\u003e\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e\u003c/sup\u003e. Participants were recruited through snowball sampling via advertisements on social media and received a monetary voucher equivalent to approximately \u003cspan\u003e$\u003c/span\u003e125 for their participation. Written informed consent was obtained from all participants. The Max Stern Yezreel Valley College Institutional Ethics Review Board approved the complete study protocol (approval number: EMEK YVC 2019-23).\u003c/p\u003e\u003c/div\u003e\n\u003ch3\u003eMeasures\u003c/h3\u003e\n\u003cp\u003e\u003cstrong\u003eDemographic Questionnaire\u003c/strong\u003e\u003cp\u003eCollected data on age, occupation and health, as well as tobacco smoking status (Yes/No), alcohol use (Yes/No) and medication use.\u003c/p\u003e\u003c/p\u003e\u003cp\u003e\u003cb\u003eADHD Rating Scale\u0026ndash;IV\u003c/b\u003e\u003csup\u003e21\u003c/sup\u003e is an 18-item questionnaire for the assessment of ADHD. The items are based on the symptoms listed in the DSM\u0026ndash;IV for ADHD diagnosis, including 9 items assessing attentiveness and 9 items assessing hyperactivity and impulsivity. In the version used in the current study\u003csup\u003e\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e\u003c/sup\u003e, participants were asked to choose whether each described symptom was correct or incorrect with respect to them. The internal consistency (Cronbach\u0026rsquo;s α) of the attentiveness section and the hyperactivity-impulsivity section of the scale in the current study were 0.82 and 0.87, respectively.\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eStructured Clinical Interview\u003c/strong\u003e\u003cp\u003eA modified version of the ADHD module from the DISC\u003csup\u003e\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e\u003c/sup\u003e was administered in order to determine suitability to the ADHD classification. The modified interview is similar to other interviews that assess ADHD in adulthood\u003csup\u003e\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e\u003c/sup\u003e, and it yields clinician-assessed symptom counts for inattentive and hyperactive-impulsive ADHD symptoms. Internal consistency (Cronbach\u0026rsquo;s α\u0026thinsp;=\u0026thinsp;0.86\u0026ndash;0.94) was consistent with prior studies.\u003c/p\u003e\u003c/p\u003e\u003cp\u003e\u003cb\u003eThe Symptom Checklist\u0026ndash;90\u0026ndash;Revised\u003c/b\u003e (SCL-90-R\u003csup\u003e26\u003c/sup\u003e): A 90-item self-report inventory assessing psychological symptoms across nine domains. Items were rated on a 0\u0026ndash;4 Likert scale, with higher scores indicating greater distress. The internal consistency (Cronbach\u0026rsquo;s α) of the Hebrew translation of the SCL-90-R was found to be within the range of .71\u0026ndash;.85\u003csup\u003e27\u003c/sup\u003e. An expert clinical psychologist examined the responses of each participant on the SCL-90-R to rule out any psychological disorder.\u003c/p\u003e\u003cp\u003e\u003cb\u003ePittsburgh Sleep Quality Index\u003c/b\u003e (PSQI\u003csup\u003e\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e\u003c/sup\u003e): A 18-item self-report questionnaire assessing seven components of sleep quality (Subjective Sleep Quality, Sleep Latency, Sleep Duration, Sleep Efficiency, Sleep Disturbance, Hypnotic Medication Use, Daytime Dysfunction) over the past month. The seven component scores are then totaled to provide a global PSQI score. The internal consistency (Cronbach\u0026rsquo;s α) of the Hebrew translation of the PSQI in the current study was .73.\u003c/p\u003e\u003cp\u003e\u003cb\u003eKarolinska Sleepiness Scale\u003c/b\u003e (KSS\u003csup\u003e\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e\u003c/sup\u003e): A scale measuring subjective sleepiness at a given time. The participant is required to rate his level of sleepiness over the last 10 min on a 9-point Likert scale ranging from 1 (\u0026ldquo;extremely alert\u0026rdquo;) to 9 (\u0026ldquo;extremely sleepy, fighting sleep\u0026rdquo;).\u003c/p\u003e\u003cp\u003e\u003cb\u003eActigraphy\u003c/b\u003e: The actigraph (Mini Motionlogger, Ambulatory Monitoring Inc., New York) is a wrist-worn ambulatory, noninvasive device designed for studies in naturalistic settings with minimal distortions. The actigraph measures wrist movements utilizing a piezoelectric element and translates them into 1-minlong epochs of sleep and wake. To that end, wrist activity levels were sampled at 10-s intervals and summed across 1-min intervals. Actigraphic raw data were translated to sleep measures using the Actigraphic Scoring Analysis program for an IBM-compatible personal computer (W2 scoring algorithm) provided by the manufacturer. Four measures of sleep were obtained: total sleep time (minutes of sleep from intended bedtime to final wake time), sleep onset latency (minutes to fall asleep from bedtime), sleep efficiency (percentage of total sleep time between falling asleep and final awakening), and wake time after sleep onset (WASO; total number of wake minutes after sleep onset). The daily actigraphy data of each subject were averaged over the five days of actigraph use in order to obtain aggregated measures that reliably characterize individuals. The participants were instructed to press a button on the actigraph when they began trying to fall asleep and when they woke up the following morning. The first button-press was used to determine bedtime and the second was used to determine wake time. For the purpose of precise analysis of the actigraph data, over the course of actigraphic recording participants were instructed to complete the Consensus Sleep Diary that included intended bedtime, initial and final wake times, number of awakenings, and lengths of awakenings.\u003c/p\u003e\n\u003ch3\u003eProcedure\u003c/h3\u003e\n\u003cp\u003eEligible participants were provided with an actigraph device five days prior to the laboratory session and instructed to wear it continuously for five nights while completing daily evening/morning sleep diaries. They were asked to sleep at least seven hours per night to avoid prior sleep deprivation.\u003c/p\u003e\u003cp\u003eOn the experimental day, participants were collected from their homes at 07:00 AM and transported to the laboratory, where the experiment began at 08:00 AM. Actigraphy data from the previous five nights were verified to ensure compliance with sleep requirements. Participants who had slept less than seven hours per night were excluded. After completing baseline questionnaires on demographics and sleep quality (PSQI), participants remained awake for approximately 25 consecutive hours under constant supervision to prevent unintended sleep. Among the ADHD group, 17 participants were medicated with their regular doses of methylphenidate (n\u0026thinsp;=\u0026thinsp;13) or amphetamine (n\u0026thinsp;=\u0026thinsp;4) at the start of the experiment (08:00 AM) and again at midnight (00:00), while 22 were unmedicated throughout the study. Subjective sleepiness was recorded hourly using the KSS. Food and non-caffeinated beverages were provided ad libitum. Upon completion of the 25-hour sleep deprivation protocol, participants were thanked, debriefed, and transported home.\u003c/p\u003e\u003cdiv id=\"Sec6\" class=\"Section2\"\u003e\u003ch2\u003eData Analysis\u003c/h2\u003e\u003cp\u003eData were analyzed using \u003cem\u003eJamovi\u003c/em\u003e version 2.5.6. Age and PSQI scores (subjective sleep quality) were compared across groups using one-way Analysis of Variance, (ANOVA). The proportion of alcohol users and smokers were compared across groups using χ2 test. Actigraphy-derived sleep variables (e.g., total sleep time, sleep latency, WASO, sleep efficiency) were compared across groups using the non-parametric Kruskal\u0026ndash;Wallis test due to non-normal data distribution. When significant differences emerged, beta regression analyses were conducted to identify predictors of sleep efficiency.\u003c/p\u003e\u003cp\u003eSubjective sleepiness (KSS) was analyzed using a linear mixed-effects model, with group (control/ADHD unmedicated/ADHD medicated) and time (25 hours) as fixed effects, and participant as a random effect. Additionally, a logistic regression analysis examined the probability of reporting a KSS score\u0026thinsp;\u0026gt;\u0026thinsp;7 at the end of the deprivation period as a function of group membership, to assess the impact of ADHD medication on subjective sleepiness under sleep deprivation conditions.\u003c/p\u003e\u003c/div\u003e"},{"header":"Results","content":"\u003cp\u003eThe study groups did not differ in age or the proportion of tobacco smokers and alcohol users (Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). Group differences in sleep variables measured via the PSQI (global scores) and actigraphy were examined (Table\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). No significant differences were found among the three groups in the PSQI scores (subjective sleep quality). In relation to actigraphy-measures sleep variables, no significant differences were found between the groups in total sleep duration [χ\u003csup\u003e2\u003c/sup\u003e\u003csub\u003e(2)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;0.39, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.822,\u003cem\u003e[\u003c/em\u003e sleep onset latency [χ\u003csup\u003e2\u003c/sup\u003e\u003csub\u003e(2)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;2.98, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.224], or WASO [χ\u003csup\u003e2\u003c/sup\u003e\u003csub\u003e(2)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;3.95, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.138]. However, a significant difference was found in sleep efficiency [χ\u003csup\u003e2\u003c/sup\u003e\u003csub\u003e(2)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;7.77, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.020]. Post-hoc analyses revealed that the control group had significantly higher sleep efficiency (M\u0026thinsp;=\u0026thinsp;0.95, SD\u0026thinsp;=\u0026thinsp;0.01) compared to both the ADHD group without medication (M\u0026thinsp;=\u0026thinsp;0.91, SD\u0026thinsp;=\u0026thinsp;0.01; Z\u0026thinsp;=\u0026thinsp;2.28, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.044) and the ADHD group with medication (M\u0026thinsp;=\u0026thinsp;0.90, SD\u0026thinsp;=\u0026thinsp;0.01; Z\u0026thinsp;=\u0026thinsp;2.69, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.020). No significant difference was found between the two ADHD groups (Z\u0026thinsp;=\u0026thinsp;0.43, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.662).\u003c/p\u003e\u003cp\u003ePearson correlations between the average sleep efficiency, as measured during the week preceding the experimental trial and the level of subjective sleepiness as measured by the KSS at the beginning of the trial (\u003cem\u003er\u003c/em\u003e = -0.05, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.71) and at its end (e.g., following sleep deprivation; \u003cem\u003er\u003c/em\u003e = -0.05, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.697) were not significant. Thus, sleep efficiency was not controlled for in subsequent sleepiness analyses.\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eDemographic Data by Group\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"5\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colname=\"c1\"\u003e\u003cp\u003eMeasure\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c2\"\u003e\u003cp\u003eControl\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c3\"\u003e\u003cp\u003eADHD\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c4\"\u003e\u003cp\u003eADHD\u0026thinsp;+\u0026thinsp;Medication\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c5\"\u003e\u003cp\u003eTest Statistic\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAge\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eMean\u0026thinsp;=\u0026thinsp;26.62\u003c/p\u003e\u003cp\u003eSD\u0026thinsp;=\u0026thinsp;4.17\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eMean\u0026thinsp;=\u0026thinsp;24.67\u003c/p\u003e\u003cp\u003eSD\u0026thinsp;=\u0026thinsp;5.22\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003eMean\u0026thinsp;=\u0026thinsp;25.05\u003c/p\u003e\u003cp\u003eSD\u0026thinsp;=\u0026thinsp;3.39\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u003cem\u003eF\u003c/em\u003e\u003csub\u003e(2,53)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;1.17\u003c/p\u003e\u003cp\u003e\u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.315\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e% Of Smokers\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e19.05\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e31.58\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e5.26\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u003cem\u003eχ\u003c/em\u003e\u003csup\u003e2\u003c/sup\u003e\u003csub\u003e(2)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;4.34\u003c/p\u003e\u003cp\u003e\u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.114\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e% Of Alcohol Users\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e42.86\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e47.37\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e73.68\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u003cem\u003eχ\u003c/em\u003e\u003csup\u003e2\u003c/sup\u003e\u003csub\u003e(2)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;4.35 \u003c/p\u003e\u003cp\u003e\u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.114\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab2\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eSubjective Sleep (PSQI scores) and Actigraphy-Based Sleep Measures by Group\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"5\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colname=\"c1\"\u003e\u003cp\u003eMeasure\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c2\"\u003e\u003cp\u003eControl\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c3\"\u003e\u003cp\u003eADHD\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c4\"\u003e\u003cp\u003eADHD\u0026thinsp;+\u0026thinsp;Medication\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c5\"\u003e\u003cp\u003eTest Statistic\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ePSQI\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eMean\u0026thinsp;=\u0026thinsp;3.90\u003c/p\u003e\u003cp\u003eSD\u0026thinsp;=\u0026thinsp;2.90\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eMean\u0026thinsp;=\u0026thinsp;5.58\u003c/p\u003e\u003cp\u003eSD\u0026thinsp;=\u0026thinsp;3.02\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003eMean\u0026thinsp;=\u0026thinsp;5.0\u003c/p\u003e\u003cp\u003eSD\u0026thinsp;=\u0026thinsp;2.55\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u003cem\u003eF\u003c/em\u003e\u003csub\u003e(2,53)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;1.76\u003c/p\u003e\u003cp\u003e\u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.182\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eSleep Duration (min)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eMed\u0026thinsp;=\u0026thinsp;417\u003c/p\u003e\u003cp\u003eIQR\u0026thinsp;=\u0026thinsp;409 ,474\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eMed\u0026thinsp;=\u0026thinsp;424\u003c/p\u003e\u003cp\u003eIQR\u0026thinsp;=\u0026thinsp;372 ,457\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003eMed\u0026thinsp;=\u0026thinsp;433\u003c/p\u003e\u003cp\u003eIQR\u0026thinsp;=\u0026thinsp;372 ,459\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u003cem\u003eχ\u003c/em\u003e\u003csup\u003e2\u003c/sup\u003e\u003csub\u003e(2)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;0.39\u003c/p\u003e\u003cp\u003e\u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.822\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eSleep Latency (min)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eMed\u0026thinsp;=\u0026thinsp;9\u003c/p\u003e\u003cp\u003eIQR\u0026thinsp;=\u0026thinsp;7.5 ,30\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eMed\u0026thinsp;=\u0026thinsp;13.75\u003c/p\u003e\u003cp\u003eIQR\u0026thinsp;=\u0026thinsp;5.8 ,35.2\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003eMed\u0026thinsp;=\u0026thinsp;7.5\u003c/p\u003e\u003cp\u003eIQR\u0026thinsp;=\u0026thinsp;5.4 ,12.5\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u003cem\u003eχ\u003c/em\u003e\u003csup\u003e2\u003c/sup\u003e\u003csub\u003e(2)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;2.98 \u003c/p\u003e\u003cp\u003e\u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.224\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eWASO\u003c/p\u003e\u003cp\u003e(min)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eMed\u0026thinsp;=\u0026thinsp;15\u003c/p\u003e\u003cp\u003eIQR\u0026thinsp;=\u0026thinsp;5 ,20\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eMed\u0026thinsp;=\u0026thinsp;20.4\u003c/p\u003e\u003cp\u003eIQR\u0026thinsp;=\u0026thinsp;14.2 ,42.6\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003eMed\u0026thinsp;=\u0026thinsp;17.8\u003c/p\u003e\u003cp\u003eIQR\u0026thinsp;=\u0026thinsp;9.7 ,28.5\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u003cem\u003eχ\u003c/em\u003e\u003csup\u003e2\u003c/sup\u003e\u003csub\u003e(2)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;3.95 \u003c/p\u003e\u003cp\u003e\u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.138\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eSleep Efficiency\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eM\u0026thinsp;=\u0026thinsp;0.95\u003c/p\u003e\u003cp\u003eSD\u0026thinsp;=\u0026thinsp;0.01\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eM\u0026thinsp;=\u0026thinsp;0.91\u003c/p\u003e\u003cp\u003eSD\u0026thinsp;=\u0026thinsp;0.01\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003eM\u0026thinsp;=\u0026thinsp;0.90\u003c/p\u003e\u003cp\u003eSD\u0026thinsp;=\u0026thinsp;0.01\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u003cem\u003eχ\u003c/em\u003e\u003csup\u003e2\u003c/sup\u003e\u003csub\u003e(2)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;7.77 \u003c/p\u003e\u003cp\u003e\u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.020\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003eNote: WASO: Wake After Sleep Onset; PSQI: Pittsburgh Sleep Quality Index (subjective sleep quality)\u003c/p\u003e\u003cdiv id=\"Sec8\" class=\"Section2\"\u003e\u003ch2\u003eSubjective Sleepiness (KSS) Over Time\u003c/h2\u003e\u003cp\u003eA linear mixed model was used to test the hypothesis that group and time interact to affect subjective sleepiness (KSS) over the 25-hour study period, and particularly following sleep deprivation. Time and group served as independent variables while participants were treated as a random variable. The random variable (σ\u003csup\u003e2\u003c/sup\u003e\u003csub\u003eIntercept\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;1.84, 95% C.I.= 1.13,1.65, ICC\u0026thinsp;=\u0026thinsp;0.48) was significant (LRT\u0026thinsp;=\u0026thinsp;760.70, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;\u0026lt;\u0026thinsp;.001). The model explained 66.29% of the variance (R\u003csup\u003e2\u003c/sup\u003e\u003csub\u003eConditional\u003c/sub\u003e), with the independent variables accounting for 35.18% (R\u003csup\u003e2\u003c/sup\u003e\u003csub\u003eMarginal\u003c/sub\u003e). A significant interaction between time and group was found [F\u003csub\u003e(48,1392.08)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;2.14, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;\u0026lt;\u0026thinsp;.001] (see Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e).\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003ePost-hoc comparisons on the KSS scores at the end point of the study (i.e., following 25 hours of sustained wakefulness) demonstrated that while there was no difference [\u003cem\u003et\u003c/em\u003e\u003csub\u003e(225.45)\u003c/sub\u003e = -0.77, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.437] between the control group (\u003cem\u003eM\u003c/em\u003e\u0026thinsp;=\u0026thinsp;6.70, \u003cem\u003eSE\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.43) and the ADHD\u0026thinsp;+\u0026thinsp;medication group (\u003cem\u003eM\u003c/em\u003e\u0026thinsp;=\u0026thinsp;6.21, \u003cem\u003eSE\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.45), the ADHD group (\u003cem\u003eM\u003c/em\u003e\u0026thinsp;=\u0026thinsp;8.42, \u003cem\u003eSE\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.45) reported significantly higher sleepiness than both the control group (\u003cem\u003et\u003c/em\u003e\u003csub\u003e(245.48)\u003c/sub\u003e = \u0026minus;\u0026thinsp;2.70, p\u0026thinsp;=\u0026thinsp;.007) and the ADHD\u0026thinsp;+\u0026thinsp;medication group (\u003cem\u003et\u003c/em\u003e\u003csub\u003e(244.96)\u003c/sub\u003e = \u0026minus;\u0026thinsp;3.43, p\u0026thinsp;\u0026lt;\u0026thinsp;.001).\u003c/p\u003e\u003cp\u003eA second linear mixed model tested the hypothesis that from 1:00 AM onward, the ADHD group would report higher sleepiness than the control and the ADHD\u0026thinsp;+\u0026thinsp;medication group, with no difference between the latter two groups. Group was the independent variable, and the participants were the random variable. The random variable (σ\u003csup\u003e2\u003c/sup\u003e\u003csub\u003eIntercept\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;2.65, 95% C.I.= 1.34,2.00, ICC\u0026thinsp;=\u0026thinsp;0.54) was significant (LRT\u0026thinsp;=\u0026thinsp;221.7, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;\u0026lt;\u0026thinsp;.001). The model explained 57.83% of the variance (R\u003csup\u003e2\u003c/sup\u003e\u003csub\u003eConditional\u003c/sub\u003e), with Group accounting for 8.25% (R\u003csup\u003e2\u003c/sup\u003e\u003csub\u003eMarginal\u003c/sub\u003e). A significant group effect was found [\u003csub\u003e(2,58.95)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;4.49, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.015]. Post-hoc comparisons demonstrated that while there was no difference [\u003cem\u003et\u003c/em\u003e\u003csub\u003e(58.60)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;0.81, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.419] between the control group (\u003cem\u003eM\u003c/em\u003e\u0026thinsp;=\u0026thinsp;6.01, \u003cem\u003eSE\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.38) and the ADHD\u0026thinsp;+\u0026thinsp;medication group (\u003cem\u003eM\u003c/em\u003e\u0026thinsp;=\u0026thinsp;5.57, \u003cem\u003eSE\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.39), the ADHD group (\u003cem\u003eM\u003c/em\u003e\u0026thinsp;=\u0026thinsp;7.16, \u003cem\u003eSE\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.38) reported significantly higher sleepiness than both the control group (\u003cem\u003et\u003c/em\u003e\u003csub\u003e(59.14)\u003c/sub\u003e = \u0026minus;\u0026thinsp;2.11, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.039) and the ADHD\u0026thinsp;+\u0026thinsp;medication group (\u003cem\u003et\u003c/em\u003e\u003csub\u003e(59.12)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;2.89, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.005).\u003c/p\u003e\u003cp\u003eAs KSS scores greater than 7 indicate extreme sleepiness with substantial difficulty remaining awake, A logistic regression tested group differences in the proportion of participants with KSS\u0026thinsp;\u0026gt;\u0026thinsp;7 at the end of the study. The model was significant [\u003cem\u003eχ\u003c/em\u003e\u003csup\u003e2\u003c/sup\u003e\u003csub\u003e(2)\u003c/sub\u003e\u0026thinsp;=\u0026thinsp;10.98, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.004, \u003cem\u003eR\u003c/em\u003e\u003csup\u003e2\u003c/sup\u003e \u003csub\u003eMcFadden\u003c/sub\u003e = .0145]. It has been revealed that while the proportion of participants with KSS\u0026thinsp;\u0026gt;\u0026thinsp;7 at the end of the study was 55.0% in the control group, it reached 88.2% in the ADHD group (see Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e), a difference that was statistically significant (\u003cem\u003eZ\u003c/em\u003e = -2.07, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.038). In the ADHD\u0026thinsp;+\u0026thinsp;medication group the proportion was 36.9%, significantly lower than ADHD without medication (\u003cem\u003eZ\u003c/em\u003e\u0026thinsp;=\u0026thinsp;2.86, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.004), and not significantly different from control (\u003cem\u003eZ\u003c/em\u003e\u0026thinsp;=\u0026thinsp;1.13, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;.258).\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003c/div\u003e"},{"header":"Discussion","content":"\u003cp\u003eThis study investigated the effects of sleep deprivation and stimulant medication (methylphenidate and amphetamine) on subjective sleepiness in young adults with ADHD, compared to individuals without ADHD. Subjective sleepiness was assessed hourly over a 25-hour experimental session using the Karolinska Sleepiness Scale (KSS). The findings support the study\u0026rsquo;s hypotheses: participants with ADHD exhibited significantly higher levels of sleepiness throughout the experiment, particularly following 25 hours of sleep deprivation. Notably, medicated ADHD participants and control participants did not differ significantly in their sleepiness levels.\u003c/p\u003e\u003cp\u003eThe observation that unmedicated individuals with ADHD experienced elevated sleepiness during sustained wakefulness, especially overnight and into the following morning, replicates our previous findings\u003csup\u003e\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e\u003c/sup\u003e and aligns with studies reporting excessive daytime sleepiness in both children and adults with ADHD\u003csup\u003e\u003cspan additionalcitationids=\"CR30 CR31\" citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR32\" class=\"CitationRef\"\u003e32\u003c/span\u003e\u003c/sup\u003e. However, our studies are among the first to systematically compare sleepiness levels throughout the day between individuals with ADHD and the general population.\u003c/p\u003e\u003cp\u003eThe sleepiness trajectory observed in the control group mirrored patterns reported in prior KSS-based studies\u003csup\u003e\u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e,\u003cspan citationid=\"CR34\" class=\"CitationRef\"\u003e34\u003c/span\u003e\u003c/sup\u003e, with relatively stable levels from morning to evening followed by a gradual increase along the night. In contrast, participants with ADHD showed a significantly steeper rise in sleepiness during the night and subsequent morning. This was further reflected in the proportion of participants scoring above 7 on the KSS the morning after sleep deprivation, 88.2% in the ADHD group versus 55% in the control group, indicating heightened vulnerability to sleep deprivation among individuals with ADHD.\u003c/p\u003e\u003cp\u003eThe differences in sleepiness in the current study between the control participants and the non-medicated ADHD participants cannot be attributed to psychiatric comorbidities that are commonly associated with ADHD\u003csup\u003e\u003cspan citationid=\"CR35\" class=\"CitationRef\"\u003e35\u003c/span\u003e\u003c/sup\u003e as individuals suffering from such psychopathologies were excluded from the study. They also cannot be explained by the tendency of ADHD patients to exhibit lower sleep quantity and quality \u003csup\u003e\u003cspan additionalcitationids=\"CR37 CR38\" citationid=\"CR36\" class=\"CitationRef\"\u003e36\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR39\" class=\"CitationRef\"\u003e39\u003c/span\u003e\u003c/sup\u003e. First, the study included only individuals without diagnosed sleep disorders and the participants were instructed to maintain a minimum of seven hours of sleep for nights prior to the experimental trial. Second, actigraphy data collected along these nights revealed that the study groups did not differ in total sleep duration or sleep onset latency. Although sleep efficiency was higher in the control group compared to the unmedicated ADHD group this difference likely did not account for the differences in subjective sleepiness as there were no significant correlation between sleep efficiency and the KSS scores at either the beginning of the experimental trial or its end. These findings are consistent with prior research suggesting that increased sleepiness in ADHD is not solely due to sleep disturbances\u003csup\u003e\u003cspan citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e,\u003cspan citationid=\"CR40\" class=\"CitationRef\"\u003e40\u003c/span\u003e\u003c/sup\u003e. Taken together, these findings support the notion that sleep deprivation exacerbates sleepiness in individuals with ADHD, indicating increased vulnerability to fatigue in this population.\u003c/p\u003e\u003cp\u003eStimulant medications, particularly methylphenidate and amphetamines, are the first-line treatment for ADHD\u003csup\u003e\u003cspan citationid=\"CR41\" class=\"CitationRef\"\u003e41\u003c/span\u003e\u003c/sup\u003e. The current findings demonstrate that these medications not only improve attention and reduce hyperactivity but also normalize subjective sleepiness levels in individuals with ADHD, making them comparable to those of non-ADHD participants. This is consistent with previous research indicating that stimulants can reduce daytime sleepiness\u003csup\u003e\u003cspan citationid=\"CR42\" class=\"CitationRef\"\u003e42\u003c/span\u003e,\u003cspan citationid=\"CR43\" class=\"CitationRef\"\u003e43\u003c/span\u003e\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003eThe findings underscore the importance of considering sleep-related factors in both the theoretical understanding and clinical management of ADHD. From a theoretical perspective, these findings support to models that conceptualize ADHD as involving dysregulation in arousal and sleep systems, in addition to cognitive and behavioral symptoms. Pharmacologically, methylphenidate and amphetamine enhance central dopamine and norepinephrine activity by inhibiting their respective transporters\u003csup\u003e\u003cspan citationid=\"CR44\" class=\"CitationRef\"\u003e44\u003c/span\u003e\u003c/sup\u003e. Given their dual efficacy in reducing ADHD symptoms\u003csup\u003e\u003cspan citationid=\"CR45\" class=\"CitationRef\"\u003e45\u003c/span\u003e,\u003cspan citationid=\"CR46\" class=\"CitationRef\"\u003e46\u003c/span\u003e\u003c/sup\u003e and sleepiness, it is plausible that dysregulation in these neurotransmitter systems underlies both domains\u003csup\u003e\u003cspan citationid=\"CR38\" class=\"CitationRef\"\u003e38\u003c/span\u003e\u003c/sup\u003e. Although the impact of stimulants on sleepiness may be independent of their cognitive effects, prior research has shown a positive correlation between daytime sleepiness and inattentiveness in ADHD\u003csup\u003e\u003cspan citationid=\"CR47\" class=\"CitationRef\"\u003e47\u003c/span\u003e\u003c/sup\u003e, suggesting that improvements in attention may be partially mediated by reductions in sleepiness. However, this intriguing hypothesis warrants further empirical investigation.\u003c/p\u003e\u003cp\u003eClinically, the study highlights the dual role of stimulant medications - not only in improving attention and reducing hyperactivity but also in alleviating daytime sleepiness, particularly under conditions of sleep deprivation. However, it is important to note that the impact of stimulant medication on sleep is complex\u003csup\u003e\u003cspan citationid=\"CR48\" class=\"CitationRef\"\u003e48\u003c/span\u003e,\u003cspan citationid=\"CR49\" class=\"CitationRef\"\u003e49\u003c/span\u003e\u003c/sup\u003e. Some studies report adverse effects when stimulants are taken late in the day, including increased sleep latency and reduced sleep efficiency\u003csup\u003e\u003cspan additionalcitationids=\"CR50 CR51\" citationid=\"CR49\" class=\"CitationRef\"\u003e49\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR52\" class=\"CitationRef\"\u003e52\u003c/span\u003e\u003c/sup\u003e. Therefore, clinicians should monitor sleep patterns and adjust medication timing and dosage to optimize therapeutic outcomes while minimizing sleep-related side effects.\u003c/p\u003e\u003cp\u003eInterpretation of the present findings should be viewed in light of a few limitations. First, due to constraints imposed by the experimental design, the study sample was limited to young adult males (ages 18\u0026ndash;30) in order to minimize variability and enhance statistical power\u003csup\u003e\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e\u003c/sup\u003e. Consequently, the generalizability of the findings to females and other age groups remains limited and warrants further investigation in future research. Second, since all ADHD participants in the current study were of the combined subtype (ADHD-C) and did not present with any psychiatric comorbidities, the applicability of these findings to individuals with other ADHD subtypes or those with co-occurring psychiatric conditions remains uncertain. Third, the experiment was conducted in a controlled laboratory setting, which may not reflect real-world conditions where environmental factors vary widely. Finally, the extreme sleep deprivation protocol (25 hours) represents an atypical scenario that may elicit exaggerated behavioral and cognitive responses.\u003c/p\u003e"},{"header":"Conclusions","content":"\u003cp\u003eThis study provides empirical support for the heightened vulnerability of individuals with ADHD to the effects of sleep deprivation on sleepiness. The stimulant medications methylphenidate and amphetamine were shown to effectively attenuate sleepiness in ADHD participants, aligning their wakefulness levels with those of non-ADHD controls. These findings highlight the dual therapeutic role of stimulants in managing both attentional deficits and sleep-related vulnerabilities in ADHD.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cdiv class=\"DefinitionList\"\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u003cb\u003eADHD\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eAttention-Deficit Hyperactivity Disorder\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u003cb\u003eADHD - C\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eCombined Type Attention-Deficit Hyperactivity Disorder\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u003cb\u003eADHD - PI\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003ePredominantly Inattentive Attention-Deficit Hyperactivity Disorder\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u003cb\u003eADHD - HI\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003ePredominantly Hyperactive-Impulsive Attention-Deficit Hyperactivity Disorder\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u003cb\u003eDISC\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eDiagnostic Interview Schedule for Children\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u003cb\u003eDSM-IV\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eDiagnostic and Statistical Manual of Mental Disorders, 4th Edition\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u003cb\u003eEEG\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eElectroencephalography\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u003cb\u003eEDS\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eExcessive Daytime Sleepiness\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u003cb\u003eKSS\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eKarolinska Sleepiness Scale\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u003cb\u003ePSQI\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003ePittsburgh Sleep Quality Index\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u003cb\u003eSCL-90\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eSymptom Checklist-90\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u003cb\u003eWASO\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eWake After Sleep Onset\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003ch2\u003eEthics approval and consent to participate\u003c/h2\u003e\u003cp\u003e The study was approved by the Max Stern Yezreel Valley College Institutional Ethics Review Board (Reference: EMEK YVC 2019-23). All participants provided informed consent to participate in the study.\u003c/p\u003e\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eClinical trial number\u003c/strong\u003e\u003cp\u003enot applicable\u003c/p\u003e\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003cp\u003eThe authors declare that they have no competing interests\u003c/p\u003e\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003cp\u003eNot applicable\u003c/p\u003e\u003c/p\u003e\u003ch2\u003eFunding\u003c/h2\u003e\u003cp\u003eThis work was supported by the Max Stern Yezreel Valley College, Emek Yezreel, Israel. The funder had no role in the conceptualization, design, data collection, analysis, decision to publish, or preparation of the manuscript\u003c/p\u003e\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eIH conceived of the study, participated in its design, data interpretation and writing the original draft; AC conceived of the study, participated in its design and data analysis, and led write-up of the manuscript; OD conceived and supervised statistical analyses and revised the original draft of the manuscript; SE conceived of the study, participated in its design, supervised data collection and participated in writing the original draft. KA performed statistical analysis, supervised data collection and participated in data curation and coordination.\u003c/p\u003e\u003ch2\u003eData Availability\u003c/h2\u003e\u003cp\u003eData is available upon reasonable request from the corresponding author.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eFaraone SV, Banaschewski T, Coghill D, et al. The World Federation of ADHD International Consensus Statement: 208 Evidence-based conclusions about the disorder. Neurosci Biobehav Rev. 2021;128:789\u0026ndash;818. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1016/j.neubiorev.2021.01.022\u003c/span\u003e\u003cspan address=\"10.1016/j.neubiorev.2021.01.022\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003ePopit S, Serod K, Locatelli I, Stuhec M. 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Published 2023 Jun 23.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eRao R, Tripathi R. Stimulants and sleep. In Sleep and neuropsychiatric disorders 2022 Feb 1 (pp. 811\u0026ndash;33). Singapore: Springer Nature Singapore.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-psychiatry","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bpsy","sideBox":"Learn more about [BMC Psychiatry](http://bmcpsychiatry.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bpsy/default.aspx","title":"BMC Psychiatry","twitterHandle":"@BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"ADHD, sleepiness, KSS, Stimulant Medications, sleep deprivation","lastPublishedDoi":"10.21203/rs.3.rs-7921122/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7921122/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e\u003cp\u003eThe present study aimed at investigating the effects of sleep deprivation and stimulant medication (methylphenidate and amphetamine) on subjective sleepiness in young adults with ADHD, compared to individuals without ADHD.\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e\u003cp\u003eFifty-nine young men (age 18\u0026ndash;35) of whom 39 were diagnosed with ADHD combined type (ADHD-C) and 20 without ADHD. The participants\u0026rsquo; sleep was monitored for 5 days via actigraphy. Subsequently, the participants were kept continuously awake in a controlled environment for 25 hours (8amtill 9am the next day). Among the ADHD group, 17 participants were medicated with their regular doses of methylphenidate (n\u0026thinsp;=\u0026thinsp;13) or amphetamine (n\u0026thinsp;=\u0026thinsp;4) at the start of the experiment (08:00 AM) and again at midnight (00:00), while 22 were unmedicated throughout the study. The sleepiness of the participants was assessed every hour by the Karolinska Sleepiness Scale (KSS) in order to obtain the sleepiness curve of both study groups.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e\u003cp\u003eUnmedicated ADHD participants reported significantly higher sleepiness throughout the protocol, especially during nighttime and early morning hours. At the end of the 25-hour wakefulness period, their KSS scores were significantly higher than both the control and medicated ADHD groups. No significant difference was found between the medicated ADHD group and controls. Additionally, 88.2% of unmedicated ADHD participants scored above 7 on the KSS (indicating extreme sleepiness), compared to 55% in controls and 36.9% in the medicated ADHD group.\u003c/p\u003e\u003ch2\u003eConclusions\u003c/h2\u003e\u003cp\u003eYoung adults with ADHD exhibit heightened vulnerability to sleep deprivation, reflected in elevated subjective sleepiness. Stimulant medications effectively attenuate sleepiness in ADHD participants, aligning their alertness levels with those of neurotypical controls. These findings support models of ADHD involving arousal dysregulation and highlight the dual therapeutic role of stimulants in managing both attentional deficits and sleep-related impairments\u003c/p\u003e","manuscriptTitle":"The Effects of Stimulant Medications on the Sleepiness Curve of Young Men with Attention-Deficit Hyperactivity Disorder (ADHD)","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-11-17 06:39:01","doi":"10.21203/rs.3.rs-7921122/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-02-27T06:23:02+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-02-26T15:37:01+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"77131663496336768454770418715863701035","date":"2026-02-09T14:08:28+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-11-20T16:09:33+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"57677920448830101954804422186515378933","date":"2025-11-07T16:22:55+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-11-06T00:59:17+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2025-10-27T19:17:45+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-10-27T12:50:54+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-10-27T12:50:00+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Psychiatry","date":"2025-10-22T06:29:14+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-psychiatry","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bpsy","sideBox":"Learn more about [BMC Psychiatry](http://bmcpsychiatry.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bpsy/default.aspx","title":"BMC Psychiatry","twitterHandle":"@BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"46c96dc8-2dda-4b88-b09b-9b25393058d8","owner":[],"postedDate":"November 17th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[],"tags":[],"updatedAt":"2026-03-30T16:28:20+00:00","versionOfRecord":{"articleIdentity":"rs-7921122","link":"https://doi.org/10.1186/s12888-026-08011-2","journal":{"identity":"bmc-psychiatry","isVorOnly":false,"title":"BMC Psychiatry"},"publishedOn":"2026-03-24 16:10:38","publishedOnDateReadable":"March 24th, 2026"},"versionCreatedAt":"2025-11-17 06:39:01","video":"","vorDoi":"10.1186/s12888-026-08011-2","vorDoiUrl":"https://doi.org/10.1186/s12888-026-08011-2","workflowStages":[]},"version":"v1","identity":"rs-7921122","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-7921122","identity":"rs-7921122","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}