The effects of sleep deprivation on cognitive flexibility: a scoping review of outcomes and biological mechanisms

Sleep supports homeostasis, glymphatic clearance, and memory consolidation, and is essential for normal brain function. A large portion of the population experiences sleep disorders leading to sleep deprivation, defined as reduced sleep duration and phases (often <4 h/24 h), whether acute or chronic. Sleep deprivation is linked to mood disturbances, fatigue, impaired immunity, cardiometabolic risks, and cognitive decline. Executive functions are particularly vulnerable, and cognitive flexibility—a core component enabling adaptation to changing conditions and rule-switching—may be altered under sleep loss. Given its importance for specialized professions (e.g., athletes, clinicians, astronauts), understanding how sleep deprivation affects cognitive flexibility and the underlying neural mechanisms is crucial. Prior work implicates prefrontal cortex hypoperfusion, glutamate-GABA imbalance, BDNF variation, reduced cortical activation, and oxidative stress after sleep loss. However, findings on cognitive flexibility have been inconsistent, motivating a scoping review to synthesize current evidence.

The review included 17 human studies published between 1998 and 2024 across multiple countries, with most published after 2018 and generally small samples. Designs comprised 6 RCTs and 11 quantitative non-randomized studies, involving children, adolescents, undergraduates, clinicians (anesthesiology residents, emergency physicians), pilots, soccer athletes, and other adults. Sleep deprivation paradigms varied: total sleep deprivation (e.g., 24–38 h awake), partial sleep restriction (e.g., 4–6 h time-in-bed), and alternating normal sleep vs. total sleep loss; one study contrasted sleep restriction with sleep extension. Sleep assessment employed polysomnography, wrist actigraphy, sleep diaries, the Karolinska Sleepiness Scale, and the Visual Analog Scale, while some studies lacked formal sleep assessment. Cognitive flexibility measures included SCWT, WCST, task-switching paradigms, DCCS, TMT, TTCT, AX-CPT-s, and a reversal learning task; only two studies used objective neuroimaging (EEG, MRI). Across studies, total sleep deprivation tended to impair cognitive flexibility, whereas partial sleep deprivation produced mixed findings, with the overweight/obesity status moderating outcomes in adolescents.

The protocol was registered on OSF (https://doi.org/10.17605/OSF.IO/YKHBT). Research questions asked whether sleep deprivation affects cognitive flexibility, which domains are impacted, and what mechanisms may link sleep loss to impaired cognitive flexibility. Comprehensive searches (from database inception to February 28, 2025) in PubMed, Web of Science, ClinicalKey, Cochrane, Scopus, SinoMed, and CNKI targeted sleep deprivation and cognitive flexibility. After deduplication using Zotero, titles/abstracts were screened, and full-texts were reviewed against predefined inclusion/exclusion criteria: observational human studies in English examining sleep deprivation (acute/transient/chronic) and cognitive flexibility outcomes; exclusions included non-English, abstracts only, systematic reviews, guidelines, commentaries, animal studies, and studies not assessing cognitive flexibility. Quality appraisal used MMAT (2018), with two initial screening questions (clarity of research question; data addressing the question) followed by five criteria scored with asterisks; two reviewers assessed independently and resolved discrepancies without excluding low-quality studies. Data extraction (Excel) captured author, year, country, design, participants, age, sample size, sleep/cognitive flexibility measures, main findings, and proposed mechanisms, followed by categorization to summarize study-level and cross-study patterns. PRISMA 2020 guidance structured the selection process (410 records identified; 271 screened after deduplication; 41 full-text reviewed; 17 included).

Study pool: 17 studies (6 RCTs, 11 non-randomized) across diverse populations; sample sizes typically small (n=7–66). Direction of effects: 8 studies reported decreased cognitive flexibility with sleep deprivation; 6 reported no significant change; 2 reported temporary improvement (likely due to acute arousal/stress). Weight moderation: Overweight/obese adolescents showed reduced cognitive flexibility after sleep restriction, whereas healthy-weight peers showed improvement (Stager et al., 2024, obesity P<0.001; healthy weight P=0.02). Accuracy vs reaction time: Multiple studies indicated greater impairment in accuracy than in speed under total sleep deprivation. Representative statistics: Honn et al. (2019) RCT: decreased flexibility in reversal learning (F=4.61, P=0.032). Zhang et al. (2024) RCT with EEG task-switching: reduced CF (P2 F=4.430, P=0.039; N2 F(1,64)=6.866, P=0.011; P3 F=5.549, P=0.022; delta power differences F=4.306–5.584, P=0.042–0.021). Chan et al. (2024) adolescent crossover (DCCS): decreased CF (β=−6.6, P=0.008); reduced CVR in temporo-occipital regions. O’Hagan et al. (2018) pilots: SCWT RT increased (F=6.475, P=0.004). Abdelhamid et al. (2020) anesthesiology residents: TMT worsened post 24-h shift (TMT-A 38.82→44.86 ms; TMT-B 63.16→72.60 ms; P<0.001). Whitney et al. (2017) adults: AX-CPT-s indicated decreased CF (F=32.0, P<0.001). Slama et al. (2018) adults: SCWT impairment (F=6.97, P=0.013). No-change examples: Randazzo et al. (1998) children TTCT (t=1.780, P=0.106); Maltese et al. (2016) ICU physicians WCST (P=0.063); Persico et al. (2018) emergency physicians WCST (P>0.05); García et al. (2021) undergraduates SCWT (F=1.90, P>0.05); Pourhassan et al. (2023) soccer athletes WCST (r=−0.11, P=0.703); Kiriş (2022) adolescents CANTAB (P=0.11). Improvement examples: Ballesio et al. (2018) task-switching improved CF after partial SD (P=0.027); Sen et al. (2023) SCWT improved (P=0.036). Mechanisms suggested: reduced cerebrovascular reactivity and localized hypoxia (MRI), decreased insular/intraparietal sulcus activity, prefrontal and hippocampal hypoactivation (BDNF Met carriers), dopamine D2 receptor binding differences (DRD2 C957T), stress-related hormone changes (cortisol, dopamine), and EEG delta/theta alterations indicating impaired interference suppression and working memory resources.

Findings indicate that total sleep deprivation robustly impairs cognitive flexibility, especially task-switching accuracy, whereas partial sleep deprivation yields mixed outcomes that may depend on individual factors (e.g., adiposity) and compensatory neural strategies. The disproportionate impact on accuracy versus reaction time suggests that while motor speed may be preserved, precise information processing and rule switching degrade under sleep loss. Neurobiological evidence supports cerebrovascular-metabolic mechanisms (reduced CVR and oxygenation), region-specific hypoactivation (prefrontal, hippocampal, insular/intraparietal areas), and neuromodulatory changes (dopamine signaling, BDNF expression) contributing to flexibility deficits. Occupational studies show variability: anesthesiology residents after 24-h shifts demonstrate clear CF impairment, while emergency physicians under partial SD show intact CF but slower processing and reduced working memory, highlighting task demands and chronicity as moderating factors. Athletes may exhibit compensatory attentional resource allocation that preserves CF under certain conditions. Adolescence emerges as a sensitive period, with sleep restriction affecting CF and CVR, and adiposity moderating outcomes. Overall, the results address the research question by demonstrating that sleep deprivation can impair cognitive flexibility via multiple mechanisms, especially under total sleep loss, while the effects of partial sleep restriction remain uncertain and context-dependent.

Most evidence indicates that sleep deprivation, particularly total sleep deprivation, hampers task-switching accuracy and cognitive flexibility. The effects of partial sleep deprivation are less consistent and may be moderated by individual factors such as weight status. The review underscores the need for precise, objective assessments (e.g., neuroimaging), larger and more diverse samples, longer and longitudinal designs, and direct comparisons between partial and total sleep deprivation to clarify short- and long-term impacts. Personalized interventions—sleep hygiene education, cognitive training, and targeted support for adolescents and high-risk professions—may mitigate adverse effects. Implementing integrated monitoring–intervention–assessment systems could enhance cognitive performance and quality of life under sleep-limited conditions.

Heterogeneous cognitive flexibility measures complicate synthesis and limit definitive conclusions. Small sample sizes restrict generalizability, and most studies rely on task-based assessments with only two employing objective neuroimaging, increasing potential bias. The participant pool is skewed toward youth, limiting applicability to older adults. Experimental durations are brief, potentially missing dynamic changes in cognitive flexibility. There is a lack of comparative studies directly contrasting partial vs. total sleep deprivation. Potential confounders (e.g., emotional states, stress, task demands, occupation-specific pressures) were not consistently controlled, which may affect accuracy and reliability of outcomes.