Utilizing neuroimaging meta-analytic techniques, we assessed structural brain alterations associated with sleep disorders, characterized the broader coactivation networks of structurally altered regions, and examined their potential behavioral implications. Across all disorders, we observed convergent structural decreases in the thalamus. More specifically, thalamic alterations were centered on the pulvinar nucleus, a region implicated in regulating attention to external stimuli and coordinating sensory integration70,76,77. Our MACM analysis indicated this thalamic region was embedded within a task-positive network comprising the medial and lateral frontal cortex, basal ganglia, and parietal cortices. Functional decoding linked this thalamic region and its broader coactivation network with behavioral domains involving task execution and goal-directed operations. Such thalamic alterations may contribute to increased error rates, attentional lapses, and risk of injury commonly observed among individuals with disrupted sleep. Across parasomnia-related studies, we identified convergent structural decreases in the PCC. Our MACM analysis indicated that this PCC region was embedded within a valuation and reward processing network, including the striatum, insula, and vmPFC. Functional decoding linked this PCC region and its broader coactivation network to reward evaluation, decision-making, and motivational regulation. Such PCC alterations within a broader PCC-centered valuation network involving the vmPFC and insula may contribute to parasomnia-related behaviors, including aberrant goal-directed actions during sleep, impaired emotional regulation, and altered motivational drives, by disrupting the integration of affective and value-based signals necessary for normal motivational regulation, reward sensitivity, and emotional control.
Disorder-general convergence (i.e., across all sleep disorders), manifested as reduced structural integrity in the thalamus, specifically within the pulvinar nucleus78,79,80,81. The thalamus plays a central role in relaying sensory and motor signals to the cortex and regulating arousal, attention, and consciousness80,81. The pulvinar is a major thalamic hub that supports visuospatial attention, sensory integration, and the regulation of cortico-cortical communication during, for example, cognitive control, working memory, and decision-making70,76,77,82,83. Via widespread projections to prefrontal, parietal, and sensorimotor cortices, this nucleus modulates top-down attention, filters distractions, and maintains task-relevant information70,76,82. Pulvinar structural alterations may contribute to impairments in the allocation of attentional resources and/or the coordination of higher-order cognition, capacities consistently compromised among individuals with sleep disorders, including insomnia and narcolepsy78,79. Thalamic structural alterations linked with sleep disorders may contribute to impaired regulation of sensory and cognitive processes70,76,80,81,82 contributing to everyday mistakes, mishaps, and accidents.
Using MACM, we delineated the broader functional neurocircuitry linked with this thalamic ROI which included the basal ganglia, medial and lateral PFC, insula, and intraparietal sulcus (IPS), key components of large-scale networks supporting goal-directed behaviors. Functionally, these regions correspond to a tripartite system involving the ECN, basal ganglia circuitry, and the SN. The ECN, anchored in the lateral frontal cortex and IPS, supports top-down attentional selection, task-set maintenance, and cognitive flexibility68,69,70,71. The basal ganglia, including the caudate, participate in cortico-striato-thalamo-cortical loops that facilitate action selection, procedural learning, and reinforcement-based adaptation83,84,85,86,87,88. The SN, encompassing the thalamus (notably the pulvinar), anterior insula, and mid-cingulate cortex, facilitates error monitoring and adaptive responding to behaviorally relevant stimuli68,69,70,71,83,88,89.
Functional decoding of this network revealed associations with terms such as sequence, execution, and task performance, consistent with mental operations required for real-world cognition. Disruptions in this integrated circuitry, as documented in sleep disorders, may therefore manifest as attentional lapses, slowed responses, and reduced cognitive flexibility68,88,89,90,91. These deficits mirror clinical observations of reduced task efficiency and increased error rates in individuals with insomnia, narcolepsy, and other sleep-related conditions68,78,79. Collectively, these findings suggest that pulvinar alterations may impact coordination across thalamocortical and cortico-subcortical circuits, weakening networks essential for sustained attention68,70,76,82,83, action execution68,69,84,85,86,87,88,92,93, and performance monitoring68,69,70,71,83,88,89,93.
Parasomnia-specific convergence was observed in the PCC, a medial limbic structure and key node of the DMN, implicated in subjective value and reward processing72,73,74,75. Functional roles of the PCC include supporting self-referential thought, autobiographical memory, and consciousness72, which contribute to affective and social cognition74,94, valuation75, and reflection on mental states of self and others94,95. Its activity is prominent during rest and introspection, aligning with its role in internally-directed thought and memory consolidation96. Beyond these canonical functions, the PCC also contributes to internal valuation processes and reward anticipation by integrating affective and motivational information relevant to guiding goal-directed behavior74,94,97,98. Consistent with this functional profile, alterations involving the PCC have been associated with disrupted reward sensitivity and maladaptive decision-making in neuropsychiatric and sleep-related disorders, including parasomnias99.
Our MACM analysis delineated the broader functional neurocircuitry linked with this PCC region, including the mid-cingulate, vmPFC, insula, and subcortical structures such as the striatum. This coactivation network is often linked with the cognitive and emotional evaluation of outcomes before (valuation) and after (reward processing) decisions are made97,98. It integrates interoceptive signals, subjective preferences, and outcome expectations to guide goal-directed behavior57,99,100,101,102,103. Within this circuitry, coordinated interactions among the vmPFC and insula have been linked with interoception, subjective preferences, and affective value representations, while co-activation with the striatum implicates dopaminergic pathways involved in reward responsivity and outcome evaluation57,97,99,100,101,102,103,104. Engagement of the mid-cingulate further suggests integration of motivational salience and performance-related signals within this valuation framework, supporting adaptive, goal-directed behavior. Functional alterations within this coactivation network have been associated with impaired reward sensitivity, maladaptive decision-making, and broader cognitive–affective disturbances observed in neuropsychiatric and sleep-related disorders, including parasomnias99,100,101,102,105,106,107.
Functional decoding of this network returned terms such as reward, preference, valence, and decision-making. In decision-making tasks, individuals select among options to maximize rewards and minimize punishments, typically expressed in a common currency (e.g., money or points), enabling assessment of relative value, discounting, and learning from outcomes98. Within the context of decision-making, reward processing serves the function of learning the subjective value (or utility) of available choices97,98. Parasomnias and sleep disruption may impact this valuation and reward processing network by altering connectivity and neurotransmitter signaling within reward-sensitive circuits. Studies have shown that sleep deprivation reduces cognitive flexibility and promotes risk-taking, especially in high-pressure and uncertain environments4,108,109,110,111,112,113. Sleep-deprived individuals also gather less information before making decisions, reflecting impaired cognitive processing114,115,116 and potential real-world consequences such as risky decision-making.
Parasomnias, including RBD, sleep-related eating disorder, sleepwalking, and nightmare disorder, have been linked to reward-processing abnormalities and reward-related personality traits such as elevated novelty seeking117,118. As parasomnias primarily manifest during transitions between non-REM sleep and wakefulness or between REM sleep and wakefulness118, these state shifts may disrupt dopamine-dependent striatal pathways104. RBD, for instance, is associated with reduced striatal dopamine and diminished responsiveness to greater rewards104. REM disruption may also impair habenula function, which integrates limbic, circadian, and reward signals to regulate monoaminergic transmission (e.g., dopamine, serotonin)119,120,121. Preclinical studies show REM fragmentation induces lateral habenula hyperactivity122, suppressing dopamine signaling and contributing to anhedonia and diminished reward sensitivity119,123. As a circadian regulator, the habenula modulates monoaminergic rhythms that may be destabilized by REM disturbances, creating a feedback loop in which REM disruption amplifies habenular output and exacerbates reward deficits120,121,122,123. Bidirectional interactions support this model, as habenula lesions reduce REM sleep, whereas REM fragmentation increases habenula activity122,123. Together, these findings underscore the importance of sleep integrity regarding the motivational functions of valuation and reward neurocircuitry; when disrupted, rewards are blunted, preferences shift, and adaptive decision-making deteriorates120,121,123,124.
Although our analyses identified disorder-general convergent structural decreases in the pulvinar and parasomnia-specific convergence in the PCC, we did not detect structural increases common across disorders or dyssomnia-specific structural decreases. Given prior meta-analytic findings, these null findings warrant consideration72,73,74,75,78,79,80,81. One plausible explanation is the heterogeneity of sleep disorder phenotypes combined with limited statistical power, which may reduce sensitivity to subtler or bidirectional structural alterations125,126. Notably, thalamic convergence emerged only in the disorder-general analysis and was absent in both the dyssomnia- and parasomnia-specific analyses, whereas PCC convergence was restricted to the parasomnia-specific analysis, indicating that structural alterations may differ depending on the level of analytic grouping68,69,70,71,83,88,89,97,98. At a neuroanatomical level, this analytic dissociation aligns with the distinct large-scale networks in which these regions are embedded: the pulvinar is situated within a task-positive network supporting attentional allocation, action execution, and performance monitoring, whereas the PCC is embedded within a network involving the vmPFC, insula, and striatum that supports internal evaluation, motivational regulation, and reward-based decision-making68,69,70,71,76,82,84,85,86,87,88,89,92,97. Together, these findings suggest that dyssomnias and parasomnias preferentially engage distinct large-scale functional systems at different levels of disorder aggregation, underscoring the importance of network-level interpretations even in the presence of regionally specific null findings57,68,69,70,71,97,98.
We identified three primary limitations in our study. First, even though the current work included more primary papers than most previous sleep disorder-related neuroimaging meta-analyses24,26,27,28,29,35, the number of available publications remains insufficient for more fine-grained ancillary analyses (e.g., disorder-specific for all disorders). Current best practices recommend a minimum of 17–20 contrasts for robust neuroimaging meta-analyses125,126. Second, our structural findings are skewed toward well-studied conditions, with no data available for multiple DSM-5-defined disorders (e.g., circadian rhythm sleep disorders, sleep-related hypoventilation). This highlights a need for further research into the neural correlates of a broader range of sleep disorders and a more comprehensive understanding of their shared and unique neurobiological mechanisms. Finally, while taxonomic groupings (e.g., parasomnias vs. dyssomnias) provide a practical organizational framework aligned with current clinical standards, we acknowledge that such classification schemes are continually evolving and may not fully capture the neurobiological complexity of sleep disorders. Alternative frameworks could offer complementary perspectives, and future work could explore the implications of alternative taxonomies to determine if more nuanced or evidence-based groupings may yield additional insights. For instance, adopting a transdiagnostic approach such as the RDoC framework, though not yet tailored for sleep disorders, could facilitate dimensional investigations of arousal regulation, circadian function, and other core sleep-related processes57,127,128. This may help elucidate more precise brain-behavior relationships and move beyond categorical diagnostic boundaries57.
This meta-analytic work enhances our understanding of neurobiological alterations associated with sleep disorders when considering structural findings across dyssomnias and parasomnias. Our outcomes suggest that regional structural alterations in the thalamus and PCC, that potentially impact larger-scale functional networks, may account for real-world behavioral consequences often linked with sleep disorders. Specifically, alterations in pulvinar integrity may affect daily functioning by increasing susceptibility to attentional lapses and task-related errors, while PCC dysfunction may contribute to reward processing and behavioral motivation alterations. Ultimately, such insights could guide development of more targeted interventions aimed at mitigating impairments and improving behavioral outcomes for those living with sleep disorders.