Abstract
Background/Aim: Pain assessment and management in children remain challenging, particularly in those with neurodevelopmental disorders. Attention-deficit/hyperactivity disorder (ADHD) is characterized by alterations in attention, executive function, emotional regulation, and reward processing. These domains are also critically involved in pain perception and expression. Emerging evidence suggests that children with ADHD may experience pain differently, display atypical pain behaviors, and face substantial challenges in pain assessment and treatment. However, the literature on pediatric ADHD and pain is fragmented across experimental, clinical, and behavioral studies.
Materials and Methods: This narrative review critically examines the neurobiological, psychological, and clinical interactions between ADHD and pain in children.
Results: We discuss proposed mechanisms linking ADHD to altered pain processing, summarize evidence on pain perception and expression, explore common pain conditions where this interaction is clinically relevant, and analyze challenges in pain assessment and management. Finally, we identify knowledge gaps and propose future directions toward function- and child-centered pain care.
Conclusion: By considering ADHD as a modifier of pain experience and a potential contributor to pain chronification rather than a mere comorbidity, this review highlights the importance of adapting pain assessment and management strategies to the specific neurodevelopmental profile of pediatric patients.
Introduction
Pain is a multidimensional experience influenced by sensory, cognitive, emotional, and contextual factors (1). In pediatric populations, accurate pain assessment is further complicated by developmental stage, communication abilities, and behavioral modulation (2). These challenges are amplified in children with neurodevelopmental disorders or other conditions of vulnerability, in whom pain may be under-recognized, misinterpreted, and consequently inadequately treated (3, 4).
Attention-deficit/hyperactivity disorder (ADHD) is among the most prevalent neurodevelopmental conditions in childhood. This complex disorder is characterized by persistent patterns of inattention, hyperactivity, and impulsivity, arising from the dynamic interplay of neurobiological, genetic, and environmental factors (5). In the general population, the prevalence of ADHD is estimated at approximately 4% among children and adolescents (6). In contrast, pooled estimates from psychiatric and clinical settings indicate substantially higher prevalence rates, reaching up to 32% in pediatric samples (7).
Beyond its core symptoms, ADHD is increasingly conceptualized as a disorder of executive control, emotional regulation, and motivational processing (8, 9). Notably, these domains substantially overlap with neural systems involved in pain modulation and chronification processes (10). Despite this theoretical convergence, pain in children with ADHD has received limited systematic attention. Clinical observations suggest that these children may manifest heightened pain complaints or, conversely, reduced pain reporting despite significant nociceptive input. This variability raises concerns regarding both pain under-treatment and inappropriate escalation of analgesic therapies (11-13). Importantly, emerging pediatric evidence indicates that pain perception in ADHD may be state-dependent, with reduced pain sensitivity in unmedicated children that appear to normalize under stimulant treatment. These findings support a central rather than peripheral modulation mechanism (12). In parallel, scoping evidence in youth suggests an association between ADHD and chronic pain, although available studies remain heterogeneous and largely observational (13). In contrast, in adult populations the association between ADHD and chronic pain is well established, particularly for pain conditions characterized by nociplastic features (14).
On these premises, this narrative review aims to synthesize and critically appraise current evidence on pain in children with ADHD, with specific objectives to: i) explore neurobiological and cognitive mechanisms linking ADHD to pain processing; ii) summarize findings on pain perception, tolerance, and behavioral expression; iii) identify clinical pain conditions where ADHD-related factors are particularly relevant; iv) discuss challenges in pain assessment and management; and v) highlight gaps in knowledge and directions for future research.
Neurobiological Links Between ADHD and Pain
Available evidence suggests that ADHD should not be conceptualized merely as a comorbid condition, but rather as a modifier of pain experience, influencing cognitive-affective processing, motor regulation, and vulnerability to pain chronification (9, 14-16). In this context, several neurobiological mechanisms have been proposed to account for altered pain processing in children with ADHD, involving pathways that are central to attentional control, emotional regulation, and sensory modulation (17). Among these, dysregulation of dopaminergic and noradrenergic systems has emerged as one of the most extensively investigated mechanisms. ADHD is consistently associated with functional and neurochemical alterations in dopamine and norepinephrine signaling, particularly within fronto-striatal and fronto-limbic circuits that play a key role in cognitive control, reward processing, and emotional regulation (17, 18). Notably, the same neurotransmitter systems play a central role in descending pain modulation, influencing nociceptive gating at both spinal and supraspinal levels, as well as the attribution of salience to sensory stimuli (19, 20). Dysregulation within these circuits may therefore lead to altered pain sensitivity, inconsistent pain reporting, or paradoxical pain behaviors, depending on contextual and motivational factors (21). In addition to catecholaminergic pathways, it is plausible that glutamatergic neurotransmission also contributes to chronic pain vulnerability in ADHD. Evidence from adult ADHD populations indicates an imbalance in glutamate signaling within key hubs of the default mode network, supporting a role for dysregulated excitatory neurotransmission in attentional lapses and impaired cognitive control (22). Importantly, glutamatergic dysregulation has been implicated in central sensitization and maladaptive plasticity, mechanisms that are central to the development and maintenance of chronic pain (23). Taken together, these alterations provide a plausible pathway through which ADHD-related network dysfunction may not only shape acute pain reporting but also increase vulnerability to pain persistence and pain-related disability (13). In this complex scenario, neuroinflammation has been proposed as a potential shared mechanism underlying both ADHD and chronic pain, particularly through its contribution to central sensitization and the maintenance of persistent pain states (15). However, direct evidence supporting this hypothesis in pediatric populations remains limited (15).
Another neurobiological mechanism underlying the link between ADHD and pain involves executive dysfunction and impaired top-down pain control. Effective pain modulation relies on higher-order cognitive processes, including sustained attention, inhibitory control, and cognitive flexibility, which enable individuals to regulate the attentional focus on pain and engage adaptive coping strategies (24). In children with ADHD, deficits in these executive domains may compromise the ability to exert top-down control over nociceptive input, leading to exaggerated pain behaviors, increased pain-related distress, or difficulty disengaging from pain once perceived (24). This impairment may be particularly evident in clinical or procedural settings requiring sustained attention and self-monitoring, where pain-related behaviors may be misattributed to oppositionality or behavioral dysregulation.
Beyond cognitive mechanisms, emotional dysregulation represents a critical bridge between ADHD and chronic pain. Emotional lability, frustration intolerance, and heightened stress reactivity are common features of ADHD and are frequently compounded by comorbid anxiety or mood symptoms (5). These affective factors are well known to amplify pain perception through interactions between limbic structures and pain-processing networks, reducing coping capacity and increasing pain-related catastrophizing (25). As a result, children with ADHD may report higher pain intensity or display disproportionate distress relative to the degree of tissue injury or nociceptive input. Nevertheless, it should be acknowledged that much of the mechanistic evidence derives from adult populations or indirect models, and pediatric-specific data remain limited, warranting cautious interpretation. The neurocognitive domains linking ADHD and pain processing are summarized in Table I. Figure 1 illustrates how ADHD may act as a modifier of pain pathways and pain chronification processes rather than a simple comorbid condition.
Neurocognitive domains in ADHD and implications for pain processing in children.
Neurobiological overlap between attention-deficit/hyperactivity disorder (ADHD) and chronic pain. ADHD-related executive dysfunction, emotional dysregulation, and altered reward and salience processing interfere with fronto-striatal and fronto-limbic circuits involved in cognitive-affective pain processing and descending pain modulation. Dysregulation of dopaminergic and noradrenergic signaling contributes to impaired top-down control and altered pain salience attribution, leading to state-dependent pain sensitivity, atypical pain behaviors, and increased functional disability. Notably, nociceptive input and ascending pain pathways remain largely intact, whereas central modulation is disrupted, increasing vulnerability to pain chronification. ACC: Anterior cingulate cortex; PAG: periaqueductal gray; RVM: rostral ventromedial medulla; DRG: dorsal root ganglion.
Pain Perception and Expression in Children With ADHD
Studies examining pain perception in children with ADHD report heterogeneous and sometimes contradictory findings, ranging from heightened pain complaints to reduced pain sensitivity (26). This heterogeneity likely reflects differences in study design, medication status, attentional demands, and outcome measures, rather than true inconsistencies in pain processing.
Experimental and population-based studies suggest that, in some children with ADHD, pain thresholds and tolerance may be altered, potentially reflecting differences in attentional engagement, reward processing, and salience attribution rather than primary abnormalities of nociceptive pathways. In particular, reduced pain perception has been reported in untreated children with ADHD, a phenomenon that has been interpreted as reflecting diminished attentional allocation to painful stimuli or altered motivational relevance of pain signals (11). Importantly, this pattern appears to be state-dependent rather than trait-like. Evidence indicates that reduced pain perception tends to normalize in children receiving stimulant medication, supporting the hypothesis that dopaminergic modulation of fronto-striatal and fronto-limbic circuits plays a central role in shaping pain experience in ADHD, rather than fixed sensory deficits (11, 12, 24). This observation aligns with broader neurobiological models implicating dopamine in pain salience, reward-related analgesia, and top-down modulation of nociceptive input (21, 24). Furthermore, consistent findings have also been reported in adult populations, where alterations in pain perception in individuals with ADHD were shown to be partially reversed by methylphenidate. This data supports, in turn, a catecholaminergic mechanism underlying state-dependent pain modulation rather than fixed sensory abnormalities (27).
Beyond pain perception per se, differences in pain expression are more consistently reported across clinical and observational studies. Children with ADHD often display impulsive or exaggerated verbal pain responses, difficulty sustaining attention during pain rating tasks, and rapid shifts between pain-related and non-pain-related behaviors (28). Such expression patterns may reflect core features of ADHD, including impaired inhibitory control, emotional lability, and reduced self-monitoring, rather than increased nociceptive drive (24). As a result, pain behaviors may appear disproportionate, poorly modulated, or contextually inappropriate, particularly in settings requiring sustained attention or delayed reporting (28). Crucially, these behavioral manifestations are at risk of being misinterpreted as oppositionality, non-compliance, or behavioral dysregulation, rather than legitimate expressions of pain (3). This misattribution complicates the clinical distinction between nociceptive pain, emotional distress, and ADHD-related behavioral symptoms, increasing the risk of both under-recognition of pain and inappropriate escalation of behavioral or pharmacological interventions.
The main patterns of pain perception and expression reported in children with ADHD are summarized in Table II.
Patterns of pain perception, mechanistic processes, and clinical implications.
ADHD in Pediatric Pain Conditions
A growing body of evidence indicates that the interaction between ADHD and pain becomes particularly salient in specific pediatric pain conditions, where attentional deficits, emotional dysregulation, and behavioral impulsivity may directly influence symptom expression and clinical outcomes (29). ADHD has been consistently associated with primary headache disorders in childhood, including migraine and tension-type headache. Meta-analytic and systematic data suggest that children with migraine exhibit significantly higher rates of ADHD compared with controls, with prevalence estimates ranging between 20% and 36% depending on diagnostic criteria and clinical setting (30, 31). By contrast, findings for tension-type headaches are less consistent (30). Shared mechanisms may include altered dopaminergic signaling, cortical excitability, and impaired sensory gating, which may predispose children with ADHD to recurrent headache and increased headache-related disability.
Functional abdominal pain disorders represent another clinical domain in which ADHD-pain interactions are highly relevant. Studies using structured psychiatric interviews have reported significantly higher rates of ADHD in children with functional abdominal pain compared with both organic pain and pain-free controls (32). Attentional dysregulation, heightened interoceptive sensitivity, and emotional reactivity may amplify visceral pain perception and contribute to symptom persistence.
Musculoskeletal pain, including multi-site and widespread pain, is frequently reported in youths with ADHD, particularly in psychiatric or tertiary care cases (13, 16). Motor regulation deficits, hyperactivity, and increased injury risk may contribute to both pain onset and maintenance. Notably, longitudinal data further suggest that childhood ADHD may be associated with an increased risk of widespread chronic pain in adulthood (26, 33).
Children with ADHD may be especially vulnerable during medical procedures, where sustained attention, behavioral inhibition, and anticipatory coping are required. In this context, pain-related behaviors may be intensified or poorly modulated, increasing distress for both patients and caregivers and complicating procedural pain management (3, 34, 35). Innovative strategies, including artificial intelligence-based approaches and gamification, could also be implemented (36).
Challenges in Pain Assessment in Children With ADHD
Pain assessment in children with ADHD presents unique challenges that extend beyond developmental considerations alone. Standard self-report pain scales assume adequate attentional capacity, sustained engagement, and introspective accuracy, domains that may be compromised in ADHD (3).
Furthermore, children with ADHD may provide inconsistent or rapidly fluctuating pain ratings, influenced by attentional shifts, emotional state, or contextual factors rather than stable nociceptive input. In this scenario, observational tools, while useful, may also be subject to bias, as hyperactivity, impulsivity, or emotional outbursts can be misinterpreted as behavioral non-compliance rather than pain-related distress (2, 3).
Moreover, the overlap between pain behaviors and ADHD-related symptoms complicates the distinction between nociceptive pain, anxiety-driven distress, and behavioral dysregulation. This diagnostic ambiguity increases the risk of both under-recognition of pain and over-medicalization of behavioral symptoms, underscoring the need for multimodal, context-sensitive pain assessment strategies that integrate caregiver input, behavioral observation, and functional impact.
In this context, reliance on single-point, intensity-based pain ratings alone is insufficient and potentially misleading in children with ADHD. Accordingly, pain assessment in children with ADHD should adopt a multimodal and context-sensitive approach that integrates repeated self-report, caregiver input, structured behavioral observation, and evaluation of functional impact over time, rather than relying on isolated intensity ratings. Such a framework facilitates the differentiation between nociceptive pain, emotional distress, and ADHD-related behavioral dysregulation, thereby reducing the risks of pain under-recognition and inappropriate medicalization of behavioral symptoms.
Implications for Pain Management and Future Directions
Given the assessment challenges, pain management in children with ADHD should be guided not only by reported pain intensity but also by functional impact and behavioral context. From a clinical perspective, the available evidence supports a function-centered and individualized approach to pain management in children with ADHD (13). In this scenario, pain assessment and treatment strategies should be integrated with the core management processes underlying ADHD care, recognizing that attentional regulation, emotional control, behavioral planning, and medication management directly influence how pain is perceived, expressed, and responded to over time (36).
Pharmacological strategies should consider the potential bidirectional effects of stimulant medications on pain perception and emotional regulation, as preliminary data suggest that stimulants may normalize altered pain sensitivity in some children (12, 13). Importantly, given the catecholaminergic modulation in pain regulation, medications commonly used for the treatment of ADHD may also exert beneficial effects on chronic pain and pain-related cognitive dysfunction, particularly when these symptoms are mediated by central sensitization mechanisms (14). First-line pharmacological options for ADHD include central stimulants such as methylphenidate and lisdexamfetamine, the selective norepinephrine reuptake inhibitor atomoxetine, and the α2-adrenergic receptor agonist guanfacine (37). Emerging clinical observations and experimental data suggest that methylphenidate, atomoxetine, and guanfacine may be associated with improvements in chronic pain symptoms and related cognitive disturbances (38, 39). Nevertheless, despite regulatory approval and widespread clinical use, treatment persistence remains a significant challenge, with more than one-third of pediatric patients discontinuing ADHD pharmacotherapy within the first year because of limited efficacy, adverse effects, or tolerability issues (37).
Non-pharmacological interventions, including behavioral therapy, cognitive-behavioral pain management strategies, and caregiver education, are particularly relevant in this population. Interventions targeting emotional regulation, attentional control, and coping skills may reduce pain-related distress even in the absence of changes in nociceptive input (40, 41). Furthermore, given the high use of analgesics among individuals with ADHD, these non-pharmacological strategies can reduce pain-related distress and functional impairment while limiting reliance on repeated analgesic intake (11).
Future research should prioritize longitudinal and mechanistic studies to clarify causal pathways between ADHD and pain, with particular attention to developmental trajectories, sex differences, and the role of neuroinflammatory processes. Other unresolved issues in this complex field, such as clinical expressions of ADHD (e.g., ADHD subtypes) and pain features, should be better clarified. For example, Berggren et al. suggested that hyperactivity and impulsivity may show a stronger association with pain outcomes than inattention-related symptoms (42).
Integrating multimodal objective measures, such as neuroimaging, digital phenotyping, and physiological biomarkers, may further enhance pain assessment and stratification in this vulnerable population (13). In this perspective, artificial intelligence (AI)-based approaches can offer a valuable help. Recent evidence in ADHD research indicates that machine learning and deep learning models applied to neuroimaging, electrophysiological, behavioral, and digital data can capture latent patterns of attentional control, emotional regulation, and network dysfunction that are not accessible through standard clinical assessment. Translated to pediatric pain care, these approaches could support the identification of ADHD-related pain phenotypes, and facilitate personalized, function-centered treatment strategies (43). Additionally, strategies for objective pain assessment could also be investigated (44). However, clinical implementation will require rigorous validation, integration of multimodal data streams, and careful consideration of ethical and developmental issues (45).
Conclusion
The available literature supports the view that ADHD modifies the pain experience and contributes to vulnerability to chronic pain, influencing how pain is perceived, expressed, and interpreted rather than constituting a simple comorbid condition. Neurobiological alterations, executive dysfunction, and emotional dysregulation contribute to heterogeneous pain presentations in children with ADHD. These mechanisms help explain the marked variability in pain sensitivity and the frequent occurrence of atypical pain behaviors, which may be disproportionate or poorly modulated and are often misattributed to behavioral dysregulation. Clinically, the interaction between ADHD and pain is particularly evident in headache disorders, functional abdominal pain, musculoskeletal pain, and procedural contexts, where attentional and emotional factors directly influence symptom burden and functional impact. Overall, effective pain assessment in children with ADHD requires multimodal, context-sensitive approaches that integrate self-report, caregiver input, behavioral observation, and functional outcomes over time.
Acknowledgements
The Authors thank the Scientific Direction of the Ospedale Pediatrico Bambino Gesù IRCCS for providing logistical support.
Footnotes
Authors’ Contributions
Conceptualization: A.V. and T.G.C.; resources: A.V. and M.C.; data curation: M.C. and V.C.; writing – original draft preparation: M.R.M and M.C.; writing – review and editing: M.R.M and M.C.; visualization: A.V and D.E.; funding acquisition: A.V. All Authors have read and agreed to the published version of the manuscript.
Conflicts of Interest
All the Authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Funding
This work was supported also by the Italian Ministry of Health with “Current Research funds”.
Artificial Intelligence (AI) Disclosure
During the preparation of this manuscript, a large language model (GPT5.2, OpenAI) was used solely for language editing and stylistic improvements in select paragraphs. No sections involving the generation, analysis, or interpretation of research data were produced by generative AI. All scientific content was created and verified by the authors.
- Received January 7, 2026.
- Revision received January 31, 2026.
- Accepted February 4, 2026.
- Copyright © 2026 The Author(s). Published by the International Institute of Anticancer Research.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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