Obsessive–compulsive disorder (OCD) is a neurobehavioral condition characterized by the presence of obsessions, intrusive, recurrent thoughts perceived as involuntary and beyond the individual’s control, and compulsions, which manifest as repetitive behaviors or mental acts aimed at reducing the distress triggered by such thoughts (1). These symptoms can cause significant impairment in daily functioning and quality of life. The global prevalence of OCD in children and adolescents is estimated at approximately 0.8–1%, with a mean age of onset around 10 years (2). However, underdiagnosis remains common, as many children do not receive timely or adequate assessment and treatment; the duration of untreated OCD remains among the longest of psychiatric disorders, with diagnostic delays averaging more than two years in pediatric samples (3). More than half of adult OCD cases have their onset during childhood or adolescence (4), supporting the disorder’s developmental continuity, although a subset of patients may achieve partial remission over time (5). Since the DSM-5-TR, OCD has been classified as distinct from anxiety disorders, within the broader category of obsessive–compulsive and related disorders (6). This reclassification reflects growing evidence that, although anxiety is a frequent component, it is not the defining feature of OCD. The disorder is instead marked by intrusive, ego-dystonic thoughts and compulsive behaviors that are phenomenologically and neurobiologically distinct from the fear and avoidance typical of anxiety disorders. Neuroimaging meta-analyses highlight altered fronto-striatal connectivity and hyperactivation in cortico-striato-thalamo-cortical networks, contrasting with the amygdala-centered dysregulation observed in anxiety (7). Moreover, OCD displays a distinct cognitive profile, characterized by impairments in executive control, response inhibition, and cognitive flexibility—core domains of self-regulation and top-down modulation of emotion (8). Clinical and epidemiological data summarized in recent reviews support the affinity of OCD with other obsessive–compulsive spectrum disorders, including body dysmorphic disorder and trichotillomania (9). Within this spectrum, a tic-related OCD subtype, often termed “Tourettic OCD”, has been increasingly recognized, particularly in developmental samples (10). Conversely, clinical presentations characterized primarily by hoarding symptoms have been separated into a distinct condition.

Beyond its categorical definition, emerging developmental and transdiagnostic perspectives suggest that pediatric OCD may be best conceptualized as a disorder of cognitive and emotional control, characterized by rigidity, impaired cognitive flexibility, and difficulties managing uncertainty and threat across development (see Figure 1) (11–13). Within this framework, emotional control refers to the set of processes that enable the child to modulate emotional arousal, distress responses, and threat-related cognitions in a flexible, goal-directed manner across development. Recent work on pediatric OCD and related emotional disorders has highlighted that difficulties in emotion regulation, heightened distress reactivity, and reduced tolerance for uncertainty represent central regulatory vulnerabilities in youth with OCD (13, 21, 73). Converging evidence from cognitive neuroscience and developmental psychopathology indicates that these deficits in executive and regulatory control contribute to the persistence and phenomenology of obsessive–compulsive symptoms in youth (11–13). These self-regulatory impairments interact with familial processes, such as parental anxiety, accommodation, and emotion-regulation styles, which may temporarily reduce distress but inadvertently maintain compulsive cycles and reinforce maladaptive coping patterns (14). Family accommodation in particular has been consistently associated with greater symptom severity and poorer treatment response, highlighting the reciprocal nature of child and parent regulation in OCD (15).

This integrative framework situates pediatric OCD within a broader network of shared neurodevelopmental, affective, and family-based mechanisms that transcend traditional diagnostic boundaries, aligning with transdiagnostic models emphasizing common processes such as emotion dysregulation, cognitive inflexibility, and intolerance of uncertainty (16, 17). From this perspective, pediatric OCD exemplifies a developmental disorder of control that bridges the domains of cognition, emotion, and interpersonal regulation.

The present mini-review aims to provide a multidimensional synthesis of pediatric OCD through this integrative lens. Specifically, it examines phenomenology, comorbidity, family dynamics, and treatment approaches to illustrate how deficits in cognitive-emotional control and family modulation jointly shape the developmental course and clinical management of OCD in youth.

Comorbidity is highly prevalent in pediatric OCD, with a meta-analysis estimating that 64% of affected youth meet criteria for at least one additional disorder (48). From a developmental–mechanistic perspective, comorbidities are not merely additive but illuminate distinct dimensions of control—from flexibility and inhibition to affective and sensory regulation—offering a transdiagnostic window into shared neurodevelopmental vulnerabilities. Broadly, these can be grouped into neurodevelopmental and affective–psychiatric domains.

Beyond individual-level vulnerabilities, these regulatory difficulties extend to the interpersonal system, where family dynamics play a critical role in maintaining or alleviating symptoms.

Family accommodation (FA) is not a primary cause of obsessive–compulsive disorder, but it reliably functions as a mechanism of external co-regulation in pediatric OCD: by assisting with rituals, providing reassurance, or avoiding triggers, caregivers reduce the child’s distress in the short term while inadvertently maintaining obsessive–compulsive cycles over time (62–65). Within this framework, FA can be understood as a dyadic regulatory loop—the child’s anxiety shapes the parent’s behavior and the parent’s accommodation shapes the child’s reliance on external control—thereby constraining opportunities for autonomous coping, corrective exposure, and learning.

Empirically, higher FA is consistently associated with greater OCD severity (especially contamination/washing), increased internalizing (anxiety, depression) and externalizing symptoms (e.g., ADHD/ODD), and poorer global, social, and role functioning independent of anxiety or cognitive level (63, 64, 66–68). FA is also linked to lower self-esteem and perceived efficacy in youth, suggesting interference with the maturation of self-regulatory capacity (68). Caregivers with elevated anxiety sensitivity or a family history of anxiety appear more prone to accommodating responses, indicating that parental emotion-regulation styles can amplify the child’s control dysregulation (63).

These observations have clear treatment implications. Family-inclusive protocols that explicitly target accommodation, such as the structured four-phase model (alliance/psychoeducation, identification and graded reduction of accommodation, ERP coaching) proposed by Demaria et al. (69) (see Table 3)—aim to shift co-regulation from accommodation to supportive non-avoidance, restoring conditions under which exposure and response prevention (ERP) can be effective. Likewise, SPACE (Supportive Parenting for Anxious Childhood Emotions) trains caregivers to respond with support rather than accommodation, by mapping key accommodating behaviors, implementing planned reductions, and managing child distress while reinforcing competence and independence (70). Viewed through a developmental, process-based lens, family accommodation is best conceptualized as external co-regulation that alleviates anxiety in the short term but sustains symptoms over time (15, 71, 72), a relational expression of impaired cognitive–emotional control in youth OCD (13) aligns with a transdiagnostic, mechanism-focused formulation of the disorder.

Recognizing family accommodation as a relational form of control dysregulation also clarifies its place within the broader therapeutic landscape. Because obsessive–compulsive symptoms are embedded in both individual and interpersonal regulatory loops, effective intervention must target control processes across levels, within the child (cognitive flexibility, tolerance of uncertainty), within the family system (patterns of co-regulation and accommodation), and within developmental context (gradual autonomy and mastery). This perspective naturally transitions from understanding family mechanisms to designing treatments that restore adaptive regulation.

International guidelines identify both pharmacological and psychological interventions as effective treatments for OCD, with cognitive-behavioral therapy (CBT) recognized as the gold-standard approach (73). Compared with medication alone, CBT produces more enduring change, lower relapse rates, and fewer side effects (74). Recent data indicate remission rates of 39.3% for CBT alone, 21.4% for SSRIs, and 53.6% for combined treatment (75). From a process-based perspective, CBT, particularly through ERP, can be understood as a means of recalibrating these same control processes that become dysregulated at both the individual and interpersonal levels.

From a process-based perspective, CBT, particularly through ERP, can be understood as a means of restoring flexible cognitive–emotional control. In adults, ERP has been shown to improve intolerance of uncertainty, cognitive rigidity, and maladaptive avoidance, mechanisms central to the persistence of obsessive–compulsive symptoms (76, 77). Consistent with this rationale, the Unified Protocols for Children and Adolescents (UP-C/A) have recently been evaluated for OCD, alongside anxiety and depression. The protocol explicitly trains emotion regulation and cognitive flexibility within a transdiagnostic, process-based framework. In a sample of 388 youth, OCD symptoms improved more slowly in the first half of treatment but caught up in the second half; youth with and without OCD showed comparable gains in anxiety, depression, and transdiagnostic targets (anxiety sensitivity, cognitive flexibility, distress tolerance). These data also suggest that introducing exposure earlier may confer additional benefit (78).

Although direct mechanistic evidence in pediatric populations is still limited, emerging developmental findings suggest that these same processes, rigidity, intolerance of uncertainty, and emotion dysregulation, play a central role in childhood OCD and may represent key therapeutic targets for age-adapted ERP (13, 79).

Within this framework, treatment is not merely symptom reduction but a gradual recalibration of maladaptive control processes, such as inflated responsibility, perfectionism, and intolerance of uncertainty, that maintain obsessive-compulsive symptoms. These cognitive shifts may also enhance emotion-regulation capacities, as emerging evidence suggests that emotion dysregulation plays a role in the maintenance and therapeutic change of pediatric OCD (13, 76, 80).

In children and adolescents, the developmental tailoring of CBT is essential to ensure emotional engagement and cognitive comprehension throughout the therapeutic process (81, 82). Early sessions typically focus on psychoeducation and the collaborative identification of feared situations and avoidance patterns, fostering a sense of agency and mastery. Subsequent stages target distorted control beliefs, such as overestimation of responsibility, perfectionism, or intolerance of uncertainty, before introducing ERP exercises that are adapted to the child’s developmental level and emotional maturity (81, 83, 84).Consistent with international recommendations, a stepped-care approach is increasingly endorsed to match treatment intensity to clinical severity. For youth with mild functional impairment, guided self-help combined with family psychoeducation may suffice, while those with moderate to severe symptoms require full CBT with ERP, caregiver involvement, and developmental adaptations (73). When psychological therapy is declined or not feasible, SSRIs remain an evidence-based adjunct, provided careful monitoring and integration with behavioral principles. While stepped-care models adjust treatment intensity according to clinical severity or response, staged-care approaches (85) organize interventions around underlying control mechanisms and developmental needs. Building on this principle, Farrell et al. (85) introduced a staged-care CBT–ERP model for pediatric OCD that operationalizes a mechanism-based hierarchy: interventions are scaled according to shared control mechanisms, such as anxiety, avoidance, and emotion dysregulation, and adjusted for developmental stage. This model bridges process-based theory and routine clinical practice, demonstrating how stepped delivery systems can translate mechanistic understanding into scalable care.

Yet, even mechanism-oriented approaches should be situated within the child’s relational environment, as family dynamics crucially shape both the onset and maintenance of obsessive-compulsive symptoms. Interventions that explicitly target family accommodation, such as the Supportive Parenting for Anxious Childhood Emotions (SPACE) program (70) or the structured four-phase family model (69), help parents shift from accommodating distress to supporting exposure-based coping, thereby restoring conditions under which ERP can be effective. Meta-analytic evidence indicates that broader family variables, including conflict, blame, overprotection, and poor cohesion, predict treatment resistance, underscoring the need for multidimensional, family-focused interventions (14).

Emerging third-wave approaches, such as Acceptance and Commitment Therapy (ACT), extend this process-based rationale by cultivating psychological flexibility, the capacity to engage with distressing internal experiences while pursuing valued goals (86–88). In younger children, behavioral and parent-mediated strategies remain preferable, focusing on reducing accommodation and scaffolding self-regulation capacities (89).

Pediatric OCD can be conceptualized as a developmental disturbance of cognitive–emotional control, rather than as a discrete categorical condition. Over the past decade, research has moved beyond traditional diagnostic boundaries toward dimensional and transdiagnostic frameworks that situate obsessive–compulsive phenomena within broader developmental pathways of internalizing psychopathology. Conventional nosological systems such as DSM and ICD often fail to capture the fluidity and overlap of symptoms commonly observed in childhood and adolescence, where anxiety, depression, and compulsivity frequently co-occur and evolve dynamically over time.

From a developmental psychopathology perspective, OCD emerges from partially shared mechanisms, such as emotion dysregulation, intolerance of uncertainty, and cognitive inflexibility, that cut across diagnostic categories. Longitudinal studies show that early behavioral rigidity and anxious traits predict later obsessive–compulsive symptoms (90), suggesting that OCD may emerge along a broader continuum of maladaptive control and internalizing distress (91). This dimensional view does not negate the specificity of OCD but instead situates it within a broader framework of developmental vulnerabilities that interact over time.

Recent theoretical advances have reinforced this perspective. Garnaat et al. (92), applying the Research Domain Criteria (RDoC) to pediatric OCD, propose that dysfunctions in the Potential Threat and Habit Formation domains may explain the transition from anxiety-driven rituals to compulsive, automatized behaviors as fronto-striatal circuits mature. Similarly, dimensional frameworks such as HiTOP integrate obsessive–compulsive phenomena within the internalizing spectrum, reflecting shared neural substrates and affective processes. The EMERGE study (93) further supports this view by demonstrating that transdiagnostic mechanisms—such as intolerance of uncertainty, behavioral avoidance, and repetitive negative thinking—predict the co-development of obsessive–compulsive, depressive, and attenuated psychotic symptoms in adolescents. Taken together, these findings underscore the importance of targeting regulatory mechanisms, rather than categorical symptoms, in both research and clinical intervention.

From a clinical standpoint, this shift has practical advantages. Transdiagnostic and process-based interventions, such as UP-C/A, directly target regulatory dysfunctions underlying OCD and related emotional disorders. Empirical findings indicate that improvements in cognitive flexibility and distress tolerance mediate symptom reduction across anxiety, depression, and OCD (94). Focusing on these core transdiagnostic processes may optimize treatment outcomes and prevent symptom migration between diagnostic categories.

Importantly, conceptualizing OCD dimensionally also aligns with its known heterogeneity. Pediatric OCD often presents with fluctuating symptom profiles, high comorbidity with anxiety and tic disorders, and variable levels of insight. Dimensional models accommodate this variability by viewing compulsivity and intrusive thinking as expressions of broader regulatory and neurocognitive dysfunctions rather than discrete disease entities. They also highlight developmental timing—showing that early emotional rigidity, maladaptive habit learning, or difficulty inhibiting prepotent responses may constitute developmental risk markers for later OCD onset.

In sum, applying transdiagnostic and developmental models to pediatric OCD allows for a more integrated understanding of its onset, course, and treatment. By clarifying the regulatory mechanisms that underlie OCD and related disorders, these models refine its conceptualization and support early, mechanism-focused interventions aimed at strengthening cognitive flexibility, enhancing emotion regulation, and improving tolerance of uncertainty across development. Together, transdiagnostic and developmental frameworks converge on the view of pediatric OCD as a disorder of cognitive–emotional control. This integrative lens not only accounts for comorbidity and heterogeneity but also informs mechanism-focused and family-integrated interventions that target maladaptive control processes within the child’s relational context.

Viewing pediatric OCD as a disorder of cognitive–emotional control, modulated by family dynamics, offers a unifying framework that reconciles developmental trajectories, comorbidity patterns, and treatment mechanisms. This perspective bridges categorical diagnosis with transdiagnostic science, clarifying how rigidity, emotion dysregulation, and intolerance of uncertainty shape symptom expression across stages of development and within relational contexts. Clinically, it supports earlier, mechanism-focused, and context-sensitive care: developmentally adapted CBT/ERP, family-integrated approaches that reduce accommodation and scaffold regulation, and flexible stepped/staged delivery that matches interventions to shared control mechanisms. Research and services aligned with this lens, linking mechanistic assessment to outcomes and prioritizing scalable, family-informed models, can improve precision in evaluation and durability of treatment gains, ultimately advancing quality of life for children and adolescents with OCD.