According to the Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition) (DSM-5) (1), the diagnosis of Attention Deficit Hyperactivity Disorder (ADHD) requires meeting three core criteria: “symptoms persist for at least 6 months”, “occur in at least 2 settings (e.g., home, school, workplace)”, and “cause significant impairment in social, academic, or occupational functioning”, with symptoms onset before 12 years of age. DSM-5 explicitly classifies ADHD into three clinical subtypes: (a) Predominantly Inattentive Presentation: Requires at least 6 inattention symptoms and fewer than 5 hyperactivity/impulsivity symptoms. Clinical manifestations often include poor academic performance (e.g., procrastinating on homework, missing test questions), weak daily planning abilities, and easily neglecting others’ signals in social interactions. (b) Predominantly Hyperactive-Impulsive Presentation: Requires at least 6 hyperactivity/impulsivity symptoms and fewer than 5 inattention symptoms. Clinical features include excessive activity in early childhood (e.g., constant running, climbing dangerous objects) and frequent conflicts from intrusive behaviors in social settings (e.g., suddenly snatching others’ toys). (c) Combined Presentation: Meets at least 6 inattention symptoms and 6 hyperactivity/impulsivity symptoms simultaneously. It presents with features of both previous subtypes, such as being easily distracted and impulsively interrupting others in social interactions.

ADHD is often comorbid with other neurodevelopmental disorders, among which Autism Spectrum Disorder (ASD) and Developmental Coordination Disorder (DCD) are particularly relevant. All three are associated with immature brain development, especially involving overlapping brain regions related to attention regulation, motor control, and social cognition (e.g., prefrontal cortex, cerebellum, cingulate gyrus). The core characteristics of ASD include social communication deficits and stereotyped behaviors, accompanied by restricted, repetitive patterns of behavior, interests, or activities. The social understanding deficits of ASD can amplify the consequences of social impulsivity in ADHD. The core feature of DCD is motor coordination significantly lower than expected for peers, which impairs academic performance, daily self-care, or social functioning. The motor coordination deficits of DCD make the “hyperactivity” of ADHD present as “clumsy hyperactivity” (e.g., frequent falls while walking, unusual pen grip) rather than mere excess energy.

The clinical symptoms of individuals with ADHD often trap them in social difficulties, which stem from impaired social cognitive abilities emerging in childhood—particularly in Theory of Mind (ToM), empathy, and emotion recognition (2, 3). Current research on the social challenges of ADHD primarily focuses on cognitive and behavioral levels, such as executive function (4) and theory of mind. Barkley proposed the inhibitory control theory, which is a classic view of the executive function of ADHD (5). That is, the core functional defect of ADHD is insufficient inhibitory control and inability to effectively inhibit dominant or irrelevant behaviors. Its neural mechanism is closely related to prefrontal cortex dysfunction (6). Defects in inhibitory control directly lead to behavioral problems such as impulsive and hyperactive externalized behaviors. At the same time, it also indirectly hinders the development of social cognitive functions such as theory of mind and cognitive empathy. For example, insufficient working memory may limit the reasoning ability of children with ADHD for complex mental states (e.g., lies and sarcasm).

However, these studies yield inconsistent results (7) and fail to explain the disorder’s complexity. On the one hand, diagnostic criteria (DSM-V) oversimplify behaviors into “attention deficits” and “hyperactivity/impulsivity” neglecting context-dependent dynamic regulation. For instance, although individuals with ADHD may appear distracted in low-stimulation environments, they may exhibit exceptional focus in high-stimulation tasks (e.g., competitive games) (8). On the other hand, clinical assessment tools (e.g., Conners scales) rely on symptom frequency statistics and fail to capture temporal fluctuations. ADHD attention levels exhibit bimodal daily fluctuations (low activation in the morning, high activation at night), which static assessments cannot reflect (9, 10). The limitations of traditional explanations demand a new perspective—a dynamic, cross-temporal interactive framework.

Because social cognition is a complex process in which the target of attention shifts rapidly and is saturated with rich behavioral and contextual information, the ADHD cognitive system struggles both in selecting what to attend to and in determining the order in which information is processed. Consequently, individuals with ADHD display inappropriate behaviors, receive negative feedback from their interaction partners, and develop more enduring socio-cognitive difficulties.

The recent emergence of vitality forms (VFs) theory (11) provides a novel lens to understand human social behavior. This theory focuses on how individuals convey dynamic information—specifically, actions, including their intensity, rhythm, temporal contours, and spatial trajectories—through body movements, facial expressions, and vocalizations during social interactions. To explain VFs more clearly, we believe that VFs includes the following concepts: (i) VFs is a set of action gestalts composed of the most basic action characteristics and involving different parts of the whole body. The same VF in different situations constitutes an individual’s certain behavior characteristic, and different behavior characteristics constitute an individual’s behavior pattern/behavior style. (ii) VFs is a set of action representations that map psychological states and personality traits. (iii) VFs is a set of continuous dynamic actions. Different from unconditioned reflexes and voluntary actions, it is an action in a preconscious state. (iv) VFs is the action process between intention and result and does not necessarily affect the result. In social interaction, the vitality form is an important carrier for transmitting emotions, attitudes and intentions. When we see a person walking with brisk steps and a relaxed posture, we may perceive that he is in a pleasant or confident state; on the contrary, if a person moves slowly and stoops, it may imply that he is in a low mood or tired. It can help individuals quickly understand the inner state of others, promote emotional resonance and communication, and plays a key role in the establishment and maintenance of interpersonal relationships. The expression and perception of ADHD’s VFs may have a unique pattern and are often difficult to be captured by consciousness. Compared with language, VFs as an action gestalt can more directly convey thoughts/intentions and emotions, and is also more likely to be chosen, especially when an individual conceals or even cannot be aware of his own thoughts. For example, a warm, enthusiastic wave versus a cold, mechanical hand gesture conveys vastly different VFs and emotional messages. In social interactions, VFs serve as critical carriers of emotions, attitudes, and intentions, enabling rapid understanding of others’ mental states, fostering emotional resonance, and underpinning relationship building and maintenance. The expression and perception of VFs in ADHD may follow unique patterns, thereby influencing intersubjective interactions. This paper aims to discuss the characteristics of VFs in ADHD, their neural mechanisms, and their potential impact on social interaction processes.

Before discussing ADHD VFs, their dimensional features need to be clarified.

Emotions and VFs are not the same. On the one hand, an emotion is typically a short-lived mental episode triggered by a specific object, whereas a vitality form is a continuous cognitive dimension present in every kind of stimulus (38). On the other hand, emotions are usually accompanied by facial expressions, whereas vitality forms are not confined to the face alone; they are revealed through the very performance or unfolding of any action. For example, “anger” is an emotion, yet it can be enacted with different vitality forms to yield finer-grained, individualized expressions. Nevertheless, the two share common ground: both carry valence—emotions can be positive or negative, and vitality forms can likewise be categorized as positive or negative. Moreover, both can coexist within the same stimulus: dance or music, for instance, is rich in vitality forms while also saturated with emotional content (39). Vitality forms and emotions are thus key non-semantic channels of human expression. Stern identifies four action dimensions—time, force, space, and directionality—with intensity and timing as core VFs dimensions (11). Chen et al. propose that VFs encompass kinematic features as well as age- and skill-related traits (14), which are refined through individuals’ life experiences. To emphasize the emotional qualities of VFs, this study categorizes their core characteristics into action features (stability, intensity, coordination) and emotional features (valence bias, stability, intensity).

The social challenges faced by individuals with ADHD stem from abnormal VFs expression and perception. Dysregulated intensity, rhythm, and emotional valence create ambiguous or inconsistent social signals. For example, excessive intensity (e.g., abrupt gestures) may be misinterpreted as aggression and rapid emotional shifts may confuse others. Bidirectional communication breakdowns occur when individuals with ADHD struggle to decode others’ VFs because of DCI–MCC dysfunction.

Specifically, when individuals with ADHD initiate interactions with unconventional vitality forms (e.g., high-intensity gestures to express friendliness), recipients may respond defensively because of mismatched expectations. Simultaneously, when individuals with ADHD misinterpret neutral actions as hostile, inappropriate reactions are triggered (e.g., withdrawal or impulsive retorts). Cumulative negative interactions may increase the risk of social exclusion, with peers distancing themselves because of unpredictability and individuals with ADHD adopting maladaptive strategies (e.g., suppressing natural expressions), further eroding social networks. In familial contexts, parent–child VFs mismatches (e.g., fragmented responses to calm instructions) exacerbate frustration and conflict (see Figure 2).

Despite their neurobiological roots, ADHD VFs can adapt with age, experience, and targeted interventions. Their plasticity suggests the following clinical approaches in motor intervention:

The social challenges of ADHD extend beyond attention deficits and hyperactivity and are closely linked with dynamic abnormalities in VFs. Individuals with ADHD exhibit significant dysregulation in action stability, coordination, and emotional valence, leading to ambiguous social signaling and comprehension errors. These issues are rooted in DCI–MCC circuit dysfunction, dopamine system dysregulation, and motor control deficits. Based on the association between the core neural mechanism of ADHD and social function deficits, we emphasize promoting the development of social functions in ADHD patients through systematic behavioral interventions and reshaping their VFs. As a key neurotransmitter, the motor control, decision-making mechanism, and reinforcement learning process regulated by dopamine essentially share the brain’s reward processing circuit. The action regulation and immediate feedback mechanism in behavioral interventions precisely rebuild this neural reward pathway and transform disorderly release of vitality into an adaptive social behavior pattern. The core logic lies in: through structured behavioral training (such as action norms in social scenes and limb strategies for emotion regulation), patients activate the dopamine-mediated reward system when performing goal-oriented behaviors, gradually establishing a virtuous cycle of “behavior adjustment - positive feedback - neural reinforcement”, thereby repairing the disorderly distribution of vitality caused by delayed neural development and ultimately achieving gradual improvement in social functions.

Future research should explore interventions that harness ADHD’s cognitive flexibility to reshape VFs dynamics and offer new pathways to improve social functioning. To clarify the causal chain between VFs deficits and ADHD social impairment, we propose the following experimental designs for further verification: (i): Longitudinal follow-up study: Conduct a 2–3-year follow-up of children with ADHD, assessing core symptoms, VFs characteristics, and social function at multiple time points. Cross-lagged panel analysis will be used to test whether VFs abnormalities can predict the persistence of subsequent social impairment—rather than being driven by pre-existing core symptoms. (ii): Two-factor controlled intervention experiment: Randomly assign ADHD patients to three groups: Group A (core symptom treatment + VFs-targeted intervention), Group B (core symptom treatment only), and Group C (usual care control). By comparing the correlations between core symptom improvement, VFs function repair and social function enhancement across the three groups post-intervention, we can verify whether VFs interventions independently contribute to social improvement—an effect that cannot be achieved by core symptom treatment alone. (iii): Neuroimaging correlation study: Combine fMRI to measure changes in DCI-MCC circuit functional connectivity before and after intervention, as well as its correlations with VFs characteristics and social function.