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From brain circuits to self-regulation: an integrative neurocognitive model of metacognition and emotion regulation
Davoud Amiri1, Lamberto Briziarelli2, Swetang J Shah3
1Specialist in Psychiatry and Social Medicine, Uppsala Region, Uppsala, Sweden.
Background:
Attention-deficit/hyperactivity disorder (ADHD) has traditionally been conceptualised as a disorder of attention and executive functioning. However, increasing evidence indicates that emotional dysregulation is highly prevalent across the lifespan and contributes substantially to functional impairment. Neuroimaging and neurochemical studies implicate abnormalities in fronto-striatal and fronto-limbic networks, including the dorsolateral prefrontal cortex, anterior cingulate cortex, amygdala, and ventral striatum. Despite these advances, existing theoretical frameworks rarely integrate neurobiological mechanisms, metacognitive control processes, emotion regulation, and clinical symptom expression within a single explanatory framework.
Objective:
This narrative review aims to synthesise evidence across neuroscience, cognitive psychology, and clinical psychiatry to propose an integrative neurocognitive model linking brain circuitry, metacognitive control, emotion regulation, and behavioural manifestations in ADHD.
Methods:
Relevant literature published between 1995 and 2025 was identified through searches of PubMed, Scopus, and Web of Science using combinations of terms related to ADHD, emotion regulation, metacognition, executive function, dopamine, glutamate, and fronto-striatal and fronto-limbic circuitry. Evidence was synthesised across four interconnected domains: neurobiological mechanisms, metacognitive control processes, emotion regulation, and clinical ADHD phenotype.
Results:
Converging evidence suggests that dysfunction within prefrontal regulatory systems may impair metacognitive monitoring and top-down control. Reduced prefrontal regulation of limbic structures, particularly the amygdala and ventral striatum, may increase emotional reactivity and impulsive behavioural responses. These interacting mechanisms provide a plausible pathway linking neural circuit dysfunction with emotional dysregulation and core behavioural manifestations of ADHD.
Conclusion:
ADHD may be conceptualised as a disorder of hierarchical self-regulation in which disturbances in neural circuitry cascade through metacognitive and emotional regulatory systems to produce characteristic behavioural symptoms. This integrative framework may inform future research and support the development of mechanism-based interventions targeting self-regulatory processes in ADHD.
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