Emotional dysregulation is common in individuals with Attention-Deficit/Hyperactivity Disorder (ADHD), and this review examines the current literature on the overlap between ADHD and emotional dysregulation. Three key findings are identified: (1) emotional dysregulation is prevalent in ADHD throughout the lifespan and is a major contributor to impairment; (2) emotional dysregulation in ADHD may arise from deficits in orienting towards, recognizing and/or allocating attention to emotional stimuli, which may involve dysfunction in the striatoamygdalo-medial prefrontal cortical network; and (3) while current treatments for ADHD often also ameliorate emotional dysregulation, focusing on this combination of symptoms could stimulate novel therapeutic approaches. Three models are considered: (1) emotional dysregulation and ADHD are correlated but distinct dimensions; (2) emotional dysregulation is a core, diagnostic feature of ADHD; and (3) the combination constitutes a nosological entity, distinct from both ADHD and emotional dysregulation alone. The differing predictions from each model can guide future research into this much-neglected population. Emotional dysregulation is a dimensional trait that is not unique to ADHD, but it undercuts the traditional divide between internalizing and externalizing diagnoses. It is also not synonymous with any single DSM-5 disorder. Emotional dysregulation is a dimensional entity, not a categorical diagnosis, and the review considers the full spectrum of emotional dysregulation within ADHD, not just extremes. The review also focuses on emotional dysregulation itself, rather than on diagnoses that may include emotional dysregulation and be comorbid with ADHD, because it is a simpler symptom construct that is familiar to clinicians and may be more readily tied to underlying neurobiological mechanisms. The review discusses the prevalence, pathophysiology, and treatment of emotional dysregulation in ADHD. Prevalence studies show that emotional dysregulation is found in around 25-45% of children and between 30-70% of adults with ADHD. It represents a major source of impairment and presages a poor clinical outcome. Pathophysiology studies suggest that emotional dysregulation in ADHD may arise from deficits at multiple levels, including abnormal early orienting to emotional stimuli, inability to recruit top-down regulatory effort or attention in response to emotional stimuli, and deficits in cognitive processes such as working memory and response inhibition. Neural mechanisms include dysfunction in the amygdala, ventral striatum, and orbitofrontal cortex, which could be regarded as the 'bottom-up' contributor. Regions at the interface of cognition and emotion (medial and ventrolateral prefrontal cortex) may underpin the abnormal allocation of attention to emotional stimuli and could thus be regarded as the major 'top-down' contributor to emotional dysregulation within ADHD. Treatment of emotional dysregulation in ADHD presents therapeutic challenges, as clinical trials often fail to assess change in emotion regulation or do soEmotional dysregulation is common in individuals with Attention-Deficit/Hyperactivity Disorder (ADHD), and this review examines the current literature on the overlap between ADHD and emotional dysregulation. Three key findings are identified: (1) emotional dysregulation is prevalent in ADHD throughout the lifespan and is a major contributor to impairment; (2) emotional dysregulation in ADHD may arise from deficits in orienting towards, recognizing and/or allocating attention to emotional stimuli, which may involve dysfunction in the striatoamygdalo-medial prefrontal cortical network; and (3) while current treatments for ADHD often also ameliorate emotional dysregulation, focusing on this combination of symptoms could stimulate novel therapeutic approaches. Three models are considered: (1) emotional dysregulation and ADHD are correlated but distinct dimensions; (2) emotional dysregulation is a core, diagnostic feature of ADHD; and (3) the combination constitutes a nosological entity, distinct from both ADHD and emotional dysregulation alone. The differing predictions from each model can guide future research into this much-neglected population. Emotional dysregulation is a dimensional trait that is not unique to ADHD, but it undercuts the traditional divide between internalizing and externalizing diagnoses. It is also not synonymous with any single DSM-5 disorder. Emotional dysregulation is a dimensional entity, not a categorical diagnosis, and the review considers the full spectrum of emotional dysregulation within ADHD, not just extremes. The review also focuses on emotional dysregulation itself, rather than on diagnoses that may include emotional dysregulation and be comorbid with ADHD, because it is a simpler symptom construct that is familiar to clinicians and may be more readily tied to underlying neurobiological mechanisms. The review discusses the prevalence, pathophysiology, and treatment of emotional dysregulation in ADHD. Prevalence studies show that emotional dysregulation is found in around 25-45% of children and between 30-70% of adults with ADHD. It represents a major source of impairment and presages a poor clinical outcome. Pathophysiology studies suggest that emotional dysregulation in ADHD may arise from deficits at multiple levels, including abnormal early orienting to emotional stimuli, inability to recruit top-down regulatory effort or attention in response to emotional stimuli, and deficits in cognitive processes such as working memory and response inhibition. Neural mechanisms include dysfunction in the amygdala, ventral striatum, and orbitofrontal cortex, which could be regarded as the 'bottom-up' contributor. Regions at the interface of cognition and emotion (medial and ventrolateral prefrontal cortex) may underpin the abnormal allocation of attention to emotional stimuli and could thus be regarded as the major 'top-down' contributor to emotional dysregulation within ADHD. Treatment of emotional dysregulation in ADHD presents therapeutic challenges, as clinical trials often fail to assess change in emotion regulation or do so