The circumplex model of affect proposes that all affective states arise from cognitive interpretations of core neural sensations that are the product of two independent neurophysiological systems. This model stands in contrast to theories of basic emotions, which posit that a discrete and independent neural system subserves every emotion. We propose that basic emotion theories no longer explain adequately the vast number of empirical observations from studies in affective neuroscience, and we suggest that a conceptual shift is needed in the empirical approaches taken to the study of emotion and affective psychopathologies. The circumplex model of affect is more consistent with many recent findings from behavioral, cognitive neuroscience, neuroimaging, and developmental studies of affect. Moreover, the model offers new theoretical and empirical approaches to studying the development of affective disorders as well as the genetic and cognitive underpinnings of affective processing within the central nervous system.The reigning experimental paradigm in affective neuroscience research posits that emotions can be divided into discrete and independent categories and that specific neural structures and pathways subserve each of these emotional categories. This theory of basic emotions has yielded significant advances in the understanding of affect and yet, in the fields of clinical psychology and psychiatry, it has left unsettled many important questions. The theory of basic emotions, for example, has not explained the near ubiquitous comorbid illnesses among mood disorders, nor has it resolved confusion over the neurophysiological underpinnings of affective disorders. Moreover, basic emotion theory is largely incompatible with recent findings in behavioral genetics and temperament research. Given these empirical and heuristic limitations of the theory of basic emotions, we propose that a shift is needed in the conceptual approaches taken to the study of emotion. We propose that clinicians and researchers move away from a strictly basic emotion model of affective states, where each emotion is thought to emerge from independent neural systems, to more dimensional models of emotions, in which all affective states are understood to arise from common, overlapping neurophysiological systems.Although poorly represented in psychiatry, dimensional models have a long history in psychology (Larsen & Diener, 1992;Russell, 2003;Schlosberg, 1952;Watson, Wiese, Vaidya, & Tellegen, 1999). One particular dimensional approach, termed the circumplex model of affect, proposes that all affective states arise from two fundamental neurophysiological systems, one related to valence (a pleasure-displeasure continuum) and the other to arousal, (Russell, 1980). Each emotion can be understood as a linear combination of these two dimensions, or as varying degrees of both valence and arousal (see Figure 1). Joy, for example, is conceptualized as an emotional state that is the product of strong activation in the neural systems associated wi...

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Background Attention deficit/hyperactivity disorder (ADHD) is a major public health concern. It has been suggested that the brain’s default network may provide a crucial avenue for understanding the neurobiology of ADHD. Evaluations of the default network have increased over recent years with the applied technique of resting-state functional connectivity MRI (rs-fcMRI). These investigations have established that spontaneous activity in this network is highly correlated at rest in young adult populations. This coherence seems to be reduced in adults with ADHD. This is an intriguing finding, as coherence in spontaneous activity within the default network strengthens with age. Thus, the pathophysiology of ADHD might include delayed or disrupted maturation of the default network. If so, it is important to determine whether an altered developmental picture can be detected using rs-fcMRI in children with ADHD. Methods The present study utilized the typical developmental context provided previously by Fair et al (1) to examine coherence of brain activity within the default network using rs-fcMRI in children with (n=23) and without ADHD (n=23). Results We found that functional connections previously shown as developmentally dynamic in the default network were atypical in children with ADHD - consistent with perturbation or failure of the maturational processes. Conclusions These findings are consistent with the hypothesis that atypical consolidation of this network over development plays a role in ADHD.

Psychopathology is increasingly viewed from a circuit perspective in which a disorder stems not from circumscribed anomalies in discrete brain regions, but rather from impairments in distributed neural networks. This focus on neural circuitry has rendered resting state functional connectivity MRI (rs-fcMRI) an increasingly important role in the elucidation of pathophysiology including attention-deficit/hyperactivity disorder (ADHD). Unlike many other MRI techniques that focus on the properties of discrete brain regions, rs-fcMRI measures the coherence of neural activity across anatomically disparate brain regions, examining the connectivity and organization of neural circuits. In this review, we explore the methods available to investigators using rs-fcMRI techniques, including a discussion of their relative merits and limitations. We then review findings from extant rs-fcMRI studies of ADHD focusing on neural circuits implicated in the disorder, especially the default mode network, cognitive control network, and cortico-striato-thalmo-cortical loops. We conclude by suggesting future directions that may help advance subsequent rs-fcMRI research in ADHD.

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The circumplex model of affect construes all emotions as linear combinations of 2 independent neurophysiological dimensions, valence and arousal. We used functional magnetic resonance imaging to identify the neural networks subserving valence and arousal, and we assessed, in 10 participants, the associations of the BOLD (blood oxygen level-dependent) response, an indirect index of neural activity, with ratings of valence and arousal during the emotional experiences induced by the presentation of evocative sentences. Unpleasant emotional experience was associated with increased BOLD signal intensities in the supplementary motor, anterior midcingulate, right dorsolateral prefrontal, occipito-temporal, inferior parietal, and cerebellar cortices. Highly arousing emotions were associated with increased BOLD signal intensities in the left thalamus, globus pallidus, caudate, parahippocampal gyrus, amygdala, premotor cortex, and cerebellar vermis. Separate analyses using a finite impulse response model confirmed these results and revealed that pleasant emotions engaged an additional network that included the midbrain, ventral striatum, and caudate nucleus, all portions of a reward circuit. These findings suggest the existence of distinct networks subserving the valence and arousal dimensions of emotions, with midline and medial temporal lobe structures mediating arousal and dorsal cortical areas and mesolimbic pathways mediating valence.

Objective-We aimed to study the neural processing of emotion-denoting words based on a circumplex model of affect, which posits that all emotions can be described as a linear combination of two neurophysiological dimensions, valence and arousal. Based on the circumplex model, we predicted a linear relationship between neural activity and incremental changes in these two affective dimensions.Methods-Using functional magnetic resonance imaging, we assessed in 10 subjects the correlations of BOLD (blood oxygen level dependent) signal with ratings of valence and arousal during the presentation of emotion-denoting words.Results-Valence ratings correlated positively with neural activity in the left insular cortex and inversely with neural activity in the right dorsolateral prefrontal and precuneus cortices. The absolute value of valence ratings (reflecting the positive and negative extremes of valence) correlated positively with neural activity in the left dorsolateral and medial pre-frontal cortex (PFC), dorsal anterior cingulate cortex, posterior cingulate cortex, and right dorsal PFC, and inversely with neural activity in the left medial temporal cortex and right amygdala. Arousal ratings and neural activity correlated positively in the left parahippocampus and dorsal anterior cingulate cortex, and inversely in the left dorsolateral PFC and dorsal cerebellum.Conclusion-We found evidence for two neural networks subserving the affective dimensions of valence and arousal. These findings clarify inconsistencies from prior imaging studies of affect by suggesting that two underlying neurophysiological systems, valence and arousal, may subserve the processing of affective stimuli, consistent with the circumplex model of affect.

Prenatal exposure to maternal depression is common and puts offspring at risk for developing a range of neuropsychiatric disorders. Despite its prevalence and adverse associations, neurobiological processes by which prenatal maternal depression (PMD) confers risk remain poorly understood. Maternal mood and fetal behavior were assessed between 34 and 37 gestational weeks. Using resting-state functional magnetic resonance imaging (fMRI) and diffusion MRI, we examined functional and structural connectivity within amygdala–prefrontal circuits in 64 infants (mean age=5.8±1.7 weeks) with (n=20) and without (n=44) in utero exposure to PMD. Resting fMRI and diffusion MRI both indicated atypical amygdala–prefrontal connectivity in PMD-exposed infants: Resting fMRI indicated increased inverse, or negative, functional connectivity between the amygdala and the dorsal prefrontal cortex (PFC), bilaterally, and diffusion MRI indicated decreased structural connectivity between the right amygdala and the right ventral PFC. Spectral dynamic causal modeling supported these findings suggesting altered amygdala–PFC effective (or directed) connectivity in PMD-exposed infants. Last, path analyses supported a mechanistic account relating PMD to a third-trimester fetal behavior: PMD alters amygdala–PFC connectivity, which in turn, is associated with an increase in fetal heart rate reactivity to in utero perturbation. These data suggest that the maturation and coordination of central and peripheral physiology are altered by prenatal exposure to maternal depression. To the best of our knowledge, this is the first study to directly associate infant MRI measures with a behavior—fetal heart rate response, and supports hypotheses that PMD-associated variations in the development of amygdala–PFC circuits are relevant for future neurobehavioral maturation.