Opinion
Cognitive-emotional interactions
Neural correlates of emotion regulation in psychopathology

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What can psychopathology and its treatment tell us about cognitive emotional interactions? Standard approaches to interactions between emotion and cognition often adopt a variant of the idea that cognitive processes, subserved by dorsal and lateral cortical circuits, exert control and regulation of ventral, limbic brain areas associated with emotional expression and experience. However, it is becoming clear from studies on depression, post-traumatic stress disorder (PTSD) and obsessive compulsive disorder (OCD), that a binary, opponent theory of cognitive emotion interaction (CEI) and the dorsal–ventral model of neurocircuitry do not fully describe the data. We summarize recent research to suggest that networks of direct and indirect pathways exist by which cognition can regulate pathological emotion, and the inter-relationships of specific nodes within the networks need to be characterized.

Introduction

In the past decade, research in cognitive and affective neuroscience has begun to link neural function, cellular physiology and even molecular genetics with higher level processes that regulate emotion 1, 2, 3. The application of this work to psychopathology has just started, providing important avenues for understanding CEI (see glossary for definition of abbreviations throughout text) in extremis, as well as the pathophysiology of psychiatric syndrome. There is probably no better demonstration of how thoughts and feelings bind together than psychiatric disorders, and the manner in which they do so provides an opportunity to understand normal CEI. In this article, we examine several psychiatric conditions in the context of CEI, focusing on the large-scale neural networks associated with the cognitive, volitional effort to modulate pathological emotions. We suggest that although a dorsal–ventral model of CEI, for example [4], characterizes much of the data, the multiple pathways by which an individual can change pathological emotion in psychotherapy requires a more complex psychological and neuroanatomical model.

Section snippets

Pathological interactions of cognition and emotion

From the earliest theoretical formulations of Freud, psychiatric thought has set cognition and emotion if not against one another, then as opposite poles of the human psyche. In general, treatment has sought to therapeutically separate, or better integrate, emotion and cognition, when they become pathologically bound together in various syndromes. For instance, depression consists of profound sadness, and cognitively, thoughts focus on themes of guilt, worthlessness and self-doubt.

Psychiatric disorders implicate emotion-processing areas of the brain

Neuroimaging studies demonstrate that emotionally evocative tasks recruit all cortical lobes, subcortical structures and the cerebellum, although activations tend to be denser in ventral cortical [particularly vmPFC], subcortical, midbrain, brainstem and cerebellar regions 10, 11 (Figure 1). Ventral and medial frontal cortex [including rACC and OFC] is particularly relevant for determining salience and generating emotional states. The anterior, dmPFC is involved in various forms of emotion

Control of dysregulated emotions: examples from psychotherapy

Psychotherapy provides instructive examples of how cognitive, volitional intention ‘regains’ control over dysregulated emotions. Strategies of emotion regulation are often divided between those that utilize attentional control (e.g. selective inattention to emotional stimuli) and those that utilize cognitive change (e.g. re-appraising a negative experience in a positive light) 2, 23. A successful psychotherapy that primarily engages cognitive change and deliberate re-appraisal is CT (cognitive

Cognitive regulation of pathological emotion in neuroanatomical systems: the dorsal–ventral model

Functional neuroanatomical studies of CEI in healthy subjects have offered a neural analogue to this ‘top down’ notion of cognition reappraising emotions. It has been suggested that frontal lobe function is divided into dorsal and ventral components 11, 28. In contrast to ventral systems that generate emotions and appraise valence, tasks that require cognitive control – the ability to volitionally order and allocate resources to meet task demands and satisfy personal goals – utilize more dorsal

Drawbacks of the dorsal–ventral model

Although only a handful of studies have examined the neural correlates of psychotherapy of depression (recently reviewed in [34]), there is no evidence that therapy bolsters dorsal activity. Two studies 35, 36 examining the effect of CT in depression reported that resting metabolism actually decreased in lateral frontal regions, along with vmPFC, dmPFC and OFC activity. Another study examined resting state metabolism before and after IPT, and found a similar pattern of decreased lateral frontal

Multiple pathways of emotion regulation in psychopathology

It is useful to consider that different types of psychotherapy suggest different methods by which cognition – in the broad sense of conscious, voluntary effort – effects therapeutic change. In other words, as Figure 2 shows, therapeutic mechanisms do not have to explicitly engage and alter emotional schemata. Therapeutic techniques that increase behavioral activity levels are also effective in depression [42]. Anxiety states, such as phobias [43], PTSD [7] and OCD [44], are treated with

Conclusion and future directions

We have suggested that the dramatic interactions of emotion and cognition in psychiatric disorders, and the multiple pathways by which cognitive, effortful behavior regulates pathological emotion, provide important insights into CEI and underlying neurocircuits. Although the paths depicted in Figure 2 are probably not exhaustive, focusing on different psychotherapeutic techniques might elucidate these hypothetical sub-systems and interactions. In turn, improved understanding of the functional

Acknowledgements

Supported by NIMH MH078281 and MH64148 to S.F.T., and MH075999 to I. L. The authors would like to thank J. Abelson for Figure I.

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