Efforts to bridge emotion theory with neurobiology can be facilitated by dynamic systems (DS) modeling. DS principles stipulate higher-order wholes emerging from lower-order constituents through bidirectional causal processes cognition relations. I then present a psychological model based on this reconceptualization, identifying trigger, self-amplification, and self-stabilization phases of emotion-appraisal states, leading to consolidating traits. The article goes on to describe neural structures and functions involved in appraisal and emotion, as well as DS mechanisms of integration by which they interact. These mechanisms (...) include nested feedback interactions, global effects of neuromodulation, vertical integration, action-monitoring, and synaptic plasticity, and they are modeled in terms of both functional integration and temporal synchronization. I end by elaborating the psychological model of emotion–appraisal states with reference to neural processes. (shrink)

Our model integrates the nativist assumption of prespecified neural structures underpinning basic emotions with the constructionist view that emotions are assembled from psychological constituents. From a dynamic systems perspective, the nervous system self-organizes in different ways at different time scales, in relation to functions served by emotions. At the evolutionary scale, brain parts and their connections are specified by selective pressures. At the scale of development, connectivity is revised through synaptic shaping. At the scale of real time, temporary networks of (...) synchronized activity mediate responses to situations. To the degree that humans share common emotional functions, neural structuration is similar across scales, giving rise to “basic” emotions. However, unique developmental and situational factors select for neural configurations mediating emotional variants. (shrink)

Intentions and emotions arise together, and emotions compel us to pursue goals. However, it is not clear when emotions become objects of awareness, how emotional awareness changes with goal pursuit, or how psychological and neural processes mediate such change. We first review a psychological model of emotional episodes and propose that goal obstruction extends the duration of these episodes while increasing cognitive complexity and emotional intensity. We suggest that attention is initially focused on action plans and their obstruction, and only (...) when this obstruction persists does focal attention come to include emotional states themselves. We then model the self-organization of neural activities that hypothetically underlie the evolution of an emotional episode. Phases of emotional awareness are argued to parallel phases of synchronization across neural systems. We suggest that prefrontal activities greatly extend intentional states while focal attention integrates emotional awareness and goal pursuit in a comprehensive sense of the self in the world. (shrink)

I applaud Fenton and Wiers' attempt to find a demarcation point between cases of addiction that fall within the range of normal function and those that may count as disease. However, I argue that continua don't offer demarcation points, the mechanisms involved are not demonstrably different, and trying to pin down subjectivity doesn't help.

Pickard’s contribution reminds me that conceptualizing choice is no simple matter. Pickard sees choice as entirely voluntary, while I argue that choice is only partially voluntary. Choices are based on appraisals of situations, which fluctuate due to external circumstances and internal states such as emotion and mood. Habit itself competes with volition, and all these parameters vary with development. Psychological factors such as delay discounting and especially one's belief in one's agency are critical for volitional choice as well.

Ainslie’s contribution offers a useful refinement of his powerful model of intertemporal bargaining. However, he focuses mostly on the cognitive mechanisms of choice. I suggest that these interact with emotional, personality, and developmental dynamics that cannot be ignored, either psychologically or neurally.

Although I reject neuronormativity -- an idea central to the Brain Disease Model of Addiction -- Henden and Gjelsvik argue that the disease definition might refer to normativity in nonneural domains. They profess that a cognitive dysfunction, or a mismatch of evolutionary intentions, could also qualify as norm violations, thus legitimizing the disease label. The need for dividing lines is questioned as well. I rebut these criticisms in turn, but I must admit they are thought provoking.

Wakefield doesn't mind my focus on parallels between addiction and love. But love can fall outside the bounds of what evolution intended. So, he claims, comparing addiction with love does not preclude a naturally defined "disorder." I counter with the argument that evolution handed us such highly general response systems, the bounds of normality cannot be defined.

Berridge's nuanced approach to the conceptualization of addiction as a disease is easier for me to accept than most others. In fact, Berridge and I agree on many core features of addiction, but still not on how to label it. When competing definitions reach a standoff on intellectual grounds, we should look at the clinical utility of each. And here I think that Berridge misses a critical insight. Yet, we end by agreeing to keep listening to each other.

Flanagan asserts that my model of addiction would apply as well to sonnet writing. Yet his most interesting point is that “addiction” is an imprecise label for a cluster of distinct phenomena. I agree with him that we need to examine these distinctions, but that doesn’t negate their shared features. Neuroscience can play an important role in advancing our understanding of both commonalities and distinctions within the phenomena of addiction.

The target article developed a dynamic systems framework that viewed the causal basis of emotion as a self-organizing process giving rise to cognitive appraisal concurrently. Commentators on the article evaluated this framework and the principles and mechanisms it incorporated. They also suggested additional principles, mechanisms, modeling strategies, and phenomena related to emotion and appraisal, in place of or extending from those already proposed. There was general agreement that nonlinear causal processes are fundamental to the psychology and neurobiology of emotion.

Frank and Nagel are very interested in the causes and consequences of moralizing about addiction. If addiction is a disease, moralistic concerns are sidelined. If it's a choice, we'd better identify clear reasons to absolve addicts from blame. While these are interesting considerations, they don't have much to do with the model of addiction I put forward in the target article.

The authors and I agree on many features of addiction, such as its developmental nature. But because I rely on much of the same data as the Brain Disease Model of Addiction, they seem to conflate my work with that of my opponents. Indeed they are generally skeptical of the use of neuroscientific data to help understand addiction, calling it "immature." Thus my work is also suspect. Hall and colleagues believe that it is impossible to look at neural and social (...) processes at the same time, yet that is exactly what I do. I suggest that interdisciplinary approaches to addiction are crucial. (shrink)

Both Matthews and I see addiction as the outcome of developmental processes that arrive at diverse levels of dysfunction for different individuals at different stages. Matthews characterizes "late-stage" addiction in terms of lost control and extreme automaticity, a degree of dysfunction he calls a "disorder" and compares to another disorder -- depersonalization. I don't mind the label "disorder." Yet addiction is no more like depersonalization than it is like other conditions, most notably obsessive-compulsive disorder. Automaticity is never pure or total. (...) My dual focus on the phenomenology and neuroscience of addiction has helped me capture these critical details and differences. In fact, I think we've had enough of comparing, classifying, and defining addiction. It's time to recognize addiction as a thing in itself, unlike anything else. (shrink)

Although these authors sometimes resort to medical terminology, we strongly agree that addiction is not a disease and that the Brain Disease Model of Addiction captures only one part of the story and distorts the big picture. Yet Satel and Lilienfeld continue to conflate a neurobiological model with a disease model. They also complain that my modeling of addiction reveals a hidden “neurocentric” bias, despite my integration of multiple levels of analysis, exactly as they recommend.

Despite its historical contribution, Heather sees the Brain Disease Model of Addiction as failing to relieve stigma, increasing fatalism, and fundamentally wrong. He also sees “choice” as partly volitional and partly unconscious, implying no moral violation. I agree on all counts. Heather then presents a disorder-of-choice model of addiction, highlighting the failure of self-regulation with respect to immediate goals. Not only do I endorse such modeling, but the neural mechanisms I describe may help to explicate it more thoroughly.

Szalavitz’s model and mine share a good many components. Foremost among them is the conviction that addiction is a developmental trajectory, not a disease. Szalavitz is correct that we should consider controlled substance use an acceptable outcome, though I would like her to shift her terminology away from the medical mainstream. Finally, I suggest that Szalavitz's important idea of a "reset" in brain development might best be addressed by the notion of kindling.

Some dynamic systems approaches posit discontinuous changes, even universal stages, in development. Conversely, Thelen and colleagues see development as gradual because it relies on real-time interactions among many components. Yet their new model hinges on one parameter, neural cooperativity, that should change discontinuously because it engenders new skills that catalyze neural connectivity. In fact, research on cortical connectivity finds development to be discontinuous, and possibly stage-like, based on experience-dependent and experience-independent factors.

Snoek, like other commentators, conflates some of my neural claims with those of the Brain Disease Model of Addiction. But she sees other details of my modeling with precision and depth. I welcome her emphasis on individual and developmental differences in addicts' capacity to recognize and deploy their personal agency. In fact we agree that belief in personal agency is a critical first step to cultivating it. Yet I wish to steer away from the disease nomenclature, to give that belief (...) its best chance to flourish. (shrink)

Rolls demonstrates how reward/punishment systems are key mediators of cognitive appraisal, and this suggests a fundamental, causal role for emotion in thought and behaviour. However, this causal role for emotion seems to drop out of Rolls's model of consciousness, to be replaced by the old idea that emotion is essentially epiphenomenal. We suggest a modification to Rolls's model in which cognition and emotion activate each other reciprocally, both in appraisal and consciousness, thus allowing emotion to maintain its causal status where (...) it matters most. (shrink)