Greg J. Siegle, PhD
Western Psychiatric Institute and Clinic, University of Pittsburgh, Pittsburgh
James Coan, PhD
University of Virginia
The goal of this chapter is to provide translational bridges from the common vocabulary of core processes in psychotherapy described throughout this book to neural mechanisms, which are increasingly the lingua franca of the rest of medical science. Success in this endeavor will ideally allow clinicians in the psychological sciences to speak with and make use of insights from the rest of medicine more effectively. In the short term this may also allow clinicians to put neuroscience behind their explanations of mechanisms of change for clients. In the longer term this type of thinking could lead to the adoption of neuroscience methods in predicting response to psychological treatments, and in designing treatments.
In this chapter, we focus specifically on qualitative associations of brain networks with key concepts. We have chosen this granularity as it is likely to have direct clinical applicability given the recent emphasis on brain networks in understanding change processes (Chein & Schneider, 2005; Lane, Ryan, Nadel, & Greenberg, 2014; Tryon, 2014). More quantitative associations, for example, what neural reactivity best predicts response to what treatments (e.g., Hofmann, 2013; Siegle et al., 2012), involve solving technical hurdles of generalizability and societal issues, such as expenses that insurance companies do not currently reimburse. If clinicians understand basic units and principles of neural change, and the empirical associations of these units with clinical concepts, this knowledge may change how they explain interventions to clients and add to the skills they can capitalize on in current interventions, and eventually it may lead to the adoption of more neurally informed methods (prediction algorithms and treatments) as they become available. Our methodology for identifying clinically relevant networks utilizes whole-brain, meta-analytic (hence, quantitative) procedures so that our described intuitions are at least defensible and externally derivable.
Increasingly, the field of cognitive neuroscience is moving away from a focus on specific brain areas putatively associated with specific discrete functions to one of networks of linked brain regions that accomplish various behavioral or psychological functions by interacting with each other (Sporns, 2010). For example, neural circuits associated with attention may modulate activity in circuits associated with emotion such that the reactions to attended emotional stimuli are different than those to unattended emotional stimuli. In this way, clinicians and therapists can conceive of a disorder not only as the activity or inactivity of a discrete neural region or circuit, but also in terms of abnormalities of communication between brain neural regions or circuits (Cai, Chen, Szegletes, Supekar, & Menon, 2015).
In this chapter we adopt the idea that change processes in psychotherapy are associated with neural change, generally described as “plasticity” or “learning” in the neuroscience literature. Neural change processes follow a few principles that are useful to highlight here. Hebbian learning (Choe, 2014) is the idea that when multiple brain mechanisms are active at the same time, the connection between them grows stronger. So, for example, the association of an event with an emotional quality could happen when neural representations of the memory for an event are coactive with neural representations of an emotion. Thus activity in brain systems associated with salience and emotion along with memory could be considered catalytic for emotional associative learning. Theoretically, change in psychotherapy could occur by systematically activating the memory without the emotional tone (extinction) when either of these associations is weakened. The idea of plasticity can seem redundant with learning, but the two terms are not conceptually identical. For example, the traditional belief that memories cannot change has largely been supplanted by the understanding that every time a memory is accessed, the neural representation of the memory itself becomes plastic and can change via reconsolidation (Axmacher & Rasch, 2017). With its emphasis on building new knowledge, lay notions of learning could be an imprecise description of memory reconsolidation. The practical outcome of this new understanding is that neurally informed therapies are increasingly working to intentionally optimize memory reconsolidation processes so as to maximize the potential for psychotherapeutic gains (Treanor, Brown, Rissman, & Craske, 2017), including the potential for integrating pharmacological and therapeutic mechanisms (Lonergan, Brunet, Olivera-Figueroa, & Pitman, 2013). In the remainder of this chapter, we concentrate on the potential effects of psychotherapeutic techniques in a handful of potential networks of interest and, in particular, the potential for change to how networks interact.
In this chapter we concentrate on a few canonical brain networks that have been identified across many studies (e.g., Bressler & Menon, 2010; K. L. Ray et al., 2013; Smith et al., 2009). Though there are many such networks, we will highlight only those that appear repeatedly in analyses of processes associated with therapeutic change, as described in the following sections. Three networks, shown in figure 1, derived using methods described in this section and consistent with those found in more traditional analyses (such as Bressler & Menon, 2010), have been particularly well characterized across multiple imaging modalities. A salience network is associated with monitoring the salience of external and internal stimuli. It consists of the insula, which is particularly associated with interoceptive processing (Craig, 2009); the dorsal anterior cingulate cortex, which is associated with the interface of emotional and cognitive information processing (Bush, Luu, & Posner, 2000); and regions traditionally considered to process emotional information, such as the amygdala (Armony, 2013). A central executive network is associated with executive control and task planning and execution. It is anchored by the dorsolateral prefrontal cortex and posterior parietal cortices. A default network (sometimes default mode) is associated with the brain’s resting state (Raichle et al., 2001); functional neuroimaging studies suggest that it activates, or becomes better synchronized, when there is no explicit task, and deactivates during explicit tasks. Its components are often detected in association with social information processing (Amodio & Frith, 2006), as well as self-referential processing (Davey, Pujol, & Harrison, 2016; Kim, 2012). It is anchored by the posterior cingulate cortex and the rostral anterior cingulate or more anterior medial structures in the orbitofrontal cortex. It also includes the hippocampus, which appears to be particularly involved in a subnetwork for learning and memory (Kim, 2012; Van Strien, Cappaert, & Witter, 2009).
Two other networks appear key to change in psychological interventions. Building on structures in the default network, researchers have observed that an expanded social information processing network (Burnett, Sebastian, Cohen Kadosh, & Blakemore, 2011) contains not only the rostral cingulate but structures such as the temporoparietal junction and superior temporal sulcus, suggesting they are involved in the perception of others’ emotions and theory-of-mind. Often discussed in the literature is the reward network, which is really a set of networks that largely reflect the brain’s responses to rewarding or positive stimuli. They are centered on the dopamine-producing ventral-tegmental area and reward-monitoring ventral striatum, or nucleus accumbens (Camara, Rodriguez-Fornells, Ye, & Münte, 2009).
By appealing to the putative function of these networks it is easy to speculate on how brain function may relate to specific therapeutic interventions. Interventions devoted to increasing reward responses might be expected to activate the reward network. Interventions devoted to decreasing self-focused processing might decrease activity in the default network. And interventions devoted to increasing social communication might activate the social information processing network. That said, these associations have not been rigorously tested, and brain reactions are often unintuitive. Thus, the forthcoming sections consist of empirical investigations of how these brain networks respond to the types of interventions discussed in this book.
For the interested methodologist, in all cases maps are shown for reverse inference (chances that the term is used, given the presence of activation in the area), which is more conservative than typical fMRI strategies of forward inference (chances the area is observed, given the term that is used). We chose this strategy as many psychological terms tend to yield similar broad patterns of activation—reverse inference allows more specificity of network activity related to psychological constructs. We used a false discovery rate criterion of 0.01 as a threshold for the images.
The curious reader can directly access the neuroimaging meta-analyses reported in this chapter online. When primary Neurosynth terms were available, we used those. Otherwise, we did “custom” analyses based on Neurosynth’s “studies” analyses; these can be accessed via the URLs listed in the appendix. The reader can thus regenerate any maps we describe. We generally show only a single representative axial, coronal, and sagittal image for each analysis; by directly regenerating the analyses, readers can see and interact with full brain maps slice by slice, as well as examine each associated study and its specific contributions to the meta-analysis. References for individual studies in the reported meta-analyses can be accessed by regenerating the associated searches.
There were four Neurosynth-nominated studies of “coping,” but we didn’t report on them because they were not strongly related to therapeutic processes (e.g., two were on repressive coping style).
The clarification of values involves an iterative process of belief refinement, which may be considered to reflect the large neuroscience literature on the adjustments of beliefs in response to errors in prediction (i.e., realizing that something you thought was incorrect and, thus, changing thinking). A Neurosynth meta-analysis of “prediction error” (figure 15) revealed reactivity almost exclusively in the basal ganglia, a key element of the reward network. Thus, we suggest that values clarification may involve the iterative refinement of what one views as rewarding or punishing, and how rewarding or punishing it is, with respect to the self.
We highlighted brain networks that are associated with concepts addressed in therapeutic change generally and the contents of this book specifically. The similarities of maps and identified networks across the sections of this chapter suggest that different therapeutic techniques may share key elements and may have critical similarities despite their nominal differences. In particular, the evidence highlights increased executive control, increased reward, and the use of somatic processing as possible routes to emotional change. Taking advantage of inherent tensions between executive control and automatic processing of salient information, as well as the potential use of executive control to increase reward valuation, are common mechanisms across intervention techniques. Keeping such common principles in mind may help clinicians to unify and promote a translational appreciation of what they are doing in the therapy room.
These custom Neurosynth meta-analyses are not among Neurosynth’s stored canonical meta-analyses. They represent searches of terms from article texts.
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