Margaret T. Lynn

Imaging volition: what the brain can tell us about the will

The question of how we can voluntarily control our behaviour dates back to the beginnings of scientific psychology. Currently, there are two empirical research disciplines tackling human volition: cognitive neuroscience and social psychology. To date, there is little interaction between the two disciplines in terms of the investigation of human volition. The aim of the current article is to highlight recent brain imaging work on human volition and to relate social psychological concepts of volition to the functional neuroanatomy of intentional action. A host of studies indicate that the medial prefrontal cortex plays a crucial role in voluntary action. Accordingly, we postulate that social psychological concepts of volition can be investigated using neuroimaging techniques, and propose that by developing a social cognitive neuroscience of human volition, we may gain a deeper understanding of this fascinating and complex aspect of the human mind.

Power to the will: How exerting physical effort boosts the sense of agency

The sense of agency refers to the experience of being in control of ones actions and their consequences. The 19th century French philosopher Maine de Biran proposed that the sensation of effort might provide an internal cue for distinguishing self-caused from other changes in the environment. The present study is the first to empirically test the philosophical idea that effort promotes self-agency. We used intentional binding, which refers to the subjective temporal attraction between an action and its sensory consequences, as an implicit measure of the sense of agency. Effort was manipulated independent of the primary task by requiring participants to pull stretch bands of varying resistance levels. We found that intentional binding was enhanced under conditions of increased effort. This suggests not only that the experience of effort directly contributes to the sense of agency, but also that the integration of effort as an agency cue is non-specific to the effort requirement of the action itself.

Co-Activation-Based Parcellation of the Lateral Prefrontal Cortex Delineates the Inferior Frontal Junction Area

The inferior frontal junction (IFJ) area, a small region in the posterior lateral prefrontal cortex (LPFC), has received increasing interest in recent years due to its central involvement in the control of action, attention, and memory. Yet, both its function and anatomy remain controversial. Here, we employed a meta-analytic parcellation of the left LPFC to show that the IFJ can be isolated based on its specific functional connections. A seed region, oriented along the left inferior frontal sulcus (IFS), was subdivided via cluster analyses of voxel-wise whole-brain co-activation patterns. The ensuing clusters were characterized by their unique connections, the functional profiles of associated experiments, and an independent topic mapping approach. A cluster at the posterior end of the IFS matched previous descriptions of the IFJ in location and extent and could be distinguished from a more caudal cluster involved in motor control, a more ventral cluster involved in linguistic processing, and 3 more rostral clusters involved in other aspects of cognitive control. Overall, our findings highlight that the IFJ constitutes a core functional unit within the frontal lobe and delineate its borders. Implications for the IFJs role in human cognition and the organizational principles of the frontal lobe are discussed.

Placebo Analgesia Affects Brain Correlates of Error Processing

Placebo analgesia (PA) is accompanied by decreased activity in pain-related brain regions, but also by greater prefrontal cortex (PFC) activation, which has been suggested to reflect increases in top-down cognitive control and regulation of pain. Here we test whether PA is associated with altered prefrontal monitoring functions that could adjust nociceptive processing to a mismatch between expected and experienced pain. We recorded event-related potentials to response errors in a go/nogo task during placebo vs. a matched control condition. Error commission was associated with two well-described components, the error-related negativity (ERN) and the error positivity (Pe). Results show that the Pe, but not the ERN, was amplified during placebo analgesia compared to the control condition, with neural sources in the lateral and medial PFC. This Pe increase was driven by participants showing a placebo-induced change in pain tolerance, but was absent in the group of non-responders. Our results shed new light on the possible functional mechanisms underlying PA, suggesting a placebo-induced transient change in prefrontal error monitoring and control functions.

The influence of high-level beliefs on self-regulatory engagement: evidence from thermal pain stimulation

Determinist beliefs have been shown to impact basic motor preparation, prosocial behavior, performance monitoring, and voluntary inhibition, presumably by diminishing the recruitment of cognitive resources for self-regulation. We sought to support and extend previous findings by applying a belief manipulation to a novel inhibition paradigm that requires participants to either execute or suppress a prepotent withdrawal reaction from a strong aversive stimulus (thermal pain). Action and inhibition responses could be determined by either external signals or voluntary choices. Our results suggest that the reduction of free will beliefs corresponds with a reduction in effort investment that influences voluntary action selection and inhibition, most directly indicated by increased time required to initiate a withdrawal response internally (but not externally). It is likely that disbelief in free will encourages participants to be more passive, to exhibit a reduction in intentional engagement, and to be disinclined to adapt their behavior to contextual needs.

Mind control? Creating illusory intentions through a phony brain–computer interface

Can one be fooled into believing that one intended an action that one in fact did not intend? Past experimental paradigms have demonstrated that participants, when provided with false perceptual feedback about their actions, can be fooled into misperceiving the nature of their intended motor act. However, because veridical proprioceptive/perceptual feedback limits the extent to which participants can be fooled, few studies have been able to answer our question and induce the illusion to intend. In a novel paradigm addressing this question, participants were instructed to move a line on the computer screen by use of a phony brain-computer interface. Line movements were actually controlled by computer program. Demonstrating the illusion to intend, participants reported more intentions to move the line when it moved frequently than when it moved infrequently. Consistent with ideomotor theory, the finding illuminates the intimate liaisons among ideomotor processing, the sense of agency, and action production.

Controlling the self: The role of the dorsal frontomedian cortex in intentional inhibition

Intentional inhibition refers to the suppression of ongoing behavior on the basis of internally-generated decisions. This ability to cancel planned actions at the last moment is thought to be critical for self-control and has been related to activation in a circumscribed region of the dorsal frontomedian cortex (dFMC). Preliminary theories of intentional inhibition were based on studies that exclusively examined the cancellation of motor responses, and consequently concluded that this region serves the suppression of motor output. Yet recent evidence suggests that the dFMC is also involved in inhibitory control over more abstract internal states such as emotions or desires that have no immediate behavioral output. In this review, we therefore wish to put forth a new integrative perspective on the role of the dFMC in human self-control. We will argue that by virtue of its anatomical location and functional connections, this area may subserve the disengagement from current urges and impulses, thus facilitating successful exertions of self-control across a wide range of contexts by overcoming a self-focused perspective. We will discuss the fit of this view of the dFMC with the existing literature, identify critical experimental determinants for engaging the dFMC in intentional inhibition, and outline promising perspectives for future research.

Voluntary inhibition of pain avoidance behavior: an fMRI study.

AbstractBehavioral inhibition has classically been considered to rely upon a neural network centered at the right inferior frontal cortex [rIFC; Aron et al. (8:170–177, 2004; 18:177–185, 2014)]. However, the vast majority of inhibition studies have entailed exogenous stop signals instructing participants to withhold responding. More recent work has begun to examine the neural underpinnings of endogenous inhibition, revealing a distinct cortical basis in the dorsal fronto-median cortex [dFMC; Brass and Haggard (27:9141–9145, 2007); Kühn et al. (30:2834–3843, 2009)]. Yet, contrary to everyday experiences of voluntary behavioral suppression, the paradigms employed to investigate action inhibition have thus far been somewhat artificial, and involve little persuasive motivation to act. Accordingly, the present fMRI study seeks to compare and contrast intentional with instructed inhibition in a novel pain paradigm that recruits ‘hot’ incentive response systems. Participants received increasing thermal stimulation to their inner wrists, and were required to occasionally withhold their natural impulse to withdraw from the compelling pain sensation at peak temperature, in both instructed and free-choice conditions. Consistent with previous research, we observed inhibition-related activity in the dFMC and the rIFC. However, these regions displayed equivalent activation levels for both inhibition types. These data extend previous research by demonstrating that under ecologically valid conditions with a strong motivation to act, both stopping networks operate in concert to enable suppression of unwanted behavior.