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Task performance was equal between the groups, with the FMD group showing full capability to carryout the sequential finger movement task during the course of the experiment. Table 2 provides a summary of the clinical characteristics of the FMD group. The FMD group was comprised of a diverse sample of ages range: 26—65 , genders 9 males, 12 females , and symptoms. Gray areas represent findings on neurological examination that are consistent with FMD. Particularly notable were the extremes where the patients claimed significant control when they had none and felt less than full control when control was complete.

Disorders of Volition

Since our cohorts were collected in series with the FMD group lagging behind the HV group, we were unable to age-match. The adjusted R 2 was 0. Whereas the behavioral task was designed to ensure paradigm validity by subjectively assessing SA experienced by participants at the end of fMRI data collection, the imaging data is intended to provide a direct assessment of how the brain responds to a loss of SA.

Despite the similarities between the groups, several key differences were present. Generally speaking, the remarkable consistency of stacking in the HV group was present in the FMD group but was less clear and only in some regions, including the right anterior insula and right TPJ. To evaluate whether individuals with FMD have impairments in their ability to judge their own intention or agency, we carried out an exploratory study to evaluate the regional blood flow responses collected by fMRI using a SA task previously carried out in a HV group to identify the brain regions modulated by changes in SA.

Despite equivalent performance on the behavior task, the FMD group showed much greater variability in their perceived level of control and an unexpected tendency to overestimate control over the virtual hand. Furthermore as real-world control was lost, making the movements truly involuntary, the FMD group lacked the ability to recognize this loss. These findings nonetheless provide additional weight to previous studies suggesting an impaired SA [ 24 — 25 ]. The validity of any subjectively reported metric is, however, questionable in a population known to inflate symptom severity and duration [ 29 ].

Although our two groups were not age-matched and the FMD group was older than the HV group mean ages of The neural network underlying SA is complex and widely distributed primarily over the right hemisphere of the brain. In our healthy volunteer cohort, we previously identified numerous brain regions that responded in a graded fashion to the loss of control during the implicit SA task. The findings within the healthy cohort are now strengthened by the results obtained from our FMD group. These findings are remarkable for at least two reasons.

First, they suggest that although fMRI lacks the temporal resolution to provide information about directional connectivity, the identification of functionally intact regions with temporally earlier hemodynamic response profiles leading to downstream areas of dysfunction is indirect evidence of the direction of information flow and the possible site s of impairment.

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While it is beyond the scope of this manuscript to review the many and various functions attributed to these ROIs, these areas are known to be functionally connected based on human neuroimaging studies [ 30 ] and structurally connected based on non-human primate labeling studies [ 31 ]. In this forward model, prefrontal and limbic areas are hypothesized to produce the drive to act. While our findings lend support to the brain regions comprising the forward model of volition, questions arise about the direction of information flow that cannot be answered by a methodology like fMRI.

For example, both the pre-SMA and DLPFC have a gradient of processing functions, whereby posterior sections manage motor actions and processing becomes more abstract and complex moving anteriorly [ 34 ]. Lau and colleagues [ 35 ] explored this connectivity while subjects performed a Libet judgment of the time of intended movement task [ 36 ].

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We speculate that this difference may represent the greater experience of SA in the FMD group that has been previously attributed to this region by others [ 8 ]. In the case of the forward model, both regions are associated with the selection and generation of the motor program, whereas in our study these areas show a differential responsivity to the degree of SA in the HV group that is no longer seen in the FMD group. This finding suggests that these regions play a larger role than the generation of the motor program and may be critical components for accurately judging volition.


The DLPFC has previously been reported to be active when conflict between intention and sensory feedback arises [ 38 ]. The right IPL and precuneus have also been previously implicated in this network as areas responsible for mismatch detection [ 5 ]. The finding of fMRI-based differences in SA between individuals with FMD and controls expands upon previous behavioral and physiologic studies in this area. While these findings may not be surprising to some, there remains a large disconnect between the causes of FMD and the associated psychiatric features.

In many cases, the psychiatric symptoms had resolved while the FMD symptoms persisted. Our findings of impaired hemodynamic responsiveness to changes in SA in critical areas of the network provide some of the strongest evidence to date for a physiological basis underlying FMD. While these findings need to be replicated and compared to an age-matched control group, future studies should focus on the roles played by different components of the network and how dysfunction in the network relates, if at all, to psychiatric comorbidities.

Further work is also needed to replicate the stacking properties of the SA network, recognizing that substantially larger sample sizes will be needed to definitively show this. Our results also provide some of the first evidence for a trait-specific rather than state-specific etiology for FMD since participants were in large part not experiencing any functional movements during the course of the experiment.

While we fully recognize the challenges of obtaining a homogeneous population using existed clinical criteria, this evidence does open the way for possible future genomics studies of FMD. We would like to acknowledge Dr. Nathan Miletta, Ms. Elaine Considine and Ms.

Barbara Kimber for their assistance in this work. Funding acquisition: MH. Investigation: FBN. Project administration: FBN.


Software: PK QS. Writing — original draft: FBN. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Abstract The sense of agency SA is an established framework that refers to our ability to exert and perceive control over our own actions. Introduction The sense of agency SA refers to our ability to exert and perceive control over our own actions [ 1 ]. Materials and methods We utilized the same experimental paradigm, scan acquisition parameters, data analysis methods, and behavioral testing as previously described in for our healthy volunteer study [ 4 ].

Subjects All aspects of this work were approved by the Institutional Review Board of the National Institute of Neurological Disorders and Stroke and all subjects provided written informed consent. Results The demographics of the study groups are listed in Table 1.

Download: PPT. Fig 1. Fig 2. Discussion To evaluate whether individuals with FMD have impairments in their ability to judge their own intention or agency, we carried out an exploratory study to evaluate the regional blood flow responses collected by fMRI using a SA task previously carried out in a HV group to identify the brain regions modulated by changes in SA.

Acknowledgments We would like to acknowledge Dr. References 1. Haggard P. Human volition: towards a neuroscience of will. Nat Rev Neurosci. Central cancellation of self-produced tickle sensation. After presenting different conceptual frameworks that identify agency, decision making, and goal pursuit as central components of volition, the book examines how impairments in these and other aspects of volition manifest themselves in schizophrenia, depression, prefrontal lobe damage, and substance abuse.

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