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Review
. 2013 Sep;229(3):313-27.
doi: 10.1007/s00221-013-3399-2. Epub 2013 Jan 18.

Neurology of volition

Affiliations
Review

Neurology of volition

Sarah M Kranick et al. Exp Brain Res. 2013 Sep.

Abstract

Neurological disorders of volition may be characterized by deficits in willing and/or agency. When we move our bodies through space, it is the sense that we intended to move (willing) and that our actions were a consequence of this intention (self-agency) that gives us the sense of voluntariness and a general feeling of being "in control." While it is possible to have movements that share executive machinery ordinarily used for voluntary movement but lack a sense of voluntariness, such as psychogenic movement disorders, it is also possible to claim volition for presumed involuntary movements (early chorea) or even when no movement is produced (anosognosia). The study of such patients should enlighten traditional models of how the percepts of volition are generated in the brain with regard to movement. We discuss volition and its components as multi-leveled processes with feedforward and feedback information flow, and dependence on prior expectations as well as external and internal cues.

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Conflict of interest statement

Conflict of Interest Statement: The authors have no conflict of interest (financial or otherwise) to report as it pertains to the present work.

Figures

Figure 1
Figure 1
The forward model framework for volition. The sense of will reflects feedforward input from motor planning as well as prior beliefs. If the execution of the movement results in perceptual feedback that matches the program and the drive to move (or motor intention), the sense of agency is generated. See text for full explanation.
Figure 2
Figure 2
Localization of the BP1 and BP2. After the drive to move originates from frontal and limbic regions among others, the BP1 is a slowly rising bilateral negativity starting >1 second prior to movement onset. The BP1 reflects activity in bilateral area 6 comprised of SMA, PMd and PMv. The faster rising negativity immediately preceding movement is BP2, reflecting additional activity in contralateral area 4, the primary motor cortex or M1. There are situations, such as tics, in which the drive to move may act on area 4 directly without much involvement of area 6, in which case only the BP2 would be seen prior to movement onset (dashed line). BP = Bereitschaftspotential, SMA = supplementary motor area, PMd = dorsal premotor cortex, PMv = ventral premotor cortex.

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