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Marked distortions in sense of agency can be induced by hypnosis in susceptible individuals, including alterations in subjective awareness of movement initiation and control. These distortions, with associated disability, are similar to those experienced with Conversion Disorder (CD), an observation that has led to the hypothesis that hypnosis and CD share causal mechanisms. The purpose of this review is to explore the relationships among motor imagery (MI), hypnotic susceptibility, and CD, then to propose how MI ability may contribute to hypnotic responding and CD. Studies employing subjective assessments of mental imagery have found little association between imagery abilities and hypnotic susceptibility. A positive association between imagery abilities and hypnotic susceptibility becomes apparent when objective measures of imagery ability are employed. A candidate mechanism to explain motor responses during hypnosis is kinaesthetic MI, which engages a strategy that involves proprioception or the "feel" of movement when no movement occurs. Motor suppression imagery (MSI), a strategy involving inhibition of movement, may provide an alternate objective measurable phenomenon that underlies both hypnotic susceptibility and CD. Evidence to date supports the idea that there may be a positive association between kinaesthetic MI ability and hypnotic susceptibility. Additional evidence supports a positive association between hypnotic susceptibility and CD. Disturbances in kinaesthetic MI performance in CD patients indicate that MI mechanisms may also underlie CD symptoms. Further investigation of the above relationships is warranted to explain these phenomena, and establish theoretical explanations underlying sense of agency., (Copyright © 2016. Published by Elsevier Ltd.)

Conversion paresis is the presence of unexplained weakness without detectable neuropathology that is not feigned. To examine the 'abnormal preparation' and 'disrupted execution' hypotheses proposed to explain the movement deficits in conversion paresis, electroencephalographic, electromyographic and kinematic measures were recorded during motor preparation and execution. Six patients with unilateral upper limb conversion weakness, 24 participants feigning weakness and 12 control participants performed a 2-choice precued reaction time task. Precues provided advance information about the responding hand or finger. Patients and feigners demonstrated similar diminished force, longer movement time and extended duration of muscle activity in their symptomatic limb. Patients showed significantly suppressed contingent negative variation (CNV) amplitudes, but only when the symptomatic limb was precued. Despite the similarity in performance measures, this CNV suppression was not seen in feigners. Diminished CNV for symptomatic hand precues may reflect engagement of an inhibitory mechanism suppressing cortical activity related to preparatory processes., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Objective: Conversion paresis patients and healthy people feigning weakness both exhibit weak voluntary movement without detectable neuropathology. Uniquely, conversion patients lack a sense of conscious awareness of the origin of their impairment. We investigated whether conversion paresis patients show distinct electroencephalographic (EEG) markers associated with their unconscious movement deficits., Methods: Six unilateral upper limb conversion paresis patients, 12 feigning participants asked to mimic weakness and 12 control participants performed a precued reaction time task, requiring movements of either hand, depending on precue information. Performance measures (force, reaction and movement time), and event-related EEG potentials (ERP) were compared, between groups and across hands or hemisphere, using linear mixed models., Results: Feigners generated the same inter-hand difference in reaction and movement time as expressed by patients, even though no specific targets were set nor feedback given on these measures. We found novel ERP signatures specific to patients. When the symptomatic hand was precued, the P3 ERP component accompanying the precue was dramatically larger in patients than in feigning participants. Additionally, in patients the earlier N1 ERP component was diminished when the precue signalled either the symptomatic or asymptomatic hand., Conclusions: These results are consistent with previous suggestions that lack of awareness of the origin of their symptoms in conversion disorder patients may result from suppression of brain activity normally related to self-agency. In patients the diminished N1 to all precues is consistent with a generalised reduction in cognitive processing of movement-related precues. The P3 enhancement in patients is unlikely to simply reflect changes required for generation of impaired movements, because it was not seen in feigners showing the same behavioural deficits. Rather, this P3 enhancement in patients may represent a neural biomarker of unconscious processes, including additional emotional loading, related to active suppression of brain circuits involved in the attribution of self-agency.