Impaired sensorimotor feedback in functional movement disorder: a resting state fMRI study (P6.080)

Abstract

OBJECTIVE: To assess the neural mechanisms underlying lack of self-agency in patients with functional movement disorder (FMD). BACKGROUND: The abnormal movements produced by patients with FMD are generated by normal voluntary motor pathways, but are strikingly perceived by patients as being involuntary. This lack of self-agency is one of the key features of FMD. The right temporo-parietal junction (TPJ) has been proposed to play an important role in self-agency by comparing internal predictions of movement with actual external events, acting as a “mismatch detector”. Task-based fMRI studies have previously demonstrated hypoactivity of the right TPJ in FMD patients; however, this region has not been examined in the resting state in these patients. DESIGN/METHODS: Resting state multi-echo BOLD fMRI and MP-RAGE images were obtained in 29 patients with clinically definite FMD and 32 age- and gender-matched healthy controls using a 3T Skyra Siemens scanner. Pre-processing was performed using the AFNI tool meica.py. Group-wise comparison between FMD patients and healthy controls was performed using AFNI GroupInstaCorr with the right TPJ as seed region-of-interest. RESULTS: As compared to controls, FMD patients demonstrated decreased functional connectivity (p<0.05 corrected) between the right TPJ and the bilateral postcentral gyri, right supplementary motor area (SMA), right posterior cingulate, right superior temporal gyrus, and left fusiform gyrus. CONCLUSIONS: We propose that the altered functional connectivity between the right TPJ and the above-mentioned sensorimotor regions reflects impaired feedforward and/or feedback with the brain’s “mismatch detector”, and may contribute to the reduced sense of agency in FMD patients.

Disclosure: Dr. Maurer has nothing to disclose. Dr. Horovitz has nothing to disclose. Dr. LaFaver has nothing to disclose. Dr. Hallett has received personal compensation for activities with Neurotoxin Institute, Cambridge University Press, Oxford University Press, Wiley-Blackwell, and Springer.