“…Across the spectrum of motor FND (mFND), which we frame as encompassing functional [psychogenic nonepileptic/dissociative] seizures (FND‐seiz) and functional movement disorders (FND‐movt), distributed corticolimbic abnormalities spanning multiple brain networks have been identified (Baizabal‐Carvallo et al, 2019; Perez et al, 2015; Pick, Goldstein, et al, 2018; Szaflarski & LaFrance, 2018). Findings include heightened amygdala reactivity to affective stimuli (Aybek et al, 2015; Aybek, Nicholson, Zelaya, et al, 2014; Voon, Brezing, et al, 2010), increased limbic‐motor control network connectivity (Aybek et al, 2015; Aybek, Nicholson, Zelaya, et al, 2014; Diez, Ortiz‐Terán, et al, 2019; van der Kruijs et al, 2012; Voon, Brezing, et al, 2010), altered right temporoparietal junction (TPJ) activity and connectivity (Arthuis, Micoulaud‐Franchi, Bartolomei, McGonigal, & Guedj, 2014; Baek et al, 2017; Maurer et al, 2016; Voon, Gallea, et al, 2010), and default‐mode network abnormalities among other findings (Monsa, Peer, & Arzy, 2018). Structural MRI studies in mFND compared to healthy controls (HCs) also report increased amygdala gray matter volume (Maurer et al, 2018), cingulo‐insular atrophy (Labate et al, 2012; Perez, Williams, et al, 2017), and changes in sensorimotor and striatothalamic areas (Aybek et al, 2014; Bègue et al, 2019; Espay, Maloney, et al, 2018).…”