Structural Organization of the Brain Connectome in Patients with Psychogenic Dystonia (I7.012)

Objective: Using diffusion tensor (DT) MRI, this study investigates the structural organization of the brain connectome in patients with psychogenic dystonia (pDYT). Background: Psychogenic dystonia is a controversial diagnosis. The neurobiological basis of psychogenic movement disorders remains poorly understood. Methods: This study included a large series of 31 pDYT (mean age 46 years; mean disease duration: 5 years; mean Fahn-Marsden rating scale score: 11.6; mean Unified Dystonia Rating Scale score: 11.2; mean Psychogenic Movement Disorder scale total score: 18.6) and 36 age- and sex-matched healthy controls. Subjects underwent 3D T1-weighted and DT MRI. The structural connectome was reconstructed based on brain parcellation and whole brain DT MRI tractography. The affected structural connections in patients relative to healthy controls were investigated using Network-Based Statistic (p<0.01, 10.000 permutations). Results: Compared to healthy controls, pDYT showed a large brainstem/basal ganglia/frontal network with decreased fractional anisotropy and increased mean diffusivity including the brainstem, left thalamus, putamen, pallidum, pre- and post-central gyri, right caudate, and anterior cingulate and middle/superior frontal cortex bilaterally. Smaller secondary networks with reduced fractional anisotropy were found in the right hemisphere connecting the right pre- and post-central gyri to the thalamus and middle frontal areas. In pDYT patients, affected connections between the right thalamus and putamen and the right thalamus and precentral gyrus correlated with the total phenomenology subscore of the Psychogenic Movement Disorder scale. Conclusions: This study points toward a structural disconnection of the brainstem/basal ganglia/frontal brain networks in patients with pDYT. Altered structural connections between basal ganglia and primary sensorimotor cortex are associated with the severity and duration of the disease. Future longitudinal studies are warranted to clarify whether these abnormalities reflect a primary disease process in these networks or are secondary effects of the disorder.