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Functional MRI of sensorimotor reorganization and plasticity in orofacial dystonia

Subject Area Human Cognitive and Systems Neuroscience
Term from 2009 to 2014
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 146249573
 
Final Report Year 2014

Final Report Abstract

During the funding period, we performed functional MRI studies in patients with different forms of focal dystonia. These included patients with blepharospasm/Meige’s syndrome, laryngeal dystonia, writer’s cramp and musicians with embouchure dystonia. Task related imaging designs (during motor imagination or standardized sensory stimulation) were combined with analyses of functional connectivity at rest to advance our understanding on abnormal sensorimotor processing already in the absence of dystonic symptoms. We found deficient basal ganglia–premotor activation as an intrinsic deficit in patients with writer’s cramp during motor imagery. Abnormal function within this network was in a next step further underlined by reduced positive functional connectivity (FC) at rest in patients with WC from the premotor cortex, pallidum and thalamus to the primary sensorimotor cortex. This analysis and a subsequent data driven whole brain analysis of FC at rest furthermore showed altered cerebello-thalamic connectivity as an important pathophysiological trait in patients with writer’s cramp. In patients with embouchure dystonia we demonstrate altered FC of clinically affected and unaffected primary sensorimotor cortices within the lateral motor network and of various auditory and sensorimotor integration areas within the auditory network. To further investigate the role of the somatosensory system we studied processing of standardized sensory stimuli in patients with different forms of focal dystonia. In all groups of patients we found signs of dysfunctional activation within primary/secondary somatosensory representations (over- or underactivity depending on the type of dystonia) of clinically affected but also unaffected body parts. Single subject analyses in patients with embouchure dystonia additionally showed topographical changes in the somatosensory cortices. Together our studies clearly show abnormal function of sensorimotor basal-gangliathalamocortical and cerebellar networks in patients with different forms of focal dystonia. Furthermore our results underline the importance of aberrant somatosensory processing in focal dystonia. Dysfunctional intracortical inhibition, sensorimotor integration and plastic reorganization are possible explanations for the observed imaging findings. Their presence at rest, i.e. without dystonic symptoms and partly for representations of clinically unaffected body parts suggest a primary predisposition for the development of symptoms of dystonia.

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