About this Special Issue
Dystonia is a motor disorder characterized by muscle contractions causing abnormal postures and/or movements, which are very disabling and painful in severe forms. Dystonia is sometimes the only symptom of the disease, but it is also present in combination with other motor dysfunctions in many neurological diseases, including Parkinson's disease and dyskinetic disorders. The possibilities of medical treatment still remain quite limited with side effects. The pathophysiologic mechanisms of dystonia concern aberrant communication within brain networks, particularly involving the basal ganglia, the sensorimotor cortex, and the cerebellum. Aberrant communication involves a combination of physiological and structural abnormalities, involving nodes that relay information between these three main actors (thalamus, brainstem nuclei, cortical nodes). However, the ways the different loops and nodes embedded in this interconnected complex system participate in explaining the symptoms are unclear, which leads to the fact that the etiology of dystonia remains poorly understood.
This Special Issue aims to publish studies in mammalian and non-mammalian phenotypic and genotypic animal models, as well as in patients. The focus is a better understanding of the pathophysiological mechanisms of dystonia, by deciphering how the functional/structural abnormalities in motor system can generate or amplify dystonic movements and postures. A better understanding of the dysfunction of each region in the network, their interactions and their link with the symptoms are important topics to address. We welcome researchers and clinicians working on animal models and/or patients (ideally translational work involving both) to participate to this issue and to shed light on novel pathophysiological processes to contribute to a deeper understanding of dystonia as a circuit disorder in relationship with motor symptoms.
Together, this Special Issue will present complementary studies in the human (including different dystonia subtypes) and animal models (including worms, fruit flies, rodents, and others) that will allow for the characterization of common physiological processes implicated in dystonia. We believe this is an important step to advance in the development of new treatments acting on motor circuits with less adverse side effects than observed with medications.
For authors, please also review the journal's information regarding Author Guidelines and Article Processing Charges, or direct any questions to the Editorial Office: dystonia.office@frontierspartnerships.org.
Manuscript Deadline: 1 October 2022
Keywords: dystonia, sensorimotor circuit, motor symptoms, humans, animals
