Vorstellung und Beobachtung von Alltagsbewegungen bei der Amyotrophen Lateralsklerose: eine multimodale Studie mittels Magnetresonanztomografie

Abstract

Amyotrophic lateral sclerosis (ALS) is characterised by progressive neuronal loss in primary motor cortex. Structural and functional changes in cortical networks have been described in the course of ALS. This study aimed at investigating compensatory neuronal processes in ALS for imagery and observation of movements of everyday life. Additionally, possible differences between ALS patients and controls in white matter integrity and in intrinsic functional connectivity were explored. Twelve ALS patients and 12 healthy controls were measured with functional magnetic resonance imaging (fMRI) during imagery and observation of 12 different movements of body parts and 1 movement of an object. Additionally, resting-state fMRI and diffusion tensor imaging data were acquired and a comprehensive neuropsychological battery was performed. Patients showed more cerebral activity than healthy controls in higher visual, motor, and association areas only for observation of movements that ALS patients are still able to execute in later disease stages. Patients displayed increased activity in the visual cortex only for visual imagery of the object movement and reduced activity for kinaesthetic imagery of body movements. More pronounced motor impairment was associated with higher cerebral activity for observation and imagery. In resting-state fMRI, patients showed increased functional connectivity compared to controls within parahippocampal and parietal areas of the default mode network (DMN). Stronger connectivity within these regions was associated with worse performance in verbal fluency and attention. Apart from the pyramidal tract, patients’ white matter integrity was reduced in frontal areas. ALS patients’ compensatory activity during movement observation and imagery and their increased connectivity within the DMN might represent cortical reorganisation in the sense of recruitment of accessory brain regions to compensate for dysfunctional motor and prefrontal networks.