Neuroplasticity with the Feldenkrais Method in Managing Multiple Sclerosis-related Ataxia

Triantafillia Reziti and Efthimios Mikropoulos

Introduction: Ataxia is a common symptom in patients with multiple sclerosis (MS). Motor-cognitive rehabilitation in such patients involves stimulation and enhancement of different brain regions, both of which rely on physiological pathways between the body and the brain, provoking brain plasticity and learning.
Objective: This study aimed at applying our recently published protocol, the neuroplasticity scale (NS), which is based on the Feldenkrais method (FM), in the context of chronic MS ataxia. Through an integrated process involving the development of a patient’s capacity to sense, think and respond in an embodied manner to external stimuli, we sought to record and reinforce brain learning during motor rehabilitation.
Method: A single MS patient presenting gait ataxia, instability, spasticity, executive dysfunction and attention deficits was selected as a case study for intervention. We applied our NS protocol for six weeks and recorded different aspects of the individual’s interaction with his environment, in terms of motor control, interoception, perception and spatial embodiment.
Results: Following our applied protocol, the individual showed clear improvement in his motor coordination, significantly reduced gait ataxia, ability to control dual-task functions, as well as improved static and dynamic balance. He also presented significantly reduced spasticity, improved sensory awareness and better embodied cognition. Overall, he showed an evident improvement in his daily functionality.
Conclusion: With further refinement, our NS protocol can provide important insights about brain learning and motor-cognitive regulation, in the context of therapeutic interventions for mild and progressive MS-related ataxia.

Published on: May 28, 2024
doi: 10.17756/jnen.2024-113
Citation: Reziti T, Mikropoulos E. 2024. Neuroplasticity with the Feldenkrais Method in Managing Multiple Sclerosis-related Ataxia. J Neurol Exp Neurosci 10(1): 10-18.