Neurorehabilitation and Neural Repair

 

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This version was published on December 1, 2007
Neurorehabilitation and Neural Repair, Vol. 21, No. 6, 518-526 (2007)
DOI: 10.1177/1545968307300698

Cortical Plasticity in Amyotrophic Lateral Sclerosis: Motor Imagery and Function

Dorothée Lulé, PhD

Section of Neurophysiology, Univeristy of Ulm, Ulm, Germany, Eberhard-Karls-University of Tübingen, Institute of Medical Psychology and Behavioral Neurobiology, Germany, dorothee.lule{at}uni-ulm.de

Volker Diekmann, PhD

Section of Neurophysiology, Univeristy of Ulm, Ulm, Germany

Jan Kassubek, MD

Department of Neurology University of Ulm, Ulm, Germany

Anja Kurt, MD

Department of Neurology University of Ulm, Ulm, Germany

Niels Birbaumer, PhD

Eberhard-Karls-University of Tübingen, Institute of Medical Psychology and Behavioral Neurobiology, Germany, National Institutes of Health, NINDS, Human Cortical Physiology, Bethesda, Maryland

Albert C. Ludolph, MD

Department of Neurology University of Ulm, Ulm, Germany

Eduard Kraft, MD

Department of Neurology University of Ulm, Ulm, Germany

Background. Cortical networks underlying motor imagery are functionally close to motor performance networks and can be activated by patients with severe motor disabilities. Objective. The aim of the study was to examine the longitudinal effect of progressive motoneuron degeneration on cortical representation of motor imagery and function in amyotrophic lateral sclerosis. Methods. The authors studied 14 amyotrophic lateral sclerosis patients and 15 healthy controls and a subgroup of 11 patients and 14 controls after 6 months with a grip force paradigm comprising imagery and execution tasks using functional magnetic resonance imaging. Results. Motor imagery activated similar neural networks as motor execution in amyotrophic lateral sclerosis patients and healthy subjects in the primary motor (BA 4), premotor, and supplementary motor (BA 6) cortex. Amyotrophic lateral sclerosis patients presented a stronger response within premotor and primary motor areas for imagery and execution compared to controls. After 6 months, these differences persisted with additional activity in the precentral gyrus in patients as well as in a frontoparietal network for motor imagery, in which activity increased with impairment. Conclusion. The findings suggest an ongoing compensatory process within the higher order motor-processing system of amyotrophic lateral sclerosis patients, probably to overcome loss of function in primary motor and motor imagery-specific networks. The increased activity in precentral and frontoparietal networks in motor imagery might be used to control brain-computer interfaces to drive communication and limb prosthetic devices in patients with loss of motor control such as severely disabled amyotrophic lateral sclerosis patients in a locked-in-like state.

Key Words: Amyotrophic lateral sclerosis (ALS) • Cortical plasticity • Motor imagery • fMRI • Brain-computer interfaces


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