Stimulation of the mesencephalic locomotor region for gait recovery after stroke

Objective One‐third of all stroke survivors are unable to walk, even after intensive physiotherapy. Thus, other concepts to restore walking are needed. Because electrical stimulation of the mesencephalic locomotor region (MLR) is known to elicit gait movements, this area might be a promising target...

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Veröffentlicht in:Annals of neurology 2017-11, Vol.82 (5), p.828-840
Hauptverfasser: Fluri, Felix, Malzahn, Uwe, Homola, György A., Schuhmann, Michael K., Kleinschnitz, Christoph, Volkmann, Jens
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Sprache:eng
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Zusammenfassung:Objective One‐third of all stroke survivors are unable to walk, even after intensive physiotherapy. Thus, other concepts to restore walking are needed. Because electrical stimulation of the mesencephalic locomotor region (MLR) is known to elicit gait movements, this area might be a promising target for restorative neurostimulation in stroke patients with gait disability. The present study aims to delineate the effect of high‐frequency stimulation of the MLR (MLR‐HFS) on gait impairment in a rodent stroke model. Methods Male Wistar rats underwent photothrombotic stroke of the right sensorimotor cortex and chronic implantation of a stimulating electrode into the right MLR. Gait was assessed using clinical scoring of the beam‐walking test and video‐kinematic analysis (CatWalk) at baseline and on days 3 and 4 after experimental stroke with and without MLR‐HFS. Results Kinematic analysis revealed significant changes in several dynamic and static gait parameters resulting in overall reduced gait velocity. All rats exhibited major coordination deficits during the beam‐walking challenge and were unable to cross the beam. Simultaneous to the onset of MLR‐HFS, a significantly higher walking speed and improvements in several dynamic gait parameters were detected by the CatWalk system. Rats regained the ability to cross the beam unassisted, showing a reduced number of paw slips and misses. Interpretation MLR‐HFS can improve disordered locomotor function in a rodent stroke model. It may act by shielding brainstem and spinal locomotor centers from abnormal cortical input after stroke, thus allowing for compensatory and independent action of these circuits. Ann Neurol 2017;82:828–840
ISSN:0364-5134
1531-8249
DOI:10.1002/ana.25086