Research Press Release

Neuroscience: Restoring movement after paralysis

Nature

May 25, 2023

An implant that restores communication between the brain and spinal cord is shown to help a patient with paralysis of the arms and legs to stand and walk naturally. The device, described in Nature this week, was also found to improve neurological recovery, and the patient was able to walk with crutches even when the implant was switched off. The findings establish a framework to restore the natural control of movement after paralysis.

Spinal cord injury can interrupt the communication between the brain and the region of the spinal cord that controls walking, leading to paralysis. Some previous approaches to restore movement in people with this type of paralysis involved electrically stimulating regions of the spinal cord to enable standing and walking. However, this required wearing motion sensors, and patients showed limited ability to adapt leg movements to changing terrains and demands. Connecting the brain and spinal cord digitally could improve the control over the timing and amplitude of muscle activity and restore more natural and adaptive control of standing and walking in these patients.

Grégoire Courtine and colleagues tested a brain–spine interface (BSI), consisting of an implanted recording and stimulation system, that establishes a direct link between the brain and spinal cord regions involved in walking. The BSI was able to calibrate within a few minutes and has remained reliable and stable for over one year, including at home without supervision. The patient reports that the BSI enables a natural control over the movements of the patient’s legs to stand, walk, climb stairs and even traverse complex terrains. Moreover, neurorehabilitation supported by the BSI improved neurological recovery and the patient regained the ability to walk with crutches over ground even when the BSI was switched off.

The concept of a digital bridge between the brain and spinal cord may help to improve the treatment of movement deficits due to neurological disorders.

doi:10.1038/s41586-023-06094-5

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