Objective: While levodopa and deep brain stimulation alleviate most of the symptoms associated with Parkinson’s Disease (PD), axial gait disorders are less responsive to these treatments. Impairments include short and slow steps, balance deficits and freezing of gait. Using MPTP-treated non-human primates, we studied the impact of a brain-spine interface on alleviating axial gait deficits observed in PD.

Background: We have established a mechanistic and technological framework that guided the design of electrical spinal cord stimulation protocols engaging extensor and flexor muscle groups. We created an interface that linked gait events decoded from leg motor cortex activity to spatially selective stimulation protocols that reinforced the movements associated with these events. As early as 6 days after spinal cord injury, this brain-spine interface restored weight-bearing locomotor movements of a paralyzed leg in a non-human primate model of spinal cord injury [1].

Methods: Three MPTP-treated Rhesus macaque monkeys, the gold standard model for PD symptomatology, were implanted with the wireless brain-spine interface. Recordings of multi-unit activity from the left and right leg motor cortex were used to detect neural states related to flexion and extension movements of both legs while the animal walked freely overground or over a horizontal ladder. The detection of these gait events triggered the delivery of spatially selective electrical stimulation protocols that reinforced the extension and flexion movements of the legs. Stimulation protocols were delivered using an implantable pulse generator with real-time triggering capability that was connected to a custom-made electrode array. The electrode layout was based on a computational model that estimated optimal locations to target the dorsal roots of each lumbar spinal cord segment.

Results: MPTP-treated monkeys exhibited moderate to severe axial gait deficits, including short and slow steps, balance deficits, freezing of gait, and poor precision of paw placement when traversing the horizontal ladder. The brain-spine interface instantly alleviated these deficits, allowing the monkeys to increase their walking speed, improved their balance and regained coordinated gait patterns. Moreover, the brain-spine interface enabled the monkeys to regain the ability to position the paws precisely on the rungs of the horizontal ladder.

Conclusions: These preliminary results illustrate the ability of the brain-spine interface to alleviate axial gait deficits and restore visuomotor control of leg movements in MPTP-treated non-human primates, standard model for PD symptomatology. These findings open promising avenues for targeting gait deficits in people with PD, which are still resistant to current treatments.

References: [1] Capogrosso M, Milekovic T, Borton D, et al. A brain-spine interface alleviating locomotor deficits after spinal cord injury. Nature 2016; 539: 284-88.

« Back to 2018 International Congress

MDS Abstracts - https://www.mdsabstracts.org/abstract/a-wireless-brain-spine-interface-alleviating-gait-deficits-of-non-human-primates-model-of-parkinsons-disease/