|Title:||Activities of cortical motor neurons trigger electrical stimulation of lower motor neurons in the spinal cord|
|Subject:||Paraplegics -- Rehabilitation.|
Spinal cord -- Wounds and injuries -- Patients -- Rehabilitation.
Neural networks (Neurobiology)
Hong Kong Polytechnic University -- Dissertations
|Department:||Department of Rehabilitation Sciences|
|Pages:||xxv, 149 leaves : ill. ; 30 cm.|
|Abstract:||Restoration of hindlimb locomotion after spinal cord injury (SCI) remains a challenging problem even though functional electrical stimulation (FES) and neuromotor prostheses (NMP) have been investigated in previous studies. Since complete lesions in the lumbar spinal cord cause caudal section below the lesion cannot receive descending signals from the brain, the volitional control of hindlimb is damaged. In this study, to restore the voluntary movement of paralyzed hindlimb, a circuit was designed that can bypass a lesion to the spinal cord, linking upper motor neurons (UMNs) and lower motor neurons (LMNs) in guinea pigs. This circuit, named as "Motolink", which contains an amplifier and a stimulator. An amplifier acquired signals from the primary motor cortex (M1) via multi-electrodes array, which triggered a programmed microprocessor to generate pulse trains that directly activated LMNs, hence produced hindlimb movements. The study was divided into two experiments. The first has been performed acutely, in which we used signals from visual cortex (VC), auditory cortex (AC) and medial geniculate body (MGB) respectively to induce hindlimb movement on anaesthetized rats with incomplete spinal cord injury. The second is chronic research, during which signals from hindlimb region of the primary motor cortex (M1HL) were acquired to induce contralateral lower limb action on guinea pigs with complete SCI, when animal slowly running on treadmill by their forelimbs with partial body support, or when animal moving freely.|
The animal's spinal cord at the level of T12 was completely transected to serve as a SCI model. The recording electrode array was implanted into special area in the right side of the brain. The stimulation electrode array was implanted into the anterior corner of the left L2-L3 segments in the spinal cord. During recording, Motolink was anchored on the skull to execute connection between cerebrum and spinal cord. Amplified cortical activities may be sent to remote computer for analyses simultaneously. One dimension of kinematics was described by Vicon system. The electromyography (EMG) activity of forelimb was recorded by another amplifier in chronic experiment part. Locations of recording and stimulating electrodes were examined by histology analyses. In the anesthetized rat, our findings showed that neural response of VC, AC or MGB to stimuli of light, sound or electrical current can be exactly acquired by the circuit as the frequency of stimuli changed. Twitching of lower limb was observed every time when neural signals were acquired to activate LMNs. In chronic experiments, the artificial circuit chronically rerouted neuronal signals around the spinal injury, enabling twitching-like movements of the paraplegic, stimulated hindlimb as animals walked at different speeds on a treadmill by forelimbs. As shown in the corresponding videos, mostly each step of forelimb is followed by one movement of left hindlimb, but sometimes followed by none or two. The time lag between the forelimb and hindlimb was shortened significantly from 153+/-42 ms to 92+/-23 ms (p<0.01) when the speed of the treadmill was increased from 5.6 cm/s to 11.1 cm/s. The UMNs were reconnected with LMNs by circuit in transected spinal cord, thus produced hindlimb movement, which electronically bypasses lesion in the spinal cord. Our finding shows the possibility of a novel therapy for functional locomotion recovery of hind limbs in patients with spinal cord injury.
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