Non-patterned electrical stimulation of the posterior structures of the lumbar spinal cord in subjects with complete, long-standing spinal cord injury, can induce patterned, locomotor-like activity. We show that epidural spinal cord stimulation can elicit step-like EMG activity and locomotor synergies in paraplegic subjects. An electrical train of stimuli applied over the second lumbar segment with a frequency of 25 to 60 Hz and an amplitude of 5-9 V was effective in inducing rhythmic, alternating stance and swing phases of the lower limbs. This finding suggests that spinal circuitry in humans has the capability of generating locomotor-like activity even when isolated from brain control, and that externally controlled sustained electrical stimulation of the spinal cord can replace the tonic drive generated by the brain.

Study design: It has been previously demonstrated that sustained nonpatterned electric stimulation of the posterior lumbar spinal cord from the epidural space can induce stepping-like movements in subjects with chronic, complete spinal cord injury. In the present paper, we explore physiologically related components of electromyographic (EMG) recordings during the induced stepping-like activity. Objectives: To examine mechanisms underlying the stepping-like movements activated by electrical epidural stimulation of posterior lumbar cord structures. Materials and methods: The study is based on the assessment of epidural stimulation to control spasticity by simultaneous recordings of the electromyographic activity of quadriceps, hamstrings, tibialis anterior, and triceps surae. We examined induced muscle responses to stimulation frequencies of 2.2-50 Hz in 10 subjects classified as having a motor complete spinal cord injury (ASIA A and B). We evaluated stimulus-triggered time windows 50 ms in length from the original EMG traces. Stimulus-evoked compound muscle action potentials (CMAPs) were analyzed with reference to latency, amplitude, and shape. Results: Epidural stimulation of the posterior lumbosacral cord recruited lower limb muscles in a segmental-selective way, which was characteristic for posterior root stimulation. A 2.2 Hz stimulation elicited stimulus-coupled CMAPs of short latency which were approximately half that of phasic stretch reflex latencies for the respective muscle groups. EMG amplitudes were stimulus-strength dependent. Stimulation at 5-15 and 25-50 Hz elicited sustained tonic and rhythmic activity, respectively, and initiated lower limb extension or stepping-like movements representing different levels of muscle synergies. All EMG responses, even during burst-style phases were composed of separate stimulus-triggered CMAPs with characteristic amplitude modulations. During burst-style phases, a significant increase of CMAP latencies by about 10 ms was observed. Conclusion: The muscle activity evoked by epidural lumbar cord stimulation as described in the present study was initiated within the posterior roots. These posterior roots muscle reflex responses (PRMRRs) to 2.2 Hz stimulation were routed through monosynaptic pathways. Sustained stimulation at 5-50 Hz engaged central spinal PRMRR components. We propose that repeated volleys delivered to the lumbar cord via the posterior roots can effectively modify the central state of spinal circuits by temporarily combining them into functional units generating integrated motor behavior of sustained extension and rhythmic flexion/extension movements. This study opens the possibility for developing neuroprostheses for activation of inherent spinal networks involved in generating functional synergistic movements using a single electrode implanted in a localized and stable region.

We report on the pathological findings in the brains of 8 Parkinson's disease patients treated with deep brain stimulation (DBS) of the thalamic ventral intermediate nucleus (6 cases) and subthalamic nucleus (2 cases). DBS was performed continuously for up to 70 months. All brains showed well‐preserved neural parenchyma and only mild gliosis around the lead track compatible with reactive changes due to surgical placement of the electrode. We conclude that chronic DBS does not cause damage to adjacent brain tissue. Ann Neurol 2000;48:372–376

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Objectives: The purpose of this study was to evaluate the eect of spinal cord stimulation (SCS) on severe spasticity of the lower limbs in patients with traumatic spinal cord injury (SCI) under close scrutiny of the site and parameters of stimulation. Materials and methods: Eight SCI patients (four women, four men) were included in the study. Levels of spasticity before and during stimulation were compared according to a clinical rating scale and by surface electrode polyelectromyography (pEMG) during passive¯exion and extension of the knee, supplemented by a pendulum test with the stimulating device switched either on or o over an appropriate period. Results: Both the clinical and the experimental parameters clearly demonstrated that SCS, when correctly handled, is a highly eective approach to controlling spasticity in spinal cord injury subjects. The success of this type of treatment hinges on four factors: (1) the epidural electrode must be located over the upper lumbar cord segment (L1, L2, L3); (2) the train frequency of stimulation must be in the range of 50 ± 100 Hz, the amplitude within 2 ± 7 V and the stimulus width of 210 ms; (3) the stimulus parameters must be optimized by clinically assessing the eect of arbitrary combinations of the four contacts of the quadripolar electrode; and (4) amplitudes of stimulation must be adjusted to dierent body positions. Conclusions: Severe muscle hypertonia aecting the lower extremities of patients with chronic spinal cord injuries can be eectively suppressed via stimulation of the upper lumbar cord segment. Spinal Cord (2000) 38, 524 ± 531