Modification of spasticity by transcutaneous spinal cord stimulation in individuals with incomplete spinal cord injury

Abstract

Context/objective: To examine the effects of transcutaneous spinal cord stimulation (tSCS) on lower-limb spasticity.

Design: Interventional pilot study to produce preliminary data.

Setting: Department of Physical Medicine and Rehabilitation, Wilhelminenspital, Vienna, Austria.

Participants: Three subjects with chronic motor-incomplete spinal cord injury (SCI) who could walk ≥10 m.

Interventions: Two interconnected stimulating skin electrodes (Ø 5 cm) were placed paraspinally at the T11/T12 vertebral levels, and two rectangular electrodes (8 × 13 cm) on the abdomen for the reference. Biphasic 2 ms-width pulses were delivered at 50 Hz for 30 minutes at intensities producing paraesthesias but no motor responses in the lower limbs.

Outcome measures: The Wartenberg pendulum test and neurological recordings of surface-electromyography (EMG) were used to assess effects on exaggerated reflex excitability. Non-functional co-activation during volitional movement was evaluated. The timed 10-m walk test provided measures of clinical function.

Results: The index of spasticity derived from the pendulum test changed from 0.8 ± 0.4 pre- to 0.9 ± 0.3 post-stimulation, with an improvement in the subject with the lowest pre-stimulation index. Exaggerated reflex responsiveness was decreased after tSCS across all subjects, with the most profound effect on passive lower-limb movement (pre- to post-tSCS EMG ratio: 0.2 ± 0.1), as was non-functional co-activation during voluntary movement. Gait speed values increased in two subjects by 39%.

Conclusion: These preliminary results suggest that tSCS, similar to epidurally delivered stimulation, may be used for spasticity control, without negatively impacting residual motor control in incomplete SCI. Further study in a larger population is warranted.

Keywords: Humans; Movement; Muscle spasticity; Paraplegia; Rehabilitation; Spinal cord injuries; Spinal cord stimulation; Tetraplegia.

Figures

Figure 1

Transcutaneous spinal cord stimulation. (A) Sketch of the placement of the stimulating and reference skin electrodes over the back and the lower abdomen, respectively, relative to the spine and the lumbosacral spinal cord. (B) The elicitation of posterior root-muscle reflexes in left (L) and right (R) quadriceps (Q), hamstrings (Ham), tibialis anterior (TA), and triceps surae (TS) was used as electrophysiological criterion to confirm the position of the stimulating paravertebral electrodes over the lumbar spinal cord. (C) The stimulation of posterior root afferents was verified by testing the recovery cycle of the evoked responses using double-stimuli at interstimulus intervals of 30, 50, and 100 ms. Electromyographic data derived from subject 2 in the supine position.

Figure 2

Wartenberg pendulum test. Electromyographic (EMG) activity from quadriceps (Q), hamstrings (Ham), tibialis anterior (TA), and triceps surae (TS) along with knee goniometric data before and after transcutaneous spinal cord stimulation in subject 3. Dotted lines mark the drop of leg from the horizontal position and the final resting knee angle reached. After stimulation, EMG activity is clearly reduced and the knee angle oscillations are a damped, pseudo-sinusoidal motion.

Figure 3

Assessment of different manifestations of spasticity before and after transcutaneous spinal cord stimulation (tSCS). (A) Manually performed hip and knee flexion and extension movements; (B) the attempt to elicit an ankle clonus; and (C) a light stroke of the plantar surface with a blunt rod. Arrow heads in (B) and (C) depict onsets of the respective mechanical stimuli. Exemplary recordings were derived from subject 2. (D) Group results (n = 6) of maneuver-induced magnitudes of ipsilateral lower limb muscle activity after tSCS relative to corresponding values before tSCS. Note the general decline in exaggerated reflex activity in the post-tSCS assessment.

Figure 4

Volitional unilateral dorsiflexion and plantar flexion in sitting position. (A) EMG patterns showing co-activation and ankle clonus (left) are reduced post-stimulation (right). Dashed lines superimposed on the ankle goniograms show the range between the neutral extended position of the ankle at rest and maximum dorsiflexion before stimulation, and a flexion bias of the rhythmic movement after stimulation is documented by the shift of the goniometric trace. Boxes are displayed with enlarged scales in (B) depicting the interference of clonus-like activity before stimulation that is eliminated after stimulation. (C) Group mean magnitudes of ipsilateral EMG activity during dorsiflexion and plantar flexion after stimulation normalized to the corresponding values before stimulation. (D) The contribution of TA to the total magnitude of ipsilateral muscle activation during dorsiflexion was increased after stimulation. TS activity during plantar flexion was at a low level before and after stimulation.