ABSTRACT
BACKGROUND: Spinal cord stimulation (SCS) is an important pain treatment modality. This study hypothesized that a novel pulsed ultrahigh-frequency spinal cord stimulation (pUHF-SCS) could safely and effectively inhibit spared nerve injury-induced neuropathic pain in rats. METHODS: Epidural pUHF-SCS (± 3V, 2-Hz pulses comprising 500-kHz biphasic sinewaves) was implanted at the thoracic vertebrae (T9 to T11). Local field brain potentials after hind paw stimulation were recorded. Analgesia was evaluated by von Frey-evoked allodynia and acetone-induced cold allodynia. RESULTS: The mechanical withdrawal threshold of the injured paw was 0.91 ± 0.28 g lower than that of the sham surgery (24.9 ± 1.2 g). Applying 5-, 10-, or 20-min pUHF-SCS five times every 2 days significantly increased the paw withdrawal threshold to 13.3 ± 6.5, 18.5 ± 3.6, and 21.0 ± 2.8 g at 5 h post-SCS, respectively (P = 0.0002, < 0.0001, and < 0.0001; n = 6 per group) and to 6.1 ± 2.5, 8.2 ± 2.7, and 14.3 ± 5.9 g on the second day, respectively (P = 0.123, 0.013, and < 0.0001). Acetone-induced paw response numbers decreased from pre-SCS (41 ± 12) to 24 ± 12 and 28 ± 10 (P = 0.006 and 0.027; n = 9) at 1 and 5 h after three rounds of 20-min pUHF-SCS, respectively. The areas under the curve from the C component of the evoked potentials at the left primary somatosensory and anterior cingulate cortices were significantly decreased from pre-SCS (101.3 ± 58.3 and 86.9 ± 25.5, respectively) to 39.7 ± 40.3 and 36.3 ± 20.7 (P = 0.021, and 0.003; n = 5) at 60 min post-SCS, respectively. The intensity thresholds for pUHF-SCS to induce brain and sciatic nerve activations were much higher than the therapeutic intensities and thresholds of conventional low-frequency SCS. CONCLUSIONS: Pulsed ultrahigh-frequency spinal cord stimulation inhibited neuropathic pain-related behavior and paw stimulation evoked brain activation through mechanisms distinct from low-frequency SCS.
ABSTRACT
OBJECTIVES: Radiofrequency has been used to suppress spasticity affecting motion in patients with cerebral palsy and spinal cord injury. This study tested spasticity suppression and locomotion change after pulsed radiofrequency (PRF) at the dorsal root ganglion of rats with spasticity. MATERIALS AND METHODS: Twenty-four rats that survived for 28 days after thoracic spinal cord injury and showed spasticity in the right hind limb were separated randomly to a PRF group or Sham operation group. PRF consisted of 2 Hz biphasic 25 msec trains of PRF (500 kHz, 5 V intensity) applied on the right L5 dorsal root ganglion for 300 sec. Muscle tension of the right triceps surae was measured at 450 deg/sec of passive ankle dorsiflexion on the day before and 3, 7, and 14 days after PRF or sham operation. Locomotive function was evaluated by obtaining Basso, Beattie, and Bresnahan (BBB) scores. RESULTS: Muscle tension of the triceps surae decreased significantly three days after PRF, and gradually returned to baseline 14 days later. In the sham operation group, muscle tension increased significantly more than 14 days. The BBB scores declined from 10 to 8 after PRF and returned to pre-PRF levels 14 days later, while scores remained constant after sham operation. CONCLUSIONS: PRF produced significant and reversible suppression in spasticity, but this was accompanied by deterioration in locomotive function. Thus, caution should be exercised in considering the benefits and costs in suppressing spasticity in ambulatory patients, and implanted devices that apply titratable doses of PRF may be best to optimize patients' needs.
