Spinal Cord Stimulation (SCS) Trial Outcomes After Conversion to a Multiple Waveform SCS System.

OBJECTIVE: Spinal cord stimulation (SCS) for chronic intractable pain is typically delivered in pulses, classically programmed between approximately 20 and 100 Hz. Though some recent studies suggest that better pain relief is obtained, with only 10 kHz stimulation, other studies show that single-therapy trials do not always lead to permanent implantation. We evaluated SCS outcomes in subjects given trials with multiple waveforms who did not experience satisfactory trial relief with 10 kHz stimulation only. METHODS: In this multicenter, open-label, real-world, observational study conducted in the United States, subjects reporting <50% pain relief with 10 kHz stimulation (i.e., failed the screening trial) received a stimulator capable of delivering multiple waveforms and/or field shapes. Pain relief and patient device preference data were collected. RESULTS: Twenty-two subjects were analyzed. Of the 16 who failed the 10 kHz trial and had numerical rating scale, visual analog scale, or percent pain relief scores available, 63% (n = 10) reported ≥50% relief with multiple waveform SCS. Additionally, 80% of subjects with ≥50% relief using multiple waveform SCS had experienced no relief with 10 kHz SCS. Among all subjects, 68% preferred multiple waveform SCS, none preferred 10 kHz SCS, and 32% had no preference. DISCUSSION: Subjects with failed SCS trials at 10 kHz experienced ≥50% relief after switching to a multiple waveform system. These results suggest that providing multiple waveforms during trials may overcome limitations of providing only 10 kHz stimulation. Thus, chronic pain's variable nature across patients and over time lends itself to variable treatment options.

Effects of Rate on Analgesia in Kilohertz Frequency Spinal Cord Stimulation: Results of the PROCO Randomized Controlled Trial.

OBJECTIVE: The PROCO RCT is a multicenter, double-blind, crossover, randomized controlled trial (RCT) that investigated the effects of rate on analgesia in kilohertz frequency (1-10 kHz) spinal cord stimulation (SCS). MATERIALS AND METHODS: Patients were implanted with SCS systems and underwent an eight-week search to identify the best location ("sweet spot") of stimulation at 10 kHz within the searched region (T8-T11). An electronic diary (e-diary) prompted patients for pain scores three times per day. Patients who responded to 10 kHz per e-diary numeric rating scale (ED-NRS) pain scores proceeded to double-blind rate randomization. Patients received 1, 4, 7, and 10 kHz SCS at the same sweet spot found for 10 kHz in randomized order (four weeks at each frequency). For each frequency, pulse width and amplitude were titrated to optimize therapy. RESULTS: All frequencies provided equivalent pain relief as measured by ED-NRS (p ≤ 0.002). However, mean charge per second differed across frequencies, with 1 kHz SCS requiring 60-70% less charge than higher frequencies (p ≤ 0.0002). CONCLUSIONS: The PROCO RCT provides Level I evidence for equivalent pain relief from 1 to 10 kHz with appropriate titration of pulse width and amplitude. 1 kHz required significantly less charge than higher frequencies.

Time-sensitive reorganization of the somatosensory cortex poststroke depends on interaction between Hebbian and homeoplasticity: a simulation study.

Together with Hebbian plasticity, homeoplasticity presumably plays a significant, yet unclear, role in recovery postlesion. Here, we undertake a simulation study addressing the role of homeoplasticity and rehabilitation timing poststroke. We first hypothesize that homeoplasticity is essential for recovery and second that rehabilitation training delivered too early, before homeoplasticity has compensated for activity disturbances postlesion, is less effective for recovery than training delivered after a delay. We developed a neural network model of the sensory cortex driven by muscle spindle inputs arising from a six-muscle arm. All synapses underwent Hebbian plasticity, while homeoplasticity adjusted cell excitability to maintain a desired firing distribution. After initial training, the network was lesioned, leading to areas of hyper- and hypoactivity due to the loss of lateral synaptic connections. The network was then retrained through rehabilitative arm movements. We found that network recovery was unsuccessful in the absence of homeoplasticity, as measured by reestablishment of lesion-affected inputs. We also found that a delay preceding rehabilitation led to faster network recovery during the rehabilitation training than no delay. Our simulation results thus suggest that homeoplastic restoration of prelesion activity patterns is essential to functional network recovery via Hebbian plasticity.