Abstract
New strategies for spinal cord stimulation (SCS) for chronic pain have emerged in recent years, which may work better via different analgesic mechanisms than traditional low-frequency (e.g., 50 Hz) paresthesia-based SCS. To determine if 10 kHz and burst SCS waveforms might have a similar mechanistic basis, we examined whether these SCS strategies at intensities ostensibly below sensory thresholds would modulate spinal dorsal horn (DH) neuronal function in a neuron type-dependent manner. By using an in vivo electrophysiological approach in rodents, we found that low-intensity 10 kHz SCS, but not burst SCS, selectively activates inhibitory interneurons in the spinal DH. This study suggests that low-intensity 10 kHz SCS may inhibit pain-sensory processing in the spinal DH by activating inhibitory interneurons without activating DC fibers, resulting in paresthesia-free pain relief, whereas burst SCS likely operates via other mechanisms.
Highlights
Differential Modulation of DorsalSince 1967, spinal cord stimulation (SCS) has been used to manage chronic intractable pain of the trunk and limbs [1]
Fundamental to the success of traditional low-frequency (e.g., 50 Hz), SCS is a concept that stimulation-induced paresthesia must be experienced by the patient and must overlap with the patient’s painful areas to result in pain relief [3]
In a previous study in rodents, we demonstrated that 10 kHz SCS at ostensibly paresthesia-free stimulation amplitudes might preferentially activate inhibitory superficial dorsal horn neurons (SDHN), which are believed to be involved in pain processing [11]
Summary
Differential Modulation of DorsalSince 1967, spinal cord stimulation (SCS) has been used to manage chronic intractable pain of the trunk and limbs [1]. Fundamental to the success of traditional low-frequency (e.g., 50 Hz), SCS is a concept that stimulation-induced paresthesia (defined as any abnormal sensation caused by A-beta fiber activation, including what is often perceived as tingling, buzzing, pins and needles, pressure, etc.) must be experienced by the patient and must overlap with the patient’s painful areas to result in pain relief [3]. In contrast to low-frequency SCS, patients receiving clinical 10 kHz SCS do not experience stimulation-induced sensations, and the A-beta-mediated paresthesia–pain overlap from 10 kHz SCS appears uncorrelated with pain relief [6,7].
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