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Burst and high frequency stimulation: underlying mechanism of action
Shaheen Ahmed1, Thomas Yearwood2, Dirk De Ridder3
1a Lab for Clinical and Integrative Neuroscience, School of Behavioral and Brain Sciences , The University of Texas at Dallas , Dallas , TX , USA.
Introduction:
Paresthesia-free spinal cord stimulation (SCS) techniques, such as burst and high-frequency (HF) SCS, have been developed and demonstrated to be successful for treating chronic pain, albeit via different mechanisms of action. The goal of this review is to discuss the mechanisms of action for pain suppression at both the cellular and systems levels for burst and HF SCS. In addition, we also discuss the neuromodulation devices that mimic these paradigms.
Areas Covered:
The authors performed a literature review to unravel the mechanisms of action for burst and HF SCS coupled with booklets and user manuals from neuromodulation companies to understand the programmable parameters and operating ranges. Burst SCS modulates the medial pathway to suppress pain. On cellular level, burst SCS is independent on activation of γ-aminobutyric acid (GABA) receptors to inhibit neuronal firing. HF SCS blocks large-diameter fibers from producing action potentials with little influence on smaller fibers, increasing pain suppression as frequency increases.
Expert Commentary:
The neuromodulation industry is in a phase of intense innovation characterized by adaptive stimulation to improve patients' experience and experiment with alternative frequencies and novel stimulation targets.
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