Burst and Tonic Spinal Cord Stimulation Differentially Activate GABAergic Mechanisms to Attenuate Pain in a Rat Model of Cervical Radiculopathy


Objective: Spinal wire stimulation (SCS) is widely used to treat neuropathic pain. Burst SCS, another mode of stimulation, reduces neuropathic pain while not paresthesia. But, the results and mechanisms of burst SCS have not been compared to standard tonic SCS in controlled investigations. This study compares the attenuation of spinal neuronal activity and tactile allodynia, and the role of γ-aminobutyric acid (GABA) signaling during burst or tonic SCS during a rat model of cervical radiculopathy. Strategies: The consequences of burst and tonic SCS were compared by recording neuronal firing before and after each mode of stimulation at day seven following a painful cervical nerve root compression. Neuronal firing was additionally recorded before and when burst and tonic SCS in the presence of the $rm GABA_rm B$ receptor antagonist, CGP35348. Results: Burst and tonic SCS both scale back neuronal firing. The impact of tonic SCS, but not burst SCS, is blocked by CGP35348. In a separate study, spinal wire stimulators were implanted to deliver burst or tonic SCS beginning on day four once painful nerve root compression; allodynia and serum GABA concentration were measured through day fourteen. Burst and tonic SCS each scale back allodynia. Tonic SCS attenuates injury-induced decreases in serum GABA, but GABA remains decreased from baseline during burst SCS. Conclusion and Significance: Together, these studies recommend that burst SCS does not act via spinal GABAergic mechanisms, despite its attenuation of spinal hyperexcitability and allodynia similar to that of tonic SCS; understanding different potential spinal inhibitory mechanisms could cause enhanced analgesia throughout burst stimulation.

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