Mechanisms Underlying Poststimulation Block Induced by High-Frequency Biphasic Stimulation

Zhong, Yihua; Wang, Jicheng; Beckel, Jonathan M.; Groat, William C. de; Tai, Changfeng

doi:10.1111/ner.13501

Cited by 7 publications

(10 citation statements)

References 25 publications

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“…At the two end segments of the modeled axon the sealed boundary conditions were implemented by setting the longitudinal axonal current to zero. This new axonal conduction model has been successfully validated in previous studies in terms of conduction velocity, refractory period, maximal firing rate, DC block, and post-stimulation block by HFBS [10,13].…”

Section: Axonal Conduction Modelmentioning

confidence: 85%

“…HFBS of 1 kHz frequency was chosen in this study to analyze the axonal conduction block because previous animal and simulation studies [7][8][9][10] showed that 1 kHz HFBS was more effective than >4 kHz HFBS to change intracellular and extracellular sodium and potassium concentrations and required a much shorter duration of stimulation to induce a poststimulation block. The 1 kHz HFBS was first applied for 59.4 s at a constant intensity of 5.4 mA.…”

Section: Simulation Protocolmentioning

confidence: 99%

“…The 1 kHz HFBS was first applied for 59.4 s at a constant intensity of 5.4 mA. These initial HFBS parameters were chosen based on a previous study [10] showing that these parameters increased the intracellular sodium concentration enough to cause a post-stimulation block. Then, the HFBS was changed to an intensity ranging between 0 mA and 5.4 mA for an additional 4 s during which the axonal conduction block was tested on a propagating AP initiated at the test electrode (see figure 1) by a single stimulus pulse (0.1 ms, 10 mA).…”

Section: Simulation Protocolmentioning

confidence: 99%

“…a post-stimulation block that can be induced by HFBS at ⩾4 kHz [7,8] as well as at 100-1000 Hz [9]. A recent modeling study [10] further revealed that the post-stimulation block is due to the accumulation of intra-axonal sodium during a long-duration stimulation. This blocking mechanism is very different from the acute block mechanism that can occur quickly after the HFBS is applied [5,6].…”

Section: Introductionmentioning

confidence: 95%

“…In this study the interaction between intracellular sodium concentration and membrane potential oscillation during axonal conduction block induced by HFBS was investigated. A newly developed axonal conduction model [10,13] that includes intracellular and extracellular sodium and potassium concentrations and ion pumps was used. The model analysis reveals the possibility to reduce HFBS intensity to a minimal level for maintaining the axonal conduction block once it has been applied at a high intensity for a period long enough to cause a post-stimulation block.…”

Section: Introductionmentioning

confidence: 99%

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Intracellular sodium concentration and membrane potential oscillation in axonal conduction block induced by high-frequency biphasic stimulation

Zhong¹,

Zhang²,

Beckel³

et al. 2022

J. Neural Eng.

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Objective. A new axonal conduction model was used to analyze the interaction between intracellular sodium concentration and membrane potential oscillation in axonal conduction block induced by high-frequency (kHz) biphasic stimulation (HFBS). Approach. The model includes intracellular and extracellular sodium and potassium concentrations and ion pumps. First, the HFBS (1 kHz, 5.4 mA) was applied for a duration (59.4 seconds) long enough to produce an axonal conduction block after terminating the stimulation, i.e., a post-stimulation block. Then, the intensity of HFBS was reduced to a lower level for 4 seconds to determine if the axonal conduction block could be maintained. Main results. The block duration was shortened from 1363 ms to 5 ms as the reduced HFBS intensity was increased from 0 mA to 4.1 mA. The block was maintained for the entire tested period (4000 ms) if the reduced intensity was above 4.2 mA. At the low intensity (<4.2 mA) the membrane potential oscillation disrupted the post-stimulation block caused by the increased intracellular sodium concentration, while at the high intensity (>4.2 mA) the membrane potential oscillation was strong enough to maintain the block and further increased the intracellular sodium concentration. Significance. This study indicates a possibility to develop a new nerve block method to reduce the HFBS intensity, which can extend the battery life for an implantable nerve stimulator in clinical applications to block pain of peripheral origin.

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Section: Axonal Conduction Modelmentioning

confidence: 85%