Introduction

Peripheral nerve stimulation (PNS) has been recognized as a treatment modality for peripheral neuropathic pain beginning with Wall and Sweet’s original description in 1967.¹ By inserting percutaneous needle electrodes into their own infraorbital regions, these authors were able to test the effects of stimulation on peripheral nerves. Through stimulation with square-wave pulses at 100 Hz and with a pulse width of 100 msec, they were able to induce diminished sensation to pin prick in the area of the stimulation. This led the way to investigations of PNS as a modality for treating neuropathic pain.

The last two decades have seen an increased interest in the use of PNS with application to occipital neuralgia, facial pain, and complex regional pain syndrome.² In addition to targeting defined peripheral nerves, clinicians are also applying the techniques of PNS to subcutaneous and regional stimulation.^3,4 This has led to a number of trials assessing the efficacy of PNS for a wide array of conditions, including lower back pain, postherniorrhaphy inguinal pain, sacral pain, and migraine headaches.⁵

Basic Science

Our understanding of the mechanism underlying PNS is still being developed. One hypothesis for achieving pain control with PNS involves the gate control theory of pain management proposed by Melzack and Wall in 1965.⁶ In their initial description of the gate theory, the authors postulated that large- and small-diameter fibers both send input to inhibitory neurons within the substantia gelatinosa. They theorized that small-diameter fibers provided inhibitory input to the substantia gelatinosa and the large-diameter fibers provided excitatory input. The summation of these inputs modulated the overall inhibitory connections from the substantia gelatinosa neurons to the dorsal horn transmission (T) cells, the projections of which formed the anterolateral system. In accordance with this theory, an increase in large-diameter afferent input would lead to increased inhibitory output from the substantia gelatinosa and consequently decreased transmission of nociceptive input to suprasegmental centers. Thus neurostimulation of peripheral nerves through its effect on the lowest threshold large-diameter fibers would act to “close the gate,” effectively inhibiting the transmission of small-diameter pain fibers. Although the gate control theory provides a framework for understanding the mechanism of PNS, the specifics have been challenged.⁷

Other investigators have shown additional mechanisms that may contribute to the potential efficacy of PNS. Campbell and Taub⁸ explored the mechanism of PNS through transcutaneous nerve stimulation of the median nerve. The authors stimulated the median nerve proximally with a 100-Hz, 1-msec stimulus. They found that the response elicited depended on the stimulus amplitude. At 10 V to 12 V touch threshold was elevated. With increased voltage pain thresholds were also elevated, and at intensities of 50 V analgesia was elicited. In addition, the development of analgesia was correlated with the loss of the Aδ portion of the compound action potential, suggesting that peripheral nerve transmission block may underlie the suppression of pain by PNS.

Ignelzi and Nyquist⁹ further explored the mechanism of PNS by placing cuff PNS electrodes around the sural and superficial radial nerves of cats. They found that, with stimulation, all of the components of the compound action potential were affected, although the Aδ fiber peak was more affected following neurostimulation than were the Aα or Aβ peaks. The changes were represented by either a reduction in amplitude or an increase in the latency of these waves. These findings also support the involvement of a more peripheral mechanism underlying the analgesic effect of PNS.

Indications/Contraindications

Equipment

The system for PNS includes the electrode through which stimulation is applied to the target nerve and the implantable pulse generator (IPG). Initial electrode designs were cuff electrodes, which were wrapped around the target nerves. This electrode design was found to lead to an increase in perineural fibrosis with some association of peripheral nerve injury. Newer electrode designs are either plate electrodes, which are surgically implanted, or wire electrodes, which may be implanted percutaneously.¹²

Both types of electrodes may be used for a trial of PNS. If the plate electrodes are used during the trial, an extension cable is externalized during the trial and is removed should the trial prove successful. If a percutaneous trial is conducted, the trial wire is removed before the implantation of the permanent system.

The IPG may be implanted in various sites, depending on the site of the stimulation electrode. Locations for the IPG include infraclavicular region, abdominal wall, gluteal region, or lateral thigh. The life span of the IPG varies, depending on the level of stimulation required for clinical efficacy, but 3 to 5 years is a reasonable estimate with current generators.

There has been significant recent research on BION (bionic neuron) technology, which is being applied to the field of PNS.¹³