Chapter Overview
Chapter Synopsis: Electrical stimulation of a peripheral nerve (PNS) can be used to treat neuropathic pain, ideally that arises from a single nerve and often follows peripheral nerve damage. This chapter considers the issues relevant to successful PNS. The conditions most amenable to PNS include occipital neuralgia, peripheral neuropathic pain, and trigeminal branch pain. With a more regional subcutaneous stimulation, PNS can affect lower back pain and migraine headache. Similar to spinal cord stimulation, our understanding of the mechanism behind PNS is rooted in Melzack and Wall’s gate control theory of pain: stimulation of large-diameter fibers decreases the pain signaling from small-fiber neurons. Other hypotheses suggest that PNS may result in peripheral nerve block or other peripheral changes in action potential kinetics to suppress pain. PNS was traditionally delivered with a cuff electrode wrapped around the target nerve, but this can lead to perineural fibrosis. Today, plate or wire electrodes are more commonly implanted, either surgically or percutaneously. An implantable pulse generator is commonly implanted in the abdominal wall or gluteal region. With surgical implantation, a piece of fascia may be implanted between the electrode and the nerve itself, fulfilling a role analogous to the dura mater in implantation of a spinal cord stimulator. Percutaneous implantation carries its own set of considerations. More recently, the leadless bionic neuron (BION) system has been developed with an eye toward PNS.
Important Points:
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PNS is most effective for neuropathic pain attributable to a single peripheral nerve.
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Some sensory preservation should be present in the region of pain.
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Implantation of PNS should be preceded by a successful trial of stimulation.
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Outcome evidence for subcutaneous and regional field stimulation is in progress.
Clinical Pearls:
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Lack of improvement with TENS is not a contraindication to a trial of PNS.
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Fascial cuff can be placed between peripheral nerve and plate electrode during surgical implantation (serves an analogous to role to the dura in spinal cord stimulation).
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Percutaneous trial of stimulation for occipital neuralgia and trigeminal branch neuralgia can be successfully performed under general anesthesia.
Clinical Pitfalls:
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Risk of infection is significant; use of local antibiotics may reduce risk.
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Incidence of lead migration can be minimized through careful anchoring and tunneling of leads.
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Cuff electrodes should not be placed around peripheral nerves because of risk of perineural fibrosis.
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. 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. In addition to targeting defined peripheral nerves, clinicians are also applying the techniques of PNS to subcutaneous and regional stimulation. 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.
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. 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.
Other investigators have shown additional mechanisms that may contribute to the potential efficacy of PNS. Campbell and Taub 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 Nyquist 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
Indications
PNS is usually indicated for patients with peripheral neuropathic pain that can be attributed to a single peripheral nerve. Candidates for PNS should have undergone multimodal therapy, including medical management, anesthetic blockade, and physical therapy. As with patients who are being evaluated for spinal cord stimulation, neuropsychological testing can be valuable. In addition, before permanent implantation of the internal pulse generator, patients should have undergone a successful trial of stimulation with a predetermined therapeutic benefit.
More recent studies of subcutaneous target stimulation (STS) and regional stimulation have broadened the traditional inclusion criteria of neuropathic pain attributable to a single peripheral nerve. Retrospective case series of subcutaneous stimulation applied to painful areas has demonstrated therapeutic benefit for lower back pain, neck pain, inguinal pain, and others. However, the longer-term efficacy for this application is unknown.
Contraindications
PNS is a well-tolerated procedure. Consequently the contraindications to implantation are generally those related to the patient’s ability to undergo a surgical procedure. Specifically the patient should not be coagulopathic and should be able to tolerate the stress of general anesthesia. Since the procedure involves the implantation of a medical device, the patient should not have an active infection, and the surgical area should be free of infection.
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.
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. BION is an implantable stimulator that can be used to target nerves and muscles. The design is quite unique from currently used technologies since it is a leadless system, in which the generator and electrode are incorporated into a single miniature apparatus. Technology is being developed to percutaneously implant these devices to be used as peripheral nerve stimulators. Reports have been published with this technique targeting the occipital and pudendal nerves, among others.
Technique
Peripheral nerve stimulators can be implanted through either an open surgical or a percutaneous approach. Box 16-1 lists nerves that are commonly targeted for PNS. If using a surgical approach, the first step is the exposure of the target nerve. An approximate 4-cm distance of the nerve is dissected free from the surrounding tissues. Care is taken not to excessively disrupt the vascularity of the nerve. Once the nerve has been dissected free, the next step is placing the electrode under the nerve so the electrode contacts lie in proximity to the nerve. The electrode can then be sutured to the surrounding tissues to prevent migration. Some authors have advocated placing a piece of fascia between the stimulating electrodes and the nerve. This is thought to be analogous to the dura in spinal cord stimulation, which separates the spinal cord–stimulating electrode from the underlying spinal cord. Fig. 16-1 illustrates the surgical technique for placement of an ulnar nerve stimulator.
Craniofacial
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Trigeminal branch nerves (supraorbital, infraorbital)
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Occipital nerves
Extremities
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Ulnar, median, radial
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Sciatic, peroneal, posterior tibial
Other Targets
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Inguinal pain (ilioinguinal, iliohypogastric)
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Chest wall (intercostal)
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