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Complications of Peripheral and Field Stimulation

Priodarshi Roychoudhury MD¹ and Peter Staats MD, MBA, FIPP²

¹University of British Columbia, Canada
²World Institute of Pain, Atlantic Beach, FL, USA

Introduction

The modern-day application of electrical stimulation to treat pain, dates back to 1965 with Melzack and Wall’s paper outlining the “gate control”, which proposed a gating mechanism in the spinal cord, whereby increased firing of the large diameter neurons “closed” the gate, for transmission of painful stimuli to the brain by small diameter neurons [1].

Since the first therapeutic application of neurostimulation [2] by neurosurgical lead implantation for peripheral nerves in 1967, peripheral nerve stimulation (PNS) and spinal cord stimulation (SCS) have evolved at different rates, with the latter dominating for a variety of reasons including reimbursement, long-term outcome studies and technologic barriers to the application of wider adoption. But it is very likely that PNS is going to have a much broader application in the years to come. The critical nature of understanding the types of complications that can occur with PNS will cross multiple disciplines.

Early advances were in the field of pain medicine, but PNS has now been successfully used in multiple non-pain related disorders including, but not limited to, obesity, migraines, Parkinson’s, asthma exacerbations in COVID, anxiety and depression, epilepsy, (vagus nerve stimulation), hypoglossal nerve stimulation for obstructive sleep apnea, carotid sinus stimulation for resistant hypertension and peroneal nerve stimulation for foot drop. Recently, PNS has received FDA approval for tibial nerve stimulation for an overactive bladder [3].

Neuromodulation has rarely recognized complications causing long-term morbidity. The aim of this chapter is to review complications observed in patients treated with PNS techniques. Despite dorsal root ganglia (DRG) arguably being considered part of the peripheral nervous system complications related to stimulation of the DRG are covered in Chapter 49: Complications of Dorsal Root Ganglion Stimulation for the Treatment of Chronic Neuropathic Pain.

Mechanism of Action for Pain

PNS delivers focused stimulation to the target nerve that innervates the painful region. Mechanistically, it causes selective activation of Aα/β fibers at frequencies (5–150 Hz) producing a comfortable sensation in the region of pain, leading to multiple analgesic mechanisms from the periphery to the dorsal horn and cortex. Larger diameter nerve fibers, activated at a lower intensity compared to smaller diameter fibers close the gate for the painful stimuli carried by the A delta and C fibers.

The original 1965 gate control theory has been critically reviewed and supplemented over time to better explain phenomenon experimentally, for example, additional proposed mechanisms for conventional stimulation for both peripheral (e.g., altering nerve fiber excitability or conduction) and central factors (modulation of expression of neuronal signaling proteins altering activity in the descending inhibitory pathway).

Although conventional PNS utilizes small electrodes immediately adjacent to a nerve, producing intense electric fields, it decays rapidly across short distances, hence fibers nearer the electrode although activated (including small diameter fibers), fibers slightly distant, deeper in or across the nerve, experience little or no stimulation at all [4]. This leads to inadequate and transient pain relief for a few days to months only.

Mechanisms of Sustained Pain Relief in Recent Technologies

A) Remote selective targeting with large open coiled electrodes

Remote selective targeting in contrast to conventional “intimate” electrodes enables more robust activation of a high proportion of large diameter fibers avoiding unintended discomfort by optimizing the strength–distance and strength–diameter relationships [4].
Remote selective targeting widens the therapeutic window by activation of motor efferent fibers resulting in strong, physiologic muscle contractions without activation of small nociceptive fibers. Muscle afferents, including proprioceptive Aα/β fibers have functional connections in the dorsal horn similar to tactile Aα/β fibers, are secondarily activated by physiologic muscle contractions contributing to the gate control mechanism of pain similar to the tactile afferent fibers that innervate the skin [5]. Stimulation of efferent fibers in mixed nerves causes primary activation of Aα/β sensory afferents, which are greater in diameter and are recruited at lower stimulation intensities than efferent fibers [6].

B) Peripherally induced reconditioning of the central nervous system

Percutaneous PNS by activation of non-nociceptive, large diameter afferent fibers, generate peripheral signals that recondition the primary somatosensory cortex (S1) cortex, which is dynamically changing as a result of shifts in afferent input, with expansion of regions that experience stronger and more frequent robust stimuli. Non-nociceptive afferent inputs to the cortex, representing a focal painful region, reduces the severity of pain by active reconditioning of the CNS as opposed to the passive deprivation of nociceptive input following nerve blocks or ablation [7, 8]. Cortical reorganization can occur in weeks [9, 10] leading to prolonged pain relief following short-term PNS treatment for a few weeks, with robust focal peripheral signals to drive beneficial plastic changes obviating the need for a permanent implant. The process is called “reconditioning” since it is not clear whether the cortex reverses or returns to its exact pre-injury architecture, as opposed to achieving a new homeostasis.

Evidence

Xu et al., in an extensive detailed review, synthesized evidence based on randomized controlled trials (RCTs) and observational studies have shown Level I (strong) and II (moderate) evidence of PNS in chronic migraine headache; Level II (moderate) evidence in cluster headache, postamputation pain, chronic pelvic pain, chronic low back and lower extremity pain; and Level IV (limited) evidence in peripheral neuropathic pain and postsurgical pain. Peripheral field stimulation has shown Level II (moderate) evidence in chronic low back pain and Level IV evidence in cranial pain [11].

Historical Complications Associated with PNS

The electrode technology available for PNS requiring placement of SCS electrodes connected had historically been limited to adaptation of SCS devices due to the market dominance of SCS. Lack of systems specifically designed for the periphery was the major reason for failure and complications.

Devices meant for SCS, including percutaneous cylindrical leads or surgical paddle-type leads, both placed immediately adjacent to, or in contact with, the targeted nerves, were subjected to greater mechanical stresses in the periphery than when placed in the epidural space, resulting in lead migration. Hence, use of these leads were limited to locations where they did not cross joints, and where they could have been exposed to high degrees of flexion or extension, leading to migration or fracture [12].

The anatomy of the peripheral nervous system is also quite varied. Having interventional pain physicians learn the various surgical techniques required of multiple PNS techniques required a steep learning curve. Moreover, to percutaneously place the device prior to the development of ultrasound (US), required advanced surgical skills. In addition, scarring has been noted when electrode arrays are placed adjacent to nervous tissue. This has led to long-term consequences including damage to neurologic tissue.

Technique

More recently, with the advent of US guidance, the use of PNS has dramatically expanded. Using image guidance allows the surgeon or operator to percutaneously place an electrode array close to the nerve without direct open visualization. This has limited the complications more frequently associated with open surgery. Current permanent leads are more flexible and have completely integrated IPGs or receivers. This has led to a decrease in the need for internally implanted batteries that, by their nature, need to cross joints. There are many different pain disorders and thus different nerves that can benefit from both temporary and permanent implantation of devices. Description of the technique of each PNS system is beyond the scope of this book, but there are several common techniques used.

Identify target nerves with US or fluoroscopic landmarks.
After prepping the track and target areas ensuring they are sterile, anesthetize the area of skin several centimeters away from the targeted nerve allowing for gentle angle of approach to the target nerve.
Make a small incision to facilitate tunneling of the receiver or extension wires.
Advance a Tuohy or other introducer needle to the target nerve.
Stimulate the target nerve (after or at the time of deploying the peripheral nerve system).
Deploy the electrode array.
Tunnel the system allowing the IPG, power source or receiver to be localized just under the skin.

Complications

Complications associated with PNS can be classified as follows [13]:

Hardware-related complications: Lead migration or fracture, extension-related complication, disconnection or misconnection and Implantable Pulse Generator (IPG)–related complications such as battery depletion, flipping and recharging difficulties.
Biological complications: Examples include infections, deep and superficial; hematoma or seroma over the device; pain over the hardware implant. Serious complications include nerve damage. Dural puncture-related headaches, spinal cord injuries, and paralysis have not been reported with PNS, although experienced in cases of SCS.
Programming or therapy-related complications: Painful or unpleasant paresthesia. These can be addressed through programming, and device removal is warranted on rare occasions.

Hardware-related Complications

Lead Migration

Lead migration is the commonest complication of peripheral nerve field stimulation (PNFS). Conventional PNS leads originally designed for SCS, including percutaneous cylindrical leads placed immediately adjacent to targeted nerves or across joints, subjected to greater mechanical stress, than those experienced in the epidural space resulted in lead migration. Migration rates as high as 100% have been reported by Schwedt et al. in cases of occipital nerve stimulation (ONS) after 3 years and 60% after one year of implantation [14]. The leads were positioned at the C1 level and secured to the fascia. Saper et al., in the ONSTIM study, recommended the use of strain-relief loops and a preference for abdominal to buttock IPG positioning to minimize lead migration [15]. Lead migration following surgical paddle lead implantation was less commonly reported compared to percutaneous cylindrical leads.

Sator-Katzenschlager [16] and Verrills [17] reported rates of 13% and 2%, respectively in the largest case series on PNFS. Although it has been mentioned that the leads were sutured to the deep fascia, the level at which the leads were placed was not clearly specified. The multicentric nature of the first study, compared to the second being conducted in a single center, and a different definition of migration, might have contributed to this wide variation in migration rates. Gazelka et al. [18], following adoption of a significant definition of lead migration, reported only 2.1% of patients requiring surgical revision in SCS patients. Hence, a concrete definition of lead migration might lead to a reduction in rates of migration.

SCS studies have reported a far smaller percentage of migration rates, probably due to the use of customized leads placed in the epidural space. Cameron et al. [19], in a 20-year-old literature review, reported 13.2% migration rates in 2753 patients. Migration rates were twice as high in the cervical region, compared to the lower dorsal spine attributed to the mobility of the cervical spine.

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