Neuromodulation for Foot and Ankle Pain
Krishna B. Shah
Daniel J. Pak
INTRODUCTION
Defined by the International Neuromodulation Society (INS) as the “alteration of nerve activity through targeted delivery of a stimulus, such as electrical stimulation or chemical agents, to specific neurological sites in the body,” neuromodulation therapies have become increasingly popular over the last several decades for the treatment of neuropathic and sympathetically mediated chronic pain.1 These therapies include noninvasive approaches, such as transcutaneous electrical nerve stimulation (TENS) units, as well as implantable devices, such as spinal cord stimulation (SCS).
Implantable neuromodulation therapies have particularly evolved since the introduction of the first SCS in the 1960s. Hardware advancements have led to the development of smaller implantable batteries with increased longevity, thereby improving patient comfort while extending the life of the power unit. The introduction of new technologies, such as dorsal root ganglion (DRG) stimulation and peripheral nerve stimulation (PNS), has also broadened the application of these devices to a vast array of chronic pain conditions, and the development of novel stimulation modes has improved the efficacy of the treatments. While these devices have traditionally been viewed as a salvage therapy, many providers are now implementing them earlier in the treatment algorithm to improve patient outcomes. This chapter aims to discuss the utility of neuromodulation therapies for the management of common chronic foot and ankle pain syndromes.
SPINAL CORD STIMULATION
Traditionally, based on the gate control theory of pain proposed by Melzack and Wall in 1965,2 SCS devices generate electrical fields between metal contact points that are placed in the epidural space on top of the dorsal column of the spinal cord. Electrical stimulation of large diameter afferent sensory nerve fibers then inhibits the ascension of nociceptive signals and suppresses pain perception.3 The gate control theory continues to serve as the core conceptual principle behind SCS though recent studies suggest other potential contributing analgesic mechanisms that are beyond the scope of this chapter.
Conventional tonic SCS delivers electrical pulses at a frequency typically less than 200 Hz with above-sensory threshold amplitudes, providing therapeutic paresthesias in the distribution of the patient’s pain. The recent emergence of subsensory threshold therapies, such as high frequency and burst SCS, now provide paresthesia-free stimulation modes, thus eliminating the uncomfortable tingling or pricking sensations associated with tonic stimulation and the need for intraoperative paresthesia
mapping (Table 19.1). High frequency SCS utilizes frequencies up to 10 kHz (HF10) while burst SCS delivers packets of higher frequency stimulation separated by pulse-free phases. The mechanisms of action for these modalities remain unclear though the activation of inhibiting interneurons and attenuation of wide dynamic range (WDR) dorsal horn neurons have been implicated.3
mapping (Table 19.1). High frequency SCS utilizes frequencies up to 10 kHz (HF10) while burst SCS delivers packets of higher frequency stimulation separated by pulse-free phases. The mechanisms of action for these modalities remain unclear though the activation of inhibiting interneurons and attenuation of wide dynamic range (WDR) dorsal horn neurons have been implicated.3
TABLE 19.1 Reported Parameters for Tonic, HF10, and Burst SCSa | ||||||||||||||||||||||||
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Indications
SCS has long been used to treat chronic neuropathic pain of the trunk and limbs. Complex regional pain syndrome (CRPS), also called reflex sympathetic dystrophy (RSD), is perhaps one of the most common indications for the therapy and is characterized by continuing pain that is disproportionate to the inciting injury with a confluence of sensory, sudomotor, vasomotor, and motor dysfunction. While the traditional treatment paradigm includes conservative measures such as physical rehabilitation, psychological therapy, medication management, and injection therapies, delays in definitive treatment have been associated with poorer functional outcomes.5,6 Therefore, a trial of SCS should be considered if patients do not respond to conventional therapies. SCS has generally been shown to be effective for CRPS, with significant improvements in visual analog scale (VAS) pain scores, functional status (including improvements in range of motion at the affected joint), and quality of life (QOL) metrics.5
Patients with refractory neuropathic pain of the lower extremities from lumbosacral radiculopathy are also excellent candidates for SCS. While most studies have been conducted in the context of chronic pain following previous spine surgery, patients treated with SCS reported significantly improved pain relief compared to those treated with medication management alone and those who underwent repeat spine surgery.7 SCS patients also had lower utilization of analgesic medications and greater improvements in QOL scores.8 More recent studies investigating the use of high frequency and burst SCS have demonstrated superior outcomes when compared to conventional tonic stimulation.9,10 Other neuropathic pain syndromes that can be treated with SCS include peripheral neuropathies (ie, painful diabetic neuropathy) and phantom limb pain.
SCS may also be utilized for the treatment of painful peripheral arterial vaso-occlusive disease, with the primary mechanism of analgesia likely secondary to alleviation of tissue ischemia. Patients with critical limb ischemia treated with SCS have demonstrated improved pain relief, regional perfusion, and limb survival compared to those treated with medical treatment alone.8
Technique
SCS implantation is a 2-stage process and is initiated with a trial period where 1 to 2 cylindrical leads are placed percutaneously in the epidural space under fluoroscopic guidance. Epidural needle entry is typically achieved at the T12-L1 or L1-L2 interlaminar spaces, and the leads are advanced along the midline dorsal epidural space so that the electrical contacts span the T8-T12 vertebral bodies for lower extremity symptoms (Figure 19.1).11 Paresthesia mapping during the procedure may be utilized to verify proper coverage of the patient’s painful areas. The leads are then secured with adhesive dressings or sutures and attached to an external
pulse generator. Patients typically spend a trial period of 7 days to determine the efficacy of the therapy. At least 50% reduction in pain is desired in order to proceed with implantation of the permanent system.
pulse generator. Patients typically spend a trial period of 7 days to determine the efficacy of the therapy. At least 50% reduction in pain is desired in order to proceed with implantation of the permanent system.
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