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Facial pain is a common condition that affects approximately 10%–25% of the worldwide adult population ( ). It is a serious health problem, and significantly affects the daily functioning of patients. The main types of facial pain are trigeminal neuralgia (TN), trigeminal neuropathic pain (TNP), and persistent idiopathic facial pain ( ). It has been reported that the lifetime prevalence of TN and persistent idiopathic facial pain is 0.3% and 0.03%, respectively ( ). Although treatments for TN are well established, TNP resulting from an injury or infection involving one or several peripheral branches of the trigeminal nerve is often difficult to control with current medical and surgical approaches ( ). Unsatisfactory results of facial pain treatment have prompted the medical community to develop new approaches to its treatment, including peripheral nerve stimulation (PNS).
Although first use of PNS for pain dates back to 1962 ( ), the first publications about PNS came out in 1967 ( ), after the introduction of the gate-control theory of pain by . More than 3 decades later, about 20 years ago, it took off as a widely accepted neuromodulation therapy. Weiner and Reed reported the first percutaneous peripheral nerve stimulators for the treatment of occipital neuralgia in 1999 ( ). Since then, the use of PNS has rapidly expanded within the neuromodulation community, and it has grown to become an invaluable modality for patients with a variety of pain conditions, including facial pain. The PNS technique is based on placement of electrodes over or near the path of the peripheral nerve that supplies the painful area and is involved in the generation of pain. Technological advances in electrode design, features of implantable pulse generators (IPGs), and refinement in surgical technique allow for implantation of PNS systems for the treatment of facial pain by using minimally invasive methods ( ). To confirm or detect the anatomical location of the nerve targeted for PNS, use of ultrasound guidance has been suggested ( ). The main reasons why PNS is one of the most attractive and diverse therapies in the field of neuromodulation for clinicians and patients are its simplicity, minimal invasiveness, reversibility, and versatility of techniques ( ). Moreover, PNS can be used as a stand-alone therapy or combined with other neuromodulation treatments, such as spinal cord stimulation (SCS) (see Chapter 38 in this volume).
Similarly to PNS in general, the history of specific use of PNS for facial pain dates back to long before the paper of Weiner and Reed. It is well known that PNS was used in the craniofacial region in by Wall and Sweet, when a reduction of facial pain perception was found by using the technique on themselves and in treating one patient with TN using electrical stimulation of the infraorbital nerve. Even earlier, in 1962, PNS was introduced as a completely novel, somewhat revolutionary approach when implanted a silicone electrode over a mandibular nerve in a patient with facial pain and treated it with electrical stimulation at a frequency of 14 kHz.
Recently the use of PNS for the treatment of intractable facial pain has been reported by multiple institutions ( ). The most common indications for PNS in the facial region remain TN in patients with postherpetic neuralgia and posttraumatic, poststroke, or postsurgical neuropathic pain. As trigeminal PNS is gaining popularity as a treatment for facial pain, it becomes apparent that this technique has limited applications and should be used mainly for patients with neuropathic pain with a clear anatomic distribution.
Overall, the use of PNS to treat facial pain, although gaining in popularity, is still a relatively understudied field. Recently multiple studies have been conducted to assess its efficacy and safety for the treatment of facial pain, but most of them are case reports or small case series, and as far as we know there have been no randomized controlled trials (RCTs) to investigate the effect of PNS on facial pain. This chapter focuses on an overview of clinical data and informs clinicians about the current use of PNS for the treatment of facial pain.
The exact mechanism(s) of pain relief using PNS is unknown. It is hypothesized that the mechanism of action (MOA) of PNS may be related to the gate-control theory of pain ( ), and may possibly involve a complex interplay between the central nervous system and the peripheral nervous system ( ). It is possible that PNS shares a similar MOA with SCS, in which electrical activation of large myelinated A-beta fibers may inhibit painful signals carried by small myelinated A-delta and unmyelinated C fibers in the same region (gate-control theory, ). It has been reported that direct stimulation of peripheral nerves results in decreased excitability, an increase in electrical thresholds, and transient slowing of conduction velocity ( ). Moreover, PNS may affect local concentrations of biochemical mediators that enhance pain responses and directly inhibit pain neurotransmission ( ). Interestingly, one study showed that PNS suppresses not only neuropathic but also nociceptive pain ( ), while SCS traditionally works on neuropathic pain only. It is obvious, however, that more research is needed to elucidate fully the mechanisms of analgesic effects of PNS. Kilohertz frequency stimulation of peripheral nerves at high intensities result in a conduction block ( ), and the MOA of that block is thought to be due to activation of K + channels or inactivation of Na + channels ( ).
It should also be stated for the sake of completeness regarding the MOA of electrical stimulation of peripheral nerves that stimulation of these nerves not only has direct effects on the nerves being stimulated but has secondary effects at the spinal cord, dorsal root ganglion ( ), and brain ( ). The end result of PNS (the perceived pain control) may be from peripheral, spinal, or cerebral effects, or a combination of these.
The success of PNS therapy, as with all neuromodulation therapies, depends on appropriate patient selection. The prerequisites for using PNS for treatment of facial pain are as follows ( ).
PNS is considered for patients with severe, chronic, refractory neuropathic pain that is affecting the patient’s quality of life.
Conservative therapies, such as pharmacotherapy, physical therapy, trigger point injections, or nerve blocks, must have been exhausted before PNS is considered.
There should be some preservation of sensation in the distribution of pain, because presence of functioning vibrotactile receptors is mandatory for PNS therapy to be successful.
The pain is within the distribution of the nerve(s) that are intended to be stimulated, and these nerves can to be covered by the length of available PNS electrode(s).
After a thorough psychologic evaluation by a qualified professional, there must be an absence of psychologic factors that would impede a favorable outcome.
There must be no coexisting chronic pain problems or neurologic diseases.
There must be no coexisting conditions/comorbidities that would increase procedural risk (e.g., uncontrolled diabetes, sepsis, coagulopathy, etc.).
A successful PNS trial is required before permanent placement of a PNS system.
In terms of indications for PNS, it is not uncommon to hear discussions among inexperienced implanters regarding using PNS for TN. Needless to say, although TN is an excellent indication for a multitude of surgical interventions (microvascular decompression, radiofrequency gasserian thermodestruction, glycerol gangliolysis, balloon compression, open rhizotomy, and stereotactic radiosurgery), it is not an indication for PNS. As a matter of fact, use of PNS in TN will worsen the patient’s pain, as electrical stimulation of the trigeminal nerve tends to trigger TN attacks instead of eliminating them ( ).
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