Accepted

Peripheral nerve stimulation is the direct electrical stimulation of named nerves outside the central neuraxis to alleviate pain in the distribution of the targeted peripheral nerve. These treatments have shown efficacy in treating a variety of neuropathic, musculoskeletal, and visceral refractory pain pathologies; although not first line, these therapies are an important part of the treatment repertoire for chronic pain. With careful patient selection and judicious choice of stimulation technique, excellent results can be achieved for a variety of pain etiologies and distributions. This article reviews current and past practices of peripheral nerve stimulation and upcoming advancements in the field.

A national crisis of opioid-related morbidity, mortality, and misuse has led to initiatives to address the appropriate role of opioids to treat pain. Deployment of a guideline from the Centers for Disease Control and Prevention to reduce the risks of opioid therapy has raised substantial clinical and public policy challenges. The agency anticipated implementation challenges and committed to reevaluating the guideline for intended and unintended effects on clinician and patient outcomes.

Nerve stimulation is a reversible technique that is used successfully for the treatment of traumatic neuropathic pain, complex regional pain syndrome, and craniofacial neuropathic pain. Nerve field stimulation targets painful regions rather than a single nerve and has expanded indications, including axial low back pain. Appropriate patient education and motivation are crucial prior to surgery. Ongoing research is necessary to provide high-level evidence for the use of nerve stimulation. Most electrodes are primarily designed for spinal cord stimulation, hence the need to develop nerve electrodes dedicated for nerve stimulation.

Temporomandibular joint (TMJ) osteoarthritis (OA) is a degenerative disease of the joint that can produce persistent orofacial pain as well as functional and structural changes to its bone, cartilage, and ligaments. Despite advances in the clinical utility and reliability of the Diagnostic Criteria for Temporomandibular Disorders, clinical tools inadequately predict which patients will develop chronic TMJ pain and degeneration, limiting clinical management. The challenges of managing and treating TMJ OA are due, in part, to a limited understanding of the mechanisms contributing to the development and maintenance of TMJ pain. OA is initiated by multiple factors, including injury, aging, abnormal joint mechanics, and atypical joint shape, which can produce microtrauma, remodeling of joint tissues, and synovial inflammation. TMJ microtrauma and remodeling can increase expression of cytokines, chemokines, and catabolic factors that damage synovial tissues and can activate free nerve endings in the joint. Although studies have separately investigated inflammation-driven orofacial pain, acute activity of the trigeminal nerve, or TMJ tissue degeneration and/or damage, the temporal mechanistic factors leading to chronic TMJ pain are undefined. Limited understanding of the interaction between degeneration, intra-articular chemical factors, and pain has further restricted the development of targeted, disease-modifying drugs to help patients avoid long-term pain and invasive procedures, like TMJ replacement. A range of animal models captures features of intra-articular inflammation, joint overloading, and tissue damage. Although those models traditionally measure peripheral sensitivity as a surrogate for pain, recent studies recognize the brain's role in integrating, modulating, and interpreting nociceptive inputs in the TMJ, particularly in light of psychosocial influences on TMJ pain. The articular and neural contributors to TMJ pain, imaging modalities with clinical potential to identify TMJ OA early, and future directions for clinical management of TMJ OA are reviewed in the context of evidence in the field.