Charles Argoff’s research while affiliated with Albany Stratton VA Medical Center and other places

OBJECTIVE This article provides an approach to the assessment, diagnosis, and treatment of central neuropathic pain. LATEST DEVELOPMENTS Recent studies of the pathophysiology of central neuropathic pain, including evidence of changes in the expression of voltage-gated sodium channels and N -methyl- d -aspartate (NMDA) receptors, may provide the basis for new therapies. Other areas of current research include the role of cannabinoid-receptor activity and microglial cell activation in various animal models of central neuropathic pain. New observations regarding changes in primary afferent neuronal activity in central neuropathic pain and the preliminary observation that peripheral nerve blocks may relieve pain due to central neuropathic etiologies provide new insights into both the mechanism and treatment of central neuropathic pain. ESSENTIAL POINTS In the patient populations treated by neurologists, central neuropathic pain develops most frequently following spinal cord injury, multiple sclerosis, or stroke. A multimodal, individualized approach to the management of central neuropathic pain is necessary to optimize pain relief and may require multiple treatment trials to achieve the best outcome.

INTRODUCTION Approximately 37 million Americans have diabetes, 1 with 25-30% experiencing PDN. 2 High-frequency (10 kHz) SCS has been shown to provide substantial symptom relief for PDN, 3 and here we report durability of these outcomes to 24 months (24M). METHODS This prospective, multicenter, RCT evaluated 10 kHz SCS with these key inclusion criteria: PDN symptoms ≥12 M refractory to medications, lower limb pain intensity ≥5 cm (0-10 cm visual analog scale [VAS]), and hemoglobin A1c ≤ 10%. Patients (n = 216) were randomized 1:1 to 10 kHz SCS plus CMM or CMM alone, with optional crossover at 6M. RESULTS At 6M, patients receiving 10 kHz SCS experienced average pain relief of 76.1% (95% CI: 70.5–81.6%), which increased to 82.0% (95% CI: 77.3–86.6%) at 24M. At 24M, 10 kHz SCS patients experienced 70% decreases in pain-associated sleep disturbance and interference with mood and daily activities. At 24M, neurological improvements were observed in 72% of patients receiving 10 kHz SCS. After 6M, 93% of eligible CMM patients elected to cross over to 10 kHz SCS, while zero 10 kHz patients crossed over. With 10 kHz SCS, both groups experienced similar, significant reductions in pain and pain-associated interference. There were zero device explants due to lack of efficacy and eight (5.2%) procedure-related infections (n = 3 resolved with antibiotics; n=5 explanted), which is within the range reported for SCS in non-diabetic patients (2.5-10%).4 CONCLUSIONS This is the largest RCT to date for SCS management of PDN. The 24M results support that 10 kHz SCS can provide safe, durable pain and symptom relief for PDN. REFERENCES 1 CDC. National Diabetes Statistics Report; 2022. 2 Finnerup et al. Lancet Neurol 2015; 14(2):162-73. 3 Petersen et al. Diabetes Care; 45(1):e3-e6. 4 Eldabe et al. Pain Med 2016; 17(2):325-36.

Objectives: A systematic review of original research articles was conducted to evaluate the safety and efficacy of lidocaine infusion in the treatment of adult patients with chronic neuropathic pain. Methods: Original research from 1970 to September 2021 describing adult patients with chronic neuropathic pain receiving at least one dose of intravenous lidocaine was included. Extracted data included study design, sample size, patient demographics and comorbidities, etiology and duration of pain, pain intensity scores, time to pain resolution, lidocaine dose and administration frequency, lidocaine serum concentration, and adverse events. Each study was evaluated for level of evidence using the 2017 American Association of Neurology classification system. Results: Twenty-seven studies evaluating lidocaine infusion treatment in chronic neuropathic pain met inclusion criteria. One class I study was identified for patients with neuropathic pain due to spinal cord injury . Two Class II studies were identified, one describing neuropathic pain due to peripheral nerve injury and another due to diabetic neuropathy. Across all studies, study design, participants, and experimental interventions were heterogenous with wide variation. Discussion: This qualitative review found insufficient, heterogenous evidence and therefore no recommendation can be made for lidocaine infusion treatment in patients with chronic neuropathic pain due to spinal cord injury, peripheral nerve injury, diabetic neuropathy, postherpetic neuralgia, or complex regional pain syndrome type II. Larger randomized, double-blind, placebo-controlled studies are required to further establish the efficacy of lidocaine infusion in patients with these etiologies of chronic neuropathic pain.