Peripheral neuropathy medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]; Anum Ijaz M.B.B.S., M.D.[3]

Overview

Peripheral neuropathy management is etiology-directed and symptom-focused, beginning with identification and treatment of reversible causes and reduction or discontinuation of neurotoxic exposures when feasible, followed by targeted management of neuropathic pain and functional impairment. Neuropathic pain is managed using a multimodal approach that may include conservative measures, topical agents (e.g., lidocaine or capsaicin), and first-line oral therapies such as gabapentin, pregabalin, serotonin–norepinephrine reuptake inhibitors, or tricyclic antidepressants, selected based on comorbidities and adverse effects. Patients with refractory symptoms may benefit from referral to a multidisciplinary pain clinic and consideration of neuromodulation, including spinal cord stimulation. Supportive care, including foot-care education and rehabilitation with physical or occupational therapy and assistive devices, is essential to reduce complications and disability.

Medical Therapy

  • Pharmacologic medical therapy is recommended among patients with peripheral neuropathy.[1]
  • Peripheral neuropathy, caused by various central and peripheral nerve disorders, is especially problematic because of its severity, chronicity and resistance to simple analgesics.[1]
  • According to the cause of the peripheral neuropathy, treatments vary from the choice drug, the dosage of drug and the time of the treatment.

Medical therapy for common etiologies of length-dependent peripheral neuropathy (LDPN)

1) LDPN associated with diabetes

  • Glycemic control (defined here as HbA1c <5.7%) is described as more effective at preventing peripheral neuropathy in type 1 diabetes than in type 2 diabetes; in established type 2 diabetic neuropathy, glycemic control has modest effects on improving symptoms or preventing progression.[2] ,[3]
  • Rapid correction of hyperglycemia, typically defined as an approximately 2% reduction in HbA1c over 3 months, can precipitate treatment-induced neuropathy of diabetes (insulin neuritis), which presents within 8 weeks with acute, severe painful small-fiber and autonomic neuropathy.[4]

2) LDPN due to nutritional imbalances

Vitamin B12 deficiency

  • Typically 1 mg vitamin B12 by subcutaneous or intramuscular injection weekly for 1 month, then 1 mg IM monthly. High-dose oral replacement (1–2 mg daily) can be similarly effective.[5]

Copper deficiency

  • Treated with oral or parenteral replacement 2–4 mg daily.[6]

Vitamin B6 (pyridoxine)

  • Toxicity: Can cause sensory neuropathy affecting dorsal root ganglia; may be irreversible; classically from very high supplement intake, but neuropathy has been reported with long-term (>~6 months) 50 mg/day use.
  • Deficiency & supplementation: Deficiency risk noted with certain medications and other states; however, there is no clear evidence that supplementation prevents peripheral neuropathy in those settings. Replacement dose is stated as 50 mg/day, and should be given only in deficiency or prophylactically in the specifically described instances.[7]

Thiamine (vitamin B1) deficiency

  • Acute replacement: Typically 100–200 mg IV three times daily for 3 days, then 100 mg orally daily long term.[6]
  • Give thiamine before glucose to avoid exacerbating deficiency (carbohydrate metabolism consumes thiamine as a co-factor), especially in Wernicke–Korsakoff syndrome.
  • Prevention in high-risk patients: 100 mg oral daily is recommended for high-risk individuals (eg, malnutrition or alcohol use disorder).

3) LDPN due to alcohol

  • Excessive alcohol use is commonly associated with LDPN; because intake is often underreported, it can be hard to separate direct alcohol neurotoxicity from vitamin deficiency effects.[8]
  • Avoidance or reduced alcohol intake is advised due to neurotoxicity.

4) Neuropathies associated with monoclonal proteins

  • People diagnosed with monoclonal gammopathy should be referred to hematology for evaluation of plasma cell disorders (eg, multiple myeloma, Waldenström macroglobulinemia, AL amyloidosis, POEMS).[9],[10]
  • In AL amyloidosis, treatment of the underlying plasma cell disorder may stabilize or improve neuropathy.[11],[12]

5) Hereditary neuropathies

  • Most inherited neuropathies lack specific therapies, but hereditary transthyretin amyloidosis is noted as treatable with:[13],[14],[15],[16],[17],[18]
    • Transthyretin stabilizers: diflunisal, tafamidis
    • Transthyretin synthesis–reducing therapies: patisiran, vutrisiran, eplontersen
  • A randomized clinical trial (130 participants) reported neuropathic stabilization in 29.7% with diflunisal vs 9.4% with placebo; phase 3 trials of transthyretin synthesis-reducing therapies reported improvements in neuropathy impairment scores and Norfolk quality of life measures at 15–18 months vs placebo.

6) LDPN due to medications (toxic neuropathies)

  • Many medications are associated with neuropathies; for chemotherapy-induced peripheral neuropathy (CIPN) there are no preventive measures.[19],[20]
  • CIPN may improve after drug cessation, but symptoms may persist for years.

7) Autoimmune/inflammatory neuropathies

Medical therapy for Neuropathy Symptoms

Management of sensory symptoms

Loss of protective sensation in length-dependent peripheral neuropathy (LDPN) predisposes patients to unrecognized injuries such as burns and cuts, which may progress to ulceration and infection. In patients with diabetes, coexisting microvascular disease further impairs wound healing.

To reduce complications related to sensory loss, patients should be counseled on preventive foot care, including:

  • Daily foot inspection
  • Wearing properly fitting footwear to prevent pressure injuries and blistering
  • Testing water temperature with the hands before foot immersion
  • Early evaluation of skin breakdown
  • Podiatric referral should be considered for patients at high risk of foot ulceration, particularly those with diabetes.

Management of neuropathic pain

Neuropathic pain associated with LDPN may be managed using a stepwise, multimodal approach, including conservative measures, topical agents, oral medications, and neuromodulation as summarized in the table below.

  • Conservative measures: Some patients experience symptom relief with simple interventions such as cool water foot soaks and regular use of moisturizing creams to prevent skin dryness.
  • Topical therapies: Topical capsaicin and lidocaine may provide benefit, though effectiveness is variable.
  • Pharmacologic therapy: FDA-approved therapies for neuropathic pain include gabapentin, pregabalin, duloxetine, topical lidocaine, topical capsaicin, and extended-release tapentadol. First-line oral pharmacologic agents for neuropathic pain include α2-δ calcium channel subunit ligands (gabapentin and pregabalin), serotonin–norepinephrine reuptake inhibitors (duloxetine and venlafaxine), and tricyclic antidepressants (amitriptyline and nortriptyline), although not all are FDA approved specifically for LDPN-associated pain.
  • Opioids: Opioids are not recommended for the treatment of neuropathic pain.[24]
  • Specialty referral and neuromodulation: Referral to a multidisciplinary pain clinic may benefit patients with refractory symptoms. Spinal cord stimulation, an implanted device delivering epidural electrical stimulation to modulate pain transmission, is FDA-approved for neuropathic pain.

Management of motor symptoms

Motor involvement in peripheral neuropathy may result in lower-extremity weakness, impaired proprioception, gait instability, and an increased risk of falls.[25]

  • Physical therapy: Gait-focused physical therapy is beneficial for patients with mild motor weakness to improve balance and reduce fall risk.
  • Occupational therapy: Occupational therapy is indicated for patients with upper-extremity weakness, particularly when fine motor skills required for daily activities (e.g., writing, buttoning, self-care) are impaired.
  • Orthopedic management: Patients who develop foot deformities or contractures may benefit from orthopedic evaluation and surgical management.
  • Assistive devices: In cases of severe motor impairment, foot orthoses, walkers, or wheelchairs may be required to maintain mobility and safety.

Treatment of Neuropathic Pain

Drug class Treatment Total daily dose and regimen Efficacy Adverse effects
Topical medications
Voltage-gated sodium channel antagonist Lidocaineᵃ 1–3 patches to region of pain daily for up to 12 h Three weeks of treatment resulted in a ≥30% reduction in weekly mean daily pain diary scores in 70% of patients with diabetic peripheral neuropathy.[26] Mild skin reactions including erythema, rash, itching (rare)
TRPV1 agonist Capsaicin 8% patchesᵃ 1–4 patches to painful area for 30–60 min every 3 mo Studies of HIV-associated LDPN showed a 22.8% reduction in pain compared with 10.7% in controls, while in postherpetic neuralgia, reductions of 42% and 30% in pain scores were reported compared with 32% in control groups.[27] Initial burning sensation and erythema of skin (common)
Oral medications
α2-δ Calcium channel subunit ligand Gabapentinᵃ 1200–3600 mg, in 3 divided doses Among patients with diabetic peripheral neuropathy, gabapentin 1200 mg daily was associated with higher rates of ≥50% pain reduction and ≥30% pain reduction at doses ≥1200 mg compared with placebo.[28] Dizziness, somnolence, peripheral edema
α2-δ Calcium channel subunit ligand Pregabalinᵃ 300–600 mg, in 2 divided doses In diabetic PN, pregabalin at 300 mg and 600 mg daily resulted in higher rates of ≥30% pain reduction compared with placebo (47% vs 42% and 63% vs 52%, respectively)[29] Somnolence, dizziness
Selective serotonin and norepinephrine reuptake inhibitor Duloxetineᵃ 60–120 mg, once daily In diabetic PN, duloxetine achieved higher rates of ≥50% improvement than placebo within 12 weeks[30], and in painful PN, duloxetine 60 mg daily was more effective than pregabalin 300 mg daily in achieving ≥50% pain reduction.[31] Headache, drowsiness, fatigue
Tricyclic antidepressant Amitriptyline 10–75 mg, once daily In a study comparing monotherapy (amitriptyline, duloxetine, pregabalin) and combination therapy in diabetic PN, 7-day mean Pain Numerical Rating Scale scores decreased from 6.6 (1.5) at baseline to 3.3 (1.8) at week 16 with both monotherapy and combination therapy, with no differences between combination treatments. [32],[33] Constipation, dizziness, dry mouth, somnolence (fewer adverse effects with nortriptyline)
Neuromodulation
Peripheral nerve stimulationᵃ Insufficient evidence for efficacy in LDPN, but is FDA approved for neuropathic pain
Spinal cord stimulationᵃ In diabetic PN, at 3 mo, 79% with spinal cord stimulation had ≥50% improvement in pain vs 5% receiving conventional medical management.[34] Headache, paresthesia, device infection

Abbreviations: LDPN= length-dependent peripheral neuropathy; TRPV1= transient receptor potential vanilloid 1.

ᵃ US Food and Drug Administration (FDA) approved for neuropathic pain.

References

  1. ↑ 1.0 1.1 Gilron I, Watson CP, Cahill CM, Moulin DE (2006). "Neuropathic pain: a practical guide for the clinician". CMAJ. 175 (3): 265–75. doi:10.1503/cmaj.060146. PMC 1513412. PMID 16880448.
  2. ↑ 2.0 2.1 "12. Retinopathy, Neuropathy, and Foot Care: Standards of Care in Diabetes-2024". Diabetes Care. 47 (Suppl 1): S231–S243. January 2024. doi:10.2337/dc24-S012. PMC 10725803 Check |pmc= value (help). PMID 38078577 Check |pmid= value (help).
  3. ↑ Callaghan BC, Little AA, Feldman EL, Hughes RA (June 2012). "Enhanced glucose control for preventing and treating diabetic neuropathy". Cochrane Database Syst Rev. 2012 (6): CD007543. doi:10.1002/14651858.CD007543.pub2. PMC 4048127. PMID 22696371.
  4. ↑ Gibbons CH, Freeman R (April 2010). "Treatment-induced diabetic neuropathy: a reversible painful autonomic neuropathy". Ann Neurol. 67 (4): 534–41. doi:10.1002/ana.21952. PMC 3057039. PMID 20437589.
  5. ↑ Vidal-Alaball J, Butler CC, Cannings-John R, Goringe A, Hood K, McCaddon A, McDowell I, Papaioannou A (July 2005). "Oral vitamin B12 versus intramuscular vitamin B12 for vitamin B12 deficiency". Cochrane Database Syst Rev (3): CD004655. doi:10.1002/14651858.CD004655.pub2. PMID 16034940.
  6. ↑ 6.0 6.1 Mauermann ML, Staff NP (January 2026). "Peripheral Neuropathy: A Review". JAMA. 335 (3): 255–266. doi:10.1001/jama.2025.19400. PMID 41247746 Check |pmid= value (help).
  7. ↑ Muhamad R, Akrivaki A, Papagiannopoulou G, Zavridis P, Zis P (June 2023). "The Role of Vitamin B6 in Peripheral Neuropathy: A Systematic Review". Nutrients. 15 (13). doi:10.3390/nu15132823. PMID 37447150 Check |pmid= value (help).
  8. ↑ Paul P, Campbell G, Zekeridou A, Mauermann M, Naddaf E (July 2024). "Diagnosing Peripheral Neuropathy in Patients With Alcohol Use Disorder". Mayo Clin Proc. doi:10.1016/j.mayocp.2024.02.024. PMID 39093265 Check |pmid= value (help).
  9. ↑ Klein CJ, Moon JS, Mauermann ML, Zeldenrust SR, Wu Y, Dispenzieri A, Dyck PJ (March 2011). "The neuropathies of Waldenström's macroglobulinemia (WM) and IgM-MGUS". Can J Neurol Sci. 38 (2): 289–95. doi:10.1017/s0317167100011483. PMID 21320835.
  10. ↑ Naddaf E, Dispenzieri A, Mandrekar J, Mauermann ML (October 2015). "Thrombocytosis distinguishes POEMS syndrome from chronic inflammatory demyelinating polyneuropathy". Muscle Nerve. 52 (4): 658–9. doi:10.1002/mus.24768. PMID 26179010.
  11. ↑ Gazzola S, Delmont E, Franques J, Boucraut J, Salort-Campana E, Verschueren A, Sagui E, Hubert AM, Pouget J, Attarian S (June 2017). "Predictive factors of efficacy of rituximab in patients with anti-MAG neuropathy". J Neurol Sci. 377: 144–148. doi:10.1016/j.jns.2017.04.015. PMID 28477685.
  12. ↑ Karam C, Klein CJ, Dispenzieri A, Dyck PJ, Mandrekar J, D'Souza A, Mauermann ML (May 2015). "Polyneuropathy improvement following autologous stem cell transplantation for POEMS syndrome". Neurology. 84 (19): 1981–7. doi:10.1212/WNL.0000000000001565. PMID 25878176.
  13. ↑ Adams D, Gonzalez-Duarte A, O'Riordan WD, Yang CC, Ueda M, Kristen AV, Tournev I, Schmidt HH, Coelho T, Berk JL, Lin KP, Vita G, Attarian S, Planté-Bordeneuve V, Mezei MM, Campistol JM, Buades J, Brannagan TH, Kim BJ, Oh J, Parman Y, Sekijima Y, Hawkins PN, Solomon SD, Polydefkis M, Dyck PJ, Gandhi PJ, Goyal S, Chen J, Strahs AL, Nochur SV, Sweetser MT, Garg PP, Vaishnaw AK, Gollob JA, Suhr OB (July 2018). "Patisiran, an RNAi Therapeutic, for Hereditary Transthyretin Amyloidosis". N Engl J Med. 379 (1): 11–21. doi:10.1056/NEJMoa1716153. PMID 29972753.
  14. ↑ Adams D, Tournev IL, Taylor MS, Coelho T, Planté-Bordeneuve V, Berk JL, González-Duarte A, Gillmore JD, Low SC, Sekijima Y, Obici L, Chen C, Badri P, Arum SM, Vest J, Polydefkis M (March 2023). "Efficacy and safety of vutrisiran for patients with hereditary transthyretin-mediated amyloidosis with polyneuropathy: a randomized clinical trial". Amyloid. 30 (1): 1–9. doi:10.1080/13506129.2022.2091985. PMID 35875890 Check |pmid= value (help).
  15. ↑ Benson MD, Waddington-Cruz M, Berk JL, Polydefkis M, Dyck PJ, Wang AK, Planté-Bordeneuve V, Barroso FA, Merlini G, Obici L, Scheinberg M, Brannagan TH, Litchy WJ, Whelan C, Drachman BM, Adams D, Heitner SB, Conceição I, Schmidt HH, Vita G, Campistol JM, Gamez J, Gorevic PD, Gane E, Shah AM, Solomon SD, Monia BP, Hughes SG, Kwoh TJ, McEvoy BW, Jung SW, Baker BF, Ackermann EJ, Gertz MA, Coelho T (July 2018). "Inotersen Treatment for Patients with Hereditary Transthyretin Amyloidosis". N Engl J Med. 379 (1): 22–31. doi:10.1056/NEJMoa1716793. PMID 29972757.
  16. ↑ Berk JL, Suhr OB, Obici L, Sekijima Y, Zeldenrust SR, Yamashita T, Heneghan MA, Gorevic PD, Litchy WJ, Wiesman JF, Nordh E, Corato M, Lozza A, Cortese A, Robinson-Papp J, Colton T, Rybin DV, Bisbee AB, Ando Y, Ikeda S, Seldin DC, Merlini G, Skinner M, Kelly JW, Dyck PJ (December 2013). "Repurposing diflunisal for familial amyloid polyneuropathy: a randomized clinical trial". JAMA. 310 (24): 2658–67. doi:10.1001/jama.2013.283815. PMID 24368466.
  17. ↑ Coelho T, Maia LF, Martins da Silva A, Waddington Cruz M, Planté-Bordeneuve V, Lozeron P, Suhr OB, Campistol JM, Conceição IM, Schmidt HH, Trigo P, Kelly JW, Labaudinière R, Chan J, Packman J, Wilson A, Grogan DR (August 2012). "Tafamidis for transthyretin familial amyloid polyneuropathy: a randomized, controlled trial". Neurology. 79 (8): 785–92. doi:10.1212/WNL.0b013e3182661eb1. PMID 22843282.
  18. ↑ Coelho T, Marques W, Dasgupta NR, Chao CC, Parman Y, França MC, Guo YC, Wixner J, Ro LS, Calandra CR, Kowacs PA, Berk JL, Obici L, Barroso FA, Weiler M, Conceição I, Jung SW, Buchele G, Brambatti M, Chen J, Hughes SG, Schneider E, Viney NJ, Masri A, Gertz MR, Ando Y, Gillmore JD, Khella S, Dyck PJ, Waddington Cruz M (October 2023). "Eplontersen for Hereditary Transthyretin Amyloidosis With Polyneuropathy". JAMA. 330 (15): 1448–1458. doi:10.1001/jama.2023.18688. PMID 37768671 Check |pmid= value (help).
  19. ↑ Shah A, Hoffman EM, Mauermann ML, Loprinzi CL, Windebank AJ, Klein CJ, Staff NP (June 2018). "Incidence and disease burden of chemotherapy-induced peripheral neuropathy in a population-based cohort". J Neurol Neurosurg Psychiatry. 89 (6): 636–641. doi:10.1136/jnnp-2017-317215. PMID 29439162.
  20. ↑ Staff NP, Grisold A, Grisold W, Windebank AJ (June 2017). "Chemotherapy-induced peripheral neuropathy: A current review". Ann Neurol. 81 (6): 772–781. doi:10.1002/ana.24951. PMID 28486769.
  21. ↑ Hattori N, Ichimura M, Nagamatsu M, Li M, Yamamoto K, Kumazawa K, Mitsuma T, Sobue G (March 1999). "Clinicopathological features of Churg-Strauss syndrome-associated neuropathy". Brain. 122 ( Pt 3): 427–39. doi:10.1093/brain/122.3.427. PMID 10094252.
  22. ↑ Hughes RA, Donofrio P, Bril V, Dalakas MC, Deng C, Hanna K, Hartung HP, Latov N, Merkies IS, van Doorn PA (February 2008). "Intravenous immune globulin (10% caprylate-chromatography purified) for the treatment of chronic inflammatory demyelinating polyradiculoneuropathy (ICE study): a randomised placebo-controlled trial". Lancet Neurol. 7 (2): 136–44. doi:10.1016/S1474-4422(07)70329-0. PMID 18178525.
  23. ↑ Tracy JA (October 2023). "Autoimmune Axonal Neuropathies". Continuum (Minneap Minn). 29 (5): 1378–1400. doi:10.1212/CON.0000000000001344. PMID 37851035 Check |pmid= value (help).
  24. ↑ Soliman N, Moisset X, Ferraro MC, de Andrade DC, Baron R, Belton J, Bennett DL, Calvo M, Dougherty P, Gilron I, Hietaharju AJ, Hosomi K, Kamerman PR, Kemp H, Enax-Krumova EK, McNicol E, Price TJ, Raja SN, Rice AS, Smith BH, Talkington F, Truini A, Vollert J, Attal N, Finnerup NB, Haroutounian S (May 2025). "Pharmacotherapy and non-invasive neuromodulation for neuropathic pain: a systematic review and meta-analysis". Lancet Neurol. 24 (5): 413–428. doi:10.1016/S1474-4422(25)00068-7. PMID 40252663 Check |pmid= value (help).
  25. ↑ Hoffman EM, Staff NP, Robb JM, St Sauver JL, Dyck PJ, Klein CJ (April 2015). "Impairments and comorbidities of polyneuropathy revealed by population-based analyses". Neurology. 84 (16): 1644–51. doi:10.1212/WNL.0000000000001492. PMID 25832668.
  26. ↑ Barbano RL, Herrmann DN, Hart-Gouleau S, Pennella-Vaughan J, Lodewick PA, Dworkin RH (June 2004). "Effectiveness, tolerability, and impact on quality of life of the 5% lidocaine patch in diabetic polyneuropathy". Arch Neurol. 61 (6): 914–8. doi:10.1001/archneur.61.6.914. PMID 15210530.
  27. ↑ Backonja M, Wallace MS, Blonsky ER, Cutler BJ, Malan P, Rauck R, Tobias J (December 2008). "NGX-4010, a high-concentration capsaicin patch, for the treatment of postherpetic neuralgia: a randomised, double-blind study". Lancet Neurol. 7 (12): 1106–12. doi:10.1016/S1474-4422(08)70228-X. PMID 18977178.
  28. ↑ "Gabapentin for chronic neuropathic pain in adults - Wiffen, PJ - 2017 | Cochrane Library".
  29. ↑ Derry S, Bell RF, Straube S, Wiffen PJ, Aldington D, Moore RA (January 2019). "Pregabalin for neuropathic pain in adults". Cochrane Database Syst Rev. 1 (1): CD007076. doi:10.1002/14651858.CD007076.pub3. PMID 30673120.
  30. ↑ Lunn MP, Hughes RA, Wiffen PJ (January 2014). "Duloxetine for treating painful neuropathy, chronic pain or fibromyalgia". Cochrane Database Syst Rev. 2014 (1): CD007115. doi:10.1002/14651858.CD007115.pub3. PMID 24385423.
  31. ↑ Tesfaye S, Wilhelm S, Lledo A, Schacht A, Tölle T, Bouhassira D, Cruccu G, Skljarevski V, Freynhagen R (December 2013). "Duloxetine and pregabalin: high-dose monotherapy or their combination? The "COMBO-DN study"--a multinational, randomized, double-blind, parallel-group study in patients with diabetic peripheral neuropathic pain". Pain. 154 (12): 2616–2625. doi:10.1016/j.pain.2013.05.043. PMID 23732189.
  32. ↑ Tesfaye S, Sloan G, Petrie J, White D, Bradburn M, Julious S, Rajbhandari S, Sharma S, Rayman G, Gouni R, Alam U, Cooper C, Loban A, Sutherland K, Glover R, Waterhouse S, Turton E, Horspool M, Gandhi R, Maguire D, Jude EB, Ahmed SH, Vas P, Hariman C, McDougall C, Devers M, Tsatlidis V, Johnson M, Rice AS, Bouhassira D, Bennett DL, Selvarajah D (August 2022). "Comparison of amitriptyline supplemented with pregabalin, pregabalin supplemented with amitriptyline, and duloxetine supplemented with pregabalin for the treatment of diabetic peripheral neuropathic pain (OPTION-DM): a multicentre, double-blind, randomised crossover trial". Lancet. 400 (10353): 680–690. doi:10.1016/S0140-6736(22)01472-6. PMID 36007534 Check |pmid= value (help).
  33. ↑ Derry S, Wiffen PJ, Aldington D, Moore RA (January 2015). "Nortriptyline for neuropathic pain in adults". Cochrane Database Syst Rev. 1 (1): CD011209. doi:10.1002/14651858.CD011209.pub2. PMID 25569864.
  34. ↑ Petersen EA, Stauss TG, Scowcroft JA, Brooks ES, White JL, Sills SM, Amirdelfan K, Guirguis MN, Xu J, Yu C, Nairizi A, Patterson DG, Tsoulfas KC, Creamer MJ, Galan V, Bundschu RH, Paul CA, Mehta ND, Choi H, Sayed D, Lad SP, DiBenedetto DJ, Sethi KA, Goree JH, Bennett MT, Harrison NJ, Israel AF, Chang P, Wu PW, Gekht G, Argoff CE, Nasr CE, Taylor RS, Subbaroyan J, Gliner BE, Caraway DL, Mekhail NA (June 2021). "Effect of High-frequency (10-kHz) Spinal Cord Stimulation in Patients With Painful Diabetic Neuropathy: A Randomized Clinical Trial". JAMA Neurol. 78 (6): 687–698. doi:10.1001/jamaneurol.2021.0538. PMID 33818600 Check |pmid= value (help).

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