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Disease/ Disorder


Diabetic neuropathy (DN) is a group of syndromes resulting from the disturbances in nerve function caused by diabetes mellitus1

Subtypes of diabetic neuropathy2

  • Symmetric and diffuse
  • Diabetic sensorimotor polyneuropathy
  • Small fiber neuropathy
  • Autonomic neuropathy
  • Treatment-induced diabetic neuropathy
  • Diabetic cachexia
  • Asymmetric and focal
  • Mononeuropathy
    • Carpal tunnel syndrome
    • Ulnar neuropathy at the elbow
    • Fibular neuropathy
  • Diabetic lumbosacral radiculoplexus neuropathy
  • Diabetic cervical radiculoplexus neuropathy
  • Thoracic radiculopathy
  • Cranial neuropathy

Epidemiology including risk factors and primary prevention

The primary risk factor for DN is the hyperglycemia of poorly controlled diabetes mellitus, and strict glycemic control may retard its progression.1 Recent observation shows even those with good glycemic control (HbA1c of less than 5.4%) are at risk. Though treatment of hyperglycemia in type 1 DM can decrease the incidence of neuropathy by up to 60 to 70%, glucose control in type 2 DM results in only a mild reduction (5-7%).3 Though Type 2 DM is much more common than type 1 DM it has a lower lifetime incidence of neuropathy (45%) as compared with type 1 DM (54-59%).Diabetic polyneuropathy (DPN) with its lifetime prevalence of approximately 50% is the most common diabetic complication. DPN causes disability due to foot ulceration leading to amputation, gait disturbance, and fall-related injury. Neuropathic pain is present in approximately 20 to 30% of patients with DPN. The total annual medical cost for diabetes is $6,632 per patient which increases to twofold ($12,492) in DPN and fourfold ($30,755) in severe painful peripheral neuropathy.3 In 2012, about 27% of healthcare costs of diabetes can be attributed to DPN in United States.3


DN is likely caused by DM-related metabolic or vascular disturbances that are interrelated or synergistic. These mechanisms lead to axonal loss via retrograde injury, as well as peripheral nerve segmental demyelination4. Long-term hyperglycemia inhibits uptake of myo-inositol and other essential molecules within the nerve, leading to the slowing of nerve conduction. The excess glucose is converted into sorbitol, which is then metabolized into fructose, both of these can cause osmotic stress on individual neurons when they accumulate.1 Excessive glucose also leads to: (i) the formation of advanced glycation end-products (AGEs) that results from the non-enzymatic glycosylation of proteins, nucleotides, or lipids; (ii) the aberrant activation of protein kinase C (PKC); (iii) the glucose shunt through the hexosamine pathway; as well as (iv) the formation of oxidative and nitrosative  stress associated with an impaired anti-oxidative defense.5 The diabetic state lowers the NAD+/NADH ratio in retina and nerve through increased flux through the polyol pathway and the elevated activity of sorbitol dehydrogenase.6

The increased intracellular glucose concentration along with impaired growth factor support by insulin causes a metabolic imbalance in adult sensory neurons. The energy sensing pathway of AMP activated protein kinase (AMPK)/sirtuin (SIRT)/peroxisome proliferator-activated receptor-γ coactivator α (PGC-1α) signaling axis is damaged. This leads to nutrient stress, and loss of insulin dependent growth factor support; this causes suppression of mitochondrial oxidative phosphorylation and shift to anaerobic glycolysis.6 All these leased to diminishment of collateral sprouting and axon regeneration in diabetic neuropathy.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Generalized symmetric polyneuropathy is a length-dependent process initially producing sensory disturbances of the distal limbs in a stocking glove distribution.  When involving large myelinated A-Type α- and β-Fibers it presents with numbness, tingling, deep-seated gnawing or aching pain, weakness, ataxia with poor balance, and falling. Exam shows impaired reflexes, loss of proprioception and perception of vibration, wasting of small muscles of hands and feet, and weakness in the feet. Clinical implications are Impaired sense of pressure and balance; susceptibility to falls, traumatic fractures, and Charcot’s arthropathy.7

When involving small myelinated and unmyelinated A-Type δ-Fibers and small unmyelinated C-Type fibers results in burning pain with sensation of stabbing and electric shocks, allodynia, hyperalgesia, and hyperesthesia. Physical exam shows impaired sensation of warm and cold temperatures and of pinprick, however, normal strength, reflexes, and nerve conduction. Impaired nociception results in susceptibility to foot ulcers, and increased risk of amputation.7

Autonomic neuropathy predominantly disrupts the cardiovascular, genitourinary, and gastrointestinal systems. Common presentations include orthostatic hypotension, absence of fluctuations in heart rate, erectile dysfunction, cardiac arrhythmias, sudomotor dysfunction, and bowel and bladder disturbances.8

Diabetic lumbosacral radiculoplexus neuropathy may present insidiously or suddenly and often begins with unilateral proximal lower limb pain, followed by intense proximal weakness. While it can evolve into a widespread paralytic disorder affecting the lower limbs, it carries a favorable prognosis, with the majority of affected patients reporting resolution of pain and weakness after several years.1,9

Diabetic cachexia can rarely occur after rapid glycemic control. This results in severe neuropathic pain with marked weight loss and sensorimotor polyneuropathy. Usually there is an improvement of the symptoms over several months.2

Treatment-induced neuropathy in diabetes (TIND) is an iatrogenic small-fiber neuropathy presenting with acute onset of neuropathic pain and/or autonomic dysfunction within 8 weeks of significant glycemic control specified as a decrease in glycosylated HbA1c of more than 2% points over 3 months. TIND was first recognized soon after the introduction of insulin and named “insulin neuritis”.2

Specific secondary or associated conditions and complications

Loss of pedal sensation from DN may result in skin wounds and ulceration. The concomitant vascular and immunologic disorders make these wounds susceptible to infection that may progress to osteomyelitis or gangrene. There are many other secondary complications including autonomic dysfunction, erectile dysfunction, gastroparesis, and neuropathic arthropathies (Charcot joints). DN may also contribute to common entrapment neuropathies, such as carpal tunnel syndrome.

Essentials of Assessment


DN may produce painful positive symptoms like squeezing, throbbing, freezing, burning, or lancinating sensations. Non-painful positive symptoms include a feeling of stiffness and thickness. Negative symptoms include numbness. History should also assess for gait disturbances, skin lesions, hypotensive symptoms, sexual dysfunction, changes in bowel or bladder function, and progressive weakness.

Distal symmetric polyneuropathy generally presents insidiously and involves the distal lower limbs in a symmetric pattern. Neurogenic or vascular claudication and other length-dependent neuropathies may mimic DN. Diabetic lumbosacral radiculoplexus neuropathy has an abrupt, painful onset, is generally accompanied by weight loss, and often is a presenting finding in newly diagnosed diabetics. It is characterized by sharp, burning, and asymmetric pain that more often presents proximally in the hip and thigh before later spreading distally.1,9

Physical examination

Gait and skin evaluations are mandatory. Proprioceptive deficits should be exposed with Romberg, tandem gait, and one-leg stand tests. Examinations with a 128 Hz tuning fork and 10-g monofilament test carry sensitivities of 62.5 and 62.8%, respectively, and specificities of 95.3 and 92.9%, respectively. Vibratory sensation is often the first sensory finding in DN, and pinprick and light touch examinations may also suggest a pattern of sensory deficit. Ankle deep tendon reflexes and strength should be documented. A skin examination should detect erythema, callouses, and ulcers, and inspection should also look for bony irregularities and muscle atrophy. Diabetic distal symmetric polyneuropathy shows sensory loss in all modalities with progression to weakness and atrophy in a distal to proximal distribution. Examination in small fiber neuropathy can show allodynia and loss of sensation to various modalities. Warm, dry skin and orthostasis may signify underlying autonomic neuropathy.

Diabetic lumbosacral radiculoplexus neuropathy generally presents with proximal deficits; motor findings are greater than sensory findings. Physical examination should be documented and serially monitored to accurately assess disease progression.1

Functional assessment

History should emphasize mobility, transfers, and other activities of daily living. Functional independence measures and the 36-item short form health survey may assist in functional assessments.

Laboratory studies

Basic laboratory evaluation of polyneuropathy includes complete blood count, erythrocyte sedimentation rate, vitamin B12, folate, comprehensive metabolic panel (including fasting blood glucose and both renal and liver function tests), thyroid function tests, and serum protein immunofixation electrophoresis. An important cause of vitamin B12 deficiency is iatrogenic, linked to cumulative doses of metformin3. Depending on the results of these studies and the patient’s history, other studies may include: methylmalonic acid with or without homocysteine, drug and toxin screens, urinalysis, and urine protein electrophoresis with immunofixation. Whether these routine studies need to be performed in known diabetics or prediabetics is unclear. Prediabetics can be identified with a fasting glucose, HbA1c, or glucose tolerance test.10


Magnetic resonance imaging of the lumbar spine and arterial studies may identify spinal or vascular etiologies of symptoms that mimic DN. Plain films may diagnose and follow the progression of neuroarthropathies, such as Charcot foot. When osteomyelitis is suspected, advanced imaging may assist in confirming the diagnosis.11

Supplemental assessment tools

Electrodiagnostic studies, including electromyography (EMG) and nerve conduction studies, may facilitate the diagnosis, monitor progression, and investigate other pathologies within the differential diagnosis of DN. In diabetic distal symmetrical polyneuropathy, conduction slowing is evidenced by prolonged latencies for distal and late responses and decreased conduction velocities. Axonal loss shows small motor and sensory amplitudes. Fibrillation potentials and positive sharp waves on needle EMG examination reveal active axonal loss. Large amplitude motor unit action potentials indicate a chronic component to the individuals with DN. Diabetic amyotrophy often shows evidence of axonal loss in the affected nerve distribution. Small fiber neuropathies frequently have normal standard electrodiagnostic studies, however skin biopsy may be useful in this diagnosis. This involves a 3 mm diameter punch biopsy usually taken from the lower extremity with measurement of intraepidermal nerve fiber density, which has 88% sensitivity. Autonomic neuropathy can be diagnosed with specialized neurophysiologic methods including sympathetic skin response and R-R variability testing on electrocardiogram.1,3,12 

Corneal confocal microscopy is a non-invasive quantitative method of detecting corneal innervation in the subbasal plexus. It has been found to be reduced early in the disease, and to be more sensitive in assessing nerve repair than other standard measures such as IENFD and NCS.13

Early predictions of outcomes

Pain, falls and foot ulcers are costly and debilitating conditions, and are important factors in patient outcomes. The presence of DPN increases the risk of falls in diabetics two to three times as compared to those without neuropathy. The increased risk of falls has been shown to occur 3 to 5 years before their diagnosis.  Those with neuropathy have a 15% increased risk of developing ulcers and 6 to 43% of these ulcers will result in an amputation.3If autonomic neuropathy is diagnosed in a diabetic individual, the chance of death increases by 25-50% over 10 years.1,14


It is important to ensure that the living environment of a patient with DN is accessible. Proper lighting at night and avoidance of throw rugs should be encouraged in order to minimize fall risk.

Rehabilitation Management and Treatments

Available or current treatment guidelines

Ultimate goals of treatment are maintenance of function, quality of life, and limb preservation. So far, no disease modifying drugs have been identified for DPN. Optimized glycemic control decreases the incidence of neuropathy in type 1 DM and was noted to show improved NCS findings and vibration sense.2 There is strong evidence that anticonvulsants are beneficial, particularly pregabalin. There is moderate evidence supporting antidepressants (tricyclic antidepressants and serotonin-norepinephrine reuptake inhibitors), capsaicin, and isosorbide dinitrate spray to treat the pain associated with DN. Medication selection generally depends on their roles in treating comorbid conditions, contraindications, and on their interactions with other medications. Patients with neuropathic pain refractory to the above treatments may be candidates for spinal cord stimulators. There is moderate evidence that percutaneous electrical nerve stimulation is beneficial.1,15  

In animal models and human trials, aerobic exercise has been shown to improve symptoms of neuropathy and facilitate re-growth of cutaneous small-diameter fibers. Similarly reduction in periods of seated, awake inactivity produces metabolic benefits similar to exercise.16

At different disease stages

Evaluations and treatments must be tailored to the specific complications and functional needs of each patient.

Coordination of care

The physiatrist coordinates diagnostic and treatment plans among orthotists, prosthetists, podiatrists, physical and occupational therapists, and surgical specialists.17

Patient & family education

The patient and family must be educated about the relationship between glycemic control and the course of diabetic neuropathies. Patients and their caretakers should be encouraged to perform daily foot inspections and bring any skin lesions to the attention of their physician. They must be educated on the complications of DN and effective methods of prevention. Routine podiatry visits must be recommended for nail care.

Emerging/unique interventions

Function should be monitored subjectively by the patient. Skin lesions must be carefully observed to resolution. For pain and other subjective neuropathic complaints, the Visual Analogue Scale, Neuropathic Pain Scale, Mcgill Pain Questionnaire, and the Leeds Assessment of Neuropathic Symptoms and Signs may also assist in assessing treatment efficacy.

Several small studies suggest that transcutaneous electrical nerve stimulation (TENS) should be considered as a treatment option for painful diabetic peripheral neuropathy (DPN) given its association with improved pain scores. An additional benefit to TENS is that it may be initiated as an adjunct therapy to other treatments.18

Of note, the FDA approved QUTENZA® (capsaicin) 8% topical system in 2009 for treatment of postherpetic neuralgia (PHN), but also recently approved its use for neuropathic pain associated with diabetic peripheral neuropathy (DPN) of the feet.19,20

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

The importance of glycemic control cannot be overstated, and patients should be continually educated about this. As vibratory sensation is lost early in DN, an examination of this should be performed if DN is suspected and serially monitored. Physiatrists must coordinate effectively with primary care and other involved physicians, providing education as appropriate for prevention and treatment techniques.

Diabetic patients should be evaluated regularly for the presence of both peripheral neuropathy and neuropathic pain, as well as the subsequent effects these conditions may have on patients’ quality of life and function.

In order to provide the best possible outcomes, it may be necessary to counsel patients on their expectations regarding pain relief. In clinical trials approximately 30% reduction in pain is considered successful. As such, when initiating pharmacologic intervention, it may be prudent to advise patients that pain reduction is the goal of intervention, and that may not necessarily mean the complete elimination of pain.21 

Mood Disorders, particularly major depression, and sleep disorders, such as obstructive sleep apnea, are more likely to occur in patients with diabetes compared to the general population. Therefore, patients with PDN should be assessed for concurrent mood and sleep disorders. Treating mood and sleep disorders may provide benefits in improving quality of life and pain reduction, apart from direct neuropathy treatment.21 

Based upon evidence of pain reduction in meta-analyses, TCAs (such as amitriptyline and nortriptyline), SNRIs (such as duloxetine and venlafaxine), gabapentinoids (such as gabapentin and pregabalin), and/or sodium channel blockers (such as carbamazepine, oxcarbazepine,lamotrigine and valproic acid) are viable options to treat painful diabetic neuropathy. The best estimates of effect sizes, and corresponding confidence intervals for these drug classes are comparable, making recommendations for one class over another difficult.18,21  

TCA, SNRI, gabapentinoid, and sodium channel blocker classes have similar efficacy regarding outcomes for reduction of neuropathic pain, however there are differences in potential adverse effects. TCAs have been associated with anticholinergic side effects, and thus should be cautioned in patients with underlying autonomic dysfunction, such as constipation, urinary retention, or orthostatic hypotension. SNRIs and sodium channel blockers have risks associated with nausea, fatigue, and dizziness. As such, patients with similar preexisting symptoms may find that these drug classes are less well-tolerated. With regard to sodium channel blockers, Valproic acid in particular has significant potential teratogenic side effects, including neural tube defects as well as hepatotoxicity, pancreatitis, hyponatremia, and pancytopenia. The administration of Valproic acid for the treatment of neuropathic pain should be approached with extreme caution. In fact, it should not be prescribed unless multiple other effective pharmacologic agents have been unsuccessful in adequately treating pain. Pre-existing peripheral edema from cardiac, renal, and/or hepatic pathologies should be considered prior to administration of Gabapentinoids, given that these medications can cause or exacerbate peripheral edema. Potential adverse effects, patient comorbidities, patient preference, and other factors outside of efficacy should be considered with regard to treatment recommendation for PDN, given that the efficacy of the aforementioned drug classes are quite similar.18,21

Patients should be informed that multiple pharmacologic interventions may need to be tried in order to achieve the most beneficial treatment regimen. An individual pharmacologic intervention is deemed ineffective for a patient if the medication has been titrated to an efficacious dose for approximately 12 weeks, and there is no clinically significant reduction in pain, or if the adverse effects from the medication outweigh the benefit for neuropathic pain reduction. In such instances, patients should be offered a trial of an alternative medication from a different drug class. Patients who experience partial improvement in neuropathic pain symptoms with an initial agent may be offered a trial of an agent from a different drug class to replace the first agent or in addition to provide a combination therapy.21

Patient preference for topical and/or nonpharmacologic treatment should be taken into account. Clinicians may offer topical medications such as capsaicin, glyceryl trinitrate spray, and Citrullus colocynthis. Nonpharmacologic options may include Cognitive Behavioral Therapy, exercise, Tai Chi, and mindfulness exercises.19,20,21

Lastly, given limited evidence of long-term efficacy, and amidst the likelihood of long-term adverse consequences, opioids and opioid/SNRI dual mechanism pharmacologic agents (such as tramadol and tapentadol) should not be used for the treatment of PDN. Patients who are taking either class of medication for PDN can be safely tapered off and offered non-opioid alternative treatment options.21

Cutting Edge/ Emerging and Unique Concepts and Practice

Cutting edge concepts and practice

Alpha lipoic acid (ALA) 600 milligrams per day was found to be the most successful antioxidant in clinical trials and has been approved for the treatment of DPN in Europe.3

Multiple trials have demonstrated that a dose of 600 mg of intravenous ALA per day improved neuropathic signs and symptoms after 3 weeks of treatment. Furthermore, there is evidence that an oral dose of ALA 600mg per day for 5 weeks improves neuropathic symptoms.22

Aldose reductase treatment showed initial promise in the treatment of DPN in several studies; but a Cochrane review of 32 randomized controlled trials showed no statistical difference between aldose reductase inhibitors and placebo.3

However, a 3-year randomized study involving the aldose reductase inhibitor, epalrestat, for the treatment of diabetic sensorimotor polyneuropathy (DSPN) showed that it was well tolerated, and it delayed the deterioration in median motor nerve conduction velocity (NCV) and vibration perception threshold (VPT). Epalrestat was more efficacious in those with less severe complications from diabetes and with adequate metabolic control.22

In both Type 1 and Type 2 Diabetes, it is not uncommon for thiamine levels to be low and thiamine clearance rates to be high. Benfotiamine is a synthetic prodrug of thiamine.  In the Benfotiamine in Diabetic Polyneuropathy (BENDIP) trial, 300mg twice daily dose of benfotiamine for 6 weeks showed a significant improvement in neuropathic symptoms. Similarly, the Benfotiamine in the treatment of Diabetic Polyneuropathy (BEDIP) trial demonstrated improvement on a dose of 100mg four times per day after 3 weeks of treatment.  Another clinical trial utilizing a therapeutic combination of benfotiamine, pyridoxine and cyanocobalamin showed that peroneal motor nerve conduction velocity was improved at 12 weeks of treatment.22  

Multiple pre-clinical and clinical studies demonstrate a pathogenic role for inflammation, especially cytokine and chemokine production, which can play a significant role in development of charcot arthropathy, and impaired wound healing in DN. Targeting low-grade inflammation via modulation of the IKKβ/NF-κB pathway could interfere with several critical pathways involved in the pathogenesis of DN and of the DN associated pain.23 One review article suggests DN in type 2 DM patients have increased serum TNF-α level than type 2 diabetic patients without peripheral neuropathy and healthy controls.24

A randomized controlled trial of fulranumab, a monoclonal antibody directed against nerve growth factor (NGF), revealed some efficacy in the reduction of daily pain when administered at 10 mg subcutaneously every 4 weeks. This study was discontinued by the Food and Drug Administration (FDA) because of the possibility that anti-NGF antibodies could be associated with increased risk of osteoarthritis or osteonecrosis.2

Gaps in the Evidence-Based Knowledge

Etiologies for DN remain controversial. Several novel theories for the pathogenesis of DN are currently in development. Neurotrophic factors, such as vascular endothelial growth factor, nerve growth factor, and insulin-like growth factor, promote the maintenance and regeneration of neurons, and low levels in diabetics may lead to neuronal apoptosis.1

The relationship between prediabetes and neuropathy remains unproven, as does the relationship between chronic inflammatory demyelinating polyneuropathy and DN.

So far there have been no preventive, or disease modifying therapy recognized to prevent the development or progression of   diabetic neuropathy. Early detection and diagnosis remain the mainstay of treatment.25


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  3. K Juster-Switlyk and A.G. Smith. Updates in diabetic peripheral neuropathy. version 1.  2016;5:F1000 Faculty Rev-738:1-7.
  4. Matti D. Allen,Timothy J. Doherty, Charles L. Rice, Kurt Kimpinski. Physiology in Medicine: neuromuscular consequences of diabetic neuropathy. J Appl Physiol (1985) 2016;121(1):1-6.
  5. Jennifer Zenker, Dan Ziegler, and Roman Chrast. Novel pathogenic pathways in diabetic neuropathy. Trends in Neurosciences. 2013;36(8):439-496.
  6. Paul Fernyhough. Mitochondrial Dysfunction in Diabetic Neuropathy: a series of unfortunate metabolic events. Curr Diab Rep. 2015;15(11):89.
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  8. Heung Yong Jin, Hong Sun Baek, Tae Sun Park. Morphologic Changes in Autonomic Nerves in Diabetic Autonomic Neuropathy. Diabetes Metab J. 2015;39:461-467.
  9. J. Dyck, A.J. Windebank. Diabetic and nondiabetic lumbosacral radiculoplexus neuropathies: new insights into pathophysiology and treatment. Muscle Nerve. 2002;25:477-491.
  10. D. England, G.S. Gronseth, G. Franklin, et al. Evaluation of distal symmetrical polyneuropathy: the role of laboratory and genetic testing. Muscle Nerve. 2009;39:116-125.
  11. Frykberg, T. Zgonis, D.G. Armstrong, et al. Diabetic foot disorders – a clinical practice guideline. J Foot Ankle Surg. 2006;45(5):1-66.
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  13. Prashanth R. J. Vas, Sanjeev Sharma, and Gerry Rayman. Distal Sensorimotor Neuropathy: Improvements in Diagnosis. The Review of Diabetic studies. 2015;12:29-47.
  14. E. Reiber, E.J. Boyko, D.G. Smith. Diabetes related amputations of lower extremities in medicare population. MMWR. 1998;47(31):649-652.
  15. Bril, J. England, G.M. Franklin, et al. Evidence-based guideline: treatment of painful diabetic neuropathy. Neurology. 2011;76(20):1758-1765.
  16. R. Singleton, A.G. Smith, R.L. Marcus. Exercise as Therapy for Diabetic and Prediabetic Neuropathy. Curr Diab Rep. 2015;15:120.
  17. A. DeLisa, B.M. Gans, et al. Physical Medicine and Rehabilitation: Principles and Practice. 2005;14:873-911.
  18. Snyder MJ, Gibbs LM, Lindsay TJ. Treating Painful Diabetic Peripheral Neuropathy: An Update. Am Fam Physician. 2016;94(3):227-234.
  19. Averitas Pharma, Inc. Qutenza (capsaicin) patch [package insert]. U.S. Food and Drug Administration. website:https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/022395s019lbl.pdf. Revised July 2020. Accessed March 25, 2022.
  20. Simpson DM, Robinson-Papp J, Van J, et al. Capsaicin 8% Patch in Painful Diabetic Peripheral Neuropathy: A Randomized, Double-Blind, Placebo-Controlled Study. J Pain. 2017;18(1):42-53. doi:10.1016/j.jpain.2016.09.008
  21. Price R, Smith D, Franklin G et al. Oral and Topical Treatment of Painful Diabetic Polyneuropathy: Practice Guideline Update Summary. Neurology. 2021;98(1):31-43. doi:10.1212/wnl.0000000000013038
  22. Ziegler D, Papanas N, Schnell O, et al. Current concepts in the management of diabetic polyneuropathy. J Diabetes Investig. 2021;12(4):464-475. doi:10.1111/jdi.13401
  23. Pop-Busui, A. Lynn, C. Holmes, K. Gallagher. Inflammation as a Therapeutic Target for Diabetic Neuropathies. Curr Diab Rep. 2016;16:29.
  24. Mu, Y. Wang, C. Li. Association Between Tumor Necrosis Factor-α and Diabetic Peripheral Neuropathy in Patients with Type 2 Diabetes: a meta-analysis. Mol Neurobiol. 2017;54(2):983-996.
  25. Anne K Schreiber, Carina FM Nones, Renata C Reis, Juliana G Chichorro, Joice M Cunha. Diabetic neuropathic pain: physiopathology and treatment. World J Diabetes. 2015;6(3):432-444.

Original Version of the Topic

Jarron I. Tilghman, MD, Kevin Komes, MD, Michael Khadavi, MD, Ebby Varghese, MD. Diabetic neuropathy. 7/25/2012

Previous Revision(s) of the Topic

Eathar A. Saad, MD, Neel Chandel, MD. Diabetic neuropathy. 11/28/2017

Author Disclosure

Sara Flores, MD
Nothing to Disclose

Michael Davis, DO, MS
Nothing to Disclose