Ulnar entrapment neuropathy in patients with type 2 diabetes mellitus: An electrodiagnostic study

Rota, Eugenia; Zavaroni, D.; Parietti, L.; Iafelice, Ilaria; Mitri, Paola De; Terlizzi, Emilio; Morelli, Nicola; Immovilli, Paolo; Guidetti, Donata

doi:10.1016/j.diabres.2014.01.024

Cited by 22 publications

(23 citation statements)

References 20 publications

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“…Moreover, in the presence of decreased SNAP amplitude of the ulnar or median nerve, the SNAP amplitude of the sural nerve was normal in 82% and 80% of the subjects respectively [3]. Such a dissociation between upper and lower limb sensory nerve involvement in DM was confirmed by another study of ours on subjects affected by Type 2 DM, where the SNAP amplitude was below the lower threshold limit in 52% of the total sample for the ulnar nerve (at the 5th finger), in 48% for the median and in 29% for the sural nerve [4]. The SNAP amplitude of the sural nerve was normal, in the presence of a decrease in the SNAP amplitude of the ulnar nerve (pattern ''abnormal ulnar/ normal sural'') in 34% of the subjects.…”

supporting

confidence: 72%

“…The SNAP amplitude of the sural nerve was normal, in the presence of a decrease in the SNAP amplitude of the ulnar nerve (pattern ''abnormal ulnar/ normal sural'') in 34% of the subjects. These findings may be only partially explained by the high prevalence of the carpal tunnel syndrome and ulnar nerve entrapments, which were diagnosed in these two studies [3,4] and, more generally, in patients with DM [5]. Indeed, a median mononeuropathy at the wrist was found in 28% and 62.5% of the two patient samples respectively, the former with DM at diagnosis, the latter with an average disease duration of 14.5 years [3,4].…”

mentioning

confidence: 58%

“…These findings may be only partially explained by the high prevalence of the carpal tunnel syndrome and ulnar nerve entrapments, which were diagnosed in these two studies [3,4] and, more generally, in patients with DM [5]. Indeed, a median mononeuropathy at the wrist was found in 28% and 62.5% of the two patient samples respectively, the former with DM at diagnosis, the latter with an average disease duration of 14.5 years [3,4]. Furthermore, subclinical ulnar entrapments were electrodiagnosed at the elbow in 34% of the patients and in 11% at the wrist [4], suggesting that the ulnar nerve is very susceptible to focal entrapment in DM, similarly to the median nerve.…”

mentioning

confidence: 72%

“…Indeed, a median mononeuropathy at the wrist was found in 28% and 62.5% of the two patient samples respectively, the former with DM at diagnosis, the latter with an average disease duration of 14.5 years [3,4]. Furthermore, subclinical ulnar entrapments were electrodiagnosed at the elbow in 34% of the patients and in 11% at the wrist [4], suggesting that the ulnar nerve is very susceptible to focal entrapment in DM, similarly to the median nerve. This is most likely due to the metabolic factors and endoneurial ischemia that occur in DM in the long preclinical stage [6] as they damage the nerve, making it more susceptible to focal entrapment at an early stage, where the focal neuropathy of the median [7] or ulnar nerve [3] may be the only manifestation of a peripheral nerve involvement.…”

mentioning

confidence: 87%

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Electrodiagnostic testing in diabetic neuropathy: Which limb?

Rota¹,

Cocito²

2015

Diabetes Research and Clinical Practice

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supporting

confidence: 72%

mentioning

confidence: 58%

mentioning

confidence: 72%

mentioning

confidence: 87%

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Electrodiagnostic testing in diabetic neuropathy: Which limb?

Rota¹,

Cocito²

2015

Diabetes Research and Clinical Practice

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“…Confirming Zhang et al [46] and Zhong et al [38], Rota et al [47] report NCV changes typical of entrapment neuropathy to be present in 70% of a consecutive series of patients referred to an Italian diabetology unit.…”

Section: Objective Outcomesmentioning

confidence: 56%

Nerve decompression and neuropathy complications in diabetes: Are attitudes discordant with evidence?

Nickerson¹

2017

Diabetic Foot & Ankle

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External neurolysis of the nerve at fibro-osseous tunnels has been proprosed to treat or prevent signs, symptoms, and complications in the lower extremity of diabetes patients with sensorimotor polyneuropathy. Nerve decompression is justified in the presence of symptomatic compressed nerves in the several fibro-osseous tunnels of the extremities, which are known to be frequent in diabetes. Quite a body of literature has accumulated reporting results after such nerve decompression in the leg, describing pain relief and sensibility improvement, as well as balance recovery, diabetic foot ulcer prevention, curtailed ulcer recurrence risk, and amputation avoidance.Historical academic hesitance to endorse surgical treatments for pain and numbness in diabetes was based primarily on the early retrospective reports’ potential for bias and placebo effects, and that the hypothetical basis for surgery lies outside the traditional etiology paradigm of length-dependent axonopathy. This reticence is here critiqued in view of recent studies using objective, measured outcome protocols which nullify such potential confounders. Pain relief is now confirmed with Level 1 studies, and Level 2 prospective information suggests protection from initial diabetic foot ulceration and most neuropathic ulcer recurrences. In view of the potential for nerve decompression to be useful in addressing some of the more difficult, expensive, and life altering complications of diabetic neuropathy, this secondary compression thesis and operative treatment methodology may deserve reassessment.

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Polydatin protects Schwann cells from methylglyoxal induced cytotoxicity and promotes crushed sciatic nerves regeneration of diabetic rats

Chen

et al. 2021

Phytotherapy Research

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Oxidative stress plays the main role in the pathogenesis of diabetes mellitus and peripheral neuropathy. Polydatin (PD) has been shown to exhibit strong antioxidative and antiinflammatory effects. At present, no research has focused on the possible effects of PD on Schwann cells and impaired peripheral nerves in diabetic models. Here, we used an in vitro Schwann cell damage model induced by methylglyoxal and an in vivo diabetic sciatic nerve crush model to study problems in such an area. In our experiment, we demonstrated that PD potently alleviated the decrease of cellular viability, prevented reactive oxygen species generation, and suppressed mitochondrial depolarization as well as cellular apoptosis in damaged Schwann cells. Moreover, we found that PD could upregulate Nrf2 and Glyoxalase 1 (GLO1) expression and inhibit Keap1 and receptor of AGEs (RAGE) expression of damaged Schwann cells. Finally, our in vivo experiment showed that PD could promote sciatic nerves repair of diabetic rats. Our results revealed that PD exhibited prominent neuroprotective effects on Schwann cells and sciatic nerves in diabetic models. The molecular mechanisms were associated with activating Nfr2 and GLO1 and inhibiting Keap1 and RAGE.

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Ulnar entrapment neuropathy in patients with type 2 diabetes mellitus: An electrodiagnostic study

Cited by 22 publications

References 20 publications

Electrodiagnostic testing in diabetic neuropathy: Which limb?

Electrodiagnostic testing in diabetic neuropathy: Which limb?

Nerve decompression and neuropathy complications in diabetes: Are attitudes discordant with evidence?

Polydatin protects Schwann cells from methylglyoxal induced cytotoxicity and promotes crushed sciatic nerves regeneration of diabetic rats

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