Diabetic neuropathy—a review

Saïd, Gérard

doi:10.1038/ncpneuro0504

Cited by 525 publications

(423 citation statements)

References 49 publications

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“…One view holds that axons degenerate “centripetally” or in a “dying‐back” fashion (ie, from distal to more proximal levels) 9, 17. This concept is mainly based on fascicular biopsies taken from distal sural nerves at the ankle level.…”

Section: Discussionmentioning

confidence: 99%

Magnetic resonance neurography detects diabetic neuropathy early and with Proximal Predominance

Pham

Oikonomou

Hornung

et al. 2015

Annals of Neurology

102

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ObjectiveThe aim of this work was to localize and quantify alterations of nerve microstructure in diabetic polyneuropathy (DPN) by magnetic resonance (MR) neurography with large anatomical coverage.MethodsPatients (N = 25) with mild‐to‐moderate (Neuropathy‐Symptom‐Score [NSS]/Neuropathy Deficit Score [NDS] 3.8 ± 0.3/2.6 ± 0.5) and patients (n = 10) with severe DPN (6.2 ± 0.6/7.4 ± 0.5) were compared to patients (n = 15) with diabetes but no DPN and to age‐/sex‐matched nondiabetic controls (n = 25). All subjects underwent MR neurography with large spatial coverage and high resolution from spinal nerve to ankle level: four slabs per leg, each with 35 axial slices (T2‐ and proton‐density–weighted two dimensional turbo‐spin‐echo sequences; voxel size: 0.4 × 0.3 × 3.5 mm3) and a three‐dimensional T2‐weighted sequence to cover spinal nerves and plexus. Nerve segmentation was performed on a total of 280 slices per subject. Nerve lesion voxels were determined independently from operator input by statistical classification against the nondiabetic cohort. At the site with highest lesion‐voxel burden, signal quantification was performed by calculating nerve proton spin density and T2 relaxation time.ResultsTotal burden of nerve lesion voxels was significantly increased in DPN (p = 0.003) with strong spatial predominance at thigh level, where average lesion voxel load was significantly higher in severe (57 ± 18.4; p = 0.0022) and in mild‐to‐moderate DPN (35 ± 4.0; p < 0.001) than in controls (18 ± 3.6). Signal quantification at the site of predominant lesion burden (thigh) revealed a significant increase of nerve proton spin density in severe (360 ± 22.9; p = 0.043) and in mild‐to‐moderate DPN (365 ± 15.2; p = 0.001) versus controls (288 ± 13.4), but not of T2 relaxation time (p = 0.49). Nerve proton spin density predicted severity of DPN with an odds ratio of 2.9 (95% confidence interval: 2.4–3.5; p < 0.001) per 100 proton spins.InterpretationIn DPN, the predominant site of microstructural nerve alteration is at the thigh level with a strong proximal‐to‐distal gradient. Nerve proton spin density at the thigh level is a novel quantitative imaging biomarker of early DPN and increases with neuropathy severity. Ann Neurol 2015;78:939–948

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Section: Discussionmentioning

confidence: 99%

Magnetic resonance neurography detects diabetic neuropathy early and with Proximal Predominance

Pham

Oikonomou

Hornung

et al. 2015

Annals of Neurology

102

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“…It causes multiple organ damage (peripheral nerves, heart, kidney, eyes), leading to an increasing prevalence and severity of several complications [2], among the most frequent of which are peripheral neuropathies [3] and cardiovascular diseases [4].…”

Section: Introductionmentioning

confidence: 99%

Regression of diabetic complications by islet transplantation in the rat

et al. 2009

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Aims/hypothesis Type 1 diabetes is a chronic disease leading to complications such as peripheral neuropathies, nephropathy and cardiovascular disease. Pancreatic islet transplantation is being extensively investigated for blood glucose control in animals and in human type 1 diabetic patients, but the question of whether it can reverse long-term diabetic complications has not been fully explored. We investigated the effects of islet transplantation on diabetic complications in a rat model of streptozotocin-induced diabetes.Methods Three groups of rats were used: healthy controls, diabetic and diabetic rats transplanted with microencapsulated islets at 2 months after diabetes induction, when neuropathy was detectable by a decrease in tail nerve conduction velocity (NCV) and impaired nociceptive thresholds. Blood glucose levels and body weight were measured weekly. The variables considered were: thermal (hot plate test) and mechanical sensitivity (Randal-Selitto paw withdrawal test), NCV and Na+, K+-ATPase activity in the sciatic nerve. At the end of the experiments hearts were removed for morphometric determination and myocyte number, and kidneys removed for histological examination. Results Islet transplantation in diabetic rats induced normoglycaemia in a few days, accompanied by a rapid rise in body weight and amelioration of impaired nociceptive thresholds, as well as normalisation of NCV and Na + , K + -ATPase, which were both about 25% below normal in diabetic rats. Myocyte loss was reduced (−34%) by islet transplantation and the observed mild kidney damage of diabetic rats was prevented. Conclusions/interpretation Besides controlling glycaemia, transplantation of microencapsulated pancreatic islets induced almost complete regression of neuropathy and prevented cardiovascular alterations.

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“…The underlying mechanism of diabetic polyneuropathy is extremely complex and likely related to various metabolic and inflammatory pathways inducing individually or superimposed on ischemic nerve lesions (Said 2007). However, it is difficult to determine the mechanism because any factor leading to cellular stress may induce an inflammatory response or inflammation that leads to polyneuropathy (Hotamisligil and Erbay 2008).…”

Section: Introductionmentioning

confidence: 99%

High Plasma Pentraxin 3 Levels in Diabetic Polyneuropathy Patients with Nociceptive Pain

Salcini

Arslan

Sünter

et al. 2016

Tohoku J. Exp. Med.

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Diabetic polyneuropathy is the most common neurologic complication of diabetes mellitus. Underlying mechanisms of diabetic polyneuropathy are related to various metabolic and inflammatory pathways. Pentraxin 3 (PTX3) is an acute phase protein that is produced locally at the inflammatory sites by several cell types. Thioredoxin binding protein 2 (TBP2) is a thioredoxin regulator involved in intracellular energy pathways and cell growth. We measured the plasma levels of PTX3 and TBP2 in type 2 diabetic patients (n = 27) with pain complaints and compared their levels with those of healthy age-and sex-matched subjects (n = 24). Moreover, the diabetic patients were divided into two groups using the Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) pain scale: patients with nociceptive pain that is caused by tissue damage and patients with neuropathic pain that is caused by nerve damage. Patients with LANSS scores of < 12 were considered to have nocicceptive pain (n = 15), while patients with LANSS scores of ≥ 12 were considered to have neuropathic pain (n = 12). We found that PTX3 levels were significantly higher in diabetic patients compared to controls (p = 0.03), but there was no significant difference in the TBP2 levels. Importantly, patients with nociceptive pain had significantly higher PTX3 levels compared to patients with neuropathic pain (p < 0.05). Thus, plasma PTX3 levels can be helpful for discrimination of nociceptive pain from neuropathic pain in diabetic patients. We propose that PTX3 may contribute to the onset of nociceptive pain.

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Diabetic neuropathy—a review

Cited by 525 publications

References 49 publications

Magnetic resonance neurography detects diabetic neuropathy early and with Proximal Predominance

Magnetic resonance neurography detects diabetic neuropathy early and with Proximal Predominance

Regression of diabetic complications by islet transplantation in the rat

High Plasma Pentraxin 3 Levels in Diabetic Polyneuropathy Patients with Nociceptive Pain

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