Classification, Differential Diagnosis, and Staging of Diabetic Peripheral Neuropathy

Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, Institute of Neurology, London, U.K.
Diabetes (Impact Factor: 8.1). 10/1997; 46 Suppl 2(supplement 1):S54-7. DOI: 10.2337/diab.46.2.S54
Source: PubMed


The peripheral nerve disorders associated with diabetes are complex and probably involve a variety of causative mechanisms. This may give rise to difficulty in the classification of individual cases. A broad separation into rapidly reversible or more persistent phenomena is helpful. The former, which can be categorized as "hyperglycemic neuropathy," include minor sensory symptoms, reduced nerve conduction velocity, and resistance to ischemic conduction failure. From analogy with experimental studies in animals, nerve hypoxia is likely to play a significant role in their origin. Of the more persistent phenomena, a distal symmetric polyneuropathy that predominantly affects sensory and autonomic function is the most common manifestation. A distal axonopathy of dying-back type may represent the underlying pathogenetic basis. Other more persistent phenomena consist of focal and multifocal lesions giving rise to cranial, thoraco-abdominal, and limb neuropathies, including proximal lower limb motor neuropathy (diabetic amyotrophy). Some of these may have an ischemic basis. Multifocal proximal lesions can summate to produce an approximately symmetric diffuse distal neuropathy. Focal lesions at sites of entrapment or external compression may reflect an abnormal susceptibility of diabetic nerve to compressive damage. There is also evidence that focal inflammatory, including vasculitic, lesions may be involved in proximal lower limb neuropathies. Finally, superimposed chronic inflammatory demyelinating polyneuropathy may occur. For the evaluation of possible treatment regimens, it is essential that cases should be correctly classified as to type. Thus, the features falling into the category of hyperglycemic neuropathy should not contaminate the assessment of distal symmetric polyneuropathy. For this type, a widely accepted scheme for staging devised by P. J. Dyck is available. Other schemes are also available for the assessment of such cases, with differing degrees of complexity. Evaluation by serial nerve biopsies has also been proposed.

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    • "The final outcome may restore microcirculation.31,32 Quantification of LPO represents an objective way of measuring oxidative stress,33 and a significant reduction was observed in the rosuvastatin group in our study. These findings could be related to improvement of DPN stage, but further studies must be done to demonstrate a correlation between LPO and clinical findings, since our sample size was too small to meet this objective. "
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    ABSTRACT: Background Diabetic neuropathy affects 50%–66% of patients with diabetes mellitus. Oxidative stress generates nerve dysfunction by causing segmental demyelinization and axonal degeneration. Antioxidants are considered to be the only etiologic management for diabetic polyneuropathy, and statins such as rosuvastatin increase nitric oxide bioavailability and reduce lipid peroxidation. The aim of this study was to evaluate the antioxidant effect of rosuvastatin in diabetic polyneuropathy. Methods We conducted a randomized, double-blind, placebo-controlled Phase IIa clinical trial in patients with type 2 diabetes and diabetic polyneuropathy (DPN) stage ≥1b. We allocated subjects to two parallel groups (1:1) that received rosuvastatin 20 mg or placebo for 12 weeks. Primary outcomes were neuropathic symptom score, disability score, and nerve conduction studies, and secondary outcomes were glycemic control, lipid and hepatic profile, lipid peroxidation, and nerve growth factor beta (NGF-β) levels. Results Both groups were of similar age and duration since diagnosis of diabetes and DPN. We observed improvement of DPN in the rosuvastatin group from stage 2a (88.2%) to stage 1b (41.2%), improvement of neuropathic symptom score from 4.5±2 to 2.4±1.8, and significant (P=0.001) reductions of peroneal nerve conduction velocity (from 40.8±2.2 to 42.1±1.6 seconds) and lipid peroxidation (from 25.4±2 to 12.2±4.0 nmol/mL), with no significant change in glycemic control or β-NGF. Conclusion The severity, symptoms, and nerve conduction parameters of DPN improved after 12 weeks of treatment with rosuvastatin. These beneficial effects appear to be attributable to reductions in lipid peroxidation and oxidative stress.
    Full-text · Article · Sep 2014 · Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy
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    • "Acute sensory neuropathy (ASN) is a variant of DSPN [13]. Many of the symptoms of ASN and DSPN are similar, but there are important differences in the onset, signs, and prognosis [14]. Severe pain, described as burning and deep aching, is the main symptom in all patients. "
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    ABSTRACT: Distal symmetric polyneuropathy (DSPN) is the most common chronic complication of diabetes mellitus. The pathogenesis of DSPN is not fully elucidated, but it is certainly multifactorial in nature and attributable to metabolic and microvessel disorders related to chronic hyperglycemia, diabetes duration, and several cardiovascular risk factors. Early diagnosis and appropriate management are extremely important, since up to 50% of DSPN cases may be asymptomatic, and patients are unaware of foot injury leading to foot ulcers and amputation. Simple, validated tests such as the Neuropathy Disability Score and/or Vibration Perception Threshold may be used to diagnose DSPN. Similarly, neurological dysfunction screening questionnaires should be used to assess the quality and severity of DSPN symptoms. Using both methods enables prediction of the prognosis of diabetic patients with DSPN. No causative treatment of DSPN is known, but the results of clinical trials indicate that several treatment options are highly effective in symptomatic treatment of painful DSPN. The appropriate treatment of DSPN may improve the outcome, preventing or delaying the development of numerous diabetic complications.
    Full-text · Article · May 2014 · Archives of Medical Science
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    • "The diabetic neuropathies represent a heterogeneous group of neuropathies affecting different parts of the nervous system, including generalized symmetric polyneuropathies, focal and multifocal neuropathies, and autonomic neuropathy [48]. "
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    ABSTRACT: An increasing body of evidence suggests that obstructive sleep apnoea (OSA) is independently associated with an increased risk of cardiovascular disease, glucose intolerance, and deteriorations in glycaemic control. Despite the knowledge of a multifactorial pathogenesis of long-term diabetes complications, there is a paucity of information on impact of comorbidities associated with chronic intermittent hypoxemia on development and progression of chronic diabetes complications. This review explores the clinical and scientific overlap of OSA and type 2 diabetes mellitus (T2DM) and its possible impact on the development and progression of diabetes macrovascular and microvascular complications. Multiple prospective observational cohort studies have demonstrated that OSA significantly increases the risk of cardiovascular disease independent of potential confounding risk factors. The current evidence further suggests that OSA with concurrent T2DM is associated with an increased risk of oxidative stress-induced damage of vulnerable endothelial and mesangial cells and peripheral nerves. Further studies are needed to validate the impact of OSA treatment on diabetes micro- and macrovascular complications. Since it is presently still unknown whether OSA treatment may provide a diabetes-modifying intervention that could delay or halt the progression of chronic diabetes complications, the emphasis is on early diagnosis and satisfactory treatment of both OSA and T2DM.
    Full-text · Article · May 2014 · Diabetes Research and Clinical Practice
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