Classification, differential diagnosis, and staging of diabetic peripheral neuropathy.
ABSTRACT 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.
- SourceAvailable from: Adolfo Daniel Rodríguez-Carrizalez[Show abstract] [Hide abstract]
ABSTRACT: 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.Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy 09/2014; 7:401-7.
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ABSTRACT: Aims/IntroductionTo elucidate the clinical significance of median neuropathy at the wrist (MN) in patients with diabetes.Materials and Methods In total, 340 patients with diabetes who were hospitalized for glycemic control were enrolled in the present study. The diagnoses of MN and diabetic polyneuropathy (DPN) were based on electrophysiological criteria. A total of 187 patients were divided into four subgroups: patients without MN or DPN; patients with MN without DPN; patients with MN and DPN; and patients with DPN without MN. Intergroup comparisons of clinical characteristics and results of nerve conduction studies were carried out.ResultsA total of 71 patients had neither MN nor DPN; 25 had MN, but no DPN; 55 had MN and DPN; and 36 had DPN, but no MN. In comparison with the MN and DPN group, the MN without DPN group included more patients in the early phase of diabetes (diagnosed within the past 5 years) and fewer patients with diabetic microangiopathy. Comparative median nerve conduction studies showed significantly lower motor and sensory nerve conduction velocities, longer F-wave latencies, and smaller sensory nerve action potentials in patients with MN and DPN than in those without DPN.ConclusionsMN in patients with diabetes could be attributed to an impairment in axonal function at common entrapment sites, and could be used to identify an early manifestation of diabetic neuropathy.Journal of Diabetes Investigation. 03/2014;
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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.Archives of medical science : AMS. 05/2014; 10(2):345-54.