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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic peripheral neuropathy (DPN) is a common complication of both type I and II diabetes mellitus. Although the exact cause remains unknown, peripheral neuropathy can cause significant health concerns and decrease the quality of life for those with this condition. Diagnosis of DPN can be made when signs and/or symptoms of peripheral nerve dysfunction are present. Patients with diabetes should be evaluated yearly for DPN with a thorough history and physical examination emphasizing the feet. Strict glycemic control and daily foot care are of utmost importance in the management and prevention of DPN. Pharmacologic therapies for pain control include tricylic antidepressants, anticonvulsants, analgesics, and capsaicin. DPN remains a frequent and serious complication of diabetes mellitus, and left unmanaged, may lead to debilitating consequences of foot ulcers and amputations.
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PMID:Peripheral neuropathy in persons with diabetes. 1115 89

Diabetic peripheral neuropathy affects 5 to 50% of people with diabetes in the United States. It is a progressive disorder that results in a gradual decrease in peripheral sensation and eventually complete loss of sensation. Patients with diabetic peripheral neuropathy are challenging to treat because of intolerable adverse medication effects and the development of tolerance to medical treatment. We present the case of a patient with peripheral neuropathy that was unresponsive to usual therapies. She experienced significant relief with the administration of topiramate. Topiramate is an anticonvulsant that is gaining recognition in the treatment of patients with neuropathic pain syndromes.
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PMID:Painful diabetic peripheral neuropathy relieved with use of oral topiramate. 1293 90

Diabetic peripheral neuropathy (DPN) is a frequent and potentially traumatic complication in diabetic individuals. The chronic nature of diabetes and its associated hyperglycemic episodes initiate a complex and inter-related series of metabolic and vascular insults that contribute to the polygenic etiology of DPN. One contributing factor in DPN is an altered neurotrophism that results from changes in the synthesis and expression of neurotrophins, insulin-like growth factor, and various cytokine-like growth factors that can directly act upon distinct subpopulations of sensory and motor neurons. Although considerable effort has focused upon examining growth factor signaling in hyperglycemically stressed neurons, myelin-forming Schwann cells also undergo substantial degenerative changes in DPN. However, scant attention has been devoted to understanding the effect of hyperglycemia on the response of Schwann cells to growth factors critical to their function. Neuregulins are gliotrophic growth factors that signal through members of the Erb B receptor-tyrosine kinase family. The neuregulin/Erb B ligand-receptor cassette can differentially influence the response of Schwann cells throughout their development by regulating cell survival, mitogenesis, and differentiation. The activity of Erb B receptors may also be affected by their interaction with caveolin-1, a protein marker of caveolae ("little caves"). However, whether neuregulin signaling may be directly or indirectly altered under conditions of hyperglycemic stress and contribute to the physiological progression of DPN is unknown. This brief review will provide a perspective on a putative role of changes in the caveolar proteome of Schwann cells in contributing to an "altered neuregulinism" in DPN.
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PMID:Altered neurotrophism in diabetic neuropathy: spelunking the caves of peripheral nerve. 1560 75

Diabetic peripheral neuropathy (DPN) is estimated to be present in 50% of people living with diabetes mellitus (DM). Comorbidities of DM, such as macrovascular and microvascular changes, also Interact with DPN and affect its course. In patients with DM, DPN Is the leading cause of foot ulcers, which in turn are a major cause of amputation in the United States. Although most patients with DPN do not have pain, approximately 11% of patients with DPN have chronic, painful symptoms that diminish quality of life, disrupt sleep, and can lead to depression. Despite the number of patients affected by DPN pain, little consensus exists about the pathophysiology, best diagnostic tools, and primary treatment choices. This article reviews the current knowledge about and presents recommendations for diagnostic assessment of DPN pain based on a review of the literature.
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PMID:Diabetic peripheral neuropathic pain: clinical and quality-of-life issues. 1660 48

Diabetic peripheral neuropathy (DPN) has been identified as a key element in the causal pathway to foot ulceration and other lower-extremity complications, impaired quality of life and increased mortality. Early detection is essential to optimise effective risk management, including adequate foot care, patient education, and future pharmacological therapy. However, data suggest that screening has been mostly sub-optimal, and many physicians remain unfamiliar with non-invasive screening tests. There is evidence in the literature to suggest that vibration perception threshold (VPT) measures can be used to easily and accurately identify at-risk diabetic patients, including those with early neuropathic deficits. These measures have been used in population-based studies and are associated with an increased risk of severe and expensive outcomes, such as ulcers and amputations. Incorporating VPT testing into clinical practice has the potential to significantly improve the outcomes in patients with DPN, thereby substantially reducing the socio-economic burden of this common and challenging disease.
Diabetes Metab Res Rev
PMID:Vibration perception threshold--a valuable assessment of neural dysfunction in people with diabetes. 1674 96

Diabetic peripheral neuropathy is the most common complication of long-standing diabetes mellitus which frequently results in clinically significant morbidities e.g. pain, foot ulcers and amputations. During its natural course it progresses from initial functional changes to late, poorly reversible, structural changes. Various interconnected pathogenetic concepts of diabetic neuropathy have been proposed based on metabolic and vascular factors, mostly derived from long-term hyperglycemia. These pathogenetic mechanisms have been targeted in several experimental and clinical trials. This review summarizes available, mainly morphological data from interventions designed to halt the progression or achieve the reversal of established diabetic neuropathy, which include the recovery of normoglycemia by pancreas or islet transplantation, polyol pathway blockade by aldose reductase inhibitors, mitigation of oxidative stress by the use of antioxidants or correction of abnormalities in essential fatty acid metabolism. Unfortunately, to date, no treatment based on pathogenic considerations has shown clear positive effects and thus early institution of optimal glycemic control remains the only available measure with proven efficacy in preventing or halting progression of diabetic neuropathy. Further experimental and clinical research employing objective reproducible parameters is clearly needed. Novel non-invasive or minimally invasive methods e.g. corneal confocal microscopy or epidermal nerve fiber counts may represent potentially useful instruments for the objective assessment of nerve damage and monitoring of treatment effects.
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PMID:Advanced Diabetic Neuropathy: A Point of no Return? 1748 38

Diabetic peripheral neuropathy (DPN) is the most common diabetic complication and is the leading cause of diabetes-related hospital admissions and non-traumatic amputations. DPN is also associated with a poor quality of life and high economic costs for both type 1 and type 2 diabetic patients. An effective treatment for DPN, besides tight glycemic control, is not yet available. The pathogenesis of DPN is complex and involves an intertwined array of mechanisms. Glucose-mediated alteration of cyclooxygenase (COX) pathway activity with subsequent impaired production and function of prostaglandins (PGs) is one mechanism that is implicated in the pathogenesis of DPN. COX-2, the inducible COX isoform, is upregulated in a variety of pathophysiological conditions including diabetes. COX-2 upregulation has tissue-specific consequences and is associated with activation of downstream inflammatory reactions. We have previously reported that COX-2 is upregulated in the peripheral nerves and dorsal root ganglia neurons in experimental diabetes and that COX-2 gene inactivation and/or selective COX-2 inhibition provides protection against various DPN deficits. This review will summarize current evidence supporting the role of COX-2 activation in inducing diabetic neurovascular dysfunction and that modulation of the COX-2 pathway is a potential therapeutic target for DPN.
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PMID:Cyclooxygenase-2 pathway as a potential therapeutic target in diabetic peripheral neuropathy. 1822 Jul 14

Longstanding diabetes mellitus targets kidney, retina, and blood vessels, but its impact upon the nervous system is another important source of disability. Diabetic peripheral neuropathy is a serious complication of inadequately treated diabetes leading to sensory loss, intractable neuropathic pain, loss of distal leg muscles, and impairment of balance and gait. Diabetes has been implicated as a cause of brain atrophy, white matter abnormalities, and cognitive impairment and a risk factor for dementia. Recent studies have incriminated advanced glycation end products (AGEs) and their receptor (RAGE) in the pathogenesis of diabetic nervous system complications. The availability of RAGE knockout mice and a competitive decoy for AGEs, soluble RAGE (sRAGE), has advanced our knowledge of the RAGE-mediated signalling pathways within the nervous system. They also provide hope for a future novel intervention for the prevention of diabetes-associated neurological complications. This review will discuss current knowledge of diabetes- and RAGE-mediated neurodegeneration, involving the distal-most level of epidermal nerve fibers in skin, major peripheral nerve trunks, dorsal root ganglia, spinal cord, and brain.
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PMID:RAGE, diabetes, and the nervous system. 1833 Dec 35

Diabetic peripheral neuropathy differs in type 1 and type 2 diabetes. The aim of this study was to evaluate how signs and symptoms of neuropathy correlated with defects in motor and sensory nerve conduction velocity (MCV and SCV) and sensory perception thresholds in patients with type 1 diabetes. MCV and SCV in peroneal and sural nerves and vibratory, warm and cold perception thresholds (VPT, WPT, CPT) were evaluated in the lower limbs of 127 patients (42+/-7.9 years old, duration of diabetes, 16+/-11 years and HbA1c, 7.7+/-1.4%). The results were compared with clinical findings (neuropathy impairment assessment, NIA) and sensory symptoms (neurological symptom assessment, NSA). Sensory symptoms were present in 24% of patients, 91% had at least one abnormal finding in the neurological examination and 84% had abnormal nerve conduction. The greatest deviation from normal was observed for CPT on the dorsum of the foot and peroneal MCV. NIA and NSA correlated with all electrophysiological measurements in the foot and big toe. It is concluded that clinical findings correlate well with electrophysiological abnormalities in patients with type 1 diabetic neuropathy. An elevated CPT for the foot was the most pronounced sensory defect.
Diabetes Res Clin Pract 2009 Sep
PMID:Abnormal cold perception in the lower limbs: a sensitive indicator for detection of polyneuropathy in patients with type 1 diabetes mellitus. 1960 94

Diabetic peripheral neuropathy is the most common peripheral neuropathy in the developed world; however, not all patients with diabetes and peripheral nerve disease have a peripheral neuropathy caused by diabetes. Several (although not all) studies have drawn attention to the presence of other potential causes of a neuropathy in individuals with diabetes; 10% to 50% of individuals with diabetes may have an additional potential cause of a peripheral neuropathy and some may have more than one cause. Neurotoxic medications, alcohol abuse, vitamin B(12) deficiency, renal disease, chronic inflammatory demyelinating neuropathy, inherited neuropathy, and vasculitis are the most common additional potential causes of a peripheral neuropathy in these series. The most common disorders in the differential diagnosis of a generalized diabetic peripheral neuropathy are discussed in this article. Prospective studies to investigate the prevalence of other disorders that might be responsible for a peripheral neuropathy in individuals with diabetes are warranted.
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PMID:Not all neuropathy in diabetes is of diabetic etiology: differential diagnosis of diabetic neuropathy. 1995 86


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