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Your search term(s) "diabetic neuropathy" returned 132 results.

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Microangiopathy, Diabetes, and the Peripheral Nervous System. IN: Veves, A.; Malik, R.A., eds. Diabetic Neuropathy: Clinical Management. 2nd ed. Totowa, NJ: Humana Press. 2007. pp 207-230.

This chapter on microangiopathy, diabetes, and the peripheral nervous system (PNS) is from a comprehensive textbook that provides general practitioners details on the latest techniques for the clinical management of diabetic neuropathy. The author explores how disease of the small nerve and ganglia microvessels, known as microangiopathy, relates to the development of diabetic peripheral neuropathy (DPN). Topics include the blood flow of nerve trunks and ganglia, acute nerve ischemia, experimental studies in this area, regeneration and microcirculation, and human studies. The author concludes that there is a relationship between microangiopathy and diabetic polyneuropathy that goes beyond direct cause and effect. The author hypothesizes that the disease of diabetes targets neural structures and vessels concurrently. 9 figures. 152 references.

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Microvascular and Macrovascular Complications. Pediatric Diabetes. 8: 163-170. 2007.

This article presents information from the International Society for Pediatric and Adolescent Diabetes (ISPAD) Clinical Practice Consensus Guidelines (2006–2007) on microvascular and macrovascular complications. The long-term vascular complications and outcomes include visual impairment and blindness due to diabetic retinopathy; renal failure and hypertension due to diabetic nephropathy; pain, muscle weakness and autonomic dysfunction due to diabetic neuropathy; and cardiac disease, peripheral vascular disease, and stroke due to macrovascular disease. This article discusses interventional studies of intensive glucose control, other risk factors for the development of complications, diabetic retinopathy, diabetic nephropathy, diabetic neuropathy, and macrovascular disease. In each of the sections discussing a particular complication, the authors address screening for and prevention of that complication, assessment, progression, and treatment options. 3 tables. 71 references.

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Neuronal and Schwann Cell Death in Diabetic Neuropathy. IN: Veves, A.; Malik, R.A., eds. Diabetic Neuropathy: Clinical Management. 2nd ed. Totowa, NJ: Humana Press. 2007. pp 113-132.

This chapter on neuronal and Schwann cell death in diabetic neuropathy is from a comprehensive textbook that provides general practitioners details on the latest techniques for the clinical management of diabetic neuropathy. The authors note that the evidence supports the idea that programmed cell death (PCD) occurs in cells of the peripheral nervous system (PNS) in the presence of diabetes, elevated glucose levels, or insulin deprivation. Most cells show evidence of mitochondrial damage and some features of apoptosis. PCD has mainly been shown in cell culture and animal models of diabetes, although there is also morphological evidence of apoptosis in Schwann cells from human sural nerve. The authors hypothesize that even nonapoptotic neurons show impaired metabolic function and protein synthesis, well before apoptosis occurs. They consider the role of diabetes-induced generation of reactive oxygen species and dysregulation of mitochondrial function. Antioxidants and certain regulators of the inner mitochondrial membrane potential, including growth factors, may prevent apoptosis in the PNS. More research on the events leading to apoptosis in the PNS would contribute to the understanding of how to intervene or prevent diabetic neuropathy. 3 figures. 115 references.

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Other Therapeutic Agents for the Treatment of Diabetic Neuropathy. IN: Veves, A.; Malik, R.A., eds. Diabetic Neuropathy: Clinical Management. 2nd ed. Totowa, NJ: Humana Press. 2007. pp 321-338.

This chapter on therapeutic agents for the treatment of diabetic neuropathy is from a comprehensive textbook that provides general practitioners details on the latest techniques for the clinical management of this diabetes complication. The authors emphasize that the pathogenesis of diabetic neuropathy is complex, and it is important to understand the underlying pathology leading to the complication to best tailor treatment for each individual patient. Drugs such as antioxidants, PKC inhibitors, and nerve growth factors can have effects on multiple systems that are compromised in diabetic neuropathy, yet even those may not be enough in and of themselves to completely restore neurological function. Specific drugs discussed include alpha-lipoic acid; tocopheral, or vitamin E; aminoguanidine; protein kinase C inhibitors; vascular endothelial growth factor; vasodilators; human intravenous immunoglobulin; neurotrophins; nerve growth factors; and topiramate. The authors conclude that combination therapy may prove to be the best long-term approach. Additional studies are needed to determine the relative roles of metabolic dysfunction, microvascular insufficiency, and autoimmunity in the diabetic neuropathy patient population. 3 figures. 1 table. 118 references.

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Painful Diabetes Neuropathy: A Management- Centered Review. Clinical Diabetes. 25(1): 6-15. Winter 2007.

This article presents a review of the epidemiology, risk factors, prevention, diagnosis, and management of painful diabetic neuropathy (PDN), focusing on the agents used in the treatment of PDN. The authors report on the effectiveness, dose, and duration for an appropriate therapeutic trial, contraindications, adverse effects, and monitoring parameters of each agent used in the treatment of PDN. Agents discussed include tricyclic antidepressants (TCAs), other antidepressants including duloxetine, antiepileptics including carbamazepine and pregabalin, and others, including capsaicin cream, tramadol, and mexilitine. The authors caution that the pain associated with PDN is difficult to treat and may not completely resolve with any of the agents discussed in this article. Combination therapies, especially those that combine centrally acting agents with peripherally acting agents, may provide increased pain relief but remain largely unstudied to date. Two case studies are used to illustrate the patient management strategies discussed. 2 tables. 82 references.

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Pathogenesis of Human Diabetic Neuropathy. IN: Veves, A.; Malik, R.A., eds. Diabetic Neuropathy: Clinical Management. 2nd ed. Totowa, NJ: Humana Press. 2007. pp 231-242.

This chapter on the pathogenesis of human diabetic neuropathy is from a comprehensive textbook that provides general practitioners details on the latest techniques for the clinical management of diabetic neuropathy. The authors consider whether hyperglycemia-mediated nerve damage may begin extremely early, even prior to overt diabetes as evidenced by several recent studies in patients with impaired glucose tolerance. Glycation is widespread and may induce a range of structural and functional changes. Glycation inhibitors are being actively developed. Treatment with ACE inhibitors has shown some benefit in both large and small vessel disease in diabetic neuropathy. Growth factors may be important in maintaining both the vascular and neuronal phenotype. 3 figures. 89 references.

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Pathophysiology of Neuropathic Pain. IN: Veves, A.; Malik, R.A., eds. Diabetic Neuropathy: Clinical Management. 2nd ed. Totowa, NJ: Humana Press. 2007. pp 339-350.

This chapter on the pathophysiology of neuropathic pain is from a comprehensive textbook that provides general practitioners details on the latest techniques for the clinical management of diabetic neuropathy. The author discusses chronic pain, noting that cerebral responses to pain are complex and dynamic in nature and can involve the entire pain-related peripheral and central nervous system. Topics include changes in the brain as a consequent of peripheral neuronal injury, functional brain responses to acute laboratory pain, chronic pain versus acute pain, and pain models. The author briefly discusses neuropathic pain research, an evolving field of study and clinical care. 1 figure. 60 references.

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Postural Hypotension and Anhidrosis. IN: Veves, A.; Malik, R.A., eds. Diabetic Neuropathy: Clinical Management. 2nd ed. Totowa, NJ: Humana Press. 2007. pp 413-432.

This chapter on postural hypotension and anhidrosis is from a comprehensive textbook that provides general practitioners details on the latest techniques for the clinical management of diabetic neuropathy. The author notes that orthostatic hypotension (OH) occurs in 10 to 20 percent of people with diabetes, presenting as lightheadedness or weakness, or fainting. The severity of symptoms correlate with autonomic deficits. Treatment of OH includes nonpharmacological and pharmacological therapy, including patient education, management of salt and fluids, sleeping with the head of the bed elevated, compression garments, physical counter maneuvers, midodrine, and pyridostigmine. Specific strategies for managing OH in the hospital, on awakening, after a meal, and at night are provided. The second section of the chapter considers sudomotor disorders in diabetes, which often manifest as distal anhidrosis––lack of sweating––followed by regional, multifocal, and other patterns of sweat loss. Sudomotor symptoms include regional hyperhydrosis and heat intolerance. 1 figure. 3 tables. 89 references.

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Punch Skin Biopsy in Diabetic Neuropathy. IN: Veves, A.; Malik, R.A., eds. Diabetic Neuropathy: Clinical Management. 2nd ed. Totowa, NJ: Humana Press. 2007. pp 293-312.

This chapter on the use of punch skin biopsy in diabetic neuropathy is from a comprehensive textbook that provides general practitioners details on the latest techniques for the clinical management of this diabetes complication. The author describes the measurement of unmyelinated C and A delta nociceptors through punch skin biopsy as an important development in this area over the past decade. Clinically, the punch biopsy technique is most often used to define a length-dependent peripheral neuropathy, but it can also be used to follow patients longitudinally over time. Epidermal nerve fibers are often lost early in diabetes or even in impaired glucose tolerance and can be the only objective measure of neuropathy in these patients. The author concludes that the superficial nature of epidermal nerve fibers allows repeated sampling of these nerves in a relatively noninvasive fashion, permitting earlier diagnosis of neuropathy and a way to measure changes over time or in response to treatment. 7 figures. 44 references.

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Spinal Cord: Structure and Function in Diabetes. IN: Veves, A.; Malik, R.A., eds. Diabetic Neuropathy: Clinical Management. 2nd ed. Totowa, NJ: Humana Press. 2007. pp 165-185.

This chapter on the structure and function of the spinal cord in diabetes is from a comprehensive textbook that provides general practitioners details on the latest techniques for the clinical management of diabetic neuropathy. The authors provide an overview of the anatomy of the spinal cord and its associated structures and review the published literature describing evidence for structural damage to the spinal cord reported in both humans with diabetes and in animal models of the disease. The authors note that the mechanisms that lead from hyperglycemia to disruption of spinal cord structure and function are only beginning to be explored. The spinal cord is not protected from diabetes-induced injury; thus, both structural and functional damage is discernable in diabetes subjects. The authors conclude that because the spinal cord is the first site of integration of sensory input from the periphery and the last site of descending control of sensory and motor systems, disruption of spinal cord function has the capacity to impede appropriate central nervous system (CNS) control systems and contribute to peripheral neuropathy. 3 figures. 1 table. 86 references.

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