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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic neuropathy contributes to the long-term complications of diabetes mellitus. Its pathogenesis is still unknown although a host of abnormalities in peripheral nerves in human diabetics and animal models has been discovered. This article emphasizes the current metabolic hypotheses: increased polyol pathway, decreased myoinositol nerve content; altered phospholipid metabolism, decreased Na+/K+ ATPase activity and non-enzymatic glycosylation of proteins. Future perspectives relevant to animal and clinical research and new therapeutic aspects are also discussed.
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PMID:Current aspects of research on the pathogenesis of diabetic neuropathy. 302 79

Diabetic neuropathy is a common complication of diabetes mellitus with significant morbidity and mortality. Hyperglycemia with its secondary metabolic, vascular, and enzymatic consequences is most likely to be the predominant cause. The clinical manifestations includes a wide range of somatic and autonomic syndromes. Painful diabetic neuropathy may require symptomatic treatment. The precise role of therapies such as continuous subcutaneous insulin therapy and aldose reductase inhibitors remains to be clarified.
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PMID:Peripheral diabetic neuropathy. 305 62

Diabetic neuropathy, long-recognized as an important but complex and poorly understood clinical complication of diabetes, is finally yielding to more than a decade of intense clinical and laboratory investigation. At least one basic biochemical mechanism involving sorbitol and MI metabolism, phosphoinositides, protein kinase C, and the (Na,K)-ATPase has been identified that can rationally account for the neurotoxicity of glucose. This biochemical sequence has been examined in some detail in vitro, but some of its elements, such as the link between abnormal sorbitol and MI metabolism, and between protein kinase C and the (Na,K)-ATPase, remain the subject of ongoing investigation. Through its effect on the (Na,K)-ATPase, this metabolic sequence can explain both the rapidly-reversible functional impairment and the early structural lesions of nerve fibers, such as paranodal swelling in acute diabetes. Extrapolation of early paranodal swelling to the more advanced stages of nerve fiber damage remains somewhat speculative, although axo-glial dysjunction is a likely intermediate step. Impaired axonal transport or microvascular dysfunction may be additional contributing factors, possibly also related to abnormal sorbitol and MI metabolism. Blunted phosphoinositide-mediated signal transduction could potentially explain a putative insensitivity to neurotrophic factors and a diminished regenerative response in diabetic neuropathy. Human morphometric studies and ARI trials support the relevance of these pathogenetic processes to human diabetic neuropathy, and suggest that specific metabolic therapy with agents such as ARIs hold promise as important new elements in the treatment and possibly prevention of diabetic neuropathy.
Diabetes Metab Rev 1988 May
PMID:Pathogenesis and prevention of diabetic neuropathy. 329 48

Diabetic neuropathy is a common complication of diabetes that may be associated both with considerable morbidity (painful polyneuropathy, neuropathic ulceration) and mortality (autonomic neuropathy). The epidemiology and natural history of diabetic neuropathy is clouded with uncertainty, largely due to confusion in the definition and measurement of this disorder. We have reviewed a variety of the clinical manifestations associated with somatic and autonomic neuropathy and discussed current views related to the management of the different abnormalities. Although unproven, the best evidence suggests that near normal control of blood glucose in the early years following onset of diabetes may help delay the development of clinically significant nerve impairment. Intensive therapy to achieve normalization of blood glucose may also lead to reversibility of early diabetic neuropathy, but again this is unproven. Our ability to manage successfully the many different manifestations of diabetic neuropathy depends ultimately on our success in uncovering the pathogenic processes underlying this disorder. The recent resurgence of interest in the vascular hypothesis, for example, has opened up new avenues of investigation for therapeutic intervention. Paralleling our increased understanding of the pathogenesis of diabetic neuropathy, there must be refinements in our ability to measure quantitatively the different types of defects that occur in this disorder. These tests must be validated and standardized to allow comparability between studies and more meaningful interpretation of study results.
Diabetes Metab Rev 1988 May
PMID:Clinical aspects of diabetic neuropathies. 329 49

Diabetic neuropathy was induced in male inbred rats by a single injection of streptozotocin. The diabetic state of the animals was prevented from detoriation by daily injections of small amounts of insulin. Before as well as 4 and 8 weeks after induction of diabetes compound action potentials evoked by electrical stimulation were repeatedly recorded from muscle and tail nerves of the same 55 animals. The motor nerve as well as the maximal proximal and distal nerve conduction velocity were determined. The neuropathy was established by comparing the increase in conduction velocity in a nondiabetic control group with the marked decrease in a group of diabetic animals receiving daily placebo injections. In a second group of diabetic animals daily injections of gangliosides (Cronassial) significantly counteracted the slowing of nerve conduction in comparison to that observed in the diabetic placebo group during the development of the neuropathy. This effect is discussed in terms of an increase of Na+-K+-ATPase or neuronal sprouting, possibly induced by the daily ganglioside application, and its usefulness in ameliorating human diabetic neuropathy.
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PMID:Effect of gangliosides on nerve conduction velocity during diabetic neuropathy in the rat. 330 67

Diabetic neuropathy includes a heterogenous group of neuropathic syndromes associated with diabetes mellitus. One form of diabetic neuropathy is distal symmetric polyneuropathy, which is characterized at a late stage by intractable pain. This pain is generally refractory to present modalities of therapy except for narcotics. Pentoxifylline offers a new approach to therapy, reducing the blood viscosity and improving perfusion of ischemic microcirculation. A case report will be presented of intractable painful peripheral neuropathy responding dramatically to pentoxifylline therapy.
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PMID:Treatment of diabetic neuropathy with pentoxifylline: case report. 336 3

Diabetic neuropathy is probably the most common and one of the most disabling complications of diabetes mellitus. Although several possible pathogenetic mechanisms for this complication have been suggested, they cannot easily be tested in man. Therefore animal models with induced or spontaneous onset of diabetes mellitus have been used. The spontaneously diabetic BB-rat may provide a valuable model, since it displays both metabolic, functional and structural abnormalities of peripheral nerve similar to those present in humans. Based on systematic studies of these abnormalities in peripheral nerve in this model, inter-relationships between diabetic dysmetabolism, dysfunction and structural changes are starting to emerge. These findings are reviewed and a scheme of proven and proposed correlations which now can be tested in this animal model is presented.
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PMID:Can the BB-rat help to unravel diabetic neuropathy? 405 70

Diabetic neuropathy is defined, and theories of its pathogenesis are reviewed. Recent studies designed to investigate the influence of plasma glucose on nerve function in noninsulin-dependent diabetic patients are summarized. Motor nerve conduction velocities in the median and peroneal nerves were measured using a double-stimulus technique, and sensory conduction velocity was measured by conventional methods before and after therapy with oral agents or insulin. The degree of hyperglycemia was assessed by measurement of fasting plasma glucose and glycosylated hemoglobin concentrations. The degree of slowing in motor nerve conduction velocity in untreated patients was found to correlate with the fasting plasma glucose and glycosylated hemoglobin concentrations, but sensory nerve function, although abnormal, did not show such correlation. Reduction of hyperglycemia was associated with improvement in motor nerve conduction velocity in the peroneal and median motor nerves of these patients, but sensory nerve conduction velocity showed no such improvement. Improvement in median motor nerve conduction velocity was directly related to the degree of reduction in fasting plasma glucose concentration. These findings suggest that metabolic factors related to hyperglycemia are important in the impaired motor nerve function seen in noninsulin-dependent patients with maturity-onset diabetes.
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PMID:Diabetic neuropathy and plasma glucose control. 745 87

One of the hallmarks of diabetes mellitus is its propensity to cause neurological complications. Diabetes is an independent risk factor of stroke. Diabetic neuropathy represents the most common type of peripheral neuropathy in our country. Improved glucose control can improve nerve function and restoration of the euglycemic state appears to stop the progression of the neuropathy. Treatment strategy of painful neuropathy with tricyclic antidepressant, anticonvulsant, anesthesia agents and topical capsaicin is discussed.
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PMID:[Neurological complications of diabetes]. 748 Dec 36

Diabetic neuropathy (DN) is chronic complication which occurs in 50% of long standing diabetes mellitus. DN is a consequence of hyperglycemia probably through the following mechanisms: a) activation of aldose-reductase, intracellular sorbitol accumulation and myoinositol depletion, reduced activity of Na+/K+ATPase, loss of Na+ channels and demyelination; b) proteins glycation; c) microangiopathy; the first mechanism being the best known and the most reliable. DN may be subclinical or clinical. The main clinical picture is a peripheral, bilateral, symmetric polyneuropathy with a "socks and gloves" sensory impairment, muscular weakness, hyporeflexia, plantar ulcers and arthropathy. Less frequent syndromes are proximal motor neuropathy and mononeuropathy of cranial nerves or thoraco-abdominal roots. Diagnosis is based on clinical data, and may be sustained on impaired nerve conduction velocity, abnormal evoked somatosensory potentials, or sural nerve biopsy. These methods are highly sensitive but unspecific. Etiopathogenic treatment is based on glycemic control and aldose reductase inhibitors. Improvement in clinical, electrophysiologic and histopathologic data have been obtained with the latter. Symptomatic treatment includes carbamazepin, phenytoin, tricyclic antidepressives and a phenotiazin. Mononeuropathies tend to complete recovery in less than 6 months. Polyneuropathy is thought to be irreversible and progressive; however, with excellent glycemic control or with aldose reductase inhibitors nerve damage may be stabilized or even reversed.
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PMID:[Diabetic neuropathy. Current concepts on etiopathogenesis, diagnosis, and treatment]. 755 46


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