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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic neuropathy is a disease of peripheral nerves, characterized by axonal atrophy and degeneration that might be preceded by a marked impairment of axonal transport and by a reduced conduction velocity. Sensory nerves are particularly susceptible to diabetes. In the present report it is shown that experimental diabetes in rats causes a significant reduction of the content of the pain-related neuropeptide substance P in sciatic nerve and lumbar spinal cord. Such a loss of substance P is fully prevented by acetyl-L-carnitine treatment. The neuroprotective pharmacological effect is selective and takes place without significant changes of hyperglycaemia and without modifications of the reduced rate of body growth typical of diabetic animals.
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PMID:Acetyl-L-carnitine prevents substance P loss in the sciatic nerve and lumbar spinal cord of diabetic animals. 128 99

Diabetic neuropathy may have a metabolic or an ischemic origin, and the pattern of nerve damage varies by cause. Treatment should address the underlying cause. Patient reassurance, relaxation techniques, glucose control, use of tricyclic antidepressants or anticonvulsants, and surgical decompression for entrapment neuropathy are currently the mainstays of treatment. Physicians must reassure these patients that neuropathic pain is temporary.
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PMID:Diabetic neuropathy. Helping patients cope with their pain. 168 27

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 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 with reduced sensitivity to pain and mechanical overloading of the joints, associated with frequently disturbed circulation in the lower extremities, are the etiopathogenetic factors of diabetic osteoarthropathy (synonyms: neuroarthropathia diabetica, Charcot joint). In the first stage there is osteonecrotic destruction of bone and cartilage. Clinically, an insidious, painless, noninflammatory hydroarthrosis with massive swelling of the soft tissues is typical. Subsequently, in stage II, irregular transformation of the bone due to multiple resorptive processes occurs. In the third stage this transformation process stabilizes and the bone ends become more pointed and more sclerotic (resembling a licked candy stick). For mechanical reasons, the tarsometatarsal and metatarsophalangeal joints and the metatarsals are primarily affected. However, destruction is also seen in Chopart's joint, the talus, the calcaneus, the ankle joint and the distal tibia. With regard to differential diagnosis, similar clinical pictures are seen in many neuropathic bony changes--tabes dorsalis, syringomyelia, myelodysplasias, congenital analgesia, congenital familial acroosteolysis. More difficult to differentiate are osteomyelitic foci, bone tuberculosis, and malignant bone tumors involving bone destruction.
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PMID:[Diabetic osteoarthropathy. Course and differential diagnosis]. 340 3

Diabetic neuropathy results from progressive nerve fibre damage with blunted nerve regeneration and repair and may be complicated by nerve hyperexcitability resulting in pain. The naturally occurring amino acid taurine functions as an osmolyte, inhibitory neurotransmitter, and modulator of pain perception. It is also known to have neurotrophic actions. The compatible osmolyte hypothesis proposes that levels of intracellular organic osmolytes including taurine and myo-inositol, respond co-ordinately in response to changes in intracellular sorbitol or external osmolality to maintain the intracellular milieu. We hypothesize that glucose-induced sorbitol accumulation in diabetes mellitus will result in taurine depletion in peripheral nerve which may potentially impair nerve regeneration and precipitate neuronal hyperexcitability and pain. This study explored the relationships of taurine, myo-inositol and sorbitol in the rat nerve and their effects on nerve conduction velocity. Osmolyte levels and nerve conduction velocity were determined in sciatic nerve from non-diabetic and streptozotocin-induced diabetic rats, with or without dietary taurine or myo-inositol supplementation. Taurine levels decreased by 31% (p < 0.01) and myo-inositol decreased by 37% (p < 0.05) in diabetic nerve as sorbitol accumulated. Taurine supplementation of diabetic animals did not affect nerve conduction velocity but further reduced nerve myo-inositol levels. Prevention of sorbitol accumulation with the aldose reductase inhibitor sorbinil increased nerve taurine levels by 22% (p < 0.05) when compared with untreated diabetic animals. Thus, we have demonstrated an interdependence of organic osmolytes within the nerve. Abnormal accumulation of one osmolyte results in reciprocal depletion of others. Diabetic neuropathy may be an example of maladaptive osmoregulation, nerve damage and instability being aggravated by taurine depletion.
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PMID:Osmotically-induced nerve taurine depletion and the compatible osmolyte hypothesis in experimental diabetic neuropathy in the rat. 835 77

Diabetic neuropathy is the most frequent complication of diabetes and the leading cause of polyneuropathy in the Western world. A distal symmetric predominantly sensory polyneuropathy is the most common of the diverse neuropathies that occur secondary to diabetes. Pain is often the most bothersome and difficult to treat symptom of diabetic neuropathy. Autonomic neuropathy is a frequent feature of diabetic neuropathy and the source of many significant problems including postural hypotension, gastroparesis, diarrhea, constipation, neurogenic bladder, and male impotence. Physicians need to be familiar with the multiple, less common forms of diabetic neuropathy, as these often mimic other medical or neurologic conditions. The cause of diabetic neuropathy is not determined, but abundant evidence suggests that both metabolic and ischemic nerve injury are likely factors. These should not be considered mutually exclusive causes of diabetic neuropathy as both factors likely operate to different degrees to produce the clinical spectrum of neuropathies that are seen in diabetes. Although no effective treatment exists to cure diabetic neuropathy, improvement is possible with glycemic control and symptomatic therapy.
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PMID:Neuropathies associated with diabetes. 841 16

Diabetic neuropathy is a common complication in diabetes mellitus. Diabetic neuropathy is accompanied by alterations in axonal excitability, which can lead to either "positive" (paresthesia, dysesthesia, pain) and/or "negative" (hypesthesia, anesthesia) symptoms. The mechanisms underlying these alterations in axonal excitability are not well understood. Clinical tests reveal reduced nerve conduction velocity and axonal loss, but fail to explain nerve excitability. Many different factors have been suggested in relation to the pathophysiology of diabetic neuropathy. There are probably as many factors as there are different clinical pictures in diabetic neuropathy. Nevertheless, it seems that hyperglycemic hypoxia is mainly responsible for the electrophysiological changes seen in damaged diabetic nerves. This article summarizes experimental data indicating that a dysfunction of ion conductances, especially voltage-gated ion channels, could contribute to abnormalities in the generation and/or conduction of action potentials in diabetic neuropathy.
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PMID:The role of axonal ion conductances in diabetic neuropathy: a review. 973 52

Estimates of the prevalence of diabetic neuropathy range from 10% to 90% of the diabetic population, depending on the criteria used to define neuropathy. Diabetic neuropathy encompasses a wide range of abnormalities affecting both the peripheral and autonomic nervous systems and causes considerable injury and death. Neurologic complications occur equally in type 1 and type 2 diabetes mellitus, as well as various forms of acquired diabetes. In this overview, we present and discuss the most recent approaches to the treatment of the common forms of diabetic neuropathy, including distal symmetric, proximal motor, and autonomic neuropathy. We also provide the reader with algorithms for recognition and management of common pain and entrapment syndromes, and a global approach to recognition of syndromes requiring specialized treatments based upon our improved understanding of their causes.
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PMID:Diagnosis and management of diabetic neuropathy. 1033 35

Diabetic neuropathy is common in patients with diabetes mellitus, and 7.5% of diabetics experience pain from diabetic neuropathy. Complications of diabetes mellitus are more common where control of the disease is not optimal. By improving the control of the disease, both the neuropathy and the pain it can produce may be improved. The pain of diabetic neuropathy can frequently be controlled using analgesics, antidepressants, anticonvulsants, topical capsaicin, and neuromodulation, either alone or in any combination.
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PMID:Treatment options in painful diabetic neuropathy. 1081 90


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