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

In the experimental rat model of diabetes a slowing of nerve conduction velocity and a resistance to ischemic conduction failure have been found as an indication of polyneuropathy. The same electrophysiological abnormalities have been demonstrated in a model in which healthy rats are kept under hypoxic conditions (10% O2) for a 10-week period. Two factors are held responsible for the development of diabetic polyneuropathy: metabolic deterioration and hypoxia. However, until now the relative roles of metabolic deterioration and hypoxia in the development of polyneuropathy have not been settled. To test both explanations further with more sophisticated electrophysiological techniques, the H-reflex (motor and sensory NVC) and the stimulated SF-EMG (measures terminal nerve branch and neuromuscular transmission) were measured in 3 groups of 10 rats, a healthy control group, a diabetic group, and a hypoxic group, every 5 weeks, for 6 months. In the control rats an age-related increase in motor and sensory conduction velocity was found, whereas in the diabetic rats as well as in the hypoxic rats a marked decrease in sensory and a slight decrease in motor nerve conduction velocity was observed. The jitter measured in the stimulated SF-EMG was significantly increased in both the diabetic and the hypoxic group. The results of the present study support the possible role of hypoxia, in addition to metabolic factors, in the development of experimental diabetic neuropathy.
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PMID:Hypoxic neuropathy versus diabetic neuropathy. An electrophysiological study in rats. 150 76

The effect of the alpha-glucosidase inhibitor acarbose on postprandial hyperglycaemia was explored in the spontaneously diabetic BB/W-rat. Acarbose-treatment (5 mg.kg body weight-1.day-1) of diabetic BB/W-rats maintained on small doses of insulin, was associated with a 40% reduction in the 24-h glucose area compared to non-treated diabetic rats. Over a 4 month treatment period this reduction in cumulative hyperglycaemia resulted in a complete prevention of autonomic polyneuropathy as indicated by R-BAR values. The development of somatic polyneuropathy in the BB/W-rat was significantly attenuated by acarbose treatment with a partial prevention of the characteristic nerve conduction velocity slowing during the first 3 months of diabetes, but no longer at 4 months. Characteristic structural abnormalities associated with diabetes in this model, such as axonal atrophy and axo-glial dysjunction, were significantly but only partially prevented in rats treated with acarbose for a diabetes duration of 4 months. These data suggest that postprandial lowering of hyperglycaemia resulting in a decrease in cumulative hyperglycaemia retards the development of diabetic polyneuropathies in the BB/W-rat.
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PMID:Long-term suppression of postprandial hyperglycaemia with acarbose retards the development of neuropathies in the BB/W-rat. 151 60

Tolrestat is an aldose reductase inhibitor that is undergoing extensive clinical investigation for the treatment of diabetic complications including polyneuropathy. As part of a larger European trial, we report here the results from a single clinical center on the efficacy of tolrestat in patients with confirmed diabetic neuropathy. The trial was conducted in two phases: a 6-month double-blind, placebo-controlled phase, and a 6-month open-label phase in which most patients were treated with tolrestat. Following the double-blind phase, motor and sensory nerve conduction velocity had significantly deteriorated in the placebo group, which did not occur during treatment with tolrestat. Deterioration of vibration threshold also occurred during placebo treatment and did not occur with tolrestat. During the open-label phase, motor nerve condition velocity and vibration threshold improved with tolrestat. Moreover, the deterioration of motor nerve conduction velocity and vibration threshold that had occurred in patients initially treated with placebo, was stopped during open-label treatment with tolrestat.
J Diabetes Complications
PMID:Long-term effects of tolrestat on symptomatic diabetic sensory polyneuropathy. 156 58

Rational treatment of diabetic polyneuropathy depends upon establishing its cause, which is at present unknown. A number of animal models of diabetes have been examined and although abnormalities are detectable in the peripheral nervous system they do not duplicate the degenerative neuropathy encountered in the human. The relevance of these abnormalities is therefore uncertain, although they may reflect the earlier changes in man. For human neuropathy, it is likely that vascular lesions or an abnormal susceptibility to mechanical injury are responsible for focal neuropathies. The evidence that ischaemia and hypoxia are responsible for the diffuse sensory neuropathy and autonomic polyneuropathy is still equivocal and it is often difficult to establish whether the vascular changes are primary or secondary. Metabolic explanations, such as sorbitol accumulation in nerve, have not so far been adequately validated by responses to treatment. The manifestations of diabetic neuropathy are complex and a single explanation should not be sought.
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PMID:Diabetic neuropathy: models, mechanisms and mayhem. 156 4

Height may increase the risk of diabetic polyneuropathy, but previous studies are inconclusive. Our purposes were to further examine the hypothesis that height (HT) is an independent risk factor for diabetic polyneuropathy and to determine which electrophysiologic measures are influenced by HT in diabetic subjects. We studied 170 Japanese American men (ages 43-73 years, mean 61) including: 69 diabetic men (mean HT 166 cm), 54 normal men (mean HT 167 cm), and 47 men with impaired glucose tolerance (IGT) (mean HT 164 cm), measuring 28 nerve conduction study (NCS) parameters. We used data from normal men in developing regression models to adjust NCS parameters for HT, age, and temperature. Factor analysis was employed to reduce the 28 NCS parameters to five physiologically meaningful factors, one of which, a factor representing median and peroneal sensory amplitudes, was significantly correlated with HT (r = -0.38, P = 0.0011) in diabetic men; taller subjects having smaller sensory nerve amplitudes. No significant correlation was found between this factor and body mass index. This factor had no correlation with HT in normal or IGT men. Our data do not confirm previous reports of associations between HT and slowed motor conduction velocities in diabetic subjects. This study does, however, support the hypothesis that HT is an independent risk factor for sensory polyneuropathy in diabetic subjects.
Diabetes Res Clin Pract 1992 May
PMID:Height is an independent risk factor for neuropathy in diabetic men. 160 Aug 57

Eighteen patients with long-standing insulin-dependent (type 1) diabetes mellitus and polyneuropathy were studied after combined pancreatic and renal transplantation. Repeated tests were performed on peripheral nerve function (electroneurography) and on autonomic function (R-R test) 6 mo and 1, 2, and 4 yr after the transplantation. Eighteen diabetic patients with only a kidney graft served as controls. After initial improvement of nerve conduction in both groups, probably caused by the elimination of uremia, further improvement was seen only in the euglycemic pancreas-graft recipients. Improvement of autonomic (parasympathetic) function was slight after 48 mo and was similar in both groups.
Diabetes 1992 Aug
PMID:Improvement of nerve conduction in diabetic neuropathy. A follow-up study 4 yr after combined pancreatic and renal transplantation. 162 68

The spontaneously diabetic BB/W-rat has emerged as an important model system for somatic and autonomic diabetic polyneuropathy. In this study we examined visual evoked potentials and the presence of morphometric and structural changes in the optic nerve and the retinal ganglion cells and their afferent axons contained in the retinal nerve fibre layer. A six-month duration of diabetes mellitus was associated with significant increases in the latencies of the visual evoked potentials. The latency of the first positive potential showed a 44% increase, and that of the first negative potential was prolonged by 41%. No significant changes were demonstrated at any of the amplitudes. In the optic nerve mean myelinated fibre size was significantly reduced to 82% of control values, which was accounted for by a significant reduction in axonal size. Axo-glial dysjunction, a prominent structural defect of diabetic somato-sensory neuropathy in both man and diabetic rodents, was non-significantly increased in the optic nerve. In diabetic animals retinal ganglion cells displayed dystrophic changes. No such changes were observed in age- and sex-matched control animals. Proximal axons of the retinal nerve fibre layer showed an increase in dystrophic axons in diabetic BB/W-rats. Morphometric analysis of optic nerve capillaries revealed no abnormalities except for basement membrane thickening. The present data suggest that the diabetic BB/W-rat develops a central sensory neuropathy, characterized functionally by prolonged latencies of the visual evoked potentials and structurally by an axonopathy of optic nerve fibres.
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PMID:Impaired visual evoked potential and primary axonopathy of the optic nerve in the diabetic BB/W-rat. 164 37

Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic patients share many clinical and biochemical characteristics. However, sural nerve biopsies from patients with advanced and chronic neuropathy show ultrastructural differences between these two groups. We investigated whether at a subclinical stage of the illness, when Type 1 and Type 2 diabetic patients are clinically uniform and the histopathological nerve alterations are not advanced, comparison between the two diabetes groups might show differences in nerve fibre involvement related to the different pathogeneses of the neuropathies. A total of 88 diabetic patients (52 Type 1 and 36 Type 2), with a subclinical form of polyneuropathy were selected. The clinical neurophysiological examination consisted of motor and sensory nerve conduction studies, Hoffmann (H)-reflex, single fibre electromyography and static as well as dynamic pupillometry. With regard to clinical neurophysiological abnormalities, the severity of the polyneuropathy appeared to be equal in both groups. Despite the absence of clinical symptoms the neurophysiological abnormalities were pronounced and it was impossible to differentiate Type 1 diabetic patients from Type 2 diabetic patients on a clinical neurophysiology basis when correcting for differences in age, height, and duration of illness. In the Type 1 diabetic group as well as in the Type 2 diabetic group the autonomic nerve fibres and nerves in the legs were more frequently affected than the thick myelinated nerves in the arms. These findings do not support the assumption that there is a difference in the manifestation of polyneuropathy between Type 1 and Type 2 diabetic patients.
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PMID:Subclinical diabetic neuropathy: similarities between electrophysiological results of patients with type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetes mellitus. 147 23

The radionuclide method was used to examine transport function of the esophagus in 24 patients suffering from diabetes mellitus and symmetric distal polyneuropathy. 99Tc-sulfocolloid was employed as a radiopharmaceutical agent. Radioactivity movement was visualized by means of a gamma chamber. In 9 patients (37.5%), measurements were made of the prolonged transit time for the whole esophagus as well as the prolonged transit time for the interior, median and upper third of the esophagus. The same patients demonstrated a delay of the rate of evacuation of the entire esophagus and respective parts thereof. The radionuclide method described is rapid and noninvasive. It may be included into the diagnostic complex for early identification of vegetative disorders in patients suffering from diabetic polyneuropathy.
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PMID:[A radionuclide study of esophageal motility disorders in patients with diabetic polyneuropathy]. 164 40

Radionuclide method was used to examine transport function of the esophagus in 24 patients with diabetes mellitus and symmetric distal polyneuropathy. 99mTc-+sulfur colloid was employed as a radiopharmaceutical agent. The movement of radioactivity was elucidated visually with the aid of a gamma-chamber. In 9 patients, measurements were made of the prolonged transit time of the whole esophagus as well as prolonged transit time for the lower, median and upper third of the esophagus. The same patients manifested deceleration of the evacuation of the entire esophagus and respective parts thereof. That method can be included into the diagnostic complex intended for early diagnosis of vegetative disorders in patients with diabetic polyneuropathy and for evaluating the intensity of autonomous neuropathy.
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PMID:[Radionuclide study of disorders of esophageal motility in patients with diabetic polyneuropathy]. 165 92


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