PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Diabetic Neuropathies”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMedDate not supplied

The epidemiology of diabetic neuropathy. Diabetic Cardiovascular Autonomic Neuropathy Multicenter Study Group.

Although neuropathy has long been recognized as a complication of diabetes, the impact of this condition has not been adequately established. The prevalence of diabetic neuropathy is virtually unknown because the published studies differ considerably with regard to definition, method of assessment, and patient selection. Furthermore, the determination of prevalence has been hampered by the fact that there is no generally accepted classification of the variety of manifestations of diabetic neuropathy. The introduction of new sensitive diagnostic methods aids in the detection of less severe stages of neuropathy, as compared with clinically based assessment, and renders the disease more prevalent. The prevalence of diabetic neuropathy in the few reported population-based studies was approximately 30%. We have evaluated the prevalence of cardiovascular autonomic neuropathy in a group of approximately 1000 diabetic patients randomly included from 21 hospitals in Germany, Austria, and Switzerland. The results of this study and those of a prospective study on the natural history of neural dysfunction during the first 5 years after diagnosis of type 1 diabetes will be presented.

Adolescent↗
PubMed1992

Diabetic neuropathies.

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 caused by confusion in the definition and measurement of this disorder. We have reviewed various clinical manifestations associated with somatic and autonomic neuropathy, and we herein discuss current views related to the management of the various abnormalities. Although unproven, the best evidence suggests that near-normal control of blood glucose in the early years after diabetes onset may help delay the development of clinically significant nerve impairment. Intensive therapy to achieve normalization of blood glucose also may 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, refinements must be made 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 Mellitus↗
PubMed1992

Clinical observations and experiments in diabetic neuropathy.

Diabetic neuropathies form a group of diverse conditions, which can be distinguished between those which recover (acute painful neuropathies, radiculopathies, mononeuropathies) and those which progress (sensory and autonomic neuropathies). These two main groups can be distinguished in several ways: sensory and autonomic neuropathies are classic diabetic complications progressing gradually in patients with long-standing diabetes who often have other specific complications, while the reversible neuropathies do not have these features. The latter are characterised by their occurrence at any stage of diabetes, often at diagnosis, they may be precipitated on starting insulin treatment, and they are more common in men; they can occur at any age, though more often in older patients, and are unrelated to other diabetic complications. The two groups of neuropathies also show differences in nerve structural abnormalities and with regard to distinctive blood flow responses. The underlying mechanisms responsible for these very different forms of neuropathy remain speculative, but evidence for an immunological basis for the development of severe symptomatic autonomic neuropathy is presented.

Diabetic Neuropathies↗
PubMed1992

Hypoxic neuropathy versus diabetic neuropathy. An electrophysiological study in rats.

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.

Afferent Pathways↗
PubMed1976

[Doubtfullness of the diagnosis diabetic neuropathy].

The diabetic neuropathy is sufficiently to be defined neither from the point of view of diabetes nor from neurological findings. There are no diagnostic criteria appliable to the individual case. Therefore, the diagnosis diabetic neuropathy is to be valuated as exclusion diagnosis. It presumes above all a careful clarification of the neurological syndrome present taking into consideration all diseases of muscles, nerves and spinal cord which are of importance in differential diagnosis. Instead of issuing from the alternative diabetogenic or nondiabetogenic, the possibility of pathogenetic combinations should rather be taken into consideration. It seems to be suitable to avoid the name diabetic neuropathy in practice and to speak only of a neuropathy or polyneuropathy (which is possibly to be described more exactly) in diabetes.

Biopsy↗
PubMed1978

A quantitative electrophysiological study of uraemic neuropathy. Diabetic and renal neuropathies compared.

The numbers of functioning motor units and the parameters of the electrically evoked motor unit potentials in the extensor digitorum brevis muscles of 30 patients on chronic haemodialysis for renal failure were obtained using recently introduced quantitative electrophysiological techniques. Measurements of the distal motor latencies and motor nerve conduction velocities in the lateral popliteal nerves of the same patients are also presented. The results support the presence of a "dying back" type of neuropathy in uraemia, with a preferential involvement of the fastest conducting motor axons. Collateral reinnervation and compensatory increase in size of surviving motor units is relatively impaired in uraemic neuropathy in comparison with a similar study on diabetic neuropathy. The significance of paranodal and segmental demyelination in producing abnormalities of conduction velocity in these neuropathies is discussed.

Action Potentials↗
PubMed1992

The influence of indomethacin and guanethidine on experimental streptozotocin diabetic neuropathy.

In diabetic animals, reduced endoneurial perfusion and oxygen content have been linked to neuropathic abnormalities and might be amenable to pharmacological manipulation. In streptozotocin-induced diabetic rats, we studied the influence of guanethidine adrenergic sympathectomy, indomethacin treatment and a combined strategy on: serial in vivo motor and sensory conduction, resistance to ischemic conduction failure, in vitro myelinated and unmyelinated conduction, endoneurial perfusion and endoneurial oxygen tension. Unlike previous work diabetic animals had normal endoneurial perfusion but lower endoneurial oxygen tensions after six months of hyperglycemia. Guanethidine worsened sensory conduction despite lower microvascular resistance and an improvement in endoneurial oxygen tension. In contrast, indomethacin improved motor and sensory conduction but not oxygen tension. These studies do not support a linkage between conduction deficits and early endoneurial microangiopathy in experimental diabetes. Indomethacin, or related agents may offer a new therapeutic approach toward diabetic neuropathy through a mechanism independent of the endoneurial microvasculature.

Animals↗
PubMed1992

Potential use of glutathione for the prevention and treatment of diabetic neuropathy in the streptozotocin-induced diabetic rat.

It has been shown that parameters of oxidative stress are increased in experimental diabetic neuropathy. The glutathione redox system is one of the intracellular scavenger systems for neutralizing free oxygen radicals. In this investigation we studied the effect of glutathione-treatment on the development of diabetic neuropathy in streptozotocin-induced diabetic rats by measuring sensory and motor nerve conduction velocities. The total study period was 10 weeks. Four groups of rats were studied: Group 1 consisted of non-diabetic, age-matched control rats; Group 2, of diabetic rats treated with placebo from week 0 to 10; Group 3, of diabetic rats treated with 200 mg glutathione/kg body weight i.v. two times per week from weeks 0 to 10; and Group 4, of diabetic rats treated with placebo from weeks 0 to 4 and as Group 3 from weeks 4 to 10. The sensory and motor nerve conduction velocity of rats treated prophylactically with glutathione (Group 3) were significantly different from those of rats treated with placebo (Group 2) or with glutathione administered at a later time point (Group 4). Complete restoration of sensory and motor nerve conduction velocity was not reached. There was a significant improvement in motor nerve conduction velocity from weeks 4 to 6 (p less than 0.005), but not in sensory nerve conduction velocity in the delayed treatment group (Group 4). In conclusion, treatment with glutathione, a free radical scavenger, is partially effective in the prevention of diabetic neuropathy in streptozotocin-induced diabetic rats, but is of limited value when the neuropathy is already present.

Animals↗
PubMedDate not supplied

[Characteristics of development of diabetic neuropathy depending on sex of diabetic patients].

The authors present the results of clinico-neurological study on 3976 patients suffering from diabetes with the use of electrophysiological, biochemical and other methods. As revealed, the sex of diabetic patients, particularly at definite age periods produced a significant influence on the time of occurrence and the rate of development of various types of the central and peripheral neuropathy. Thus, at the age of under 30 years almost all the types of diabetic neuropathy originated earlier and developed more rapidly in women, and after the age of 50 years some of these types of neuropathies were more frequent and more pronounced in men. No significant differences in the incidence of many types of diabetic neuropathy were revealed at the age of from 30 to 50 years both in men and in women. The mentioned regularity was most distinctly traced in analysis of distal pelyneuropathy. A hypothesis is put forward on the causes inducing peculiarities of the diabetic neuropathy development depending on the sex factor.

Adolescent↗
PubMed1976

Diabetic neuropathy: clinical aspects.

The importance of diabetic neuropathy derives from its remarkable frequency and its clinical impact. In view of the varying underlying pathogenetic mechanisms and the resulting diversity of clinical representations, it becomes apparent that there are diabetic neuropathies, rather than a single entity of diabetic neuropathy. The scope of involvement is widespread with virtually every system at risk. Although peripheral neuropathy is by far the most common expression, visceral neuropathy is also highly significant. It may affect every part of the gastrointestinal tract, the genitourinary tract, and sexual function, as well as direct autonomic nerve pathology. Clearly, neuropathy in diabetes offers a specific and important diagnostic challenge to the clinician and plays a definitive role in differential diagnosis. The problem is heightened by the fact that any and all of the diabetic neuropathic syndromes may be the initial clinical manifestation of diabetes in the absence of covert manifestations of carbohydrate metabolic disorder. It is to be stressed that the diagnosis is more than an academic exercise, since each diabetic neuropathic syndrome carries with it some beneficial therapeutic modality to aid the patient.

Arm↗
PubMedDate not supplied

Hypothesis: low Na/K-ATPase activity in the red cell membrane, a potential marker of the predisposition to diabetic neuropathy.

OBJECTIVES: The development of diabetic complications does not depend entirely on diabetes duration and control. Predisposing and aggravating factors, either constitutional or environmental, seem to play a role. We have previously observed that polyneuropathy is more frequent, of earlier onset, and more severe among North African insulin-dependent diabetic patients than among Europeans matched for sex, duration and control of diabetes. The Na/K-ATPase activity displays sex and ethnic differences and a dysfunction of this enzyme is probably involved in the pathogenesis of diabetic neuropathy. We have therefore postulated that the predisposition of some diabetic patients to develop a polyneuropathy could be related to a low Na/K-ATPase activity. DESIGN: Red cell membrane Na/K-ATPase activity was studied in European men presenting with insulin-dependent diabetes mellitus for more than 15 years. 10 patients with neuropathy were matched to 10 patients void of neuropathy on duration of diabetes and HbA1c values. Thirteen healthy European men and 13 North African men born and living in France were also studied. RESULTS: Na/K-ATPase activity was lower in patients with neuropathy (200 +/- 31 vs 289 +/- 42 nmol Pi.mg protein-1.h-1 mean +/- SD; p less than 0.05). When compared to that of 13 European healthy men, Na/K-ATPase activity was lower in the whole group of diabetic patients but appeared to be in the normal range for patients without neuropathy and decreased in those with neuropathy. The 13 North African healthy men had lower values than the European healthy men (227 +/- 46 vs 298 +/- 60 nmol Pi.mg protein -1.h-1, p less than 0.05). CONCLUSION: Red cell membrane Na/K-ATPase activity is low in insulin dependent patients with neuropathy compared to those without neuropathy. This finding probably reflects a constitutional difference. This association could be explained if red cell and nerve membrane Na/K-ATPase abnormalities behave similarly according to glycaemic control in diabetic subjects. It is suggested that the predisposition to neuropathy of North African insulin-dependent diabetic patients may be related to lower Na/K-ATPase activity. A high level of activity of this enzyme may protect from diabetic neuropathy. This enzyme activity could be a marker of predisposition towards diabetic polyneuropathy.

Adult↗
PubMed1992

The use of gamma-linolenic acid in diabetic neuropathy.

EF4 is an entirely new approach to the management of diabetic neuropathy. EF4 (providing gamma-linolenic acid or gamolenic acid, GLA) has been shown to reverse existing diabetic neuropathy in trials in seven centres. Diabetic animals and humans have a reduced ability to convert dietary linoleic acid to GLA. GLA and its metabolites are required for normal neuronal structure and function and a normal microcirculation. The lack of GLA and its metabolites may play a major role in the development of the neuropathy. EF4 helps to correct the biochemical defects, restores levels of GLA metabolites towards normal and produces highly significant clinical and neurophysiological improvements in diabetic neuropathy.

Animals↗
PubMed1977

"Intrinsic" heart rate in diabetic neuropathy.

Changes of heart frequency have been studied in diabetic neuropathy by blocking autonomic innervation of the heart with atropine and propranolol (intrinsic rate). It was found that in diabetic neuropathy the initial heart rate was higher than in the controls and in non-neutropathic diabetics, but this higher frequency could not be increased any further by the administration of atropine and propranolol compared to the values registered in the other two groups.

Adolescent↗
PubMed1992

Exercise-induced conduction velocity increment: a marker of impaired peripheral nerve blood flow in diabetic neuropathy.

Severe microvascular disease exists at the stage of clinical diabetic neuropathy. A non-invasive test that will identify those diabetic subjects who will eventually develop neuropathy is essential for early intervention. Sural sensory conduction velocity was recorded (x3) in 12 non-neuropathic diabetic subjects, 15 diabetic subjects with established neuropathy and 16 age-matched normal control subjects, before and after exercise to 80% age/sex predicted maximum heart rate. Fixed sural electrodes were used. Subcutaneous temperature was recorded by a needle thermocouple placed near the sural nerve. Sural sensory conduction velocity increased significantly after exercise in normal subjects (p less than 0.01, mean increase 5.07 m/s) and non-neuropathic diabetic subjects (p less than 0.02, mean increase 3.99 m/s) but not in neuropathic subjects (mean increase 0.99 m/s). Subcutaneous temperature rose significantly in normal subjects (p less than 0.01, mean increase 2.07 degrees C) and non-neuropathic diabetic subjects (p less than 0.001, mean increase 2.52 degrees C) but not in neuropathic subjects (mean increase 0.15 degree C). However, sural sensory conduction velocity increased by 1.2 m.s-1.degree C-1 following direct warming of the limb in six neuropathic subjects which was comparable to that of normal and non-neuropathic subjects (1.49 and 1.48 m.s-1. degree C-1). The impairment of exercise conduction increment in diabetic neuropathy suggests impaired nerve blood flow in diabetic neuropathy.

Adult↗
PubMedDate not supplied

Diabetic neuropathy, A review of clinical manifestations.

Diabetic neuropathy in some form or other afflicts a majority of patients with diabetes mellitus. Neuropathic disturbance of sensory, motor or autonomic nerves may occur singly or in combination. Cranial nerve and other mononeuropathies generally resolve spontaneously. Autonomic neuropathy which can result in orthostatic hypotension, gastroparesis diabeticorum, nocturnal diarrhea, atonic bladder and impotence, although chronic, may wax and wane in clinical severity. Neuritis, disesthesias and painful sensory neuritis may resolve with good diabetic control; on occasion, diphenylhydantoin has been of therapeutic benefit.

Adolescent↗
PubMed1976

Subacute proximal diabetic neuropathy.

The results of clinical, electrophysiologic, and histologic studies in three patients with a type of diabetic peripheral neuropathy, subacute proximal diabetic neuropathy (diabetic amyotrophy), are presented. On the basis of our findings, we suggest that diabetic amyotrophy is a clinical and pathologic entity separate from mononeuritis multiplex. These patients have a generalized neuropathy, and it is postulated that disordered neuron-axonal metabolism forms the basis for the pathologic and clinical changes. Histochemical changes in the muscle biopsy showed type 1 predominance. We suggest that this phenomenon represents a conversion of surviving fibers of whatever type, to a type 1 oxidative metabolism because of the change in use of these fibers.

Aged↗