Explore the vast range of titles available.

Diabetic neuropathies (DNs) differ in clinical course, distribution, fiber involvement (type and size), and pathophysiology, the most typical type being a length-dependent distal symmetric polyneuropathy (DSP) with differing degrees of autonomic involvement. The pathogenesis of diabetic DSP is multifactorial, including increased mitochondrial production of free radicals due to hyperglycemia-induced oxidative stress. Mechanisms that impact neuronal activity, mitochondrial function, membrane permeability, and endothelial function include formation of advanced glycosylation end products, activation of polyol aldose reductase signaling, activation of poly(ADP ribose) polymerase, and altered function of the Na + /K + -ATPase pump. Hyperglycemia-induced endoplasmic reticulum stress triggers several neuronal apoptotic processes. Additional mechanisms include impaired nerve perfusion, dyslipidemia, altered redox status, low-grade inflammation, and perturbation of calcium balance. Successful therapies require an integrated approach targeting these mechanisms. Intensive glycemic control is essential but is insufficient to prevent onset or progression of DSP, and disease-modifying treatments for DSP have been disappointing. Atypical forms of DN include subacute-onset sensory (symmetric) or motor (asymmetric) predominant conditions that are frequently painful but generally self-limited. DNs are a major cause of disability, associated with reduced quality of life and increased mortality.

Boulton et al provide a relevant information on diabetic neuropathies, a heterogeneous, affecting different parts of the nervous system that present with diverse clinical manifestations. Most common among the neuropathies are chronic sensorimotor distal symmetric polyneuropathy and the autonomic neuropathies. Details of its classifications, diagnosis, and clinical aspects are also presented.

One of the fundamental challenges when dealing with medical imaging datasets is class imbalance. Class imbalance happens where an instance in the class of interest is relatively low, when compared to the rest of the data. This study aims to apply oversampling strategies in an attempt to balance the classes and improve classification performance. We evaluated four different classifiers from k-nearest neighbors (k-NN), support vector machine (SVM), multilayer perceptron (MLP) and decision trees (DT) with 73 oversampling strategies. In this work, we used imbalanced learning oversampling techniques to improve classification in datasets that are distinctively sparser and clustered. This work reports the best oversampling and classifier combinations and concludes that the usage of oversampling methods always outperforms no oversampling strategies hence improving the classification results.

OBJECTIVE:--To compare populations with and outcomes of diabetic foot ulcers managed in the U.K., Germany, Tanzania, and Pakistan and to explore the use of a new score of ulcer type in comparing outcomes among different countries. RESEARCH DESIGN AND METHODS--Data from a series of 449 patients with diabetic foot ulcers managed in the U.K. were used to evaluate the new simplified system of classification and to derive an aggregate score. The use of the score was then explored using data from series managed in Germany (n = 239), Tanzania (n = 479), and Pakistan (n = 173). RESULTS:--A highly significant difference was found in time to healing between ulcers of increasing score in the U.K. series (Kruskal-Wallis test; P = 0). When data from all centers were examined, a step-up in days to healing was noted for those with scores of >=3 (out of 6). Examination of baseline variables contributing to outcome revealed the following differences among centers: ischemia, ulcer area, and depth contributing to outcome in the U.K.; ischemia, area, depth, and infection in Germany; depth, infection, and neuropathy in Tanzania; and depth alone in Pakistan. CONCLUSIONS:--Any system of classification designed for general implementation must encompass all the variables that contribute to outcome in different communities. Adoption of a simple score based on these variables, the Site, Ischemia, Neuropathy, Bacterial Infection, and Depth (SINBAD) score, may prove useful in predicting ulcer outcome and enabling comparison among different centers.

Background Electromyography (EMG) alterations during gait, supposedly caused by diabetic sensorimotor polyneuropathy, are subtle and still inconsistent, due to difficulties in defining homogeneous experimental groups with a clear definition of disease stages. Since evaluating these patients involve many uncertainties, the use of a fuzzy model could enable a better discrimination among different stages of diabetic polyneuropathy and lead to a clarification of when changes in muscle activation start occurring. The aim of this study was to investigate EMG patterns during gait in diabetic individuals with different stages of DSP severity, classified by a fuzzy system. Methods 147 subjects were divided into a control group (n = 30) and four diabetic groups: absent (n = 43), mild (n = 30), moderate (n = 16), and severe (n = 28) neuropathy, classified by a fuzzy model. The EMG activity of the vastus lateralis, tibialis anterior, and gastrocnemius medialis were measured during gait. Temporal and relative magnitude variables were compared among groups using ANOVA tests. Results Muscle activity changes are present even before an established neural involvement, with delay in vastus lateralis peak and lower tibialis anterior relative magnitude. These alterations suggest an impaired ankle shock absorption mechanism, with compensation at the knee. This condition seems to be more pronounced in higher degrees of neuropathy, as there is an increased vastus lateralis activity in the mild and severe neuropathy groups. Tibialis anterior onset at terminal stance was anticipated in all diabetic groups; at higher degrees of neuropathy, the gastrocnemius medialis exhibited activity reduction and peak delay. Conclusion EMG alterations in the vastus lateralis and tibialis anterior occur even in the absence of diabetic neuropathy and in mild neuropathic subjects, seemingly causing changes in the shock absorption mechanisms at the heel strike. These changes increase with the onset of neural impairments, and the gastrocnemius medialis starts presenting altered activity in the later stages of the disease (moderate and severe neuropathy). The degree of severity of diabetic neuropathy must be taken into account when analyzing diabetic patients’ biomechanical patterns of locomotion; we recommend the use of a fuzzy model for classification of disease stages.

Vinik et al discuss several common entrapment neuropathies involving the median, ulnar, peroneal nerves, the lateral cutaneous of the thigh, and the tibial nerve in the tarsal canal, which are used for diabetics with carpal tunnel syndrome and tarsal tunnel syndrome. These include the ulnar entrapment, radial nerve entrapment, and common peroneal entrapment.

This article describes the different conditions that embrace the diagnosis of diabetic neuropathies—the Cinderella complication of diabetes. Distinction between the proximal and distal large and small fiber, focal mononeuritides and entrapments is essential since each has a unique presentation and requires specific therapeutic intervention for a successful outcome. Diabetic neuropathies are a heterogeneous group of disorders that include a wide range of abnormalities. They can be focal or diffuse, proximal or distal, affecting both peripheral and autonomic nervous systems, causing morbidity with significant impact on the quality of life of the person with diabetes, and can result in early death. Distal symmetric polyneuropathy, the most common form of diabetic neuropathy, usually involves small and large nerve fibers. Small-nerve-fiber neuropathy often presents with pain but without objective signs or electrophysiologic evidence of nerve damage, and is recognized as a component of the impaired glucose tolerance and metabolic syndromes. The greatest risk resulting from small-fiber neuropathy is foot ulceration and subsequent gangrene and amputation. Large-nerve-fiber neuropathies produce numbness, ataxia and uncoordination, impairing activities of daily living and causing falls and fractures. A careful history and detailed physical examination are essential for the diagnosis. Symptomatic therapy has become available and newer and better treatment modalities, based on etiologic factors, are being explored with potential for significant impact on morbidity and mortality. Preventive strategies and patient education still remain key factors in reducing complication rates and mortality. Key Points Diabetic neuropathies are among the commonest, long-term complications of diabetes although often are not recognized by physicians A thorough history and detailed physical examination, with the aid of simple tests that can be done in the clinic, are essential for the diagnosis Management of the disease is complex and the key to success depends, in part, on discovering the underlying pathological processes in each particular clinical presentation There has been increasing understanding of the pathogenesis of diabetic neuropathies over the last decades and new therapies are emerging that hold promise for the treatment of this disease

Children who develop cerebral edema (CE) during diabetic ketoacidosis (DKA) exhibit definable signs and symptoms of neurological collapse early enough to allow intervention to prevent brain damage. Our objective was to develop a model for early detection of CE in children with DKA. A training sample of 26 occurrences of DKA complicated by severe CE and 69 episodes of uncomplicated DKA was reviewed. Signs of neurological disease were incorporated into a bedside evaluation protocol that was applied to an independent test sample of 17 patients previously reported to have developed symptomatic CE during treatment for DKA. Head computed tomograms and their reports were reviewed. The protocol allowed 92% sensitivity and 96% specificity for the recognition of CE sufficiently early for intervention. The diagnostic criteria were fulfilled in two temporal patterns, defining early- and late-onset CE. Although initial computed tomograms were often normal, the findings also included diffuse CE and focal brain injury, the latter only in patients with an early onset of abnormal neurological signs. CE may occur in the absence of acute changes on head computed tomograms. Early detection of CE at the bedside using an evidence-based protocol permits intervention in time to prevent permanent brain damage.

To review the clinical manifestations and current treatment options for diabetic neuropathies, one of the most common complications of diabetes mellitus. We performed a MEDLINE search of the English-language literature using a combination of words (diabetic neuropathy, diabetic autonomic neuropathy, diagnosis and treatment) to identify original studies, consensus statements, and reviews on diabetic neuropathies published in the past 25 years. Emphasis was placed on clinical manifestations of distal polyneuropathy and its treatment, especially new therapies. Distal symmetric polyneuropathy, the most common form of diabetic neuropathy, usually involves small and large nerve fibers. Small-nerve fiber neuropathy often presents with pain and loss of intraepidermal nerve fibers, but without objective signs or electrophysiologic evidence of nerve damage. This type of neuropathy is a component of impaired glucose tolerance and the metabolic syndrome. The greatest risk from small-fiber neuropathy is foot ulceration and subsequent gangrene and amputation. Large-nerve fiber neuropathy produces numbness, ataxia, and incoordination, thus impairing activities of daily living and causing falls and fractures. Successfully treating diabetic neuropathy requires addressing the underlying pathogenic mechanisms, treating symptoms to improve quality of life, and preventing progression and complications of diabetes mellitus. Two new drugs, duloxetine hydrochloride and pregabalin, have recently been approved for treatment of neuropathic pain associated with diabetes mellitus. Symptomatic therapy has become available and newer and better treatment modalities, based on etiologic factors, are being explored with potential for clinically significant reduction of morbidity and mortality. Preventive strategies and patient and physician education still remain key factors in reducing complication rates and mortality.

Diabetic neuropathy is a debilitating disorder that occurs in nearly 50 percent of patients with diabetes. It is a late finding in type 1 diabetes but can be an early finding in type 2 diabetes. The primary types of diabetic neuropathy are sensorimotor and autonomic. Patients may present with only one type of diabetic neuropathy or may develop combinations of neuropathies (e.g., distal symmetric polyneuropathy and autonomic neuropathy). Distal symmetric polyneuropathy is the most common form of diabetic neuropathy. Diabetic neuropathy also can cause motor deficits, silent cardiac ischemia, orthostatic hypotension, vasomotor instability, hyperhidrosis, gastroparesis, bladder dysfunction, and sexual dysfunction. Strict glycemic control and good daily foot care are key to preventing complications of diabetic neuropathy.