Home About us Contact
|
Home About us Contact | ||
|
|
||
Diabetic Neuropathy (diabetic + neuropathy)
Kinds of Diabetic Neuropathy Selected AbstractsAbstracts of the Joint 8th International Symposium on Diabetic Neuropathy and 19th Annual Meeting of the Diabetic Neuropathy Study Group of the EASDJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 20092009 Toronto, Canada, October 1 [source] Textbook of Diabetic NeuropathyJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2004Nigel A. Calcutt Ph.D. [source] Favorable Impact of a Vegan Diet with Exercise on Hemorheology: Implications for Control of Diabetic NeuropathyJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2003MF McCarty A little-noticed clinical report indicates that a low-fat, whole-food vegan diet, coupled with daily walking exercise, leads to rapid remission of neuropathic pain in the majority of type 2 diabetics expressing this complication. Concurrent marked improvements in glycemic control presumably contribute to this benefit, but are unlikely to be solely responsible. Consideration should be given to the possibility that improved blood rheology , decreased blood viscosity and increased blood filterability , plays a prominent role in mediating this effect. There is considerable evidence that neural hypoxia, secondary to impaired endoneurial microcirculatory perfusion, is a crucial etiologic factor in diabetic neuropathy; the unfavorable impact of diabetes on hemorheology would be expected to exacerbate endoneurial ischemia. Conversely, measures which improve blood fluidity would likely have a beneficial impact on diabetic neuropathy. There is indeed evidence that vegan diets, as well as exercise training, tend to decrease the viscosity of both whole blood and plasma; reductions in hematocrit and in fibrinogen may contribute to this effect. The fact that vegan diets decrease the white cell count is suggestive of an improvement in blood filterability as well; filterability improves with exercise training owing to an increase in erythrocyte deformability. Whether these measures influence the activation of leukocytes in diabetics , an important determinant of blood filterability , remains to be determined. There are various reasons for suspecting that a vegan diet can reduce risk for other major complications of diabetes , retinopathy, nephropathy, and macrovascular disease , independent of its tendency to improve glycemic control in type 2 patients. The vegan diet/exercise strategy represents a safe, ,low-tech' approach to managing diabetes that deserves far greater attention from medical researchers and practitioners. [source] Electrophysiological Changes In Diabetic Neuropathy: From Subclinical Alterations To Disabling AbnormalitiesJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000M. Baba Clinical spectrum of diabetic neuropathy is variable; it may be asymptomatic, but once established, it becomes irreversible and disabling. Some investigators suggested that earliest change in diabetic nerve function is alteration in axonal excitability due to alterations in ion conductance of axon membrane, although these functional changes of ion channels necessarily cause permanent damage or degeneration of nerve fibers. Among various parameter of nerve conduction study in diabetics, prolonged F-wave latency in the peroneal and tibial nerve seems the commonest abnormality in asymptomatic patients. Decrease in amplitude of compound sensory action potential of sural nerve is another earlier abnormality, which is, then, accompanied by a fall in motor amplitude of peroneal and tibial nerves in advanced patients. In disabled patients no motor response is often elicited in the legs. Previous electrophysiological studies could not make clear if central axons were involved or not in diabetic neuropathy. Recently, our group has demonstrated that somatosensory central conduction from the spinal cord to the sensory cortex is delayed in diabetics as well as in the peripheral conduction, which might be partly responsible for the irreversible clinical presentation of diabetic neuropathy. [source] Future Progress In Diabetic NeuropathyJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000Jd Ward Over three decades much knowledge regarding the pathogenesis of diabetic neuropathy has been gathered but sadly this has led to very little understanding. This final review lecture of the symposium will attempt to analyse why progress has been so slow and look to the future for signs of inventive improvement. Papers presented during the symposium will be reviewed to allow estimate of future success and where perhaps efforts should be focused. At present the best we can do for our patients is to control blood glucose as rigidly as possible for preventative therapy and logical interventional drugs are not available. Hopefully the symposium will provide new insights into future investigations and potential pathways. [source] Microcirculatory Responses To Electrical Spinal Cord Stimulation In Painful Diabetic Neuropathy And Other Painful ConditionsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000Nd Harris Electrical spinal cord stimulation (ESCS) has been used to provide pain relief in a number of conditions, including painful diabetic neuropathy (PDN). ESCS has also been shown to increase microvascular blood flow in peripheral vascular disease. If nerve hypoxia contributes to pain in PDN, ESCS may relieve this by increasing nerve blood flow. We have therefore investigated skin and sural nerve microvascular responses to ESCS. We studied subjects implanted with ESCS for pain relief, 4 had PDN and 7 were controls with other painful conditions. Blood flow, before and during stimulation, was assessed using Laser Doppler flowmetry. Only one (PDN) subject showed a statistically significant increase in skin blood flow during stimulation. The three remaining PDN subjects showed significant reductions in skin blood flow, as did 3/7 of controls. Sural nerve blood flow was measured on a separate occasion. During stimulation nerve blood flow increased in 1 (control) subject, decreased in 1 (PDN) subject and did not change in the other 5 tested (3 PDN and 2 control). In summary, ESCS did not produce any consistent increase in skin or nerve microvascular blood flow. ESCS reduces pain in a variety of different conditions, however this does not appear to be mediated by changes in blood flow. Until a thorough understanding of the pathogenic mechanisms causing PDN is achieved, therapy will be limited to providing symptomatic relief. [source] C-Peptide Deficiency: An Important Pathogenetic Factor In Type 1 Diabetic NeuropathyJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000Aaf Sima Background: C-peptide has insulin-like effects and ameliorates the acute nerve conduction defect (NCD) in experimental and human type 1 diabetic neuropathy (DN). Methods: In this study, diabetic BB/Wor-rats were treated with rat C-peptide (75 ng/kg) from onset of diabetes for 8 months (prevention-group, PG). In a separate experiment, 5-mo untreated diabetic BB/Wor-rats were started on the same C-peptide treatment continued to 8 mo of diabetes (intervention group, IG). Results: In the PG, the NCD was significantly decreased (p < 0.001) compared to untreated BB/Wor-rats and was similar to that of normo-C-peptidemic and isohyperglycemic type 2 BBZ rats. This effect was associated with significant preventions of nodal changes (p < 0.001) including axo-glial dysjunction (p < 0.001), which was not different from non-diabetic control rats. Axonal atrophy and Wallerian degeneration were significantly prevented (both p < 0.05). In the IG, the NCD decreased significantly (p < 0.01) during the 3 mo treatment period. Associated with the functional improvement, nodal changes improved significantly (p < 0.001) as did axonal degenerative changes (p < 0.01). C-peptide treatment in the IG resulted in a significant increase in the frequency of regenerating fibers (p < 0.001) compared with untreated 5 mo diabetic rats. Conclusion: These studies demonstrate that C-peptide replacement in type 1 diabetes prevents the chronic NCD and structural changes. Furthermore, C-peptide treatment significantly improves the already established functional and structural abnormalities of DN. This is the first demonstration of a therapeutic improvement of established neuropathy in experimental diabetes. We conclude that C-peptide deficiency in type 1 diabetes is an important pathogenetic component of DN and that its replacement may provide a valuable adjunct to intensive insulin treatment. [source] A Sonic Hedgehog (SH) Fusion Protein Corrects Multifocal Defects In Experimental Diabetic NeuropathyJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000Dr Tomlinson Diabetic neuropathy develops from defective interactions between nerve axons and other cells in the endoneurium; such interactions are influenced in development by hedgehog proteins. This study explored the possibility that this might be maintained in the adult and form a basis for therapy in diabetic neuropathies. Streptozotocin-diabetic rats were treated (final 5 weeks of 10 weeks diabetes) with a SH-IgG fusion protein (either 0.3mg/kg or 3.0mg/kg s.c. 3 times per week); control diabetic and non-diabetic rats received vehicle. Conduction velocity (MNCV, SNCV) data and sciatic nerve levels of nerve growth factor (NGF) and neuropeptide Y (NPY) are presented below. Diabetes caused significant (p < 0.05 by ANOVA with SNK tests) reductions in all variables and treatment with SH-IgG either attenuated or prevented (p < 0.05) these reductions. Since it is well-established that the conduction deficits are unrelated to neurotrophic deficits (NGF depletion) and that NPY depletion derives from a neurotrophic defect distinct from NGF, this treatment clearly acts at multiple components of the aetiology of diabetic neuropathy. [source] Diabetic neuropathy and oxidative stressDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 4 2006Rodica Pop-Busui Abstract This review will focus on the impact of hyperglycemia-induced oxidative stress in the development of diabetes-related neural dysfunction. Oxidative stress occurs when the balance between the production of reactive oxygen species (ROS) and the ability of cells or tissues to detoxify the free radicals produced during metabolic activity is tilted in the favor of the former. Although hyperglycemia plays a key role in inducing oxidative stress in the diabetic nerve, the contribution of other factors, such as endoneurial hypoxia, transition metal imbalances, and hyperlipidemia have been also suggested. The possible sources for the overproduction of ROS in diabetes are widespread and include enzymatic pathways, auto-oxidation of glucose, and mitochondrial superoxide production. Increase in oxidative stress has clearly been shown to contribute to the pathology of neural and vascular dysfunction in diabetes. Potential therapies for preventing increased oxidative stress in diabetic nerve dysfunction will be discussed. Copyright © 2006 John Wiley & Sons, Ltd. [source] Prevalence and impact of pain in diabetic neuropathyEUROPEAN DIABETES NURSING, Issue 2 2009M Geerts M Abstract Background: Diabetic neuropathy (DNP) is a serious and common complication of diabetes mellitus, with a prevalence of around 30-50%. Aims: To describe the prevalence, severity and medical treatment of painful DNP (PDNP) experienced by patients treated in secondary care; to determine quality of life (QoL) impact and the relationship between severity of pain and severity of DNP. Methods: Cross-sectional, two-phase survey. First, a pain interview was conducted by telephone (219 DNP patients), which covered types of pain, location and duration. Secondly, 50 patients were visited at home. Patients completed the Brief Pain Inventory, the Short Form Health Survey (SF-36) and the Hospital Anxiety and Depression Scale. Results: Prevalence of PDNP was 57.5%. Average and worst pain scores were 5.3 ± 2.1 and 6.4 ± 2.2, respectively (0-10 scale, 10 = worst pain imaginable). In 70% of patients, average pain was severe (score ,5). Substantial interference by pain (score ,4) was found in walking ability, sleep and normal activities. PDNP patients had a decreased QoL for all SF-36 domains (p,0.01) except for health change. Moreover, symptoms of anxiety (36%) and depression (34%) were reported frequently. Medical treatment was prescribed in 46% of patients, in whom treatment was ineffective in 39%. Physical functioning scores were lower in patients with severe versus moderate DNP (p,0.01). Conclusions: The prevalence of severe PDNP was high. Severity of DNP was not related to pain severity. PDNP was associated with loss of QoL and with symptoms of anxiety and depression. A considerable proportion of patients did not have medical treatment and, if treatment was given, its impact was disappointing. Medical treatment of PDNP was unsatisfactory and clearly needs to be improved. Copyright © 2009 FEND [source] Diabetic neuropathy: therapies on the horizonJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 9 2009Danish Mahmood Abstract Objectives This is a review of emerging interventions from the recent preclinical and clinical literature that demonstrate the potential for effectiveness in the therapy of diabetic neuropathy (DN). DN is the most common complication of diabetes mellitus and up to 50% of patients with type 1 and type 2 forms have some or other form of neuropathy. The pathology of DN is characterized by progressive nerve fibre loss that gives rise to positive and negative clinical signs and symptoms such as pain, paraesthesiae and loss of sensation. Key findings There are very few drugs available to directly treat DN. Those that are clinically indicated provide symptomatic relief but do not repair or reverse underlying nerve damage. However, some agents are in clinical development that may support adult neurons and direct reparative processes after injury stages. Several disease modifying drugs such as aldose reductase inhibitors and protein kinase C inhibitors are in phase III development. Agents on the horizon include neurotrophic factors, growth factors, gene therapy, immunotherapy, poly(ADP-ribose) polymerase inhibitors and non-immunosuppressive immunophilin ligands. Summary Progress has been made toward understanding the biochemical mechanisms leading to diabetic neuropathy, and as a result, new treatment modalities are being explored. The pathogenesis, types and approaches for treating DN together with the newer therapeutic interventions on the horizon are discussed. [source] A Sonic Hedgehog (SH) Fusion Protein Corrects Multifocal Defects In Experimental Diabetic NeuropathyJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000Dr Tomlinson Diabetic neuropathy develops from defective interactions between nerve axons and other cells in the endoneurium; such interactions are influenced in development by hedgehog proteins. This study explored the possibility that this might be maintained in the adult and form a basis for therapy in diabetic neuropathies. Streptozotocin-diabetic rats were treated (final 5 weeks of 10 weeks diabetes) with a SH-IgG fusion protein (either 0.3mg/kg or 3.0mg/kg s.c. 3 times per week); control diabetic and non-diabetic rats received vehicle. Conduction velocity (MNCV, SNCV) data and sciatic nerve levels of nerve growth factor (NGF) and neuropeptide Y (NPY) are presented below. Diabetes caused significant (p < 0.05 by ANOVA with SNK tests) reductions in all variables and treatment with SH-IgG either attenuated or prevented (p < 0.05) these reductions. Since it is well-established that the conduction deficits are unrelated to neurotrophic deficits (NGF depletion) and that NPY depletion derives from a neurotrophic defect distinct from NGF, this treatment clearly acts at multiple components of the aetiology of diabetic neuropathy. [source] Critical review of oral drug treatments for diabetic neuropathic pain,clinical outcomes based on efficacy and safety data from placebo-controlled and direct comparative studiesDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 3 2005Hugo Adriaensen Abstract The present review aims to evaluate the efficacy and safety of a selection of oral treatments for the management of painful diabetic neuropathy. A literature review was conducted retrieving placebo-controlled and direct comparative studies with a selection of oral treatments for painful diabetic neuropathy. All studies were analyzed with regard to efficacy and tolerability. Efficacy was evaluated as the percentage improvement in pain intensity between baseline and endpoint. Tolerability was evaluated by means of study discontinuations due to adverse events and by incidence of drug-related adverse events. The analyzed trials enrolled different patient populations with mostly small numbers of patients. The great variability in dosages and dose titration schemes, cross-over designs with variable wash-out periods, and other design schemes made comparison between the different studies difficult. Gabapentin, lamotrigine, tramadol, oxycodone, mexiletine, and acetyl-L-carnitine were the only treatments studied in large (at least 100 patients), placebo-controlled parallel group trials. It is concluded that standardization in design and reporting for comparison of treatments is needed. Validated questionnaires for evaluation of the efficacy and safety should be further developed. Based on the reviewed randomised controlled trials, gabapentin shows good efficacy, a favourable side-effect profile with lack of drug interactions and therefore it may be a first choice treatment in painful diabetic neuropathy, especially in the elderly. However, head to head trials of current treatments are lacking and therefore randomized controlled trials are required to address this issue. Copyright © 2005 John Wiley & Sons, Ltd. [source] Understanding the impact of painful diabetic neuropathyDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue S1 2003Cristian Quattrini Abstract Painful neuropathy is a common and often distressing complication of diabetes. It has considerable impact on the social and psychological well-being of affected individuals. There are two distinct forms of painful neuropathy: an acute and self-limiting form that resolves within a year or a chronic form that can go on for years. There are now a number of drugs available for the treatment of neuropathic pain. However, some may fail to respond to these drugs or may have unacceptable adverse side effects. When this is the case, the patient's quality of life can be severely affected. Health care professionals need to assess the full impact of painful neuropathy. In this article we review a number of instruments that are used to assess the severity of painful neuropathy and its impact on the quality of life. Copyright © 2003 John Wiley & Sons, Ltd. [source] Neuropathic pain and diabetesDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue S1 2003Dilip Kapur Abstract Neuropathic pain is a common phenomenon resulting from injury to the central or peripheral nervous system. The means by which diabetes results in nerve injury is unclear but the effect is to cause injury at all levels of the nervous system from the level of the peripheral nerves to the brain. Nerve injury causes pain through a cascade of mechanisms resulting in altered processing of sensory input into the nervous system. This alteration occurs through chemical and anatomical changes in the nervous system that are similar to some of the processes seen in central sensitisation following acute pain. Following nerve injury, neuropathic pain occurs not only when these mechanisms are activated but also when sensitisation is maintained. Other processes occurring in neuropathic pain appear to be a loss of normal inhibitory controls as seen by a reduction in local GABA-ergic and descending monoaminergic influences. There are also important changes mediated via glial cells that can maintain neuropathic pain. Diabetes affects all areas of the nervous system and the contribution of higher levels of the nervous system is often overlooked. Neurophysiological and MRI evidence strongly suggest that these may contribute to the pain of diabetic neuropathy. Psychological dysfunction in diabetic patients is an important factor in increasing the suffering associated with all aspects of the disease, but treatment and control of pain can greatly improve the quality of life. Copyright © 2003 John Wiley & Sons, Ltd. [source] Treatment of symptomatic diabetic neuropathyDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue S1 2003Andrew J. M. Boulton Abstract Painful diabetic neuropathy is a common and particularly unpleasant long-term complication of diabetes that affects a significant minority of patients with distal polyneuropathy. After exclusion of other causes of neuropathic pain, attention should be focused on achieving optimal and stable glycaemic control avoiding flux of blood glucose levels, which have been shown to aggravate pain. Most patients will require pain control therapy and whilst the tricyclic drugs remain a first-line approach, their use is often hampered by predictable but troublesome side effects. Gabapentin, the only agent specifically licensed for the treatment of neuropathic pain in the United Kingdom, is useful in diabetic neuropathy and is generally better tolerated than the tricyclics. Additionally, other pharmacological and non-pharmacological pain management approaches may be useful. Patient education has a significant role to play in the avoidance of late neurological complications. Copyright © 2003 John Wiley & Sons, Ltd. [source] Plantar pressures in diabetic patients with foot ulcers which have remained healedDIABETIC MEDICINE, Issue 11 2009T. M. Owings Abstract Aims, The recurrence of foot ulcers is a significant problem in people with diabetic neuropathy. The purpose of this study was to measure in-shoe plantar pressures and other characteristics in a group of neuropathic patients with diabetes who had prior foot ulcers which had remained healed. Methods, This was an epidemiological cohort study of patients from diabetes clinics of two Swedish hospitals. From a database of 2625 eligible patients, 190 surviving patients with prior plantar ulcers of the forefoot (hallux or metatarsal heads) caused by repetitive stress were identified and 49 patients agreed to participate. Barefoot and in-shoe plantar pressures were measured during walking. Data on foot deformity, activity profiles and self-reported behaviour were also collected. Results, Mean barefoot plantar peak pressure at the prior ulcer site (556 kPa) was lower than in other published series, although the range was large (107,1192 kPa). Mean in-shoe peak pressure at this location averaged 207 kPa when measured with an insole sensor. Barefoot peak pressure only predicted ,35% of the variance of in-shoe peak pressure, indicating variation in the efficacy of the individual footwear prescriptions (primarily extra-depth shoes with custom insoles). Conclusions, We propose that the mean value for in-shoe pressures reported in these patients be used as a target in footwear prescription for patients with prior ulcers. Although plantar pressure is only one factor in a multifaceted strategy to prevent ulcer recurrence, the quantitative focus on pressure reduction in footwear is likely to have beneficial effects. [source] Healthcare charges and utilization associated with diabetic neuropathy: impact of Type 1 diabetes and presence of other diabetes-related complications and comorbiditiesDIABETIC MEDICINE, Issue 1 2009Y. Zhao Abstract Aims The aim was to examine the impact of Type 1 diabetes and having any other diabetes-related complication or comorbidity on healthcare charges and utilization in patients with diabetic neuropathy (DN). Methods We selected individuals aged < 65 years who continuously enrolled in a large US commercial plan from July 2004 to June 2006 and who received at least one diagnosis of DN at any time from July 2004 to June 2005. We compared the prevalence of other diabetes-related complications or comorbidities between patients with Type 1 and with Type 2 diabetes. In patients with DN with or without any other diabetes-related complication or comorbidity, we used multivariate regression to assess the marginal contribution of Type 1 diabetes on healthcare charges and utilization from July 2005 until June 2006. Results The majority of DN patients had at least one other diabetes-related complication or comorbidity. Most of the DN patients had Type 2 diabetes. DN patients with Type 1 diabetes had more comorbid medical conditions than those with Type 2 diabetes. Compared with Type 2, Type 1 patients had a higher prevalence of each individual non-DN diabetes-related complication or comorbidity, except heart disease. Controlling for comorbidities, Type 1 and Type 2 patients with DN but no other diabetes-related complication or comorbidity had similar healthcare utilization. However, Type 1 patients had significantly higher charges than those with any other diabetes-related complication or comorbidity. Conclusions Many patients with DN have Type 1 diabetes and other common diabetes-related complications or comorbidities, which can have a significant impact on healthcare charges and utilization. [source] Stratified analyses for selecting appropriate target patients with diabetic peripheral neuropathy for long-term treatment with an aldose reductase inhibitor, epalrestatDIABETIC MEDICINE, Issue 7 2008N Hotta Abstract Aims The long-term efficacy of epalrestat, an aldose reductase inhibitor, in improving subjective symptoms and nerve function was comprehensively assessed to identify patients with diabetic peripheral neuropathy who responded to epalrestat treatment. Methods Stratified analyses were conducted on data from patients in the Aldose Reductase Inhibitor,Diabetes Complications Trial (ADCT). The ADCT included patients with diabetic peripheral neuropathy, median motor nerve conduction velocity , 40 m/s and with glycated haemoglobin (HbA1c) , 9.0%. Longitudinal data on HbA1c and subjective symptoms of the patients for 3 years were analysed (epalrestat n = 231, control subjects n = 273). Stratified analyses based on background variables (glycaemic control, grades of retinopathy or proteinuria) were performed to examine the relationship between subjective symptoms and nerve function. Multiple logistic regression analyses were conducted. Results Stratified subgroup analyses revealed significantly better efficacy of epalrestat in patients with good glycaemic control and less severe diabetic complications. In the control group, no improvement in nerve function was seen regardless of whether symptomatic benefit was obtained. In the epalrestat group, nerve function deteriorated less or improved in patients whose symptoms improved. The odds ratio of the efficacy of epalrestat vs. control subjects was approximately 2 : 1 (4 : 1 in patients with HbA1c , 7.0%). Conclusion Our results suggest that epalrestat, an aldose reductase inhibitor, will provide a clinically significant means of preventing and treating diabetic neuropathy if used in appropriate patients. [source] Nitroglycerin spray rapidly improves pain in a patient with chronic painful diabetic neuropathyDIABETIC MEDICINE, Issue 9 2004M. Higa No abstract is available for this article. [source] The value of the Rydel-Seiffer tuning fork as a predictor of diabetic polyneuropathy compared with a neurothesiometerDIABETIC MEDICINE, Issue 6 2004T. Kästenbauer Abstract Aims The aim of the study was to investigate the predictive value of the Rydel-Seiffer tuning fork for detecting diabetic neuropathy and to compare it with an electronic neurothesiometer. Methods In 2022 consecutive diabetic subjects, peripheral polyneuropathy was diagnosed by vibration perception threshold (VPT) at the tip of both great toes using a 128-Hz tuning fork and a neurothesiometer, by simple bedside tests and by the presence of neuropathic symptoms. These evaluations were further combined to diagnose peripheral nerve dysfunction (abnormal bedside tests) and symptomatic neuropathy. VPT was also measured in 175 non-diabetic control subjects to define normal values. Results VPT was normal in 1917 subjects and abnormal in 105 (5.2%) patients when measured by the tuning fork. Patients with an abnormal vibration test were significantly (P < 0.0001) older than subjects with a normal vibration sense, while diabetes duration and HbA1c of the former were also significantly elevated. The same was true for the percentages of an abnormal 10-g monofilament test (66.7% vs. 7.2%, P < 0.0001) and a missing Achilles' tendon reflex (68.6% vs. 24.8%, P < 0.0001). Finally, the VPT measured by the neurothesiometer was 2.5 times higher in patients with an abnormal tuning fork test (32.0 ± 9.8 vs. 12.5 ± 6.4 V, P < 0.0001). The plot of the difference of both methods against their mean yielded a good agreement of the two VPT measurements, and the tuning fork had a high sensitivity and positive predictive value for the diagnosis of abnormal bedside tests and for symptomatic neuropathy. Conclusion The tuning fork reliably detected peripheral neuropathy in comparison with the neurothesiometer. A tuning fork is a useful screening test for diabetic neuropathy. [source] How should peripheral neuropathy be assessed in people with diabetes in primary care?DIABETIC MEDICINE, Issue 5 2003A population-based comparison of four measures Abstract Aims To test the accuracy of four measures of peripheral diabetic neuropathy in a primary care population. Methods Type 2 diabetic (n = 544) and 544 non-diabetic participants aged 45,76 years were randomly selected from general practice registers. Neuropathy was assessed using vibration threshold (VT) and scores for light touch, thermal sense and modified Michigan Neuropathy Screening Instrument questionnaire. These measures were assessed for variation with diabetes status, age, diabetes duration, HbA1c, and presence of retinopathy and nephropathy. Light touch, thermal sense and questionnaire scores were assessed against VT using ROC curve analysis. Results Only VT and light touch were different between diabetic and non-diabetic groups (P = 0.02 and < 0.0001, respectively). All measures were significantly associated with diabetes duration and retinopathy, and all except questionnaire score (P = 0.14) with age. None was associated with nephropathy and only questionnaire score was associated with HbA1c (P = 0.033). VT varied as expected across scores of light touch (,2 = 41.65, P = 0.0001), thermal sense (,2 = 15.86, P = 0.015) and questionnaire (,2 = 21.22, P = 0.047). Area under the curve values for light touch, thermal and questionnaire scores were 0.72 (95% confidence interval (CI) 0.63, 0.82), 0.63 (95% CI 0.52, 0.73) and 0.64 (95% CI 0.53, 0.74), respectively. Conclusions All measures had associations with risk factors for neuropathy, but light touch score (monofilament) had the strongest association with vibration threshold (the chosen gold standard) and thus appeared the most appropriate tool for use in primary care, because of its validity and simplicity of use. Diabet. Med. 20, 368,374 (2003) [source] ,Numbness of the feet' is a poor indicator for polyneuropathy in Type 2 diabetic patientsDIABETIC MEDICINE, Issue 2 2000L. V. Franse Summary Aims To identify neuropathic sensory symptoms associated with a clinical neurological examination (CNE) and to investigate whether these symptoms could be used as a diagnostic or screening tool for diabetic polyneuropathy in general practice. Methods Five hundred and eighty-eight patients with Type 2 diabetes, recruited from 26 general practices in the Netherlands, underwent a CNE and completed a diabetes symptom checklist that included 10 items on neuropathic sensory symptoms. Linear regression analyses were performed to assess the association between neuropathic symptoms and CNE. Receiver operating characteristic (ROC) curves were created to assess the diagnostic properties of neuropathic symptoms. Results In this population, with a mean age of 66.8 years, 32% were identified with diabetic polyneuropathy according to the CNE. Variables that showed the strongest association with CNE score were age (, = 0.41), symptoms of sensory alteration (, = 0.27), and the item ,numbness of the feet' (, = 0.35) in particular. ROC curves showed that prediction of diabetic polyneuropathy from these symptoms was unsatisfying. The sensitivity and specificity of daily symptoms of ,numbness of the feet' were 28% and 93%, respectively, in patients <,68 years, and 22% and 92%, respectively, in patients ,,68 years. Conclusions Identification of neuropathic sensory symptoms is not useful as a diagnostic or even a screening tool in the assessment of diabetic neuropathy in daily practice. Therefore, the results reported in this paper mandate an annual foot examination by the general practitioner. [source] Prevalence and impact of pain in diabetic neuropathyEUROPEAN DIABETES NURSING, Issue 2 2009M Geerts M Abstract Background: Diabetic neuropathy (DNP) is a serious and common complication of diabetes mellitus, with a prevalence of around 30-50%. Aims: To describe the prevalence, severity and medical treatment of painful DNP (PDNP) experienced by patients treated in secondary care; to determine quality of life (QoL) impact and the relationship between severity of pain and severity of DNP. Methods: Cross-sectional, two-phase survey. First, a pain interview was conducted by telephone (219 DNP patients), which covered types of pain, location and duration. Secondly, 50 patients were visited at home. Patients completed the Brief Pain Inventory, the Short Form Health Survey (SF-36) and the Hospital Anxiety and Depression Scale. Results: Prevalence of PDNP was 57.5%. Average and worst pain scores were 5.3 ± 2.1 and 6.4 ± 2.2, respectively (0-10 scale, 10 = worst pain imaginable). In 70% of patients, average pain was severe (score ,5). Substantial interference by pain (score ,4) was found in walking ability, sleep and normal activities. PDNP patients had a decreased QoL for all SF-36 domains (p,0.01) except for health change. Moreover, symptoms of anxiety (36%) and depression (34%) were reported frequently. Medical treatment was prescribed in 46% of patients, in whom treatment was ineffective in 39%. Physical functioning scores were lower in patients with severe versus moderate DNP (p,0.01). Conclusions: The prevalence of severe PDNP was high. Severity of DNP was not related to pain severity. PDNP was associated with loss of QoL and with symptoms of anxiety and depression. A considerable proportion of patients did not have medical treatment and, if treatment was given, its impact was disappointing. Medical treatment of PDNP was unsatisfactory and clearly needs to be improved. Copyright © 2009 FEND [source] The role of neuropeptides and neuropeptide-degrading enzymes in wound healingEXPERIMENTAL DERMATOLOGY, Issue 9 2004John E. Olerud Thirty to 40% of diabetic patients develop sensory neuropathy. Neuropathy is a major causal factor in diabetic ulcers. Only 31% of neuropathic diabetic ulcers heal in 20 weeks. Patients with neuropathy have a 15.5-fold excess risk of amputation. Diabetic patients with neuropathy particularly lose epidermal and papillary dermal sensory nerves which release neuropeptides such as substance P (SP). Neutral endopeptidase (NEP), the enzyme that degrades SP, is dramatically over expressed in patients with diabetic neuropathy. SP has positive effect on wound healing. Treatment strategies related to the nervous system for prevention and treatment of diabetic ulcers currently being studied include prevention of neuropathy with tight control of blood glucose, application of neuropeptides, nerve growth factors (NGF), and antagonists of NEP. [source] Migraine and Psychiatric Comorbidity: From Theory and Hypotheses to Clinical ApplicationHEADACHE, Issue 9 2002Fred D. Sheftell MD Objective.,To review psychiatric issues that accompany migraine and means of addressing these issues. Background.,Psychiatric factors and migraine may interact in three general ways, etiologically, psychophysiologically or biobehaviorally, and comorbidly (the two disorders coexist), which is the present focus. There are several possible mechanisms of comorbidity. The relation between two disorders may be a result of chance. One disorder can cause another disorder: Diabetes can cause diabetic neuropathy. There might be shared environmental risks: Head trauma can cause both posttraumatic epilepsy and posttraumatic headache. And there may be environmental or genetic risk factors that produce a brain state giving rise to both conditions, that is, there may be some common biology underlying both conditions. This last mechanism seems to be the most likely one underlying comorbidity of migraine and psychiatric disorders. We introduce a possible role for classical paradigms of learned helplessness in regard to psychiatric comorbid depressive and anxiety disorders and migraine. Results.,There appears to be an association between migraine and affective disorders, particularly depression and anxiety. There are a number of formal tools for recognizing depression, but clinical evaluation should not be overlooked. Once diagnosed, depression and anxiety should be treated, both to improve the success of migraine treatment and to improve the patient's quality of life. Patients with recurring headaches are much more likely to overuse and misuse, rather than abuse, pain medications. It is important to be alert for signs that the patient may be misusing medication. Behavioral approaches can surround and support pharmacological therapy. Conclusions.,Migraine is often comorbid with psychiatric disorders, particularly depression and anxiety. The relationship is likely based on shared mechanisms and successful treatment is possible. [source] Epidermal transient receptor potential vanilloid 1 in idiopathic small nerve fibre disease, diabetic neuropathy and healthy human subjectsHISTOPATHOLOGY, Issue 5 2007E P Wilder-Smith Aims:, The transient receptor potential vanilloid 1 (TRPV1) plays an important role in mediating pain and heat. In painful neuropathies, intraepidermal TRPV1 nerve fibre expression is low or absent, suggesting that pain generated is not directly related to sensory nerve fibres. Recent evidence suggests that keratinocytes may act as thermal receptors via TRPV1. The aim was to investigate epidermal TRPV1 expression in patients with neuropathic conditions associated with pain. Methods and results:, In a prospective study of distal small nerve fibre neuropathy (DISN; n = 13) and diabetic neuropathy (DN; n = 12) intraepidermal nerve fibre density was assessed using the pan axonal marker PGP 9.5 and epidermal TPVR1 immunoreactivity compared with controls (n = 9). Intraepidermal nerve fibres failed to show TRPV1 immunoreactivity across all groups. There was moderate and strong TRPV1 reactivity of epidermal keratinocytes in 41.8% and 6% for DISN, 32.9% and 2.9% for DN and 25.4% and 5.1% for controls, respectively. Moderate keratinocyte TRPV1 expression was significantly increased in DISN compared with controls (P = 0.01). Conclusion:, Our study suggests that in human painful neuropathies, epidermal TRPV1 expression is mainly in keratinocytes. [source] Relationship between fascicle size and perineurial collagen IV content in diabetic and control human peripheral nerveHISTOPATHOLOGY, Issue 6 2000P E Williams Aim: The relationship between perineurial collagen IV content and fascicle size was determined in diabetic and control human peripheral nerve. Methods and results Age-matched diabetic and control sural nerve samples were immunostained using antibodies to collagen IV. The number of cell layers and the perimeter of the fascicle were measured and the collagen IV content of the perineurium determined. Using this method, a comparison could be made of collagen IV content in the perineuria of fascicles of different size. A positive linear relationship was found between fascicle size and the amount of collagen IV per unit of perineurium. The number of perineurial cell layers and the collagen IV content of the diabetic nerve did not differ from control values. Conclusions The linear relationship between fascicle size and perineurial collagen IV content per unit of perineurium underlines the importance of taking fascicle size into account when determining changes in basement membrane components associated with neuropathy. The results indicate that increased deposition of collagen IV is not involved in the early changes in the perineurial cell basement membrane and is thus not the primary factor involved in altered nerve function associated with diabetic neuropathy. [source] Penile vibratory stimulation and electroejaculation in the treatment of ejaculatory dysfunction,INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 6 2002JENS SØNKSEN Summary The purpose of this review is to present the current understanding of penile vibratory stimulation (PVS) and electroejaculation (EEJ) procedures and its clinical use in men with ejaculatory dysfunction. Unfortunately, the record of treating such individuals has been quite poor, but within recent years development and refinement of PVS and EEJ in men with spinal cord injury (SCI) has significantly enhanced the prospects for treatment of ejaculatory dysfunction. The majority of spinal cord injured men are not able to produce antegrade ejaculation by masturbation or sexual stimulation. However, approximately 80% of all spinal cord injured men with an intact ejaculatory reflex arc (above T10) can obtain antegrade ejaculation with PVS. Electroejaculation may be successful in obtaining ejaculate from men with all types of SCI, including men who do not have major components of the ejaculatory reflex arc. Because vibratory stimulation is very simple in use, non-invasive, it does not require anaesthesia and is preferred by the patients when compared with EEJ, PVS is recommended to be the first choice of treatment in spinal cord injured men. Furthermore, EEJ has been successfully used to induce ejaculation in men with multiple sclerosis and diabetic neuropathy. Any other conditions which affect the ejaculatory mechanism of the central and/or peripheral nervous system including surgical nerve injury may be treated successfully with EEJ. Finally, for sperm retrieval and sperm cryopreservation before intensive anticancer therapy in pubertal boys, PVS and EEJ have been successfully performed in patients who failed to obtain ejaculation by masturbation. Nearly all data concerning semen characteristics in men with ejaculatory dysfuntion originate from spinal cord injured men. Semen analyses demonstrate low sperm motility rates in the majority of spinal cord injured men. The data give evidence of a decline in spermatogenesis and motility of ejaculated spermatozoa shortly after (few weeks) an acute SCI. Furthermore, it is suggested that some factors in the seminal plasma and/or disordered storage of spermatozoa in the seminal vesicles are mainly responsible for the impaired semen profiles in men with chronic SCI. Home insemination with semen obtained by penile vibratory and introduced intravaginally in order to achieve successful pregnancies may be an option for some spinal cord injured men and their partners. The majority of men will further enhance their fertility potential when using either penile vibratory or EEJ combined with assisted reproduction techniques such as intrauterine insemination or in-vitro fertilization with or without intracytoplasmic sperm injection. [source] Chronic, painful lower extremity wounds: postoperative pain management through the use of continuous infusion of regional anaesthesia supplied by a portable pump deviceINTERNATIONAL WOUND JOURNAL, Issue 3 2010Christy L Scimeca Reducing and preventing postoperative pain are currently a topic of great interest. There are different modalities for providing analgesia that can provide an alternative or adjunct to opioid therapy. One mode of therapy involves the use of portable pain pump devices that can deliver continuous local anaesthesia directly to the site of interest. A considerable amount of attention in literature has been dedicated to using regional anaesthesia postoperatively for various surgical applications. However, to our knowledge, little or no work has been published concerning the use of infusion of regional anaesthesia in the treatment of painful lower extremity wounds. We present a case report of a 55-year-old gentleman with a complex past medical history, 2-year history of opioid dependency and a 2-week history of intractable pain associated with the combination of debilitating painful diabetic neuropathy and painful lower extremity wounds. After surgical debridement of the lower extremity wounds, substantial analgesia was achieved postoperatively through the implantation of a portable direct infusion pump device. The device supplied 2 ml/hour of 0·25% bupivacaine and resulted in a reduction in pain within the first hour of implantation. Although the device achieved maximal analgesia at 6 hours, we found that this could have been likely reduced through the use of a 5-ml bolus dose of 0·25% bupivacaine at the time of implantation. The device provided sufficient analgesia to the patient without any observed adverse effects, and showed significant potential in avoiding an increase in his requirement for other systemic analgesia including opioids. [source] | |||||||||||||||||||||||||||||||