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Motor Nerve Conduction Velocity (motor + nerve_conduction_velocity)
Selected AbstractsDiet-induced obesity in Sprague,Dawley rats causes microvascular and neural dysfunctionDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 4 2010Eric P. Davidson Abstract Background The objective of this study was to determine the effect of diet-induced obesity (DIO) on microvascular and neural function. Methods Rats were fed a standard or high fat diet for up to 32 weeks. The following measurements were carried out: vasodilation in epineurial arterioles using videomicroscopy, endoneurial blood flow using hydrogen clearance, nerve conduction velocity using electrical stimulation, size,frequency distribution of myelinated fibres of the sciatic nerve, intraepidermal nerve fibre density using confocal microscopy and thermal nociception using the Hargreaves method. Results Rats fed a high fat diet for 32 weeks developed sensory neuropathy, as indicated by slowing of sensory nerve conduction velocity and thermal hypoalgesia. Motor nerve conduction velocity and endoneurial blood flow were not impaired. Mean axonal diameter of myelinated fibres of the sciatic nerve was unchanged in high fat-fed rats compared with that in control. Intraepidermal nerve fibre density was significantly reduced in high fat-fed rats. Vascular relaxation to acetylcholine and calcitonin gene-related peptide was decreased and expression of neutral endopeptidase (NEP) increased in epineurial arterioles of rats fed a high fat diet. In contrast, insulin-mediated vascular relaxation was increased in epineurial arterioles. NEP activity was significantly increased in the skin of the hindpaw. Markers of oxidative stress were increased in the aorta and serum of high fat-fed rats but not in epineurial arterioles. Conclusion Chronic obesity causes microvascular and neural dysfunction. This is associated with increased expression of NEP but not oxidative stress in epineurial arterioles. NEP degrades vasoactive peptides, which may explain the decrease in microvascular function. Copyright © 2010 John Wiley & Sons, Ltd. [source] Electrophysiological features in the distinction between hereditary demyelinating and chronic acquired demyelinating neuropathiesJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2004F Poglio We carried out an electrophysiological retrospective study in 55 patients with chronic demyelinating acquired and hereditary neuropathies. Alterations of motor nerve conduction velocities (MNCV), distal motor latencies (DML), conduction blocks (CB) and compound muscle action potential (CMAP) were compared, considering the whole number of nerves for each disease. MNCV, DML, CB and CMAP were considered suggestive of demyelination when meeting the American Academy of Neurology (AAN) criteria. Abnormally slow MNCV was found respectively in the 46% of all the CMTX female nerves studied, in the 56.5% of CMTX males, 84% of CMT1A, 74% CIDP and 70% of MAG-PNP. Prolonged DML was observed in the 25% of the CMTX female nerves studied, in the 49.5% of CMTX males, 81% of CMT1A, 63% of CIDP and 71% of MAG-PNP. Moreover, CB were quite often evidenced in CIDP and MAG-PNP nerves (respectively in 48% and 29%) and rarely in hereditary neuropathies. Finally, we observed CMAP reduction in the 45% of all the CMTX female nerves studied, in the 50% of CMTX males, 63% of CMT1A, 49% of CIDP and 60% of MAG-PNP. A well-characterized pattern generally allows an electrophysiological distinction between CMT1A, CMTX males, MAG-PNP on one side and CIDP and CMTX females on the other side. A clear electrodiagnostic distinction result is often hard between CMTX males and MAG-PNP and between CIDP and CMTX females. [source] ROSS SYNDROME: CLINICAL AND LABORATORY EVALUATION OF TWO CASESJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2000G. De Joanna We describe two males, aged 41 and 55, come to our observation complaining of heat intolerance, abnormal increase in body temperature with minimal exercising, reduced sweating and, generalized fatigability; one of them had distal paresthesias. Neurologic evaluation showed bilateral Adie's tonic pupil and an absence of deep-tendon jerks. A diagnosis of Ross' Syndrome was advanced. Autonomic tests, nerve conduction study, H-reflex, computerized termoregulatory and pain thresholds, laser CO2 cortical evoked potentials, and skin biopsy were performed. One of them performed a histamine test and hand photopletismography resulted positive for sympathetic impairment, and pilocarpine pupil test that showed a parasympathetic denervation hypersensitivity. The following tests gave the same results in both patients: parasympathetic and most sympathetic tests were normal. Sympathetic skin response was absent and Minor test showed an almost complete absence of sweating. Sweating was possible only in two or three small areas. Positive pilocarpine test suggested a postganglionic involvement of sympathetic nervous system. Sensitive and motor nerve conduction velocities were normal, while H-reflex was not detectable. Termoregulatory and pain thresholds were abnormal. Laser CO2 cortical evoked potentials showed the absence of C fibre potentials, whereas A-, fibres response was abnormal in one of them. Hairy skin biopsy showed a definite reduction of sweat glands and of small vessel innervation; glabrous skin biopsy performed in one of them showed a reduced number of Meissner corpuscles. These findings suggest that in Ross' Syndrome the degenerative process can involve, besides the autonomic fibres, myelinated somatosensory fibres also. [source] C-peptide: new findings and therapeutic implications in diabetesCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 4 2004John Wahren Summary In contrast to earlier views, new data indicate that proinsulin C-peptide exerts important physiological effects and shows the characteristics of an endogenous peptide hormone. C-peptide in nanomolar concentrations binds specifically to cell membranes, probably to a G-protein coupled receptor. Ca2+ - and MAP-kinase dependent signalling pathways are activated, resulting in stimulation of Na+, K+ -ATPase and endothelial nitric oxide (NO) synthase, two enzyme systems known to be deficient in diabetes. C-peptide may also interact synergistically with insulin signal transduction. Studies in intact animals and in patients with type 1 diabetes have demonstrated multifaceted effects. Thus, C-peptide administration in streptozotocin-diabetic animals results in normalization of diabetes-induced glomerular hyperfiltration, reduction of urinary albumin excretion and diminished glomerular expansion. The former two effects have also been observed in type 1 diabetes patients given C-peptide in replacement dose for up to 3 months. Peripheral nerve function and structure are likewise influenced by C-peptide administration; sensory and motor nerve conduction velocities increase and nerve structural changes are diminished or reversed in diabetic rats. In patients with type 1 diabetes, beneficial effects have been demonstrated on sensory nerve conduction velocity, vibration perception and autonomic nerve function. C-peptide also augments blood flow in several tissues in type 1 diabetes via its stimulation of endothelial NO release, emphasizing a role for C-peptide in maintaining vascular homeostasis. Continued research is needed to establish whether, among the hormones from the islets of Langerhans, C-peptide is the ugly duckling that , nearly 40 years after its discovery , may prove to be an endogenous peptide hormone of importance in the treatment of diabetic long-term complications. [source] Protein kinase C beta inhibitor prevents diabetic peripheral neuropathy, but not histopathological abnormalities of retina in Spontaneously Diabetic Torii ratDIABETES OBESITY & METABOLISM, Issue 11 2009T. Sasase Spontaneously Diabetic Torii (SDT) rat shows severe ocular complications such as tractional retinal detachment. In the present study, effect of protein kinase C beta (PKC,) inhibitor JTT-010 was evaluated to clarify the involvement of PKC, in complications of SDT rat. SDT rats were administered JTT-010 (10 or 50 mg/kg/day) for 48 weeks. SDT rats showed delayed oscillatory potentials in electroretinogram. Delayed motor nerve conduction velocity, decreased coefficients of variation of R,R intervals in electrocardiogram and thermal hypoalgesia were also observed. These functional disorders were prevented by administration of JTT-010. Abnormal retinal vascular was formed and the optic disc was protruded in SDT rat; however, JTT-010 did not prevent these hyperglycaemia-induced retinal abnormalities. These findings indicate that PKC, is intimately involved in diabetic complications; however, it seems that other factor(s) are primary contributors to histopathological abnormalities in retina. Therefore, PKC, inhibitors require concurrent administration of antihyperglycaemic drugs to achieve maximum effect on diabetic complications. [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] Age-Induced Neuropathy In RatsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000S Yagihashi We studied the effects of exogenously administered advanced glycation end-products (AGE) on the peripheral nerve function and structure in normal rats. Normal Wistar rats aged 6 weeks were injected intraperitoneally with purified AGE (20 mg/kg/day) produced by incubation of glucose with bovine serum albumin (BSA) for 12 weeks. Control rats were treated with BSA alone. One of AGE-treated groups was co-treated with 50 mg/kg aminoguanidine (AG). During the experimental period, body weight and blood glucose levels were not affected in AGE-treated rats. Serum AGE levels were elevated two fold in AGE-treated group whereas BSA treated rats maintained normal levels, whereas tissue AGE levels in sciatic nerve were not increased in treated group. AG did not alter the levels of serum AGE. AGE-treated rats exhibited significant delay of motor nerve conduction velocity by 30% and reduction of sciatic nerve in Na,K-ATPase activity by 25% in AGE-treated rats. AG treatment significantly inhibited these changes. Immunostains on the cross-sections of sciatic nerve demonstrated significant increase in cells positive for 8 hydroxy-deoxyguanosine, a marker of oxidative stress-induced DNA injury, in AGE-treated group. AG treatment significantly inhibited this reaction. There was no difference in morphometric data on myelinated fibers in sural nerve among the experimental groups. AGE-injected rats thus showed the neuropathic changes, similar to those found in experimentally-induced diabetic animals and it is therefore suggested that AGE have a pathogenetic role in the development of diabetic neuropathy through induction of excessive oxidative stress. Supported by Juvenile Diabetes Foundation International (1-2000-263), Japan Diabetes Foundation, Japanese Ministry of Science, Education, Sports and Culture. [source] Sural Nerve Pathology In Asymptomatic Minimally Neuropathic Diabetic PatientsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000Ra Malik 12 diabetic patients aged 47.5 ± 9.4 yr., duration of diabetes (14.6 ± 10.3 yr.) and 15 control subjects were studied. In diabetic patients neuropathy symptom score =0, neuropathy deficit score = 4.5 + 0.7/30, vibration = 12.0 + 1.8 V, thermal perception (2.0 + 0.8°C), heart rate variation during deep breathing (17.8 + 2.3), 30:15 ratio (1.31 + 0.07) was normal. Baseline (n=12) and repeat neurophysiology (n=10) performed 8.7 + 0.6 years after sural nerve biopsy demonstrated normal values at baseline, with progression of neuropathy (peroneal motor nerve conduction velocity (ms,1) (42.3 + 2.9 v 39.4 +2.0), sural nerve conduction velocity (45.4 + 3.7 v 43.6 + 1.7). Myelinated fibre density, fibre and axonal area and g-ratio were not significantly reduced. Teased fibre studies showed paranodal abnormalities (p < 0.001), segmental demyelination (P < 0.01) with remyelination (P < 0.01) without axonal degeneration. Unassociated Schwann cell profile density (p < 0.04) and axon density (P < 0.001) were increased and axon diameter was decreased (P < 0.007) with a shift of the size frequency distribution to the left (skewness- 0.89 v 0.64, P < 0.03) suggestive of unmyelinated axonal atrophy/regeneration. Endoneurial capillary basement membrane thickening (P < 0.006), endothelial cell hyperplasia (P < 0.004) and luminal narrowing (P < 0.007) occurred. Current measures of neuropathy are too insensitive to detect significant nerve fibre pathology. The presence of microangiopathy provides support for a microvascular basis of diabetic neuropathy. [source] SUB-CLINICAL PERIPHERAL NERVE INVOLVEMENT IN PSORIATIC ARTHRITISJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2000C. Di Girolamo Immunological studies document the role of HLA in psoriasis and the correlation between neuropeptides, psoriasis, and related arthritis. Some anecdotal case reports, moreover, describe a noncasual association between peripheral neuropathy and psoriatic manifestations. To verify a possible subclinical peripheral nerve involvement in this disimmune pathology, we started a pilot study in twenty patients with psoriatic arthritis and in whom other common causes of peripheral neuropathies had been ruled out. We performed a complete clinical neurological examination and a neurophysiological examination (orthodromic sensory and motor nerve conduction velocity in median and tibial nerves; antidromic sensory nerve conduction velocity in sural nerve). In 40% of the patients there was a mild but definite "glove-stocking" hypoesthesia, while hypopallesthesia was detected in only 20%. Electrophysiologic examinations were less informative borderline distal conduction velocities in 30% of patients. These preliminary data suggest a peripheral nerve involvement in this pathology, mainly affecting the small nerve fibres. [source] Chronic treatment of silymarin improves hyperalgesia and motor nerve conduction velocity in diabetic neuropathic ratPHYTOTHERAPY RESEARCH, Issue 8 2010Tourandokht Baluchnejadmojarad Abstract The effect of chronic silymarin (SM) treatment on hyperalgesia, sciatic motor nerve conduction velocity (MNCV) and oxidative stress in streptozotocin (STZ)-diabetic neuropathic rat was evaluated. Rats were divided into control, diabetic, SM-treated control and diabetic, and sodium salisylate (SS)-treated control and diabetic. SM was administered daily at a dose of 100,mg/kg for two months. Finally, hyperalgesia and sciatic MNCV and oxidative stress markers were assessed. Diabetic rats showed a significant deficit in MNCV and markedly exhibited chemical and thermal hyperalgesia, indicating development of diabetic neuropathy. Antioxidant enzyme superoxide dismutase (SOD) level significantly reduced and malondialdehyde (MDA) level significantly increased in diabetic rats compared to control rats; SM treatment significantly ameliorated the alteration in MNCV, hyperalgesia, MDA level and antioxidant enzyme SOD in diabetic rats. These results clearly suggest the potential effect of SM in prevention and treatment of diabetic neuropathy. Copyright © 2009 John Wiley & Sons, Ltd. [source] A Novel Drug Therapy for Recurrent Laryngeal Nerve Injury Using T-588,THE LARYNGOSCOPE, Issue 7 2007Yuko Mori MD Abstract Objectives/Hypothesis: We have previously shown that gene therapy using Insulin-like growth factor (IGF)-I, glial cell line-derived neurotrophic factor (GDNF), and brain-derived neurotrophic factor (BDNF), or a combination of these trophic factors, is a treatment option for recurrent laryngeal nerve (RLN) palsy. However, there remain some difficulties preventing this option from becoming a common clinical therapy for RLN injury. Thus, we need to develop novel treatment option that overcomes the problems of gene therapy. R(,)-1-(benzothiophen-5-yl)-2-[2-N,N-diethylamino]ethoxy]ethanol hydrochloride (T-588), a synthetic compound, is known to have neuroprotective effects on neural cells. In the present study, the possibility of new drug treatments using T-588 for RLN injury was assessed using rat models. Study Design: Animal study. Methods: Animals were administered T-588 for 4 weeks. The neuroprotective effects of T-588 administration after vagal nerve avulsion and neurofunctional recovery after recurrent laryngeal nerve crush were studied using motoneuron cell counting, evaluation of choline acetyltransferase immunoreactivity, the electrophysiologic examination, and the re-mobilization of the vocal fold. Results: T-588 administration successfully prevented motoneuron loss and ameliorated the choline acetyltransferase immunoreactivity in the ipsilateral nucleus ambiguus after vagal nerve avulsion. Significant improvements of motor nerve conduction velocity of the RLN and vocal fold movement were observed in the treatment group when compared to controls. Conclusion: These results indicate that oral administration of T-588 might be a promising therapeutic option in treating peripheral nerve injury. [source] | ||||||||||