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Sensory Nerve Conduction Velocity (sensory + nerve_conduction_velocity)
Selected AbstractsEffect of pneumatic power tool use on nerve conduction velocity across the wristHUMAN FACTORS AND ERGONOMICS IN MANUFACTURING & SERVICE INDUSTRIES, Issue 4 2005John Rosecrance The purpose of this study was to determine if the use of pneumatic power tools altered electrophysiologic properties of the median and ulnar nerves at the wrist during the work shift. Sensory nerve conduction velocities were measured in hands of workers before work and then at 2-hour intervals during the workday. Ten workers exposed to pneumatic power tool use and 10 workers not exposed to intensive hand activity were evaluated. The conduction velocities slowed significantly across the wrist in the median and ulnar nerves among workers using pneumatic tools but not among control workers. This investigation demonstrated that short-term exposure to highly intensive hand tasks causes significant slowing in nerve conduction velocity across the wrist. © 2005 Wiley Periodicals, Inc. Hum Factors Man 15: 339,352, 2005. [source] Electrophysiological sensory demyelination in typical chronic inflammatory demyelinating polyneuropathyEUROPEAN JOURNAL OF NEUROLOGY, Issue 7 2010Y. A. Rajabally Background:, The presence of electrophysiological demyelination of sensory nerves is not routinely assessed in the evaluation of suspected chronic inflammatory demyelinating polyneuropathy (CIDP). Whether this can be useful is unknown. Methods:, We compared, using surface recording techniques, in 19 patients with typical CIDP and 26 controls with distal large fibre sensory axonal neuropathy, the forearm median sensory conductions, sensory nerve action potential (SNAP) amplitudes and durations and sensory nerve conduction velocities (SNCVs) of median, radial and sural nerves. Results:, Median nerve sensory conduction block (SCB) across the forearm was greater in CIDP patients than in controls (P = 0.005). SNAP durations were longer in CIDP patients for median (P = 0.001) and sural nerves (P = 0.004). Receiver operating characteristic (ROC) curves provided sensitive (>40%) and specific (>95%) cut-offs for median nerve SCB as well as median and sural SNAP durations. SNCVs were significantly slower for median and sural nerves in CIDP patients, but ROC curves did not demonstrate cut-offs with useful sensitivities/specificities. Median SCB or prolonged median SNAP duration or prolonged sural SNAP duration offered a sensitivity of 73.7% for CIDP and specificity of 96.2%. Used as additional parameters, they improved diagnostic sensitivity of the American Academy of Neurology (AAN) criteria for CIDP of 1991, from 42.1% to 78.9% in this population, with preserved specificity of 100%. Discussion:, Sensory electrophysiological demyelination is present and may be diagnostically useful in typical CIDP. SCB detection and SNAP duration prolongation appear to represent more useful markers of demyelination than SNCV reduction. [source] Electrophysiological studies in a mouse model of Schwartz,Jampel syndrome demonstrate muscle fiber hyperactivity of peripheral nerve originMUSCLE AND NERVE, Issue 1 2009Andoni Echaniz-Laguna MD Abstract Schwartz,Jampel syndrome (SJS) is an autosomal-recessive condition characterized by muscle stiffness and chondrodysplasia. It is due to loss-of-function hypomorphic mutations in the HSPG2 gene that encodes for perlecan, a proteoglycan secreted into the basement membrane. The origin of muscle stiffness in SJS is debated. To resolve this issue, we performed an electrophysiological investigation of an SJS mouse model with a missense mutation in the HSPG2 gene. Compound muscle action potential amplitudes, distal motor latencies, repetitive nerve stimulation tests, and sensory nerve conduction velocities of SJS mice were normal. On electromyography (EMG), neuromyotonic discharges, that is, bursts of motor unit action potentials firing at high rates (120,300 HZ), were constantly observed in SJS mice in all muscles, except in the diaphragm. Neuromyotonic discharges were not influenced by general anesthesia and disappeared with curare administration. They persisted after complete motor nerve section, terminating only with Wallerian degeneration. These results demonstrate that perlecan deficiency in SJS provokes a neuromyotonic syndrome. The findings further suggest a distal axonal localization of the generator of neuromyotonic discharges. SJS should now be considered as an inherited disorder with peripheral nerve hyperexcitability. Muscle Nerve, 2009 [source] Diet-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] Workshop 5: NAAG and NAALADase: Functional Properties in the Central and Peripheral Nervous SystemJOURNAL OF NEUROCHEMISTRY, Issue 2002D. Bacich Glutamate carboxypeptidase II (GCPII, also known as N-acetylated-alpha-linked acidic dipeptidase or NAALADase) knockout (KO) mice were generated by inserting a GCPII targeting cassette containing a PGK-Neo resistance marker and stop codons in exons 1 and 2, and removal of exons 1 and 2 intron/exon boundary sequence. Embryonic stem cells were injected into C57BL6 blastocysts, and chimeric offspring born. Germline transmission was confirmed by mating the chimeras to generate heterozygous KO mice. Crossing heterozygous mice generated F2 generation mice homozygous for the null mutant, as confirmed by loss of GCPII protein. NAAG hydrolyzing activity was minimal (0.07 pmol/mg/min) in KO tissue, with normal levels (4.82 pmol/mg/min) in wild types and intermediate levels (1.73 pmol/mg/min) in heterozygotes. Preliminary neuropathy experiments showed KO mice are less affected by nerve-crush and recover faster from the damage-induced neuropathy, as indicated by EMG recording and nerve morphology. Similarly, GCPII KO mice subjected to high dose vitamin B6 displayed less severe neuropathy than wild types, as indicated by reduced sensory nerve conduction velocity and morphological deficits. Also, in a transient middle cerebral artery occlusion model, GCPII KO mice were significantly more resistant to the effects of cerebral ischemia than their wildtype littermates. Findings support GCPII involvement in stroke and in mediating chronic neuropathic conditions and suggest GCPII inhibitors may be useful in treatment of brain ischemia as well as peripheral neuropathies. [source] Towards development of a nonhuman primate model of carpal tunnel syndrome: Performance of a voluntary, repetitive pinching task induces median mononeuropathy in Macaca fascicularisJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 6 2007Carolyn M. Sommerich Abstract This study investigated changes in median sensory nerve conduction velocity (SNCV) over several weeks of exposure to a voluntary, moderately forceful, repetitive pinching task performed for food rewards by a small sample of young adult female monkeys (Macaca fascicularis). SNCV, derived from peak latency, decreased significantly in the working hands of three of the four subjects. The overall decline in NCV was 25%,31% from baseline. There was no decrease in SNCV in the contralateral, nonworking hands. Several weeks after being removed from the task, SNCV returned to within 87%,100% of baseline. MRI showed enlargement of the affected nerves near the proximal end of the carpal tunnel, at the time of maximal SNCV slowing. This new animal model demonstrates a temporally unambiguous relationship between exposure to a moderately forceful, repetitive manual task and development of median mononeuropathy at the wrist, and recovery of SNCV following termination of task exposure. This study contributes to the pattern of evidence of a causal relationship between manual work, median mononeuropathy, and carpal tunnel syndrome in humans. In the future, this new animal model could be used to characterize dose,response relationships between risk factors and carpal tunnel syndrome. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 25: 713,724, 2007 [source] Sodium Valproate in the Management of Painful Neuropathy in Type 2 Diabetes , a Randomized Placebo Controlled StudyJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2003DK Kochar OBJECTIVE: To study the effectiveness and safety aspects of sodium valproate in the management of painful neuropathy in patients of type 2 diabetes mellitus. MATERIAL AND METHODS: A randomized double-blind placebo controlled trial of sodium valproate was done in type 2 diabetic patients to assess its efficacy and safety in the management of painful neuropathy. We screened 60 patients but eight patients could not complete the study; hence, the present study was done on 52 patients. Each patient was assessed by clinical examination, pain score by short form of the McGill pain questionnaire (SF-MPQ) and electrophysiological examination, which included motor and sensory nerve conduction velocity, amplitude and H-reflex initially and at the end of 1 month of treatment. RESULTS: Significant improvement was noticed in the pain score of patients receiving sodium valproate in comparison to patients receiving placebo at the end of 1 month (P < 0.05). The changes in electrophysiological data were not significant. The drug was well tolerated by all patients except one who developed a raised aspartate transaminase (AST)/alanine transaminase (ALT) level after 15 days of treatment. CONCLUSION: Sodium valproate is a well-tolerated drug and provides significant subjective improvement in painful diabetic neuropathy. These data provide a basis for future trials of longer duration in a larger group of patients. [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] ELECTROPHYSIOLOGICAL ABNORMALITIES IN DIABETIC PATIENTSJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2000B. Lanzillo We studied 476 patients affected by diabetes: 166 male (mean age 61.6 ± 10 years, range 27,91) and 310 female (mean age 61.5 ± 8.4 years, range 25,82). Mean disease duration was 11.3 ± 7.6 years, range 0.3,37). All patients underwent surface motor and sensory nerve conduction along median, popliteal, and sural nerve. Results. Median nerve: in 3.1% of subjects sensory action potentials (SAP) was absent; sensory nerve conduction velocity (SNCV) was reduced in 41.8% in distal segment and in 27.5% in the proximal segment. Motor nerve conduction (MNCV) was reduced in 29.9% of the subjects. Sural nerve: SAP was absent in 24.4% and SNCV was reduced in 32.7%. Popliteal nerve: MNCV was abnormal in 30.4% of the subjects. Combining electrophysiological data we observed that: 1. 28.6% of the subjects resulted normal 2. 12.8% were affected by a lower limbs sensory neuropathy 3. 0.2% had a lower limbs motor neuropathy 4. 5.9% had a lower limbs sensory-motor neuropathy 5. 6.1% had a diffused sensory neuropathy 6. 30.2% had a diffused sensory-motor neuropathy 7. 16.2% had a carpal tunnel syndrome. Patients were divided in 2 groups: patients with and patients without neuropahy: the latter showed a significantly shorter disease duration (12.7 ± 8.1 vs 9.0 ± 6.3; p < 0.0001). In addition, we observed a significant correlation between disease duration and distal latency, median and popliteal MNCV, and SNCV in median and sural nerve (Regression test; p < 0.0001). Patients on insulin showed a longer disease duration and more severe electrophysiological abnormalities. [source] High insulin levels are positively associated with peripheral nervous system functionACTA NEUROLOGICA SCANDINAVICA, Issue 2 2009H. Isojärvi Objective,,, The aim of this study was to analyze peripheral nervous system (PNS) function in overweight and obese individuals. Materials and Methods,,, Forty-four adult non-diabetic overweight individuals were recruited. Peroneal motor nerve conduction and radial, sural, and medial plantar sensory nerve conduction were studied. Insulin and glucose levels were determined twice (over a 2- to 3-year period) with an oral glucose tolerance test (OGTT). Multiple stepwise linear regression models adjusted for age, height, weight, and skin temperature were used to analyze the data. Results,,, Analysis revealed that baseline insulin levels measured 120 min after an OGTT explained 18% of the variation in peroneal F -wave minimum latency, 8% of peroneal F -wave maximum latency variation, 15% of sural sensory latency variation, 13% of sural sensory nerve conduction velocity (NCV) variation, and 10% of the variation in medial plantar sensory NCV. Discussion and Conclusion,,, Our study shows that serum insulin levels measured 120 min after an OGGT are positively associated with PNS function. High insulin levels without notably high glucose levels appear to be beneficial for the function of the PNS. [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] | |||||||||||||