Decrease In Nerve Conduction Velocity Research Articles

Genetic and Functional Analyses of Patients with Marked Hypo-High-Density Lipoprotein Cholesterolemia.

This study aimed to analyze two cases of marked hypo-high-density lipoprotein (HDL) cholesterolemia to identify mutations in ATP-binding cassette transporter A1 (ABCA1) and elucidate the molecular mechanism by which these novel pathological mutations contribute to hypo-HDL cholesterolemia in Tangier disease. Wild type and mutant expression plasmids containing a FLAG tag inserted at the C-terminus of the human ABCA1 gene were generated and transfected into HEK293T cells. ABCA1 protein expression and cholesterol efflux were evaluated via Western blotting and efflux assay. The difference in the rate of change in protein expression was evaluated when proteolytic and protein-producing systems were inhibited. In case 1, a 20-year-old woman presented with a chief complaint of gait disturbance. Her HDL-C level was only 6.2 mg/dL. Tangier disease was suspected because of muscle weakness, decreased nerve conduction velocity, and splenomegaly. Whole-exome analysis showed compound heterozygosity for a W484* nonsense mutation and S1343I missense mutation, which confirmed Tangier disease. Cholesterol efflux decreased by a mixture of W484* and S1343I mutations. The S1343I mutation decreased the protein production rate but increased the degradation rate, decreasing the protein levels. This patient also had Krabbe disease. The endogenous ABCA1 protein level of macrophage cell decreased by knocking down its internal galactocerebrosidase.Case 2, a 51-year-old woman who underwent tonsillectomy presented with peripheral neuropathy, corneal opacity, and HDL-C of 3.4 mg/dL. Whole-exome analysis revealed compound heterozygosity for R579* and R1572* nonsense mutations, which confirmed Tangier disease. Case 1 is a new ABCA1 mutation with complex pathogenicity, namely, a W484*/S1343I compound heterozygote with marked hypo-HDL cholesterolemia. Analyses of the compound heterozygous mutations indicated that decreases in ABCA1 protein levels and cholesterol efflux activity caused by the novel S1343I mutation combined with loss of W484* protein activity could lead to marked hypo-HDL cholesterolemia. Galactocerebrosidase dysfunction could also be a potential confounding factor for ABCA1 protein function.

Blocking CCN2 Reduces Established Palmar Neuromuscular Fibrosis and Improves Function Following Repetitive Overuse Injury.

The matricellular protein cell communication factor 2/connective tissue growth factor (CCN2/CTGF) is critical to development of neuromuscular fibrosis. Here, we tested whether anti-CCN2 antibody treatment will reduce established forepaw fibro-degenerative changes and improve function in a rat model of overuse injury. Adult female rats performed a high repetition high force (HRHF) task for 18 weeks. Tissues were collected from one subset after 18 wks (HRHF-Untreated). Two subsets were provided 6 wks of rest with concurrent treatment with anti-CCN2 (HRHF-Rest/anti-CCN2) or IgG (HRHF-Rest/IgG). Results were compared to IgG-treated Controls. Forepaw muscle fibrosis, neural fibrosis and entheseal damage were increased in HRHF-Untreated rats, compared to Controls, and changes were ameliorated in HRHF-Rest/anti-CCN2 rats. Anti-CCN2 treatment also reduced phosphorylated-β-catenin (pro-fibrotic protein) in muscles and distal bone/entheses complex, and increased CCN3 (anti-fibrotic) in the same tissues, compared to HRHF-Untreated rats. Grip strength declines and mechanical sensitivity observed in HRHF-Untreated improved with rest; grip strength improved further in HRHF-Rest/anti-CCN2. Grip strength declines correlated with muscle fibrosis, entheseal damage, extraneural fibrosis, and decreased nerve conduction velocity, while enhanced mechanical sensitivity (a pain-related behavior) correlated with extraneural fibrosis. These studies demonstrate that blocking CCN2 signaling reduces established forepaw neuromuscular fibrosis and entheseal damage, which improves forepaw function, following overuse injury.

Through Its Powerful Antioxidative Properties, L-Theanine Ameliorates Vincristine-Induced Neuropathy in Rats.

L-theanine (LT), which is a major amino acid found in green tea, was shown to alleviate Vincristine (VCR)-induced peripheral neuropathy and associated neuronal functional changes in rats. To induce peripheral neuropathy, rats were administered VCR at a dose of 100 mg/kg/day intraperitoneally on days 1-5 and 8-12, while control rats received LT at doses of 30, 100, and 300 mg/kg/day intraperitoneally for 21 days or saline solution. Electrophysiological measurements were taken to evaluate the nerve functional loss and recovery through motor and sensory nerve conduction velocities. The sciatic nerve was examined for several biomarkers, including nitric oxide (NO), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), total calcium, IL-6, IL-10, MPO, and caspase-3. The results showed that VCR caused significant hyperalgesia and allodynia in rats; decreased nerve conduction velocity; increased NO and MDA levels; and decreased GSH, SOD, CAT, and IL-10 levels. LT was found to significantly reduce VCR-induced nociceptive pain thresholds, decrease oxidative stress levels (NO, MDA), increase antioxidative strength (GSH, SOD, CAT), and reduce neuroinflammatory activity and apoptosis markers (caspase-3). LT's antioxidant, calcium homeostasis, anti-inflammatory, anti-apoptotic, and neuroprotective properties make it a potential adjuvant to conventional treatment in VCR-induced neuropathy in rats.

α-Synuclein induces prodromal symptoms of Parkinson’s disease via activating TLR2/MyD88/NF-κB pathway in Schwann cells of vagus nerve in a rat model

BackgroundIncreasing evidence suggests that patients with Parkinson's disease (PD) present with peripheral autonomic dysfunction (AutD) that even precedes motor deficits, through which α-synuclein can spread to the central nervous system. However, the pathological mechanisms underlying AutD in prodromal PD remain unclear. Here, we investigated the role of α-synuclein and its interplay with the activation of Schwann cells (SCs) of the vagus nerve in AutD.MethodsRats were subjected to injection with adeno-associated viruses containing the human mutated A53T gene (AAV-A53T) or an empty vector into the left cervical vagus nerve and evaluated for gastrointestinal symptoms, locomotor functions, intestinal blood flow, and nerve electrophysiology. Further, we examined the impact of α-synucleinopathy on vagus nerves, SCs, and central nervous system neurons using electron microscopy, immunofluorescence, immunohistochemistry, and western blot. Finally, the role of Toll-like receptor 2 (TLR2) in regulating the neuroinflammation in the vagus nerve via MyD88 and NF-κB pathway was determined using genetic knockdown.ResultsWe found that rats injected with AAV-A53T in the vagus nerve exhibited prominent signs of AutD, preceding the onset of motor deficits and central dopaminergic abnormalities by at least 3 months, which could serve as a model for prodromal PD. In addition, reduced intestinal blood flow and decreased nerve conduction velocity were identified in AAV-A53T-injected rats, accompanied by disrupted myelin sheaths and swollen SCs in the vagus nerve. Furthermore, our data demonstrated that p-α-synuclein was deposited in SCs but not in axons, activating the TLR2/MyD88/NF-κB signaling pathway and leading to neuroinflammatory responses. In contrast, silencing the TLR2 gene not only reduced inflammatory cytokine expression but also ameliorated vagal demyelination and secondary axonal loss, consequently improving autonomic function in rats.ConclusionsThese observations suggest that overexpression of α-synuclein in the vagus nerve can induce symptoms of AutD in prodromal PD, and provide support for a deeper understanding of the pathological mechanisms underlying AutD and the emergence of effective therapeutic strategies for PD.

Decreased nerve conduction velocity may be a predictor of fingertip dexterity and subjective complaints

We examined the causes of decreased fingertip dexterity in elderly individuals with an aim to improve their quality of life by improving their activities of daily living. We calculated nerve conduction velocity, absolute error during force adjustment tasks, and fingertip dexterity test scores for 30 young (21–34 years old) and 30 elderly (60–74 years old) participants to identify age-related changes. We also assessed subjective complaints of pain, motor function, and numbness. Motor nerve (young: 55.8 ± 3.7 m/s; elderly: 52.2 ± 5.0 m/s) and sensory nerve (young: 59.4 ± 3.4 m/s; elderly: 55.5 ± 5.3 m/s) conduction velocities decreased in an age-dependent manner. Moreover, the decrease of motor nerve conduction velocity was associated with decreased fingertip dexterity (objective index), while the decrease of sensory nerve conduction velocity was associated with subjective complaints of pain and motor function (subjective index).

Effect of body mass index on ulnar nerve conduction velocity among medical students

Background: Obesity and overweight incidence is increasing among the medical students. The main reason for obesity among medical students is sedentary lifestyle, unhealthy food intake and stress. Increase in subcutaneous fat impairs the conduction in nerve fibers. Body mass index (BMI) is an easy tool to assess the obesity as it is noninvasive and non-expensive. Nerve conduction studies are the tools for assessing the performance of the nervous system. Aims and Objectives: The aim of the study was to evaluate the effect of obesity on the ulnar nerve conduction velocity among medical students. Materials and Methods: A total of 50 medical students were recruited for the study and the study was done in the Department of Physiology, ESIC Medical College, Hyderabad. Two groups were made Group A (n = 25 with BMI 18.5–24.9) and Group B (n = 25 with BMI >25). AD instrument was used for data acquisition for right ulnar nerve conduction velocity in both the groups. Results from both the groups were compared. Results: Nerve conduction velocity among the Group B students (50.95 ± 15.91) was decreased compared to Group A students (57.56 ± 14.79) but the decrease in nerve conduction velocity was not significant (P = 0.28). Conclusions: Nerve conduction velocity gets impaired with obesity among medical students, but further studies need to be done with more sample size.

Nomophobia and the psycho-physiological effects of PUBG gaming on medical college student’s health and academic performance

Introduction and Aim: Nomophobia is a psychological condition, where people have a fear of being detached from mobile phone connectivity. The medical college students are suffering from PUBG addiction which affects their psycho-physiological parameters. The aim is to assess the prevalence of nomophobia in the medical college students, to assess the stress and anxiety in the absence of smartphone and correlate it with the conduction velocity of median nerve. Materials and Methods: A cross-sectional study was conducted in the physiology department of a tertiary care teaching hospital for a period of 2 months involving 169 medical students using smartphones. For studying nomophobia, the students in the study group were divided into groups A and B according to their smartphone usage and on the basis of a Smartphone Addiction Scale (SPAS) Questionnaire. Results: Out of the 169 students, 80 were subjected for the assessment of the variability in the median nerve conduction velocity as a quantitative measurement to detect the decrease in the terminal latency index, motor distal latency and the conduction velocity due to excessive gaming or chronic smartphone usage. As per our hypothesis 94.37 % of the study sample had decreased terminal latency index and about 85.62 % of students had a decreased nerve conduction velocity. Conclusion: The prevalence of nomophobia in our study was 37.39 % as per the ICD-10 diagnostic criteria for dependence syndrome. Hence medical education to school-going children, teenagers and adolescents about the risks of excessive smartphone usage should be given as they are the most vulnerable to this disorder.

460-P: Cellular Communication of Schwann Cell Subtypes in Metabolically-Acquired Neuropathy

The prevalence of the metabolic syndrome (MetS) is increasing worldwide due in part to the increased consumption of a Western diet. MetS is associated with peripheral neuropathy (PN) . PN develops in a cell non-autonomous manner with involvement of axons, Schwann cells (SC) and nerve tissue- infiltrating macrophages (TIM) . SC are divided into subtypes with different roles in nerve injury. Our aim in the current study was to determine how gene expression of different types of SC and macrophages are affected in MetS and how these cells communicate with one another. C57BL6/j male mice (6-weeks old) were fed either a standard diet (SD, 10% fat) or high fat diet (HFD, 60%) for 17 weeks. Metabolic and PN phenotyping were performed for all mice and SC were extracted from sciatic nerves for single cell RNA sequencing (scRNA-seq) . Cellular communication was determined using the CellChat tool. Mice on HFD had higher fasting blood glucose (FBG) , glycated hemoglobin (HbA1c) and decreased nerve conduction velocities and intraepidermal nerve fiber densities consistent with PN compared to mice on SD. Analysis of SC scRNA-seq data revealed unique RNA expression signatures for TIM and 4 subpopulations of SC denoted as myelinating SC (mySC) , non-myelinating SC (nmSC) , SC precursors (SCP) and regenerating SC. Inflammatory genes such as Ptprc and Il1b were significantly more expressed in both TIM and mySC in HFD mice compared to SD mice. CellChat analysis of cellular communication revealed more crosstalk between TIM and various types of SC in HFD animals and identified multiple metabolic and inflammatory pathways that were activated in HFD compared to SD mice. In conclusion, our study shows that there are many subtypes of SC that behave differently in MetS. Their communication with each other and with TIM strongly implicates these two cell types in the pathogenesis of metabolically acquired PN. Disclosure S.Eid: None. M.H.Noureldein: None. F.Mendelson: None. E.L.Feldman: None. Funding Funding was provided by the National Institutes of Health (NIH) (1R24082841 to ELF) , Novo Nordisk Foundation (NNF14OC0011633 to ELF) , the Nathan and Rose Milstein Research Fund (to SAE) , NeuroNetwork for Emerging Therapies at the University of Michigan (to SAE, MHN, and ELF) , and the A. Alfred Taubman Medical Research Institute (to SAE, MHN, and ELF) .

Diyabetik ve Non-Diyabetik Hastalarda Total İntravenöz Anestezi ve Sevofluran Anestezisinin Rokuronyumun Klinik Etki Süresi Üzerine Olan Etkilerinin Retrospektif Olarak Karşılaştırılması: Retrospektif Gözlemsel Çalışma

Objective: Due to the decrease in nerve conduction velocity, the clinical effect of rocuronium may be prolonged in diabetic patients receiving inhalation anesthesia, and its postoperative residual muscle relaxant effect may lead to complications. We compared the effects of total intravenous anesthesia and sevoflurane anesthesia on the clinical duration of action of rocuronium in diabetic and nondiabetic patients. Material and Methods: Patients between the ages of 18-65, who underwent general anesthesia for elective surgery in the general surgery department of our hospital (0.6 mg of rocuronium was used for tracheal intubation), with Type 2 diabetes and with the American Society of Anesthesiologists Physical Condition Classification (ASA) I-II were included in the study. Non-diabetic patients (ASA I-II) of the same age were included in the study as the control group. The duration of the clinical effect of rocuronium between the time of administration of the first dose of rocuronium and the time of administration of the additional rocuronium dose (time recorded in TOFcount 2-TOFc2) was evaluated. Results: The clinical duration of action of rocuronium was longer in both diabetic groups than in nondiabetic groups (p=0.000). When the diabetic patient groups were compared, the clinical duration of action of rocuronium was longer in the diabetic sevoflurane group than in the diabetic group that received total intravenous anesthesia (p=0.012). Conclusion: It was determined that the duration of rocuronium action was longer in diabetic patients who were administered sevoflurane anesthesia than in patients who received total intravenous anesthesia and in non-diabetic patients.

Comparison of the Effects of Electroacupuncture and Melatonin on Nerve Regeneration in Experimentally Nerve-Damaged Rats.

Development of methods to accelerate nerve regeneration in peripheral nerve damage is important. Electroacupuncture is a new therapeutic method that combines traditional acupuncture with modern electrotherapy. Melatonin has been shown to reduce nerve damage. Objectives: In this study, we aimed to determine and compare the therapeutic effects of electroacupuncture and melatonin on rat sciatic nerve injury. A total of 56 adult male Wistar Albino rats were divided into four study groups with 14 animals in each group: intact control (group I), subcutaneous saline (group II), subcutaneous melatonin (group III), and electroacupuncture (group IV). Surgical procedure including unilateral (right) sciatic nerve injury was applied to groups II, III, and IV. Saline and melatonin started immediately after surgery for six weeks, while electroacupuncture was given two weeks after surgery for 3 weeks. Functional and histological assessments were used as outcome measurements. Sciatic nerve damage caused a significant decrease in nerve conduction velocity. Both electroacupuncture treatment and melatonin treatment significantly increased the nerve conduction velocity. Both sciatic functional recovery and histological regeneration were faster in these treatment groups compared to the saline. However, no significant difference was observed between the two treatment groups. Electroacupuncture and melatonin are promising alternative treatment strategies for peripheral nerve damage and can be examined in detail in future studies.

Neuroprotective effect of l-theanine in a rat model of chronic constriction injury of sciatic nerve-induced neuropathic pain

We investigated the protective efficacy of l-theanine (LT), the major amino acid components of green tea, on chronic constriction injury (CCI) of sciatic nerve-induced neuropathic pain (NP) development and neuronal functional changes in rats. Rats with NP induced by CCI of the left sciatic nerve and sham-operated rats received LT or saline solution, with pain sensitive tests of thermal hyperalgesia and mechanical allodynia. Motor and sensory nerve conduction velocities were measured after surgery. Subsequently, the rats were sacrificed; the sciatic nerve was excised, homogenized, prepared and subjected for estimation of nitric oxide (NO), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), myeloperoxidase (MPO), and caspase-3. CCI produced a significant increase in hyperalgesia and allodynia, an increase in SFI, a decrease in nerve conduction velocity, increases in NO, MDA, TNF-α, IL-1β, IL-6, MPO, and caspase-3 levels, as well as reduction of GSH, SOD, and CAT in the rat sciatic nerve. LT treatment significantly and dose-dependently alleviated CCI-induced nociceptive pain thresholds and ameliorated abnormal nerve conduction and functional loss in rats with CCI. Moreover, LT treatment reduced NO and MDA levels, increased antioxidative strength, and markedly suppressed the levels of neuroinflammatory and apoptotic markers in injured sciatic nerves. This is the first report on the ameliorative effect of LT in CCI-induced NP in rats. This effect might be attributed to its anti-oxidative, anti-inflammatory, anti-apoptotic, and neuroprotective, thus making it potentially useful as an adjuvant to conventional treatment.

Показники стимуляційної електронейроміографії в пацієнтів iз первинним гіпотиреозом

Мета дослідження — виявити електронейроміографічні особливості ураження периферичної нервової системи в пацієнтів iз первинним гіпотиреозом на фоні автоімунного тиреоїдиту (АІТ) та післяопераційного гіпотиреозу шляхом проведення стимуляційної електрoнейроміографії (ЕНМГ). Матеріали та методи. Обстежено 56 хворих на гіпотиреоз на фоні АІТ та 19 пацієнтів iз післяопераційним гіпотиреозом. Контрольну групу становили 20 практично здорових осіб. П’ятдесят сім (76 %) пацієнтів отримували замісну терапію синтетичними похідними L-тироксину, у 18 (24 %) хворих був субклінічний гіпотиреоз. Проведено комплексне клініко-неврологічне та електрофізіологічне обстеження хворих, що включало ЕНМГ-тестування моторних (малогомілкові, великогомілкові, серединні) та сенсорних (малогомілкові, литкові) нервів. При дослідженні моторних нервів оцiнювали наступні показники: амплітуду та тривалість М-відповіді, площу М-відповіді на стимуляцію нерву в дистальній та проксимальній точках, термінальну латентність, резидуальну латентність, швидкість проведення збудження (ШПЗ), при вивченні сенсорних нервів — амплітуду потенціалу дії та ШПЗ. Результати. За АІТ спостерігалось ураження сенсорних нервів нижніх кінцівок (поверхневi малогомілковi та литковi) за змішаним типом. Аксонопатія проявлялась у зменшенні амплітуди потенціалу дії поверхневого малогомілкового нерва на 32,7 % (p < 0,05) та литкового на 27,5 % (p < 0,05) порівняно з контрольною групою, також відмічали зниження ШПЗ малогомілковими нервами на 21,9 % (p < 0,05), що свідчить про пошкодження мієлінової оболонки. У пацієнтів iз післяопераційним гіпотиреозом спостерігалися переважно ознаки аксонопатії, про що свідчило зменшення амплітуди потенціалу дії поверхневого малогомілкового нерва на 27,9 % (p < 0,05). При дослідженні функції рухових волокон периферичних нервів (сере­динний, малогомілковий та великогомілковий) виявлено, що ураження моторних волокон мало демієлінізуючий характер у 78,8 % випадків, у решти хворих (22,2 %) полінейропатія була змішаною (з ознаками ураження мієлінової оболонки та аксонів). Пошкодження ліктьових та великогомілкових нервів було облігатним, у той же час ознаки ураження серединного нерва спостерігалися в 72,8 % випадків. Про демієлінізацію швидкопровідних волокон малогомілкових та великогомілкових нервів свідчило подовження резидуальної латентності на 31,7 % (p < 0,05) та 31,6 % відповідно (p < 0,05), зниження ШПЗ при тестуванні малогомілкових нервів на 21,5 % (p < 0,05) та на 19,4 % — при дослiдженні великогомілкових нервів. З боку серединних нервів відмічалося незначне зниження амплітуди дистальної М-відповіді, на ураження мієлінової оболонки вказувало статистично вірогідне підвищення резидуальної латентності та незначне зниження ШПЗ. У 22,2 % хворих з АІТ відмічалися ознаки поєднаного ураження мієлінової оболонки та аксонального пошкодження, коли крім зниження ШПЗ руховими волокнами великогомілкового та малогомілкового нервів на 21,7 та 21,4 % та деякого підвищення резидуальної латентності спостерігалося вірогідне зниження амплітуди М-відповіді на 15,6 та 14,8 % відповідно. У пацієнтів iз післяопераційним гіпотиреозом відмічалися лише ознаки мієлінопатії. Висновки. ЕНМГ дозволила виявити демієлінізуючий та змішаний характер ураження моторних волокон та аксональний характер ураження сенсорних периферичних нервів, причому більш виражені зміни спостерігалися при АІТ, ніж при полінейропатії на фоні післяопераційного гіпотиреозу.

Treatment of diabetic peripheral neuropathy with engineered mesenchymal stromal cell-derived exosomes enriched with microRNA-146a provide amplified therapeutic efficacy

Diabetic peripheral neuropathy (DPN) is one of the most prevalent chronic complications of diabetes mellitus with no effective treatment. We recently demonstrated that mesenchymal stromal cell (MSC)-derived exosomes (exo-naïve) alleviate neurovascular dysfunction and improve functional recovery. MicroRNA (miRNA), one of the exosomal cargos, downregulates inflammation-related genes, resulting in suppression of pro-inflammatory gene activation. In the present study, we developed engineered MSC-exosomes loaded with miR-146a (exo-146a) and compared the therapeutic effects of exo-146a with exo-naïve in diabetic (db/db) mice with DPN. Exo-146a possesses a high loading capacity, robust ability to accumulate in peripheral nerve tissues upon systemic administration, and evokes substantially enhanced therapeutic efficacy on neurological recovery compared with exo-naïve. Treatment of DPN in diabetic mice with exo-146a for two weeks significantly increased and decreased nerve conduction velocity, and thermal and mechanical stimuli threshold, respectively, whereas it took four weeks of exo-naive treatment to achieve these improvements. Compared with exo-naïve, exo-146a significantly suppressed the peripheral blood inflammatory monocytes and the activation of endothelial cells via inhibiting Toll-like receptor (TLR)-4/NF-κB signaling pathway. These data provide a proof-of-concept about both the feasibility and efficacy of the exosome-based gene therapy for DPN. The translation of this approach to the clinic has the potential to improve the prospects for people who suffer from DPN.

Effects of brief and prolonged cold application on maximal isometric handgrip strength

IntroductionNeuromuscular effects of cold highlight a decrease in nerve conduction velocity, which supports its analgesic impact, and muscle tone and strength reduction. However, it has been suggested that cold could increase strength with short-time applications. The study aimed to compare the effects of brief and prolonged cold application on maximal isometric handgrip strength.MethodsThe controlled randomized clinical trial involved 112 volunteers (56 men and 56 women, mean age: 22 ± 2.1 years), randomly assigned to brief cooling group (BC, <i>n</i> = 36), prolonged cooling group (PC, <i>n</i> = 40), and control group (<i>n</i> = 36). BC received quick icing in anterior forearm, while PC and control group received ice pack application and no treatment, respectively. Three sessions with 3-day intervals were performed. Handgrip strength was assessed with hand-held dynamometry before and after treatment. The main outcome was maximal isometric strength difference (MISdiff).ResultsThere were statistically significant between-group differences in MISdiff in the 3 sessions (S1: <i>p</i> = 0.018; S2: <i>p</i> < 0.001; S3: <i>p</i> < 0.0001), showing a strength increase in BC (<i>p</i> < 0.0001) and decrease in PC (<i>p</i> = 0.025) at the end of the sessions. In addition, a post-intervention strength increase in BC was highlighted when analysing the sessions individually (S1: <i>p</i> = 0.0003; S2: <i>p</i> = 0.00147; S3: <i>p</i> = 0.0001).ConclusionsBrief cold seems a good strategy to increase maximal isometric strength, although the underlying neurophysiological mechanisms must be further studied. Brief cooling could be considered as an ergogenic low-cost support when isometry training is required. In turn, a strength decrease after prolonged cooling was observed.

Curcumin–cyclodextrin/cellulose nanocrystals improve the phenotype of Charcot-Marie-Tooth-1A transgenic rats through the reduction of oxidative stress

The most prevalent form of Charcot-Marie-Tooth disease (CMT type 1A) is characterized by duplication of the PMP22 gene, peripheral dysmyelination and decreased nerve conduction velocities leading to muscle weakness. Recently, oxidative stress was reported as a feature in CMT1A patients. Curcumin exhibits antioxidant activities and has shown beneficial properties on peripheral nerves. However, curcumin presents unfavorable pharmacokinetics. We developed curcumin-cyclodextrin/cellulose nanocrystals (Nano-Cur) to bypass this limitation. The present study investigated the therapeutic potential of Nano-Cur in vitro in Schwann cells (SCs) and in vivo in the transgenic CMT1A rat model. In vitro, Nano-Cur treatment (0.01 μM for 8 h) reduced reactive oxygen species and improved mitochondrial membrane potential in CMT1A SCs. Moreover, Nano-Cur treatment (0.01 μM for 1 week) increased the expression of myelin basic protein in SC/neuron co-cultures. Preliminary in vivo experiments carried out in WT rats showed that intraperitoneal (i.p.) injection of Nano-Cur treatment containing 0.2 mg/kg of curcumin strongly enhanced the bioavailability of curcumin. Afterwards, in 1-month-old male CMT1A rats, Nano-Cur treatment (0.2 mg/kg/day, i.p. for 8 weeks) significantly improved sensori-motor functions (grip strength, balance performance, and mechanical and thermal sensitivities). Importantly, sensory and motor nerve conduction velocities were improved. Further histological and biochemical analyses indicated that myelin sheath thickness and myelin protein expression (myelin protein zero and PMP22) were increased. In addition, oxidative stress markers were decreased in the sciatic nerve and gastrocnemius muscle. Finally, Nrf2 expression and some major antioxidant enzymes were increased in sciatic nerve. Therefore, Nano-Cur significantly improved cellular, electrophysiological, and functional features of CMT1A rats.

Correlation Between Forearm Positions Across Elbow Joint and Ulnar Nerve Conduction Velocity Among Mobile Hand-Held Users

Abstract: Background: Extensive use of mobile hand-held devices with prolonged forearm pronation and elbow flexion could result in pain and weakness with decreased nerve conduction velocities (NCV) of peripheral nerves. Purpose: To identify the ulnar nerve conduction velocity at different forearm positions across elbow joint in mobile-hand held devices users. Design of the study: One shot case study Subjects: Fifty healthy subjects from both genders, Their age ranged from 20 to 40 years old. All subjects had body mass index BMI between 18.5 and 24.9 Kg/m2. Method: Electromyography (EMG) was used for measuring ulnar NCV across elbow joint at different angles (0, 45, and 90,120) degrees of elbow flexion with different forearm positions (supination and pronation). Result: Multivariate Analysis of Variance (MANOVA) revealed that there was a statistical significant difference in mean values of ulnar nerve conduction velocities at different angles of elbow flexion with forearm supination and pronation (P=0.001). There was a statistical significant difference in mean values of ulnar nerve conduction velocities between forearm pronation and supination at the different angles of elbow flexion (P=0.001). Conclusion: forearm supination with full extension elbow position showed the most significant increase in ulnar nerve conduction velocity than other positions. As well as the best position for elbow joint during using mobile hand held devices is 0°-45° elbow flexion with elbow supinated.

ЭЛЕКТРОНЕЙРОМИОГРАФИЧЕСКИЕ ИЗМЕНЕНИЯ У ДЕТЕЙ С ОТСТАВАНИЕМ РАЗВИТИЯ ДВИГАТЕЛЬНЫХ ФУНКЦИЙ

ENMG was held in order to make sure the status of motor analyzer and, particularly, peripheral nerves in arms and legs of children with motor developmental delay, and also asa differential diagnostic with cerebrospinal and cerebral groups. Detected changes of ENMG in somatic nerves ofarms and legs as a symmetric decrease of nerve conduction velocity and muscular activity in young children with spinal pathology have helped to connect the results with abnormality and progression of ischemia of peripheral nerves' structure of arms and legs

Mechanisms of changes in the spinal segmental level in patients with post-traumatic cervical myelopathy

To study the neurophysiological mechanisms of motor deficit in patients with post-traumatic cervical myelopathy. A retrospective clinical and neurophysiological study was conducted for the period 2008-2018. The study included 190 patients with post-traumatic cervical myelopathy (39 women and 159 men, mean age 27 (21,0; 36,0) years, time after spinal cord injury 3 [1,0; 8,0] years). A spinal cord injury was the cause of cervical myelopathy in 92,5% of the patients. The International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) was administered at admission and during rehabilitation. A motor nerve conduction study (NCS) was conducted as well. Compound muscle action potentials (CMAP) amplitude and nerve conduction velocity (NCV) in the distal segment of 160 left and 145 right median nerves, 161 left and 151 right tibial nerves, 90 left and 66 right ulnar nerves were recorded. Re-examination (n=95 patients) was performed 6 (3,0; 10,0) years after injury. The time between examinations was 2,9 (1,0; 4,0) years. The control groups for the median nerve and the tibial nerve consisted of age- and sex-matched 10 patients with traumatic paraplelegia and 12 healthy subjects, respectively. In the main group, the SMAP amplitude for the median nerve was 4,1 [1,6; 6,1] mV, NCV 56 [51,0; 61,0] m/s; in the control group the SMAP was 11 [7,50; 16,40] mV (p=00), NCV 59 [58,0; 6,0] m/s (p=00), in the main group the SMAP amplitude for the tibial nerve was 4,3 [0,65; 7,95] mV, NCV 43 [39,0; 48,0] m/s, in the control group SMAP was 8,4 [6,4; 10,1] mV (p=00), NCV 50 [47,0 ; 51,0] m/s (p=00). About 20% of patients had severe denervation changes. In patients with clinically complete spinal cord injury, axonal neuropathy (a decrease in SMAP) was more pronounced in all nerves than in incomplete patients, and a decrease in NCV was observed in both tibial nerves. In patients with C7-Th1 level, the SMAP amplitude was reduced on the left (2,5 [0,55; 5,65] mV) and right (2,7 [0,80; 6,30] mV) sides compared to those with C4-C6, in which CMAP was 4,6 [2,30; 6,20] mV on the left (p=0.03) and 4,7 [2,80; 6,10] mV on the right sides (p=0.03). The main neurophysiological mechanisms of motor deficit in patients with post-traumatic cervical myelopathy are the combination of the primary neuronal damage at the level of spinal cord injury and the development of secondary axonal neuropathy more caudally at the first three years after spinal cord injury.

Effect of Watermelon Extract on Nerve Conduction Velocity, Memory, and T4 Level in Rats.

Background:Watermelon is a fruit with the thirst-quenching effect and especially is consumed in summer. In this study, the effect of consumption of watermelon extract (in drinking water) on thyroid hormone level (TT4), animals' weight, water and food consumption, nerve conduction velocity (NCV), and memory in Wistar rats were investigated.Materials and Methods:Twenty-four male Wistar rats were divided into three groups: control, CT 1500 mg/kg, and CT 3000 mg/kg (n = 8, in each group). Watermelon extract was administered for 42 days. The results measured in this study were analyzed with repeated measures or one-way analysis of variance and compared by the least significant difference post hoc. P < 0.05 was considered as significant difference.Results:The results showed that animals' weight in both the treatment groups decreased compared to the control group (P < 0.05 and P < 0.01, respectively). Water and food consumption and the level of TT4 increased when compared to the control group in both the treated groups (both P < 0.001). NCV in both the treated groups decreased in comparison with the control group (both P < 0.001). Spatial memory did not change significantly, but passive avoidance memory in both the treated groups significantly decreased in comparison to the control group (respectively, with P < 0.05 and P < 0.01).Conclusion:Based on these finding, in spite of increase in food and water consumption in the treated groups, animal weight did not increase significantly. Impairment in memory and decrease in NCV were also occurred, but TT4 level was increased in animals treated with watermelon extract.

AGE-RELATED PRESERVATION OF MOTOR NERVE CONDUCTION VELOCITY IN NEURONAL MTORC1 KNOCKDOWN MICE

With age, peripheral nerves undergo demyelination along with overall decrease in peripheral nerve conduction velocity in both sensory and motor nerves. Loss of innervation in muscles is thought to be a major factor in causing age-related sarcopenia including a decrease in muscle function. Dietary restriction attenuates the detrimental effects of aging in mice. Reduction of mTOR signaling is hypothesized to have overlapping mechanisms with dietary restriction. Furthermore, inhibition of mTOR via rapamycin treatment is known to extend lifespan in mice as well as improve peripheral nerve myelination. Therefore, I hypothesized that reducing mTORC1 signaling in neurons would be able to ameliorate the deleterious effects of aging in peripheral nerves. An overall decrease in nerve conduction velocity was observed in both tail sensory and sural nerves with age (15 vs. 30 months). In neuronal mTORC1 KD animals, there was an age-related preservation of both sural and sciatic nerve conduction. Rapamycin treatment produced similar effects with a trend towards increased sciatic nerve conduction velocity in rapamycin-treated wild-type mice at 19 months. The preserve sciatic nerve conduction velocity could be partially explained by preserved myelination. Neuronal mTORC1 knockdown animals had more myelin in the sciatic nerve at 30 mo. as compared to age-matched controls. Overall, these data indicate that mTORC1 signaling plays a role in the age-related decline in peripheral nerve myelination as well as nerve conduction velocity. Future therapeutics could utilize rapamycin or other rapalogs to combat the decline in peripheral nerve function associated with age and other diseases as well.