Decrease In Conduction Velocity Research Articles

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.

The bradycardic agent ivabradine decreases conduction velocity in the AV node and in the ventricles in-vivo

Ivabradine blocks hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels, thereby lowering the heart rate, an action that is used clinically for the treatment of heart failure and angina pectoris. We and others have shown previously that ivabradine, in addition to its HCN channel blocking activity, also inhibits voltage-gated Na channels in vitro at concentrations that may be clinically relevant. Such action may reduce conduction velocity in cardiac atria and ventricles.Here, we explore the effect of administration of ivabradine on parameters of ventricular conduction and repolarization in the surface ECG of anesthetized mice. We found that 5 min after i.p. administration of 10 mg/kg ivabradine spontaneous heart rate had declined by ~13%, which is within the range observed in human clinical studies. At the same time a significant increase in QRS duration by ~18% was observed, suggesting a reduction in ventricular conduction velocity. During transesophageal pacing at heart rates between 100 and 220 beats/min there was no obvious rate-dependence of ivabradine–induced QRS prolongation. On the other hand, ivabradine produced substantial rate-dependent slowing of AV nodal conduction. We conclude that ivabradine prolongs conduction in the AV-node and in the ventricles in vivo.

Evaluation of peripheral nerves of upper limb and its correlation with blood sugar levels: A electrophysiological study in type 2 diabetics

Introduction: Peripheral neuropathy is a complication of diabetes which causes considerable indisposition and frailty. Metabolic derangement in diabetes affects nerve. Aim: To carry out electrophysiological study of nerves in diabetics and to correlate it with blood sugar. Materials and Methods: Nerves of upper limb were assessed for motor nerve conduction with the help of surface electrodes and windows based (Neuro perfect software) computerized system in 50 type 2 diabetic male patients and 50 healthy males. The nerves chosen for study were median and ulnar. Parameters studied were distal latency and conduction velocity. Results: Observation revealed increased distal latency and decreased conduction velocity in diabetics with statistically significant difference. These parameters also showed association with blood sugar levels in diabetics. Conclusions: Diabetes affect nerves as indicated by declined motor nerve function through electrophysiological testing. Elevated blood sugar levels are related with nerve damage. Keywords: Peripheral neuropathy, Diabetes, Electrophysiological tests, Conduction velocity.

VITAMINS B1 AND B12 DEFICIENCY AS A PREDICTOR OF TUBERCULOSIS SEVERITY AND PERIPHERAL NERVOUS SYSTEM DAMAGE

Background: It is known that vitamin status plays one of the leading roles in the normal functioning of the immune system. Vitamins deficiency leads to the weakening of immunity and can provoke the occurrence of severe infectious diseases, including tuberculosis. The purpose of the study was to investigate the role of vitamins B1 and B12 deficiency as a predictor of tuberculosis severity and development of peripheral nervous system damage. Materials and methods. 89 patients with pulmonary tuberculosis and 12 healthy persons were included in the study. The patients were examined and treated according to current guidelines of Ministry of Health of Ukraine. Additionally, the concentration of vitamins B1 and B12 was measured by ELISA in blood serum in all the patients at the treatment onset and in all healthy persons. To find the damage of peripheral nervous system we performed stimulation electroneuromyography of lower limbs. Results. The level of vitamin B12 was 0.19±0.01 nmol/L (median - 0.19 nmol/L) in patients with destruction of lung tissue and 0.22±0.01 nmol/L (median - 0.21 nmol/L) in patients without destruction, p <0.05. MNCV was 49.25±0.80 mm/s (median - 49.40 mm/s) in patients with destruction of lung tissue and 53.41±0.99 mm/s (median - 53.10 mm/s) in patients without destruction, p<0.01. SNCV was 43.41±1.14 mm/s (median - 42.05 mm/s) in patients with destruction of lung tissue and 45.91±0.94 mm/s (median - 46.00 mm/s) in patients without destruction, p<0.05. Conclusions. Pulmonary tuberculosis leads to the disturbances in the metabolism of vitamins B1 and B12, causing their deficiency and the associated violation of impulse conduction along peripheral nerve fibers. More severe tuberculous lesions with destruction of lung tissue and massive bacterial excretion are associated with a more pronounced deficiency of vitamins B1 and B12, as well as decrease of motor and sensory conduction velocity.

A survey of pathways for mechano-electric coupling in the atria

Mechano-electric coupling (MEC) in atrial tissue has received sparse investigation to date, despite the well-known association between chronic atrial dilation and atrial fibrillation (AF). Of note, no fewer than six different mechanisms pertaining to stretch-activated channels, cellular capacitance and geometric effects have been identified in the literature as potential players. In this mini review, we briefly survey each of these pathways to MEC. We then perform computational simulations using single cell and tissue models in presence of various stretch regimes and MEC pathways. This allows us to assess the relative significance of each pathway in determining action potential duration, conduction velocity and rotor stability. For chronic atrial stretch, we find that stretch-induced alterations in membrane capacitance decrease conduction velocity and increase action potential duration, in agreement with experimental findings. In the presence of time-dependent passive atrial stretch, stretch-activated channels play the largest role, leading to after-depolarizations and rotor hypermeandering. These findings suggest that physiological atrial stretches, such as passive stretch during the atrial reservoir phase, may play an important part in the mechanisms of atrial arrhythmogenesis.

The Mechanical Cost of Decreasing Conduction Velocity: A Mathematical Model of Pacing-Induced Lower Strain.

To simulate the effect of decreasing conduction velocity (Cvel) on average segmental myocardial strain using mathematical modeling. The simulation was run using MatLab version 7.4 (The MathWorks, Inc. Natick, Massachusetts). A normal strain-time curve pattern was sampled from a normal human echo study using the 2D strain imaging software (GE Healthcare, Milwaukee, Wisconsin). Contraction was simulated from simultaneous segmental activation (Cvel=∞) through normal activation (Cvel=400cm/sec) to pacing Cvel (100 to 10cm/sec). The simulation generated average segmental strain-time waveforms for each velocity and peak strain as a function of Cvel and time to peak strain as a function of Cvel curves. With decreasing Cvel, average peak segmental strain was found to be decreased and delayed. The following correlation equation represents the correlation betweenpeak strain and Cvel : strain= -20.12+27.65 x e (-0.29 x Cvel). At the highest pacing Cvel (100cm/sec) average peak segmental strain dropped by 10%, at 50cm/sec by 30% and at the lowest pacing Cvel (10cm/sec) peak strain dropped by >90%. Time to peak segmental strain was minimally longer with decreasing Cvel down to 70cm/sec (pacing velocity range). Further decreased velocity dramatically increased time to peak strain of the simulated segment. The simulation yielded a predictive correlation between slower conduction velocities and decreased and delayed segmental strain.

Deficiency of glucagon gene-derived peptides induces peripheral polyneuropathy in mice

Although diabetic polyneuropathy (DPN) is the commonest diabetic complication, its pathology remains to be clarified. As previous papers have suggested the neuroprotective effects of glucagon-like peptide-1 in DPN, the current study investigated the physiological indispensability of glucagon gene-derived peptides (GCGDPs) including glucagon-like peptide-1 in the peripheral nervous system (PNS). Neurological functions and neuropathological changes of GCGDP deficient (gcg−/−) mice were examined. The gcg−/− mice showed tactile allodynia and thermal hyperalgesia at 12–18 weeks old, followed by tactile and thermal hypoalgesia at 36 weeks old. Nerve conduction studies revealed a decrease in sensory nerve conduction velocity at 36 weeks old. Pathological findings showed a decrease in intraepidermal nerve fiber densities. Electron microscopy revealed a decrease in circularity and an increase in g-ratio of myelinated fibers and a decrease of unmyelinated fibers in the sural nerves of the gcg−/− mice. Effects of glucagon on neurite outgrowth were examined using an ex vivo culture of dorsal root ganglia. A supraphysiological concentration of glucagon promoted neurite outgrowth. In conclusion, the mice with deficiency of GCGDPs developed peripheral neuropathy with age. Furthermore, glucagon might have neuroprotective effects on the PNS of mice. GCGDPs might be involved in the pathology of DPN.

A novel missense pathogenic variant in NEFH causing rare Charcot-Marie-Tooth neuropathy type 2CC.

The purpose of this research is to explore the underlying genes of Charcot-Marie-Tooth (CMT). Technologies such as electrophysiological testing and gene sequencing have been applied. We identified a novel variant NEFH c.2215C>T(p.P739S)(HGNC:7737) in a heterozygous state, which was considered to be pathogenic for CMT2CC(OMIM:616924).The proband and his brothers presented with muscle atrophy of hand and calf and moderately decreased conduction velocities. By whole exome sequencing analysis, we found the novel missense pathogenic variant in the proband, his brother and mother. This report broadened current knowledge about intermediate CMT and the phenotypic spectrum of defects associated with NEFH. In addition, the proband carried other five variants {HSPD1c.695C>A (p.S232X), FLNCc.1073A>G (p.N358S), GUSBc.323C>A (p.P108Q), ACY1 c.1063-1G>A and APTX c.484-2A>T}, which have not been reported until now. The NEFH c.2215C>T (p.P739S) give us a new understanding of CMT, which might provide new therapeutic targets in the future.

Exendin-4 inhibits atrial arrhythmogenesis in a model of myocardial infarction-induced heart failure via the GLP-1 receptor signaling pathway.

Glucagon-like peptide-1 receptor (GLP-1 receptor) agonists are considered to exert cardioprotective effects in models of acute and chronic heart disease. The present study aimed to investigate the role of exendin-4 (a GLP-1 receptor agonist) in atrial arrhythmogenesis in a model of myocardial infarction (MI)-induced heart failure and to elucidate the mechanisms underlying its effects. For this purpose, male Sprague-Dawley rats underwent sham surgery or left anterior descending artery ligation prior to being treated with saline/exendin-4/exendin-4 plus exendin9-39 (an antagonist of GLP-1 receptor) for 4 weeks. The effects of exendin-4 on atrial electrophysiology, atrial fibrosis and PI3K/AKT signaling were assessed. Rats with MI exhibited depressed left ventricular function, an enlarged left atrium volume, prolonged action potential duration, elevated atrial tachyarrhythmia inducibility, decreased conduction velocity and an increased total activation time, as well as total activation time dispersion and atrial fibrosis. However, these abnormalities were attenuated by treatment with the GLP-1 receptor agonist, exendin-4. Moreover, the expression levels of collagen I, collagen III, transforming growth factor-β1, phosphorylated PI3K and AKT levels in atrial tissues were upregulated in rats with MI. These changes were also attenuated by exendin-4. It was also found that these exedin-4-mediated attenutations were mitigated by the co-administration of exendin9-39 with exendin-4. Overall, the findings of the present study suggested that exendin-4 decreases susceptibility to atrial arrhythmogenesis, improves conduction properties and exerts antifibrotic effects via the GLP-1 receptor signaling pathway. These findings provide evidence for the potential use of GLP-1R in the treatment of atrial fibrillation.

Prolonged duration of repolarization and decreased conduction velocity in the atrial myocardium after hypothermic ischemia-reperfusion may be related to expressions of inward rectifier potassium channel 2.1 protein and connexin 40.

The study aimed to determine the role of inward rectifier potassium channel 2.1 protein and connexin 40 expressions in regulating the duration of repolarization and conduction velocity of right atrial myocardium in rats following hypothermic ischemia-reperfusion. The Langendorff isolated rat cardiac perfusion models were divided into control (C) and hypothermic ischemia-reperfusion groups, with 8 models in group C and 16 models in group ischemia-reperfusion. Depending on the incidence of atrial arrhythmia after reperfusion, the models in group ischemia-reperfusion were further divided into reperfusion non-atrial arrhythmia or reperfusion atrial arrhythmia subgroup. Right atrial monophasic action potential duration at 50% and 90% of repolarization after 30 minutes of continuous perfusion in group C and group ischemia-reperfusion (T0), 105 minutes of continuous perfusion in group C or after 15 minutes of reperfusion in group ischemia-reperfusion (T1) and 120 minutes of continuous perfusion in group C or 30 minutes of reperfusion in group ischemia-reperfusion (T2) were recorded. Right atrial conduction velocity and effective refractory period were recorded at T2. Then, the expressions of inward rectifier potassium channel 2.1 protein and connexin 40 in the right atrial myocardium were detected. Monophasic action potential duration at 50% and 90% were higher at T1 and T2 than those at T0 in subgroup reperfusion atrial arrhythmia (p < 0.05); monophasic action potential duration at 50% in subgroup reperfusion atrial arrhythmia were larger than group C and subgroup reperfusion non-atrial arrhythmia at T1 and T2 (p < 0.05); monophasic action potential duration at 90% in subgroup reperfusion atrial arrhythmia were larger than group C and subgroup reperfusion non-atrial arrhythmia at T1 and T2 (p < 0.05); effective refractory period in subgroup reperfusion atrial arrhythmia was greater than that in group C and subgroup reperfusion non-atrial arrhythmia, and the conduction velocity and the expressions of inward rectifier potassium channel 2.1 protein and connexin 40 were significantly lower than group C and subgroup reperfusion non-atrial arrhythmia (p < 0.05). The prolonged duration of repolarization and a decrease in conduction velocity of the atrial myocardium occur in rats after hypothermic ischemia-reperfusion. These observed effects may be related to the downregulated expressions of connexin 40 and inward rectifier potassium channel 2.1.

Peripheral nerve injury and sensitization underlie pain associated with oral cancer perineural invasion.

Cancer invading into nerves, termed perineural invasion (PNI), is associated with pain. Here, we show that oral cancer patients with PNI report greater spontaneous pain and mechanical allodynia compared with patients without PNI, suggesting that unique mechanisms drive PNI-induced pain. We studied the impact of PNI on peripheral nerve physiology and anatomy using a murine sciatic nerve PNI model. Mice with PNI exhibited spontaneous nociception and mechanical allodynia. Perineural invasion induced afterdischarge in A high-threshold mechanoreceptors (HTMRs), mechanical sensitization (ie, decreased mechanical thresholds) in both A and C HTMRs, and mechanical desensitization in low-threshold mechanoreceptors. Perineural invasion resulted in nerve damage, including axon loss, myelin damage, and axon degeneration. Electrophysiological evidence of nerve injury included decreased conduction velocity, and increased percentage of both mechanically insensitive and electrically unexcitable neurons. We conclude that PNI-induced pain is driven by nerve injury and peripheral sensitization in HTMRs.

Clinical and neurophysiological correlation in axonal and demyelinating polyneuropathy

BackgroundThe neurophysiological examination provides valuable pathophysiological information for the diagnosis, prognosis, and therapy of patients with polyneuropathy (Fuglsang- Fredriksen A., Pugdahl K. Clin Neurophysilogy 122:440–455, 2011). Nerve conduction study (NCS) is the most objective and reliable measure of peripheral nerve function and is considered the gold standard for the diagnosis of most neuropathies.Aim of the studyTo evaluate the clinical usefulness of nerve conduction study (NCS) in the differentiation between axonal and demyelinating polyneuropathies.MethodsIn the present study, 125 patients with polyneuropathy were studied ranging age from 9 to 79 years. Thirty-six patients were classified as axonal polyneuropathy, 23 patients as demyelinating, and 9 as mixed, while 57 patients were classified as neuropathic. Nerve conduction study (NCS) and electromyography (EMG) were performed using Nihon Kochden electromyography machine with surface recording and stimulating electrodes.ResultsThere is statistically significant linear correlation between reduction in sensory nerve action potential (SNAP) amplitude and decrease in sensory conduction velocity (SCV) of median and ulnar nerves. Also, there is statistically significant inverse correlation between reduction in compound motor action potential (CMAP) amplitude and increase in distal motor latency (DML). There is statistically significant linear correlation between reduction in compound motor action potential (CMAP) amplitude and decrease in motor conduction velocity (MCV). There is statistically significant linear correlation between reduction in compound motor action potential (CMAP) amplitude and decreased grade of power in both axonal and demyelinating polyneuropathy; statistically significant linear correlation was found between decrease in conduction velocity and decrease in grade of power.ConclusionThe present study demonstrates significant correlation between amplitude reduction and conduction slowing in demyelinating as well as axonal polyneuropathy.

Age related changes in surface myoelectric signals

The initial values and the time course of muscle fiber conduction velocity and of surface myoelectric signal spectral variables were studied during voluntary or electrically elicited contractions of the tibialis anterior muscle of 15 healthy elderly human subjects. Age ranged from 65 to 84 years. Isometric voluntary contractions were performed at 20% MVC (Maximal Voluntary Contraction) and 80% MVC for 20 s. Tetanic electrical stimulation was then applied to the main muscle motor point for 20 s with surface electrodes. Two stimulation rates (20 Hz and 40 Hz) and two stimulation amplitudes were used to induce different degrees of fatigue. One stimulation amplitude was supramaximal, the second was adjusted to induce a response (M-wave) about 30% of the maximal. Results were compared with those reported in previous work on healthy adults (age range 18 to 43 years). The main findings of this work are: (a) when voluntary contraction level is increased from 20% MVC to 80% MVC conduction velocity and spectral variables increase; this increase is significantly smaller in elderly subjects, (b) during sustained contractions at 80% MVC the decrease of conduction velocity and spectral variables is significantly smaller in elderly subjects, (c) during contractions induced by supramaximal stimulation at 40 Hz the decrease of conduction velocity and spectral variables is not significantly different in the two age groups. It is concluded that points a and b reflect the age related decrease of number and size of fast twitch fibers indicated by histological data. Point c is discussed and possible explanations are suggested.

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

The proarrhythmic features of pathological cardiac hypertrophy in neonatal rat ventricular cardiomyocyte cultures.

Different factors may trigger arrhythmias in diseased hearts, including fibrosis, cardiomyocyte hypertrophy, hypoxia, and inflammation. This makes it difficult to establish the relative contribution of each of them to the occurrence of arrhythmias. Accordingly, in this study, we used an in vitro model of pathological cardiac hypertrophy (PCH) to investigate its proarrhythmic features and the underlying mechanisms independent of fibrosis or other PCH-related processes. Neonatal rat ventricular cardiomyocyte (nr-vCMC) monolayers were treated with phorbol 12-myristate 13-acetate (PMA) to create an in vitro model of PCH. The electrophysiological properties of PMA-treated and control monolayers were analyzed by optical mapping at day 9 of culture. PMA treatment led to a significant increase in cell size and total protein content. It also caused a reduction in sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2 level (32%) and an increase in natriuretic peptide A (42%) and α1-skeletal muscle actin (34%) levels, indicating that the hypertrophic response induced by PMA was, indeed, pathological in nature. PMA-treated monolayers showed increases in action potential duration (APD) and APD dispersion, and a decrease in conduction velocity (CV; APD30 of 306 ± 39 vs. 148 ± 18 ms, APD30 dispersion of 85 ± 19 vs. 22 ± 7 and CV of 10 ± 4 vs. 21 ± 2 cm/s in controls). Upon local 1-Hz stimulation, 53.6% of the PMA-treated cultures showed focal tachyarrhythmias based on triggered activity (n = 82), while the control group showed 4.3% tachyarrhythmias (n = 70). PMA-treated nr-vCMC cultures may, thus, represent a well-controllable in vitro model for testing new therapeutic interventions targeting specific aspects of hypertrophy-associated arrhythmias.NEW & NOTEWORTHY Phorbol 12-myristate 13-acetate (PMA) treatment of neonatal rat ventricular cardiomyocytes (nr-vCMCs) led to induction of many significant features of pathological cardiac hypertrophy (PCH), including action potential duration prolongation and dispersion, which provided enough time and depolarizing force for formation of early afterdepolarization (EAD)-induced focal tachyarrhythmias. PMA-treated nr-vCMCs represent a well-controllable in vitro model, which mostly resembles to moderate left ventricular hypertrophy (LVH) rather than severe LVH, in which generation of a reentry is the putative mechanism of its arrhythmias.

Electromyographic Evaluation of Early Stage Results of Exoscopic Microdecompressive Spinal Surgery in Dogs

Background: Spinal surgical interventions are generally used in the treatment of various spinal pathologies such as vertebral fracture, luxation-subluxation, congenital vertebral deformities, discal hernia, infection and tumor. Minimally invasive spinal surgery contributes to rapid recovery by reducing iatrogenic muscle damage and postoperative pain. In minimally invasive spinal surgery, a new hybrid imaging technique, the exoscope, has been developed in the last decade The purpose of this study was to report efficacy of the exoscopic microdecompressive spinal surgery (MDSS) and its early postoperative electromyography (EMG) results in dogs.Materials, Methods &amp; Results:The material of this study consisted of the owned 10 dogs with spinal cord injury resulted from the different etiologies. On the basis of examinations, medical support (fluid therapy, corticosteroid, etc.) was applied to the required dogs. Exoscopic MDSS was performed under general anesthesia in dogs. The neurologic, radiologic and EMG examination were completed at pre- and postoperative periods. EMG results at postoperative 1st week showed increased conduction velocity and amplitudes in 3 cases. There was no significant change in a case. And, there was a slight slowdown in conduction velocity and significant decrease in amplitudes in a case. At postoperative 4th week, ther was increased conduction velocity and amplitudes in 8 cases and needle EMG showed that spontan muscle activity was normal in 5 cases, mild in 2 cases, moderate a case and severe in a case. But spontan muscle activity was unfollowed in a case. Postoperative outcomes were poor in 3 cases, fair in 3 cases, good in 3 cases and unfollowed in a case. Discussion: Spinal cord injuries encountered in veterinary medicine have significant morbidity and mortality. In spinal patients, in addition to neurological examination, lesion localization can be determined using imaging techniques such as radiology, computed tomography, and MRI. EMG and somatosensory evoked potentials examinations are used to evaluate quantitative functional recovery, especially in spinal cord injuries. EMG also provides an opportunity to evaluate muscle activation patterns during recovery. Exoscopic spinal surgery is the newest hybrid imaging technique. Exoscopic MDSS facilitated manipulation by providing adequate illumination and vision at the exploration site. Exoscopic MDSS has the advantages of microscopic surgery and is a new technique that can be applied in dogs with spinal pathology.

Acute Motor Sensory Axonal Neuropathy: A Variant of Guillain&amp;ndash;Barr&amp;eacute; Syndrome&amp;mdash;A Rare Case Report

ABSTRACT Background Guillain–Barré syndrome (GBS) is an immune-mediated disorder of the nervous system that shows acute or subacute onset. It is also known as Landry's paralysis. It is characterized by muscle weakness of legs and arms, limb paresthesias, and total or relative areflexia. Acute motor sensory axonal neuropathy (AMSAN) is a distinct subtype of GBS. It is not only a rare but severe variant that involves axonal degeneration in motor and sensory nerve fibers and has a prolonged recovery course. Case description A 60-year-old male presented to the emergency department having complaints of weakness, numbness, and tingling sensation in feet for the last fortnight, which ascended gradually towards the calves. He was observed to have a sensory disorder in hands, but not flaccid paralysis. The patient history and nerve conduction studies were indicative of AMSAN variant of GBS. Discussion In patients of AMSAN, the reduction of sural nerve amplitude is more pronounced as compared to acute inflammatory demyelinating polyneuropathy (AIDP) patients. In case of our patient, the electrophysiological feature indicated a more than 50% decrease in SNAP. A marked reduction in sensory nerve action potential and compound muscle action potential with only slightly decreased conduction velocities is a requirement for the diagnosis of axonal neuropathies, which is the trait seen in the reported case. How to cite this article Saggar SK, Thaman RG, Mohan G. Acute Motor Sensory Axonal Neuropathy: A Variant of Guillain–Barré Syndrome—A Rare Case Report. MEI's Curr Trends Diagn Treat 2020;4(2):110–111.

Melatonin Ameliorates Radiation-induced Sciatic Nerve Injury

Background: Radiotherapy is a treatment method for cancer mostly utilized for about 60% of cancer patients. Peripheral neuropathy is one of the severe complications of radiotherapy. Two stages of neuropathy will occur following irradiation; electrophysiological and biochemical variations as the first stage, while the second stage involves fibrosis of soft tissues surrounding the exposed nerve. This novel study aimed to investigate the radioprotective effects of melatonin against ionizing radiation-induced sciatic nerve damage. Methods: 60 rats were randomly assigned to four groups; C (Control), M (Melatonin), R (Radiation), MR (Radiation + Melatonin). Their right legs were exposed to 30 Gy single dose gamma rays. Melatonin (100 mg/kg) was administered 30 min before irradiation and once daily (5 mg/kg) till the day of rats’ sacrifice. Their exposed nerve tissues were evaluated for biochemical changes in addition to Electromyography (EMG) and Nerve Conduction Study (NCS). Results: 4, 12 and 20 weeks post-irradiation, EMG and NCS examinations in R group showed reduced Compound Muscle Action Potential (CMAP) representing axonal degeneration when compared with C and M groups. Prolonged latency and a decrease in Conduction Velocity (CV) gave an indication of demyelinating neuropathy at 12 and 20 weeks. EMG and NCS results of R group showed partial nerve lesion. Biochemical assessments showed that irradiation of sciatic nerve led to increased MDA level, as well as decreased CAT and SOD activities. However, in all cases, treatment with melatonin can reverse these effects. Conclusion: We conclude that melatonin can improve electrophysiological, oxidative stress and antioxidant defense features of irradiated rats’ sciatic nerves. We would also recommend the use of melatonin in an optimal and safe dose. It should be administered over a long period of time for effective protection of the peripheral nerve tissues, as well as improving the therapeutic ratio of radiotherapy.

Minimally invasive techniques for sensory and motor nerve conduction in Wistar albino rats

Decrease in motor and/or sensory conduction velocities, or a decrease in the amplitude of muscle or nerve potential indicates certain peripheral nerve system disorders. Techniques for the measurement of motor and sensory conduction velocities are well established in humans as well as in numerous animal models such as the rat and the monkey. Scientists widely use rats as experimental animals for scientific research for their viability, fast reproduction and simplicity, which makes them indispensable in experimental researches. Particularly, rats are used for investigation of models of peripheral axonal and demyelinating neuropathies, neural tissue injury and regeneration.[1-3] In rats, motor nerve conduction velocity (NCV) is measured at the level of the sciatic nerve[4] or less frequently at the tail.[5-6] The sensory nerve conduction velocity (SNCV) has been measured on the external saphenous nerve and sural nerve.[7]

NS5806 Induces Electromechanically Discordant Alternans and Arrhythmogenic Voltage-Calcium Dynamics in the Isolated Intact Rabbit Heart.

Background: NS5806 activates the transient outward potassium current Ito, and has been claimed to reproduce Brugada Syndrome (BrS) in ventricular wedge preparations. Ito modulates excitation-contraction coupling, which is critical in alternans dynamics. We explored NS5806-arrhythmogenic effects in the intact whole heart and its impact on alternans.Methods: Langendorff-perfused rabbit hearts (n = 20) underwent optical AP and Ca mapping during pacing at decremental cycle lengths (CL). Spontaneous arrhythmias and pacing-induced alternans was characterized at baseline (BL), after perfusing with NS5806, before and after adding verapamil (VP), and SEA0400 (SEA, n = 5 each), to modulate Ca-current and Na-Ca exchange, the main AP-Ca coupling mechanisms.Results: NS5806 induced BrS-like ECG features in 6 out of 20 hearts. NS5806 prolonged steady-state (3 Hz) action potential duration (APD) by 16.8%, Ca decay constant by 34%, and decreased conduction velocity (CV) by 52.6%. After NS5806 infusion, spontaneous ventricular ectopy (VE) and AP/Ca alternans occurred. Pacing-induced alternans during NS5806 infusion occurred at longer CL and were AP/Ca discordant from its onset. Spatially discordant alternans after NS5806 infusion had non-propagation-driven nodal line distribution. No spontaneous phase-2 reentry occurred. Under NS5806 + VP, alternans became AP/Ca concordant and only induced in two out of five; NS5806 + SEA did not affect alternans but suppressed spontaneous ectopy.Conclusions: NS5806 disrupts AP-Ca coupling and leads to Ca-driven, AP/Ca-discordant alternans and VE. Despite BrS-like ECG features, no spontaneous sustained arrhythmias or phase-2 reentry occurred. NS5806 does not fully reproduce BrS in the intact rabbit heart.