Proper Understanding of the Nerve Impulses and the Action Potential

Neurologists define the transmission of nerve impulses across the membranes of the neural cells as a result of difference in the concentration of ions while they measured an electric potential, called as an action potential, which allows the propagation of such nerve impulses as electrical signals. Such measurements should guide them to a logical explanation of the nerve impulses as electric charges driven by the measured action potential. However, such logical conclusion, or explanation, is ignored due to a wrong definition of the flow of electric charges as a flow of electrons that cannot pass through neural networks. According to recent studies, electric charges are properly defined as electromagnetic (EM) waves whose energy is expressed as the product of its propagating electric potential times their entropy flow which is adhered to the flow of such energy. Such definition matches the logical conclusion of the nerve impulses as electric charges, as previously explained, and defines the entropy of the neural network, measured by Ammeters, in Watt or Joule/Volt. The measured entropy represents a neurodiagnostic property of the neural networks that measures its capacity to allow the flow of energy per unit action potential. Theoretical verification of the innovative definition of nerve impulses is presented by following an advanced entropy approach. A proper review of the machine records of the stimulating electric charges, used in the diagnosis of the neural networks, and the stimulated nerve impulses or stimulated responses, represents practical verifications of the innovative definitions of the electric charges and the nerve impulses. Comparing the functioning of the thermoelectric generators and the brain neurons, such neurons are defined as thermoelectric generators of the electric nerve impulses and their propagating, or action, potential.

Promising application of a new ulnar nerve compound muscle action potential measurement montage in amyotrophic lateral sclerosis:a prospective cross-sectional study

Previous studies have shown that ulnar nerve compound muscle action potential recorded by the conventional“belly-tendon”montage does not accurately and completely reflect the action potential of the ulnar nerve dominating the abductor digiti minimi muscle due to the effects of far-field potentials of intrinsic hand muscles.A new method of ulnar nerve compound muscle action potential measurement was developed in 2020,which adjusts the E2 electrode from the distal tendon of the abductor digitorum to the middle of the back of the proximal wrist.This new method may reduce the influence of the reference electrode and better reflect the actual ulnar nerve compound muscle action potential.In this prospective cross-sectional study,we included 64 patients with amyotrophic lateral sclerosis and 64 age-and sex-matched controls who underwent conventional and novel ulnar nerve compound muscle action potential measurement between April 2020 and May 2021 in Peking University Third Hospital.The compound muscle action potential waveforms recorded by the new montage were unimodal and more uniform than those recorded by traditional montage.In the controls,no significant difference in the compound muscle action potential waveforms was found between the traditional montage and new montage recordings.In amyotrophic lateral sclerosis patients presenting with abductor digiti minimi spontaneous activity and muscular atrophy,the amplitude of compound muscle action potential-pE2 was significantly lower than that of compound muscle action potential-dE2(P<0.01).Using the new method,damaged axons were more likely to exhibit more severe amplitude decreases than those measured with the traditional method,in particular for patients in early stage amyotrophic lateral sclerosis.In addition,the decline in compound muscle action potential amplitude measured by the new method was correlated with a decrease in Revised Amyotrophic Lateral Sclerosis Functional Rating Scale scores.These findings suggest that the new ulnar nerve compound muscle action potential measurement montage reduces the effects of the reference electrode through altering the E2 electrode position,and that this method is more suitable for monitoring disease progression than the traditional montage.This method may be useful as a biomarker for longitudinal follow-up and clinical trials in amyotrophic lateral sclerosis.

The optimal distance between two electrode tips during recording of compound nerve action potentials in the rat median nerve

The distance between the two electrode tips can greatly influence the parameters used for record- ing compound nerve action potentials. To investigate the optimal parameters for these recordings in the rat median nerve, we dissociated the nerve using different methods and compound nerve action potentials were orthodromically or antidromically recorded with different electrode spac- ings. Compound nerve action potentials could be consistently recorded using a method in which the middle part of the median nerve was intact, with both ends dissociated from the surrounding fascia and a ground wire inserted into the muscle close to the intact part. When the distance be- tween two stimulating electrode tips was increased, the threshold and supramaximal stimulating intensity of compound nerve action potentials were gradually decreased, but the amplitude was not changed significantly. When the distance between two recording electrode tips was increased, the amplitude was gradually increased, but the threshold and supramaximal stimulating intensity exhibited no significant change. Different distances between recording and stimulating sites did not produce significant effects on the aforementioned parameters. A distance of 5 mm between recording and stimulating electrodes and a distance of 10 mm between recording and stimulating sites were found to be optimal for compound nerve action potential recording in the rat median nerve. In addition, the orthodromic compound action potential, with a biphasic waveform that was more stable and displayed less interference （however also required a higher threshold and higher supramaximal stimulus）, was found to be superior to the antidromic compound action potential.

Character of diaphragm compound muscle action potential and phrenic nerve conduction time in patients with obstructive sleep apnea-hypopnea syndrome

BACKGROUND： Both hypoxia and.carbon dioxide retention can damage phrenic nerve and muscle conduction, as well as diaphragm function. Diaphragm compound muscle action potential and phrenic nerve conduction time are reliable indicators for measuring phrenic nerve and diaphragm function. OBJECTIVES： To verify the hypothesis that changes of phrenic nerve conduction time （PNCT） and diaphragm compound muscle action potential （CMAP） in obstructive sleep apnea-hypopnea syndrome （OSAHS） patients might contribute to the decline of phrenic nerve and diaphragm function. PNCT and CMAP were measured with multipair esophageal electrodes combined with unilateral magnetic stimulation. DESIGN, TIME AND SETTING： Case controlled study. The experiment was carried out in Guangzhou Institute of Respiratory Disease, Guangzhou MediCal College, from June 2005 to April 2006. PARTICIPANTS： Twenty seven OSAHS patients and eight primary snoring subjects from Guangzhou Institute of Respiratory Disease, Guangzhou Medical College were recruited and all subjects were diagnosed by polysomnography （PSG）. Sixteen healthy, non-snoring subjects in the hospital for medical examination during the same time period were selected as the control group. METHODS： Esophageal electrodes, made by Guangzhou Institute of Respiratory Disease, combined with unilateral magnetic stimulation, were used to measure PNCT and CMAP of all subjects. PNCT was defined as the time from stimulation artifact to the onset of CMAP and diaphragm CMAP amplitude was measured from peak to peak. Oxygen desaturation index and apnea-hypopnea index were measured using PSG, and their relevance to PNCT and CMAP were analyzed. PNCT and CMAP in five OSAHS patients were repeatedly measured after effective nasal continuous positive airway pressure treatment for more than 2 months. MAIN OUTCOME MEASURES： （1） PNCT and diaphragm CMAP of subjects in each group. （2） Relevance of oxygen desaturation index and apnea-hypopnea index to PNCT and CMAP. （3） Changes of PNCT and CMAP of OSAHS patients before and after treatment. RESULTS： All subjects were included in the analyzed results. （1） PNCT of the OSAHS group was significantly longer compared to that of the control and primary snore groups, while CMAP of the OSAHS group was significantly lower （P 〈 0.05）. （2） PNCT and CMAP recorded from both sides correlated significantly with oxygen desaturation index and with apnea-hypopnea index （P 〈 0.01 ）. （3） PNCT shortened significantly after effective nasal continuous positive airway pressure treatment for more than 2 months （ P 〈 0.05）. CONCLUSION： Prolongation of PNCT and decrease of CMAP might contribute to the decline of phrenic nerve and diaphragm function caused by repeated nocturnal hypoxia and carbon dioxide retention. The impairment of the phrenic nerve might also decrease diaphragm function.

Effects of dexmedetomidine and dexketoprofen on the conduction block of rat sciatic nerve

Dexmedetomidine is a selective α2-adrenoceptor agonist that is used because of its sedative,anxiolytic,and analgesic effects.Dexketoprofen,which is used as an analgesic,is a nonselective nonsteroidal anti-inflammatory drug (NSAID).The use of dexmedetomidine and dexketoprofen as adjuvants to local anesthetics for the peripheral nerve is gradually increasing.In this study,we aimed to investigate the effects of different doses of dexmedetomidine and dexketoprofen on conduction block of rat sciatic nerve.The isolated sciatic nerve from adult rats was transferred to a nerve chamber.The compound action potentials (CAPs) were recorded from stimulated nerve with electrophysiological methods.Dexmedetomidine (n = 8) and dexketoprofen (n = 8) were administered in the chamber with cumulative concentrations of 10–9 to 10–5 M,and the CAPs were recorded for 5 and 10 minutes.The CAP parameters were calculated.Both dexmedetomidine and dexketoprofen significantly depressed all CAP parameters in a dose-dependent manner compared with the control group,i.e.,the group in which rats did not receive treatment.CAP parameters showed there was no significant difference in nerve conduction inhibition between dexmedetomidine and dexketoprofen.Higher doses of dexmedetomidine suppressed the conduction in the fast-conducting fibers;however,dexketoprofen was found to suppress the conduction in the slow-conducting fibers in a time-dependent manner and suppress the conduction in the medium- and slow-conducting fibers in a dose-dependent manner.These findings suggest that dexmedetomidine and dexketoprofen exhibit better anesthetic effects on peripheral nerve through different ways of action.The experimental procedures were approved by the Necmettin Erbakan University on January 30,2013 (approval No.2013-024).

Stimulating effect of thyroid hormones in peripheral nerve regeneration:research history and future direction toward clinical therapy

Injury to peripheral nerves is often observed in the clinic and severe injuries may cause loss of motor and sensory functions.Despite extensive investigation,testing various surgical repair techniques and neurotrophic molecules,at present,a satisfactory method to ensuring successful recovery does not exist.For successful molecular therapy in nerve regeneration,it is essential to improve the intrinsic ability of neurons to survive and to increase the speed of axonal outgrowth.Also to induce Schwann cell phenotypical changes to prepare the local environment favorable for axonal regeneration and myelination.Therefore,any molecule that regulates gene expression of both neurons and Schwann cells could play a crucial role in peripheral nerve regeneration.Clinical and experimental studies have reported that thyroid hormones are essential for the normal development and function of the nervous system,so they could be candidates for nervous system regeneration.This review provides an overview of studies devoted to testing the effect of thyroid hormones on peripheral nerve regeneration.Also it emphasizes the importance of combining biodegradable tubes with local administration of triiodothyronine for future clinical therapy of human severe injured nerves.We highlight that the local and single administration of triiodothyronine within biodegradable nerve guide improves significantly the regeneration of severed peripheral nerves,and accelerates functional recovering.This technique provides a serious step towards future clinical application of triiodothyronine in human severe injured nerves.The possible regulatory mechanism by which triiodothyronine stimulates peripheral nerve regeneration is a rapid action on both axotomized neurons and Schwann cells.

Temporal sequential correlation analysis on compoundaction potentials of the auditory nerve versus the stimulating AM-sound envelope

Compound action potentials of the auditory nerve in response to amplitude modulating tones were recorded in guinea pigs with electrode implanted to the exit of the internal auditory meatus and temporal sequential correlation between the responses and the modulators was studied in a paradigm of systematically changing acoustic parameters. Three kinds of modulators were used. continuous or burst sinusoids of fixed frequency (in the range of 40 Hz-5 kHz), short bursts of sinusoids with changing frequency and short segments of speech signal. Ranges of parametric variation were 500 Hz-20 kHz for carrier frequency, 5%-95% for modulation depth and 20 dB-90 dB SPL for intensity. For continuous or burst sinusoidal modulators of fixed frequencies, the correlation coefficient (r) remained quite high in most parametric conditions, ranging from 0.80 to 0.95. It became smaller mainly in instances of decreased response amplitude on account of unfavourable parameters. For burst modulators of changing frequency, r varied around 0.66-0.86. When segments of speech signal served as the modulators, significant correlation (r around 0.50 ) also existed, indicating the validity of the timing mode of information encoding for speech sound at the cochlear nerve level. Some theoretical and technical points in studying the timing mechanism of audition is discussed.

CHARACTERISTIC OF FACIAL MUSCLE AND EFFERENT NERVE ON PHYSIOLOGY AND ANATOMY

Objective.To study the speciality of orbicularis oculi muscles, nerves and oris muscles, nerves and mechanism of difference of faclal muscular injury in facial paralysis deeply.Methods. The conductive velocity of the efferent nerves of orbicularis oculi and oris muscles of the health human beings and guinea pigs is measured with electromyogram (EMG) apparatus.Results. The conductive velocity of orbicularis oculi nerve is quicker and oris muscles are controlled by facial nerves on both sides. Measuring the threshold of Strength-Duration (S-D) curves of the motor point of orbicularis oculi and oris muscles shows the threshold of the former is lower. Measuring the diameter of orbicularis oculi and oris nerve fibers on the guinea pigs and rabbits shows the diameter of orbicularis oculi nerve fiber is bigger. The area of secondary synapse space of orbicularis oculi motor end plate is larger than that of oris under scanning electromicroscope.Conclusions. Orbicularis oculi muscles,orbicularis oculi nerves and oris muscles,oris nerves all have their own characteristic on physiology and anatomy. It elucidated the mechanism that orbicularis oculi muscle is easy to be injuried.

Brainstem auditory evoked potential combined with high resolution cranial base CT can optimize the diagnosis of auditory nerve injury

Purpose:Auditory nerve injury is one of the most common nerve injury complications of skull base fractures.However,there is currently a lack of auxiliary examination methods for its direct diagnosis.The purpose of this study was to find a more efficient and accurate means of diagnosis for auditory nerve injury.Methods:Through retrospectively analyzing the results of brainstem auditory evoked potential(BAEP)and high-resolution CT(HRCT)in 37 patients with hearing impairment following trauma from January 1,2018 to July 31,2020,the role of the two inspection methods in the diagnosis of auditory nerve injury was studied.Inclusion criteria were patient had a clear history of trauma and unilateral hearing impairment after trauma;while exclusion criteria were:(1)severe patient with a Glasgow coma scale score<5 because these patients were classified as severe head injury and admitted to the intensive care unit,(2)patient in the subacute stage admitted 72 h after trauma,and(3)patient with prior hearing impairment before trauma.According to Goodman's classification of hearing impairment,the patients were divided into low/medium/severe injury groups.In addition,patients were divided into HRCT-positive and negative groups for further investigation with their BAEP results.The positive rates of BEAP for each group were observed,and the results were analyzed by Chi-square test(p<0.05,regarded as statistical difference).Results:A total of 37 patients were included,including 21 males and 16 females.All of them were hospitalized patients with GCS score of 6-15 at the time of admission.The BAEP positive rate in the medium and severe injury group was 100%,which was significantly higher than that in the low injury group(27.27%)(p<0.01).The rate of BEAP positivity was significantly higher in the HRCT-positive group(20/30,66.7%)than in the HRCT-negative group(1/7,14.3%)(p<0.05).Twenty patients(54.05%)were both positive for BEAP and HRCT test,and considered to have auditory nerve damage.Six patients(16.22%)were both negative for BEAP and HRCT test,and 10 patients(27.03%)were BAEP-negative but HRCT-positive:all the 16 patients were considered as non-neurological injury.The rest 1 case(2.70%)was BAEP-positive but HRCT-negative,which we speculate may have auditory nerve concussion.Conclusion:By way of BAEP combining with skull base HRCT,we may improve the accuracy of the diagnosis of auditory nerve injury.Such a diagnostic strategy may be beneficial to guiding treatment plans and evaluating prognosis.

健康豚鼠不同直径刺激电极圆窗ECAP比较分析

目的比较分析不同直径刺激电极对健康豚鼠圆窗电诱发复合动作电位(electrically evoked auditory nerve compound action potentials,ECAP)的影响。方法选取健康豚鼠12只(24耳),随机分为A组和B组,每组6只(12耳),A组使用直径为0.7mm的银球电极,B组使用直径为1mm的银球电极。吸入麻醉后打开听泡,刺激电极正极置于圆窗膜,在电刺激条件下通过体表电极记录ECAP波形,比较两组ECAP引出率、阈值、幅值、潜伏期;总和电位(electrically evoked summating potentials,ESP)幅值、潜伏期。结果刺激电极直径愈大,ESP阈值愈小,潜伏期愈长,差异有统计学意义(P=0.021,P<0.05)。但刺激电极直径不同时ECAP的引出率、阈值、幅值与潜伏期及ESP幅值、阈值无显著性差异。结论全麻下豚鼠圆窗ECAP可以稳定地记录到,其引出率、阈值与刺激电极直径大小无明显相关性。与直径为1 mm的银球电极相比,使用直径为0.7 mm的银球电极可以更快引出ESP,但刺激电极直径为1 mm时ECAP、ESP波形分化更好。

六价铬对牛蛙心脏、骨骼肌和坐骨神经干生理功能的影响

【目的】从电生理学角度研究六价铬对牛蛙心脏、腓肠肌和坐骨神经干动作电位的影响,探讨六价铬的毒性作用机制。【方法】将不同浓度重铬酸钾溶液通过腹腔注射和离体心脏灌流法处理牛蛙心脏,测定六价铬对在体和离体心脏心率和收缩力的影响。用重铬酸钾溶液浸润好的纱布包裹腓肠肌,测定腓肠肌收缩力变化。采用细胞外电极引导法,测定六价铬对坐骨神经干动作电位传导速度的影响。【结果】结果显示:重铬酸钾对心率和收缩力具有抑制作用,机制分别与六价铬抑制T型钙通道活性和L型钙通道活性有关;然而1 mg/L铬对在体蛙心作用15 min至30 min后,心率增加,可能是“毒物兴奋效应”所致;0.001 mg/L至10 mg/L六价铬对腓肠肌收缩力具有浓度依赖性增强作用,表现为正性变力效应,可能是“毒物兴奋效应”的结果;100 mg/L六价铬抑制了腓肠肌收缩力,表现为负性变力效应,机制与六价铬对兰尼碱受体(Ryanodine receptor,RyR)的抑制作用有关;六价铬以质量浓度和时间依赖性降低了神经干动作电位传导速度,机制与六价铬对电压门控Na+通道产生的失活作用有关。【结论】六价铬对心肌、骨骼肌和神经均具有毒性作用,结果可为六价铬的毒性作用研究提供一定的电生理实验依据。

蛇床子素通过阻断钙通道降低蛙坐骨神经复合动作电位幅度

目的探讨蛇床子素对蛙坐骨神经复合动作电位的作用以及离子机制。方法通过细胞外空气间隔法诱导蛙坐骨神经复合动作电位,观察蛇床子素作用及其机制。结果蛇床子素剂量依赖降低蛙坐骨神经复合动作电位幅度。胞外0钙能够减小蛇床子素的抑制效应。广谱钙通道阻断剂氯化镉,氯化镧阻断蛇床子素的抑制效应。L型钙通道阻断剂地尔硫卓、维拉帕米,P/T型钙通道阻断剂氯化镍都能阻断蛇床子素的抑制效应。结论蛇床子素通过抑制钙通道降低蛙的坐骨神经复合动作电位幅度。

Mechanism of persistent hyperalgesia in neuropathic pain caused by chronic constriction injury

Transmembrane member 16 A(TMEM16 A) is involved in many physiological functions, such as epithelial secretion, sensory conduction, nociception, control of neuronal excitability, and regulation of smooth muscle contraction, and may be important in peripheral pain transmission. To explore the role of TMEM16 A in the persistent hyperalgesia that results from chronic constriction injury-induced neuropathic pain, a rat model of the condition was established by ligating the left sciatic nerve. A TMEM16 A selective antagonist(10 μg T16 Ainh-A01) was intrathecally injected at L5–6. For measurement of thermal hyperalgesia, the drug was administered once at 14 days and thermal withdrawal latency was recorded with an analgesia meter. For measurement of other indexes, the drug was administered at 12 days,once every 6 hours, totally five times. The measurements were performed at 14 days. Western blot assay was conducted to analyze TMEM16 A expression in the L4–6 dorsal root ganglion. Immunofluorescence staining was used to detect the immunoreactivity of TMEM16 A in the L4–6 dorsal root ganglion on the injured side. Patch clamp was used to detect electrophysiological changes in the neurons in the L4–6 dorsal root ganglion. Our results demonstrated that thermal withdrawal latency was shortened in the model rats compared with control rats.Additionally, TMEM16 A expression and the number of TMEM16 A positive cells in the L4–6 dorsal root ganglion were higher in the model rats, which induced excitation of the neurons in the L4–6 dorsal root ganglion. These findings were inhibited by T16 Ainh-A01 and confirm that TMEM16 A plays a key role in persistent chronic constriction injury-induced hyperalgesia. Thus, inhibiting TMEM16 A might be a novel pharmacological intervention for neuropathic pain. All experimental protocols were approved by the Animal Ethics Committee at the First Affiliated Hospital of Shihezi University School of Medicine, China(approval No. A2017-170-01) on February 27, 2017.

Neuroprotective effect of interleukin-6 regulation of voltage-gated Na^+ channels of cortical neurons is time-and dose-dependent

Interleukin-6 has been shown to be involved in nerve injury and nerve regeneration, but the effects of long-term administration of high concentrations of interleukin-6 on neurons in the central nervous system is poorly understood. This study investigated the effects of 24 hour expo-sure of interleukin-6 on cortical neurons at various concentrations （0.1, 1, 5 and 10 ng/mL） and the effects of 10 ng/mL interleukin-6 exposure to cortical neurons for various durations （2, 4, 8, 24 and 48 hours） by studying voltage-gated Na＋ channels using a patch-clamp technique. Volt-age-clamp recording results demonstrated that interleukin-6 suppressed Na＋ currents through its receptor in a time- and dose-dependent manner, but did not alter voltage-dependent activation and inactivation. Current-clamp recording results were consistent with voltage-clamp recording results. Interleukin-6 reduced the action potential amplitude of cortical neurons, but did not change the action potential threshold. The regulation of voltage-gated Na＋channels in rat corti-cal neurons by interleukin-6 is time- and dose-dependent.

Olfactory ensheathing cells promote nerve regeneration and functional recovery after facial nerve defects

Olfactory ensheathing cells from the olfactory bulb and olfactory mucosa have been tbund to increase axonal sprouting and pathfinding and promote the recovery of vibrissae motor performance in facial nerve transection injured rats. However, it is not yet clear whether olfactory ensheathing cells promote the reparation of facial nerve defects in rats. In this study, a collagen sponge and silicone tube neural conduit was implanted into the 6-mm defect of the buccal branch of the facial nerve in adult rats. Olfactory ensheathing cells isolated from the olfactory bulb of newborn Sprague-Dawley rats were injected into the neural conduits connecting the ends of tile broken nerves, the morphology and function of the regenerated nerves were compared between the rats implanted with olfactory ensheathing cells with the rats injected with saline. Facial paralysis was assessed. Nerve electrography was used to measure facial nerve-induced action potentials. Visual inspection, anatomical microscopy and hematoxylin-eosin staining were used to assess the histomorphology around the trans planted neural conduit and the morphology of the regenerated nerve. Using fluorogold retrograde tracing, toluidine blue staining and lead uranyl acetate staining, we also measured the number of neurons in the anterior exterior lateral f：acial nerve motor nucleus, the number of myelinated nerve fibers, and nerve fiber diameter and myelin sheath thickness, respectively. After surgery, olfactory ensheathing cells de- creased facial paralysis and the latency of the facial nerve-induced action potentials. There were no differences in the general morphology of the regenerating nerves between the rats implanted with olfactory ensheathing cells and the rats injected with saline. Between-group results showed that olfactory ensheathing cell treatment increased the number of regenerated neurons, improved nerve fiber morphology, and increased the number of myelinated nerve fibers, nerve fiber diameter, and myelin sheath thickness. In conclusion, implantation of olfactory ensheathing cells can promote regeneration and functional recovery after facial nerve damage in rats.

Genetic factors for nerve susceptibility to injuries – lessons from PMP22 deficiency

Genetic factors may be learnt from families with gene mutations that render nerve-injury sus- ceptibility even to ordinary physical activities. A typical example is hereditary neuropathy with liability to pressure palsies （HNPP）. HNPP is caused by a heterozygous deletion of PMP22 gene. PMP22 deficiency disrupts myelin junctions （such as tight junction and adherens junctions）, leading to abnormally increased myelin permeability that explains the nerve susceptibility to injury. This finding should motivate investigators to identify additional genetic factors contribut- ing to nerve vulnerability of injury.

Surgical treatment for severe cubital tunnel syndrome with absent sensory nerve conduction

For severe cubital tunnel syndrome, patients with absent sensory nerve action potential tend to have more severe nerve damage than those without. Thus, it is speculated that such patients generally have a poor prognosis. How absent sensory nerve action potential affects surgical outcomes remains uncertain owing to a scarcity of reports and conflicting results. This retrospective study recruited one hundred and fourteen cases(88 patients with absent sensory nerve action potential and 26 patients with present sensory nerve action potential) undergoing either subcutaneous transposition or in situ decompression. The minimum follow-up was set at 2 years. Primary outcome measures of overall hand function included their McGowan grade, modified Bishop score, and Disabilities of the Arm, Shoulder, and Hand Questionnaire(DASH) score. For patients with absent sensory nerve action potential, 71 cases(80.7%) achieved at least one McGowan grade improvement, 76 hands(86.4%) got good or excellent results according to the Bishop score, and the average DASH score improved 49.5 points preoperatively to 13.1 points postoperatively. When compared with the present sensory nerve action potential group, they showed higher postoperative McGowan grades and DASH scores, but there was no statistical difference between the modified Bishop scores of the two groups. Following in situ decompression or subcutaneous transposition, great improvement in hand function was achieved for severe cubital tunnel syndrome patients with absent sensory nerve action potential. The functional outcomes after surgery for severe cubital tunnel syndrome are worse in patients with absent sensory nerve action potential than those without. This study was approved by the Ethical Committee of Huashan Hospital, Fudan University, China(approval No. 2017142).

Repairing whole facial nerve defects with xenogeneic acellular nerve grafts in rhesus monkeys

Acellular nerve allografts conducted via chemical extraction have achieved satisfactory results in bridging whole facial nerve defects clinically,both in terms of branching a single trunk and in connecting multiple branches of an extratemporal segment.However,in the clinical treatment of facial nerve defects,allogeneic donors are limited.In this experiment,we exposed the left trunk and multiple branches of the extratemporal segment in six rhesus monkeys and dissected a gap of 25 mm to construct a monkey model of a whole left nerve defect.Six monkeys were randomly assigned to an autograft group or a xenogeneic acellular nerve graft group.In the autograft group,the 25-mm whole facial nerve defect was immediately bridged using an autogenous ipsilateral great auricular nerve,and in the xenogeneic acellular nerve graft group,this was done using a xenogeneic acellular nerve graft with trunk-branches.Examinations of facial symmetry,nerve-muscle electrophysiology,retrograde transport of labeled neuronal tracers,and morphology of the regenerated nerve and target muscle at 8 months postoperatively showed that the faces of the monkey appeared to be symmetrical in the static state and slightly asymmetrical during facial movement,and that they could actively close their eyelids completely.The degree of recovery from facial paralysis reached House-Brackmann grade II in both groups.Compound muscle action potentials were recorded and orbicularis oris muscles responded to electro-stimuli on the surgical side in each monkey.Fluoro Gold-labeled neurons could be detected in the facial nuclei on the injured side.Immunohistochemical staining showed abundant neurofilament-200-positive axons and soluble protein-100-positive Schwann cells in the regenerated nerves.A large number of mid-graft myelinated axons were observed via methylene blue staining and a transmission electron microscope.Taken together,our data indicate that xenogeneic acellular nerve grafts from minipigs are safe and effective for repairing whole facial nerve defects in rhesus monkeys,with an effect similar to that of autologous nerve transplantation.Thus,a xenogeneic acellular nerve graft may be a suitable choice for bridging a whole facial nerve defect if no other method is available.The study was approved by the Laboratory Animal Management Committee and the Ethics Review Committee of the Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University,China(approval No.2018-D-1)on March 15,2018.

Acrylamide inhibits nerve sprouting induced by botulinum toxin type A

Botulinum toxin type A is a potent muscle relaxant that blocks the transmission and release of acetylcholine at the neuromuscular junction. Intramuscular injection of botulinum toxin type A has served as an effective and safe therapy for strabismus and focal dystonia. However, muscular weakness is temporary and after 3-4 months, muscle strength usually recovers because function- al recovery is mediated by nerve sprouting and reconstruction of the neuromuscular junction. Acrylamide may produce neurotoxic substances that cause retrograde necrotizing neuropathy and inhibit nerve sprouting caused by botulinum toxin type A. This study investigated whether acrylamide inhibits nerve sprouting after intramuscular injection of botulinum toxin type A. A tibial nerve sprouting model was established through local injection of botulinum toxin type A into the right gastrocnemius muscle of Sprague-Dawley rats. Following intramuscular injection, rats were given intraperitoneal injection of 3% acrylamide every 3 days for 21 days. Nerve sprout- ing appeared 2 weeks after intramuscular injection of botulinum toxin type A and single-fiber electromyography revealed abnormal conduction at the neuromuscular junction I week after intra- muscular injection of botulinum toxin type A. Following intraperitoneal injection of acrylamide, the peak muscle fiber density decreased. Electromyography jitter value were restored to normal levels 6 weeks after injection. This indicates that the maximal decrease in fiber density and the time at which functional conduction of neuromuscular junction was restored were delayed. Addition- ally, the increase in tibial nerve fibers was reduced. Acrylamide inhibits nerve sprouting caused by botulinum toxin type A and may be used to prolong the clinical dosage of botulinum toxin type A.