Nerve Conduction Block Research Articles

Supramaximal stimulation during intraoperative facial nerve monitoring as a simple parameter to predict early functional outcome after parotidectomy

Conclusion: A supramaximal stimulation at 2 mA during intraoperative electromyographic (EMG) facial nerve monitoring appears to be a simple and effective parameter to predict immediate postoperative injury. Objectives: To assess the role of systematic intraoperative facial nerve monitoring in predicting the early functional outcomes obtained after parotidectomy. Methods: Data were collected from patients who underwent parotidectomy. Intraoperative EMG monitoring of the facial nerve was performed by registering two parameters, event intensity (>100 μV) and amplitude of response after a supramaximal stimulation at 2 mA, at the beginning and end of gland removal. Early postoperative clinical functional facial nerve disorder was assessed at day 2. Results: Overall, 50 patients were included and an early facial dysfunction was detected in 27 cases (54%). The maximal response amplitude after supramaximal stimulation at the trunk of the facial nerve was higher in patients with normal facial function compared with those with poor outcomes at the end of surgery (p < 0.01). The postdissection to predissection ratios of maximal response amplitude, but not the stimulation thresholds, were indicative of a nerve conduction block and were significantly lower in the patient group with a poor outcome compared with the group with a normal facial outcome (p < 0.02).

Calculation skills for nurses: Local anaesthetic agents

M clinical scenarios require the administration of local anaesthetic. Local anaesthetics are generally viewed as safe drugs, with a low risk of systemic adverse drug reactions when prescribed and administered correctly (Faccenda and Finucane, 2001). However, if toxicity arises—as a result of exceeding the maximum safe dose (MSD), inappropriate use, or inadvertent intravascular administration—the consequences for the neurological and/or cardiovascular systems can be serious (Cox et al, 2003). The aim of this article is to assist nurse prescribers to administer safe levels of injectable local anaesthetic agents. Allergic reactions are not included, as they are unrelated to the calculation of safe doses. Agents predominantly for dental use and topical agents are also excluded. All local anaesthetics reversibly block nerve conduction at a local level without impeding consciousness. Most local anaesthetics in routine use in the UK are amide compounds (e.g lidocaine and bupivacaine), which undergo hepatic metabolism and predominantly renal excretion (Edgcombe and Hocking, 2006). The speed of onset, potency, and duration of action depend upon the active agent, the percentage concentration and the addition of vasoconstrictors. Vasoconstrictors, such as adrenaline, alter drug kinetics and hence may impact on the permitted dose. They shrink local vasculature and slow the rate of absorption of the anaesthetic into the circulation, prolonging the anaesthetic effect. A temporal decrease in systemic absorption means that toxic concentrations are less likely, and this is reflected in higher MSDs for some agents (Table 1). Formally, there is no change for bupivacaine with adrenaline, to minimise the cardiotoxic risk. Despite this, some sources advise that the MSD can increase to 2.5 mg/kg with adrenaline (Anaesthesia UK, 2009).

In vivo optical spectroscopy monitoring in a new model of muscular compartment syndrome

Muscular compartment syndrome (MCS) is a rare but serious postoperative complication. In vivo optical spectroscopy (INVOS) monitors continuously and non-invasively regional oxygen saturation (rSO(2)), and could predict the development of MCS. In 10 healthy volunteers, we inflated a tourniquet to the mean arterial pressure to produce slight venous congestion and arterial hypoperfusion. Comparisons were made between the relative reduction in rSO(2) with baseline (deltaINVOS) and the time to observe motor nerve block (with non-invasive electromyography). Neurological symptoms, pain, and invasive intracompartmental pressure (ICP) were assessed. In the eight volunteers completing the protocol, we observed a profound motor nerve conduction block, immediately reversible. Baseline values were: [mean (sd)] INVOS: 73.3 (8.9)% and ICP: 16.9 (8.6) mm Hg. At the time of the block, values were: INVOS: 46.4 (10.9)%, deltaINVOS: 28.7 (10.6)%, and ICP: 70.0 (5.5) mm Hg. The time to reach the block was 33.0 (10.9) min, and to a deltaINVOS>10%: 27.4 (10.4) min. Receiver-operating characteristic curves demonstrated a similar accuracy of ICP and INVOS to predict the occurrence of the block. Twenty minutes with a deltaINVOS>10% or ICP>30 mm Hg were associated with a sensitivity and a specificity of 95% and 70%; or 91% and 65%, respectively. We have developed a model of acute immediately reversible MCS. Monitoring using the INVOS technology is as accurate as measurement of ICP, and could be a useful tool to prevent development of intraoperative MCS.

Effect of Local Anesthesia on Trigeminal Somatosensory-evoked Magnetic Fields

For objective neurophysiological evaluation of the function of the trigeminal system, magnetoencephalography- based TSEF (trigeminal somatosensory-evoked field) assessment would be valuable in providing spatial and temporal profiles of cortical responses. However, this necessitates knowledge of how TSEF varies with trigeminal nerve dysfunctions. We introduced a conduction block of the trigeminal nerve using local anesthesia (lidocaine) to temporally mimic nerve dysfunctions, and monitored TSEF changes. Following an electrical stimulation of the lower lip, a magnetic response with peak latency of approximately 20 ms was identified in all participants. Dipole for the peak was estimated on the post-central gyrus in the participant’s own magnetic resonance image. After normalization to Montreal Neurological Institute (MNI) space and inter-participant data integration, the summary equivalent current dipole localization among participants remained in the post-central gyrus, suggesting validity of the use of MNI space. Partial anesthesia of the lower lip led to a loss of the waveform characteristics of TSEF for electrical stimulation to the trigeminal nerve. We verified that the 20-ms latency cortical response of TSEF components localized at the primary sensory cortex can serve as a robust neurofunctional marker of experimental trigeminal nerve dysfunction.

Role of Activity-Dependent Conduction Block in the Diagnosis of Primary Demyelinating Polyneuropathy

Motor conduction block is one of the well-known neurophysiologic features of primary demyelinating polyneuropathy. In contrast, activity-dependent conduction block (motor conduction block after brief maximum voluntary contraction) is a "rare" neurophysiologic finding in primary demyelinating polyneuropathy. We are reporting the first known case of multifocal acquired demyelinating sensory and motor polyneuropathy with a well-documented activity-dependent conduction block of the ulnar nerve at the forearm segment that transformed into a typical motor response with abnormal temporal dispersion.

Use of High Surface Area Electrodes for Safe Delivery of Direct Current for Nerve Conduction Block

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Dimethylsulfoxide potentiates the nerve conduction–blocking effect of lidocaine without augmentation of the intracellular lidocaine concentration in the giant axon of crayfish in vitro

The purpose of this study was to investigate how dimethylsulfoxide (DMSO) potentiates the blocking action of lidocaine. A giant axon removed from a crayfish was used to investigate nerve conduction and intracellular lidocaine concentration. The maximum values of the differential waveform (dV/dt max) calculated from evoked action potentials were used for evaluating an inhibition of nerve conduction. The inhibition of the dV/dt max in low-frequency stimulation (tonic block) and high-frequency stimulation (phasic block) after perfusion of 1 mm lidocaine with or without 0.2 vol % DMSO, in which the concentration of DMSO alone had no anesthetic effect, was measured to evaluate the potentiating action of DMSO. The intracellular lidocaine concentration was measured via a lidocaine-sensitive glass microelectrode during 30 min of perfusion of 1 mm lidocaine alone or in combination with DMSO. When applied without lidocaine, DMSO caused a dose-dependent nerve conduction block when used at concentrations >1 vol %. The dV/dt max in the tonic block was significantly decreased when 0.2 vol % DMSO was added to the lidocaine solution (P = 0.004). In the phasic block, there was no significant potentiating action of DMSO. There were no significant differences in the intracellular lidocaine concentrations with or without DMSO. The potentiating effects of DMSO were observed only in the condition of low-frequency stimulation and were not related to the intracellular lidocaine concentration in the giant axon of crayfish in vitro.

High frequency sacral root nerve block allows bladder voiding

Dyssynergic reflexive external urethral sphincter (EUS) activity following spinal cord injury can prevent bladder voiding, resulting in significant medical complications. Irreversible sphincterotomies or neurotomies can prevent EUS activation and allow bladder voiding, but may cause incontinence or loss of sacral reflexes. We investigated whether kilohertz frequency (KF) electrical conduction block of the sacral roots could prevent EUS activation and allow bladder voiding. The S2 sacral nerve roots were stimulated bilaterally to generate bladder pressure in six cats. One S1 nerve root was stimulated proximally (20 Hz biphasic pulse trains) to evoke EUS pressure, simulating worst-case dyssynergic EUS reflexes. KF waveforms (12.5 kHz biphasic square wave) applied to an electrode implanted distally on the S1 nerve root blocked nerve conduction, preventing the increase in EUS pressure and allowing voiding. Applying KF waveforms increased bladder voiding in single, limited-duration trials from 3 ± 6% to 59 ± 12%. Voiding could be increased to 82 ± 9% of the initial bladder volume by repeating or increasing the duration of the trials. Sacral nerve block can prevent EUS activation and allow complete bladder voiding, potentially eliminating the need for a neurotomy. Eliminating neurotomy requirements could increase patient acceptance of bladder voiding neuroprostheses, increasing patient quality of life and reducing the cost of patient care.

Neurophysiological diagnosis of hereditary neuropathy with liability to pressure palsies

Objective To explore the neurophysiological properties of hereditary neuropathy with liability to pressure palsies(HNPP),so as to provide evidence for the diagnosis of HNPP.Methods Three families(8 individuals) with clinically affected and asymptomatic HNPP patients underwent routine electrodiagnostic tests,including median,ulnar,radial,tibial and proneal motor and sensory nerve conduction,and the results were compared with those of 30 healthy subjects.Results(1)Prolongation of the distal nerve conduction latencies was the most seen abnormality(92.1%),mainly found in the median and common peroneal nerves,including those with and without symptoms.(2)The rate of motor nerve conduction slowing was 63.2%,mostly seen in the median and common peroneal nerves.(3)The rate of sensory nerve conduction slowing was 89.6%,mostly affecting the sural and median nerves.(4)The conduction block of the ulnar nerve at the elbow was more commonly seen than that of the proneal nerve at the fibular head.Conclusion Neurophysiological examination is a noninvasive,fast,simple and accurate diagnosis way for clinically suspected HNPP patients,and it can be used for screening the family members of HNPP patients and for prevention of HNPP.

Dysfunction of nodes of Ranvier: A mechanism for anti-ganglioside antibody-mediated neuropathies

Autoantibodies against gangliosides GM1 or GD1a are associated with acute motor axonal neuropathy (AMAN) and acute motor-sensory axonal neuropathy (AMSAN), whereas antibodies to GD1b ganglioside are detected in acute sensory ataxic neuropathy (ASAN). These neuropathies have been proposed to be closely related and comprise a continuous spectrum, although the underlying mechanisms, especially for sensory nerve involvement, are still unclear. Antibodies to GM1 and GD1a have been proposed to disrupt the nodes of Ranvier in motor nerves via complement pathway. We hypothesized that the disruption of nodes of Ranvier is a common mechanism whereby various anti-ganglioside antibodies found in these neuropathies lead to nervous system dysfunction. Here, we show that the IgG monoclonal anti-GD1a/GT1b antibody injected into rat sciatic nerves caused deposition of IgG and complement products on the nodal axolemma and disrupted clusters of nodal and paranodal molecules predominantly in motor nerves, and induced early reversible motor nerve conduction block. Injection of IgG monoclonal anti-GD1b antibody induced nodal disruption predominantly in sensory nerves. In an ASAN rabbit model associated with IgG anti-GD1b antibodies, complement-mediated nodal disruption was observed predominantly in sensory nerves. In an AMAN rabbit model associated with IgG anti-GM1 antibodies, complement attack of nodes was found primarily in motor nerves, but occasionally in sensory nerves as well. Periaxonal macrophages and axonal degeneration were observed in dorsal roots from ASAN rabbits and AMAN rabbits. Thus, nodal disruption may be a common mechanism in immune-mediated neuropathies associated with autoantibodies to gangliosides GM1, GD1a, or GD1b, providing an explanation for the continuous spectrum of AMAN, AMSAN, and ASAN.

Selective silencing of Na(V)1.7 decreases excitability and conduction in vagal sensory neurons.

There has been much information learned in recent years about voltage gated sodium channel (Na(V)) subtypes in somatosensory pain signalling, but much less is known about the role of specific sodium channel subtypes in the vagal sensory system. In this study, we developed a technique using adeno-associated viruses (AAVs) to directly introduce shRNA against Na(V)1.7 subtype gene into the vagal sensory ganglia of guinea pigs in vivo. Na(V)1.7 gene expression in nodose ganglia was effectively and selectively reduced without influencing the expression of other sodium channel subtype genes including Na(V)1.1, 1.2, 1.3 1.6, 1.8, or 1.9. Using a whole cell patch-clamp technique, this effect on Na(V)1.7 gene expression coincided with a reduction in tetrodotoxin-sensitive sodium current, a requirement for much larger depolarizing stimulus to initiate action potentials, and reduction in repetitive action potential discharge. Extracellular recordings in the isolated vagus nerve revealed that the conduction of action potentials in sensory A- and C-fibres in many neurons was effectively abolished after Na(V)1.7 shRNA introduction. Moreover, bilateral Na(V)1.7 shRNA injected animals survived for several months and the vagal reflex behaviour, exemplified by citric acid-induced coughing, was significantly suppressed. These data indicate that selectively silencing Na(V)1.7 ion channel expression leads to a substantial decrease in neural excitability and conduction block in vagal afferent nerves.

Functional electrical stimulation of intrinsic laryngeal muscles under varying loads in exercising horses.

Bilateral vocal fold paralysis (BVCP) is a life threatening condition and appears to be a good candidate for therapy using functional electrical stimulation (FES). Developing a working FES system has been technically difficult due to the inaccessible location and small size of the sole arytenoid abductor, the posterior cricoarytenoid (PCA) muscle. A naturally-occurring disease in horses shares many functional and etiological features with BVCP. In this study, the feasibility of FES for equine vocal fold paralysis was explored by testing arytenoid abduction evoked by electrical stimulation of the PCA muscle. Rheobase and chronaxie were determined for innervated PCA muscle. We then tested the hypothesis that direct muscle stimulation can maintain airway patency during strenuous exercise in horses with induced transient conduction block of the laryngeal motor nerve. Six adult horses were instrumented with a single bipolar intra-muscular electrode in the left PCA muscle. Rheobase and chronaxie were within the normal range for innervated muscle at 0.55±0.38 v and 0.38±0.19 ms respectively. Intramuscular stimulation of the PCA muscle significantly improved arytenoid abduction at all levels of exercise intensity and there was no significant difference between the level of abduction achieved with stimulation and control values under moderate loads. The equine larynx may provide a useful model for the study of bilateral fold paralysis.

An electrophysiological study of Hirayama disease

Objective To analyze the electrophysiological characteristics of Hirayama disease and explore their significance for its diagnosis. Methods Electrophysiological tests were performed on 18 patients who fulfilled the clinical criteria for Hirayama disease. Sixteen were males and 2 were females. The mean age was 24.9years old ( 19-58 years), and the mean case history was 5.2 years ( 1-40 years). The Hirayama disease was clearly unilateral in 10 patients and bilateral in 3, with 5 cases suspected of being bilateral. Motor neuron conduction velocity (MCV) and sensory neuron conduction velocity (SCV) were measured in the median and ulnar nerves.Electromyograms (EMGs) of the abductor digiti minimi, abductor pollicis brevis, extensor digitorum communis,brachioradialis muscle, biceps brachii and sternocleidomastoid were recorded in all cases. The MCV and SCV of the common peroneal nerve and an EMG of the tibialis anterior muscle were examined in one leg. The MCV and SCV of the ulnar nerve and EMGs of the abductor digiti minimi, extensor digitorum communis and brachioradialis muscles were inspected on the contralateral sides of 8 cases, including the patients suspected of suffering bilateral Hirayama disease. The MCVs of the median and ulnar nerves were examined segmentally by stimulating the nerves distally as well as proximally, and recording the amplitude, duration and area of compound muscle action potentials (CMAP) and changes in wave form, then determining whether there was a nerve conduction block. Results (1) No conduction block was detected in any median nerve or ulnar nerve among the 18 cases. (2) All the SCVs and sensory nerve action potentials of the median and ulnar nerves were normal. ( 3 ) All the MCVs and SCVs of the common peroneal nerve and the EMGs of the anterior tibialis muscles were normal. (4) MCV slowing in the upper limbs accounted for 41.3％ (19/44) of the examined nerves. The rates of MCV decrease were 72.2％ (13/18)in the ulnar nerve on the affected sides, 33.3％ (6/18) in the median nerve on the affected sides and 0％ (0/8)in the ulnar nerve on the contralateral sides. (5) Amplitude reduction in the CMAP in the upper limbs accounted for 81.8％ (36/44) of the examined nerves. The rates of amplitude decrease were 100％ (18/18) in the ulnar nerves of the affected sides, 77.8％ (14/18) of median nerves on the affected side and 50％ (4/8) of ulnar nerves on the contralateral side. ( 6 ) Upper limb EMGs revealed a rate of neurogenic damage of 47.0％ ( 62/132). The EMGs decreased in 100％ (18/18) of the abductor digiti minimi and abductor pollicis brevis on the affected side, 88.9％ (16/18) of extensor digitorum communis on the affected side, 62.5％ (5/8) of the abductor digiti minimi on the contralateral side, 37.5％ (3/8) of the extensor digitorum communis on the contralateral side,5.6％ ( 1/18 ) of the brachioradialis and biceps brachii muscles on the affected sides. There was no neurogenic damage of the contralateral brachioradialis muscle or the sternocleidomastoid on the affected side. Conclusions The electrophysiological features of Hirayama disease include unilateral or bilateral neurogenic damage in the upper limbs. According to the abnormal EMGs, spinal anterior horn cells on the affected sides were injured at C7-T1. C6and above C6 were rarely involved. The electrophysiological characteristics of Hirayama disease could provide a clear basis for localization and differentiation in Hirayama disease diagnosis. Key words: Hirayama disease; Electrophysiology

Electromyography and Ultrasonography in the Diagnosis of A Rare Double-Crush Ulnar Nerve Injury

Akyuz M, Yalcin E, Selcuk B, Onder B, Özçakar L. Electromyography and ultrasonography in the diagnosis of a rare double-crush ulnar nerve injury. Reported here is a 46-year-old man who was seen for pain, numbness, and weakness in his left upper limb and hand. Electromyographic studies demonstrated denervation of ulnar-innervated muscle groups except for the flexor carpi ulnaris. A localized nerve conduction block could not be depicted because of severe axonal loss. Ultrasonographic evaluation showed enlargement of the ulnar nerve at 2 sites: at the level of the epicondylar groove and the inside of the flexor carpi ulnaris muscle. Herein, we would like to emphasize the complementary role of an ultrasound in peripheral nerve pathologies, not only does it confirm the entrapment but it also displays the underlying cause(s).

P5.5 Partial conduction block of ulnar nerve at the wrist

P5.5 Partial conduction block of ulnar nerve at the wrist

Electrical conduction block in large nerves: high-frequency current delivery in the nonhuman primate.

Recent studies have made significant progress toward the clinical implementation of high-frequency conduction block (HFB) of peripheral nerves. However, these studies were performed in small nerves, and questions remain regarding the nature of HFB in large-diameter nerves. This study in nonhuman primates shows reliable conduction block in large-diameter nerves (up to 4.1 mm) with relatively low-threshold current amplitude and only moderate nerve discharge prior to the onset of block.

Mechanism of conduction block in amphibian myelinated axon induced by biphasic electrical current at ultra-high frequency

The mechanism of axonal conduction block induced by ultra-high frequency (≥ 20 kHz) biphasic electrical current was investigated using a lumped circuit model of the amphibian myelinated axon based on Frankenhaeuser-Huxley (FH) equations. The ultra-high frequency stimulation produces constant activation of both sodium and potassium channels at the axonal node under the block electrode causing the axonal conduction block. This blocking mechanism is different from the mechanism when the stimulation frequency is between 4 kHz and 10 kHz, where only the potassium channel is constantly activated. The minimal stimulation intensity required to induce a conduction block increases as the stimulation frequency increases. The results from this simulation study are useful to guide future animal experiments to reveal the different mechanisms underlying nerve conduction block induced by high-frequency biphasic electrical current.

Sustained Enzymatic Correction by rAAV-Mediated Liver Gene Therapy Protects Against Induced Motor Neuropathy in Acute Porphyria Mice

Acute intermittent porphyria (AIP) is characterized by a hereditary deficiency of hepatic porphobilinogen deaminase (PBGD) activity. Clinical features are acute neurovisceral attacks accompanied by overproduction of porphyrin precursors in the liver. Recurrent life-threatening attacks can be cured only by liver transplantation. We developed recombinant adeno-associated virus (rAAV) vectors expressing human PBGD protein driven by a liver-specific promoter to provide sustained protection against induced attacks in a predictive model for AIP. Phenobarbital injections in AIP mice induced porphyrin precursor accumulation, functional block of nerve conduction, and progressive loss of large-caliber axons in the sciatic nerve. Hepatocyte transduction showed no gender variation after rAAV2/8 injection, while rAAV2/5 showed lower transduction efficiency in females than males. Full protection against induced phenobarbital-attacks was achieved in animals showing over 10% of hepatocytes expressing high amounts of PBGD. More importantly, sustained hepatic expression of hPBGD protected against loss of large-caliber axons in the sciatic nerve and disturbances in nerve conduction velocity as induced by recurrent phenobarbital administrations. These data show for the first time that porphyrin precursors generated in the liver interfere with motor function. rAAV2/5-hPBGD vector can be produced in sufficient quantity for an intended gene therapy trial in patients with recurrent life-threatening porphyria attacks.

Concurrence of Multifocal Motor Neuropathy and Hashimoto's Thyroiditis

BackgroundMultifocal motor neuropathy (MMN) is an immune-mediated disorder that is characterized by slowly progressive and asymmetrical weakness, but its pathophysiological mechanism is uncertain. The hypothesis that MMN is an immunological disease has been supported by the proven therapeutic effects of intravenous immunoglobulin and the detection of antiganglioside antibodies in MMN patients. The coexistence of MMN with other immune diseases has been rarely reported.Case ReportA 37-year-old woman visited our hospital complaining of weakness in both hands. The clinical manifestations coincided well with MMN: predominantly distal upper-limb weakness, asymmetric involvement, a progressive course, absence of sensory symptoms, absence of pyramidal signs, and sparing of the cranial muscles. The electrophysiological findings also supported a diagnosis of MMN, with motor nerve conduction block in the median, ulnar, and radial nerves, without sensory nerve involvement. The patient was simultaneously diagnosed as having Hashimoto's thyroiditis, which is a well-known immune-mediated disease.ConclusionsThe concurrence of MMN and Hashimoto's thyroiditis in our patient is significant for understanding the immunological characteristics of the two diseases.

Design, fabrication and evaluation of a conforming circumpolar peripheral nerve cuff electrode for acute experimental use

Nerve cuff electrodes are a principle tool of basic and applied electro-neurophysiology studies and are championed for their ability to achieve good nerve recruitment with low thresholds. We describe the design and method of fabrication for a novel circumpolar peripheral nerve electrode for acute experimental use. This cylindrical cuff-style electrode provides approximately 270° of radial electrode contact with a nerve for each of an arbitrary number of contacts, has a profile that allows for simple placement and removal in an acute nerve preparation, and is designed for adjustment of the cylindrical diameter to ensure a close fit on the nerve. For each electrode, the electrical contacts were cut from 25 μm platinum foil as an array so as to maintain their positions relative to each other within the cuff. Lead wires were welded to each intended contact. The structure was then molded in silicone elastomer, after which the individual contacts were electrically isolated. The final electrode was curved into a cylindrical shape with an inner diameter corresponding to that of the intended target nerve. The positions of these contacts were well maintained during the molding and shaping process and failure rates during fabrication due to contact displacements were very low. Established electrochemical measurements were made on one electrode to confirm expected behavior for a platinum electrode and to measure the electrode impedance to applied voltages at different frequencies. These electrodes have been successfully used for nerve stimulation, recording, and conduction block in a number of different acute animal experiments by several investigators.