Nerve Compound Action Potential Research Articles

Effect of vasopressin as a local anesthetic in mice.

We sought to elucidate how the local administration of mepivacaine hydrochloride and vasopressin via the tail affects the peripheral blood flow volume, tissue dynamics, and mepivacaine's anesthetic effect in mice. Two-hundred and twenty-six male ICR mice were used in this study. Blood flow was measured after administering mepivacaine alone or mepivacaine with either 0.03, 0.3, or 3.0 U/mL vasopressin or 10µg/mL epinephrine via the tail tissue. The tail tissue and blood dynamics were measured using 3H-labeled mepivacaine hydrochloride with vasopressin or epinephrine. The compound nerve action potential (CNAP) was measured to clarify the anesthetic effect after administering mepivacaine with 0.3 U/mL vasopressin. The statistical methods employed were Steel-Dwass test, Mann-Whitney U test, Dunnett's test, and Tukey test. P < 0.05 indicated statistical significance. The results revealed that the local administration of ≥ 0.03 U/mL vasopressin reduced local blood flow and prolonged 3H-M localization in the tail tissue in a concentration-dependent manner. Addition of 0.3 U/mL vasopressin enhanced and prolonged the anesthetic effect of mepivacaine. The findings suggest that adding vasopressin to a local anesthetic regimen may be effective, and thus it could be applied as a vasoconstrictor.

Deep brain drug-delivery control using vagus nerve communications

Vagus nerve stimulation (VNS) uses electrical impulses applied at the neck in order to mitigate the effects of, for example, epileptic seizures. We propose using VNS to provide data pulses to communicate with a drug-delivery system embedded near the brainstem. We model the generation of a vagus nerve compound action potential (CAP), calculating the signal attenuation and the resulting transmission range. The metabolic cost of CAP transmission in terms of the use of adenosine triphosphate (ATP) is also calculated. The channel capacity for on-off keying (OOK) is computed from the CAP characteristics, the neural refractory period and the level of background neural noise. The resulting low bit-rate, unidirectional asynchronous transmission system is analysed for the use of different methods of forward error correction (FEC) to improve bit-error rate (BER). We show a proposed data packet structure that could deliver instructions to an embedded drug-delivery system with multiple addressable drug reservoirs. We also analyse the scope for powering the drug-delivery system with energy harvested from cerebrospinal glucose.

Experimental Basis for Creating an Osseointegrated Neural Interface for Prosthetic Control: A Pilot Study in Rabbits.

While debate persists over how to best prevent or treat amputation neuromas, the more pressing question of how to best marry residual nerves to state-of-the-art robotic prostheses for naturalistic control of a replacement limb has come to the fore. One potential solution involves the transposition of terminal nerve ends into the medullary canal of long bones, creating the neural interface within the bone. Nerve transposition into bone is a long-practiced, clinically relevant treatment for painful neuromas. Despite neuropathic pain relief, the physiological capacity of transposed nerves to conduct motor and sensory signals required for prosthesis control remains unknown. This pilot study addresses the hypotheses that (1) bone provides stability to transposed nerves and (2) nerves transposed into bone remain physiologically active, as they relate to the creation of an osseointegrated neural interface. New Zealand white rabbits received transfemoral amputation, with the sciatic nerve transposed into the femur. Morphological examination demonstrates that nerves remain stable within the medullary canal, while compound nerve action potentials evoked by electrical stimulation of the residual nerve within the bone could be achieved at 12 weeks (p<0.0005). Transposed nerves retain a degree of physiological function suitable for creating an osseointegrated neural interface.

The Spatial Origins of Cochlear Amplification Assessed by Stimulus-Frequency Otoacoustic Emissions

Cochlear amplification of basilar membrane traveling waves is thought to occur between a tone’s characteristic frequency (CF) place and within one octave basal of the CF. Evidence for this view comes only from the cochlear base. Stimulus-frequency otoacoustic emissions (SFOAEs) provide a noninvasive alternative to direct measurements of cochlear motion that can be measured across a wide range of CF regions. Coherent reflection theory indicates that SFOAEs arise mostly from the peak region of the traveling wave, but several studies using far-basal suppressor tones claimed that SFOAE components originate many octaves basal of CF. We measured SFOAEs while perfusing guinea pig cochleas from apex to base with salicylate or KCl solutions that reduced outer-hair-cell function and SFOAE amplification. Solution effects on inner hair cells reduced auditory nerve compound action potentials (CAPs) and provided reference times for when solutions reached the SFOAE-frequency CF region. As solution flowed from apex to base, SFOAE reductions generally occurred later than CAP reductions and showed that the effects of cochlear amplification usually peaked ∼1/2 octave basal of the CF region. For tones ≥2 kHz, cochlear amplification typically extended ∼1.5 octaves basal of CF, and the data are consistent with coherent reflection theory. SFOAE amplification did not extend to the basal end of the cochlea, even though reticular lamina motion is amplified in this region, which indicates that reticular lamina motion is not directly coupled to basilar membrane traveling waves. Previous reports of SFOAE-frequency residuals produced by suppressor frequencies far above the SFOAE frequency are most likely due to additional sources created by the suppressor. For some tones <2 kHz, SFOAE amplification extended two octaves apical of CF, which highlights that different vibratory motions produce SFOAEs and CAPs, and that the amplification region depends on the cochlear mode of motion considered. The concept that there is a single “cochlear amplification region” needs to be revised.

Threshold dynamics of the auditory nerve electrically evoked compound action potential in implanted children

To study the dynamics of thresholds of the electrically evoked compound action potential of the auditory nerve (ECAP) during neural responce telemetry (NRT) intraoperatively, at the time of activation of the cochlear implantation system (CI) and after 3 and 6 months. The study included 50 children aged 1 year to 4 years with bilateral sensorineural deafness, operated on by Nucleus CI512 Profile + CP900 CI systems («Cochlear», Australia). In all patients, the electrode array was fully inserted. The dynamics and thresholds of ECAP were recorded and assessed in dynamics: when performing NRT intraoperatively, when the CI system was activated, and after 3 and 6 months. To assess the thresholds, the 1st, 6th, 11th, 16th and 22nd electrodes of the multichannel electrode array were selected. The average threshold values and the NRT threshold profile determined intraoperatively and during measurements at different times after the activation of the CI system were significantly different (p<0.001), while the average postoperative results were characterized by relative stability. It was shown that the thresholds determined on the electrodes located in the middle of the electrode lattice are more stable than the thresholds determined on the apical and basal electrodes. In most patients, the NRT threshold values determined at the time of the activation of the CI system and after 3 and 6 months were significantly lower than the thresholds determined intraoperatively. The data obtained allow us to conclude that NRT is a stable and accurate technique that allows you to objectify the process of setting up an individual card for the stimulation of the speech processor at the rehabilitation stage after cochlear implantation.

Effects of Static Magnetic Field on Compound Action Potential of Isolated Frog Sciatic Nerve

The use of Static Magnetic Field (SMF) in medicine is currently under consideration. In this experimental study, the aim is to investigate the possible effects of SMF on nerve excitation and conduction characteristics. Our objectives are to take Compound Action Potential (CAP) measurements from an isolated frog sciatic nerve under SMF, and to calculate the amplitude and latency parameters of the CAP in order to assess possible effects. The experimental study was carried on twelve Rana Ridibundas. The sciatic nerve of the frogs were isolated from their locations and transferred to the nerve chamber. The nerve was stimulated with an electrical impulse of 0.2 ms duration and 1.4 V amplitude at the proximal end and its response was recorded at the distal end. The possible effects of SMF on the frog sciatic nerve were examined. A sequence of CAP measurements were taken with and without SMF exposure. Changes in four variables were observed. Two of the measurement variables were peak-to-peak amplitudes. The other two variables were the durations of stimulus artifact from the onset to the appearance of the first negative and first positive peaks respectively. After the first, second and third SMF exposure periods, there was a significant increase in the height of PP-1 and PP-2 which are peak-to-peak variables of CAP in both during and after exposure. Similarly, after the first, second and third SMF exposure periods, there was a significant increase in the length of Latency-1 and Latency-2 which are linked with the duration of CAP. In this study, it was observed that SMF exposure increases both the amplitude and duration of nerve CAP. Our study gave a different perspective on the effects of SMF on neuronal excitation mechanism of sciatic nerves. Besides, it provided a better understanding of the pain perception phenomenon based on transmembrane Na+ channel dynamics and nerve conduction velocity.

LSP5-2157 a new inhibitor of vesicular glutamate transporters

Vesicular glutamate transporters (VGLUT1-3) mediate the uptake of glutamate into synaptic vesicles. VGLUTs are pivotal actors of excitatory transmission and of almost all brain functions. Their implication in various pathologies has been clearly documented. Despite their functional importance, the pharmacology of VGLUTs is limited to a few dyes such as Trypan Blue, Rose Bengal or Brilliant Yellow type. Here, we report the design and evaluation of new potent analogs based on Trypan Blue scaffold. Our best compound, named LSP5-2157, has an EC50 of 50 nM on glutamate vesicular uptake. Using a 3D homology model of VGLUT1 and docking experiments, we determined its putative binding subdomains within vesicular glutamate transporters and validated the structural requirement for VGLUT inhibition. To better estimate the specificity and potency of LSP5-2157, we also investigated its ability to block glutamatergic transmission in autaptic hippocampal cells. Neither glutamate receptors nor GABAergic transmission or transmission machinery were affected by LSP5-2157. Low doses of compound reversibly reduce glutamatergic neurotransmission in hippocampal autpases. LSP5-2157 had a low and depressing effect on synaptic efficacy in hippocampal slice. Furthermore, LSP5-2157 had no effect on NMDA-R- mediated fEPSP but reduce synaptic plasticity induced by 3 trains of 100 Hz. Finally, LSP5-2157 had the capacity to inhibit VGLUT3-dependent auditory synaptic transmission in the guinea pig cochlea. In this model, it abolished the compound action potential of auditory nerve at high concentration showing the limited permeation of LSP5-2157 in an in-vivo model. In summary, the new ligand LSP5-2157, has a high affinity and specificity for VGLUTs and shows some permeability in isolated neuron, tissue preparations or in vivo in the auditory system. These findings broaden the field of VGLUTs inhibitors and open the way to their use to assess glutamatergic functions in vitro and in vivo.

Methodology for creating a chronic osseointegrated neural interface for prosthetic control in rabbits

BackgroundChronic stability and high degrees of selectivity are both essential but somewhat juxtaposed components for creating an implantable bi-directional PNI capable of controlling of a prosthetic limb. While the more invasive implantable electrode arrays provide greater specificity, they are less stable over time due to compliance mismatch with the dynamic soft tissue environment in which the interface is created. New MethodThis paper takes the surgical approach of transposing nerves into bone to create neural interface within the medullary canal of long bones, an osseointegrated neural interface, to provide greater stability for implantable electrodes. In this context, we describe the surgical model for transfemoral amputation with transposition of the sciatic nerve into the medullary canal in rabbits. We investigate the capacity to create a neural interface within the medullary canal histolomorphologically. In a separate proof of concept experiment, we quantify the chronic physiological capacity of transposed nerves to conduct compound nerve action potentials evoked via an Osseointegrated Neural Interface. Comparison with Existing Method(s)The rabbit serves as an important animal model for both amputation neuroma and osseointegration research, but is underutilized for the exploration neural interfacing in an amputation setting. ResultsOur findings demonstrate that transposed nerves remain stable over 12 weeks. Creating a neural interface within the medullary canal is possible and does not impede nerve regeneration or physiological capacity. ConclusionsThis article represents the first evidence that an Osseointegrated Neural Interface can be surgically created, capable of chronic stimulation/recording from amputated nerves required for future prosthetic control.

Novel functional imaging technique for the brachial plexus based on magnetoneurography

ObjectiveTo visualize neural activity in the brachial plexus using magnetoneurography (MNG). MethodsUsing a 124- or 132-channel biomagnetometer system with a superconducting quantum interference device, neuromagnetic fields above the clavicle and neck region were recorded in response to electrical stimulation of the median and ulnar nerves in five asymptomatic volunteers (four men and one woman; age, 27–45 years old). Equivalent currents were computationally reconstructed from neuromagnetic fields and visualized as pseudocolor maps. Reconstructed currents at the depolarization site and compound nerve action potentials (CNAPs) at Erb’s point were compared. ResultsNeuromagnetic fields were recorded in all subjects. The reconstructed equivalent currents propagated into the vertebral foramina, and the main inflow levels differed between the median nerve (C5/C6–C7/T1 vertebral foramen) and the ulnar nerve (C7/T1–T1/T2). The inward current peaks at the depolarization site and CNAPs showed high linear correlation. ConclusionsMNG visualizes neural activity in the brachial plexus and can differentiate the conduction pathways after median and ulnar nerve stimulations. In addition, it can visualize not only the leading and trailing components of intra-axonal currents, but also inward currents at the depolarization site. SignificanceMNG is a novel and promising functional imaging modality for the brachial plexus.

Extraction of Evoked Compound Nerve Action Potentials from Vagus Nerve Recordings.

Cervical vagus nerve stimulation (VNS) is a neuromodulation therapy for the treatment of several chronic disorders. The effects of VNS are mediated by activation of nerve fibers of different types. In order to maximize the desired and minimize the undesired effects of VNS, assessing activation of vagal fiber types by VNS is essential. Evoked compound nerve action potentials (CNAPs) are commonly used as a method to estimate vagal fiber activation in the context of neurostimulation. However, vagal CNAPs are frequently contaminated by signals from non-neural sources, like electrocardiography (ECG), stimulus artifacts and evoked electromyographic (EMG) activity. In this study, we present a systematic methodology for suppressing non-neural signals in CNAP recordings from the rat vagus. The methodology involves intravenous infusion of vecuronium under ventilation, for suppressing EMG, and digital and analog signal processing, for suppressing ECG and stimulus artifacts, respectively. We compiled A-, B- and C-type fiber activation profiles with and without this methodology and found that our method significantly increased the reliability of CNAPs. We found that the A-component is obscured by the stimulus artifact, whereas the B- and C-components are frequently contaminated by evoked EMG. We extracted CNAPs evoked by square pulses of different polarities and amplitudes and documented effects consistent with well-established biophysical attributes of VNS.

Nerve Conduction and Neuromuscular Transmission in C57Bl/6 Mice with Genetically Determined Peripheral Neuropathy

Charcot–Marie–Tooth disease is one of the most widespread forms of hereditary peripheral neuropathy in humans. C57Bl/6 mice are considered the most appropriate animal model for studies of this disease. We measured the conduction velocity in the sciatic nerve (NCV) and amplitude of the M-wave in mice of strains C57Bl/6 and C57Bl. It was found that the mean conduction velocity in the right and left sciatic nerves of C57Bl/6 mice was about 3.5-fold lower than that in C57Bl animals. In the former mice, the mean amplitude of compound nerve action potentials (CNAPs) and that of the M-wave in the m. gastrocnemius-soleus after stimulation of the sciatic nerve were 5- and 4-fold, respectively, lower, than those in the control (C57B1). Thus, the data obtained show that the genetically determined pathology of the peripheral nervous system caused by a mutation of the PMP22 gene results in dramatic negative shifts of the characteristics of conduction via the peripheral nerves and of neuromuscular trans-mission.

The anti-stress effects of therapy dogs on college students

The relationship between dysmyelination and the progression of neuropathy in Charcot–Marie–Tooth (CMT) hereditary polyneuropathy is unclear. Mice heterozygously deficient for the myelin protein P0 gene (P0+/−) are indistinguishable from wild-type (WT) at birth and then develop a slowly progressing demyelinating neuropathy reminiscent of CMT Type 1b. Accumulating evidence suggests that impulse conduction can become lethal to acutely demyelinated central and peripheral axons. Here we investigated the vulnerability of motor axons to long-lasting, high-frequency repetitive stimulation (RS) in P0+/− mice as compared to WT littermates at 7, 12, and 20 months of age. RS was carried out in interrupted trains of 200 Hz trains for 3 h. Tibial nerves were stimulated at the ankle while the evoked compound muscle action potentials (CMAPs) and the ascending compound nerve action potentials (CNAPs) were recorded from plantar muscles and the sciatic nerve, respectively. In 7-month old mice, there was recovery of CMAP and CNAP following RS. When mice were about one year old, electrophysiological recovery following RS was incomplete and in P0+/− also associated with morphological signs of partial Wallerian degeneration. The effect of RS was larger in P0+/− as compared to age-matched WT. When mice were about 2 years old, the effect was stronger and became similar between WT and P0+/−. RS was followed by a transient hyperpolarization, which decreased with age and was smaller in P0+/− than in WT. Our data suggest that both aging and the dysmyelinating disease process may contribute to the susceptibility to activity-induced axonal degeneration. It is possible that in aging mice and in P0+/− there is inadequate energy-dependent Na+/K+ pumping, as indicated by the reduced post-stimulation hyperpolarization, which may lead to a lethal Na+ overload in some axons.

Dependence of c-fos Expression on Amplitude of High-Frequency Spinal Cord Stimulation in a Rodent Model

Clinical high-frequency spinal cord stimulation (hfSCS) (>250 Hz) applied at subperception amplitudes reduces leg and low back pain. This study investigates, via labeling for c-fos-a marker of neural activation, whether 500 Hz hfSCS applied at amplitudes above and below the dorsal column (DC) compound action potential (CAP) threshold excites dorsal horn neurons. DC CAP thresholds in rats were determined by applying single biphasic pulses of SCS to T12 -T13 segments using pulse widths of 40 or 200 μsec via a ball electrode placed over the left DC and increasing amplitude until a short latency CAP was observed on the L5 DC and sciatic nerve. The result of this comparison allowed us to substitute sciatic nerve CAP for DC CAP. SCS at T12 -T13 was applied continuously for two hours using: sham or hfSCS at 500 Hz SCS, 40 μsec pulse width, and 50, 70, 90, or 140% CAP threshold. Spinal cord slices from T11 -L1 were immunolabeled for c-fos, and the number of c-fos-positive cells was quantified. 500 Hz hfSCS applied at 90 and 140% CAP threshold produced substantial (≥6 c-fos + neurons on average per slice per segment) c-fos expression in more segments between T11 and L1 than did sham stimulation (p < 0.025, 90% CAP; p < 0.001, 140% CAP, Fisher's Exact Tests) and resulted in more c-fos-positive neurons on average per slice per segment ipsilateral to than contralateral to the SCS electrode at 70, 90, and 140% CAP threshold (p < 0.01, Wilcoxon Signed Rank Tests). The finding of enhanced c-fos expression in the ipsilateral superficial dorsal horn provides evidence for activation/modulation of neuronal circuitry associated with subperception hfSCS.

Cochlear compound action potentials from high-level tone bursts originate from wide cochlear regions that are offset toward the most sensitive cochlear region.

Little is known about the spatial origins of auditory nerve (AN) compound action potentials (CAPs) evoked by moderate to intense sounds. We studied the spatial origins of AN CAPs evoked by 2- to 16-kHz tone bursts at several sound levels by slowly injecting kainic acid solution into the cochlear apex of anesthetized guinea pigs. As the solution flowed from apex to base, it sequentially reduced CAP responses from low- to high-frequency cochlear regions. The times at which CAPs were reduced, combined with the cochlear location traversed by the solution at that time, showed the cochlear origin of the removed CAP component. For low-level tone bursts, the CAP origin along the cochlea was centered at the characteristic frequency (CF). As sound level increased, the CAP center shifted basally for low-frequency tone bursts but apically for high-frequency tone bursts. The apical shift was surprising because it is opposite the shift expected from AN tuning curve and basilar membrane motion asymmetries. For almost all high-level tone bursts, CAP spatial origins extended over 2 octaves along the cochlea. Surprisingly, CAPs evoked by high-level low-frequency (including 2 kHz) tone bursts showed little CAP contribution from CF regions ≤ 2 kHz. Our results can be mostly explained by spectral splatter from the tone-burst rise times, excitation in AN tuning-curve "tails," and asynchronous AN responses to high-level energy ≤ 2 kHz. This is the first time CAP origins have been identified by a spatially specific technique. Our results show the need for revising the interpretation of the cochlear origins of high-level CAPs-ABR wave 1. NEW & NOTEWORTHY Cochlear compound action potentials (CAPs) and auditory brain stem responses (ABRs) are routinely used in laboratories and clinics. They are typically interpreted as arising from the cochlear region tuned to the stimulus frequency. However, as sound level is increased, the cochlear origins of CAPs from tone bursts of all frequencies become very wide and their centers shift toward the most sensitive cochlear region. The standard interpretation of CAPs and ABRs from moderate to intense stimuli needs revision.

CK prognostic factor in fast/slow progressive Amyotrophic Lateral Sclerosis (ALS)

To measure serum creatine kinase (CK) and myoglobin in ALS and Chronic Inflammatory Demyelinating Neuropathy (CIDP) patients with secondary axonal damage to investigate mechanisms of muscular damage and to assess whether CK in ALS is correlated with clinical features and disease progression. CK and myoglobin were quantified in 116 ALS and 46 CIDP. Patients with ALS were followed for 20 months, subdivided in fast or slow disease progressors according to mean monthly reduction of functional scale (ALSFRS score), whereas CK was measured at different times. Relationship with onset site, proximal and distal nerve compound action potential (cMAP) was analyzed. At baseline CK was raised in ALS patients with spinal compared to bulbar onset. CK in CIDP patients was normal. Myoglobin was normal in both diseases. Slow progressive patients showed higher CK than fast progressive (p

Effect of low-level 1800 MHz radiofrequency radiation on the rat sciatic nerve and the protective role of paricalcitol.

The nervous system is an important target of radiofrequency (RF) radiation exposure since it is the excitable component that is potentially able to interact with electromagnetic fields. The present study was designed to investigate the effects of 1,800 MHz RF radiation and the protective role of paricalcitol on the rat sciatic nerve. Rats were divided into four groups as control, paricalcitol, RF, and RF + paricalcitol. In RF groups, the rats were exposed to 1,800 MHz RF for 1 h per day for 4 weeks. Control and paricalcitol rats were kept under the same conditions without RF application. In paricalcitol groups, the rats were given 0.2 μg/kg/day paricalcitol, three times per week for 4 weeks. Amplitude and latency of nerve compound action potentials, catalase activities, malondialdehyde (MDA) levels, and ultrastructural changes of sciatic nerve were evaluated. In the RF group, a significant reduction in amplitude, prolongation in latency, an increase in the MDA level, and an increase in catalase activity and degeneration in the myelinated nerve fibers were observed. The electrophysiological and histological findings were consistent with neuropathy, and the neuropathic changes were partially ameliorated with paricalcitol administration. Bioelectromagnetics. 39:631-643, 2018. © 2018 Wiley Periodicals, Inc.

Influence of Cholecystokinin-8 on Compound Nerve Action Potentials from Ventral Gastric Vagus in Rats.

Vagus Nerve Stimulation (VNS) has shown great promise as a potential therapy for a number of conditions, such as epilepsy, depression and for Neurometabolic Therapies, especially for treating obesity. The objective of this study was to characterize the left ventral subdiaphragmatic gastric trunk of vagus nerve (SubDiaGVN) and to analyze the influence of intravenous injection of gut hormone cholecystokinin octapeptide (CCK-8) on compound nerve action potential (CNAP) observed on the same branch, with the aim of understanding the impact of hormones on VNS and incorporating the methods and results into closed loop implant design. The cervical region of the left vagus nerve (CerVN) of male Wistar rats was stimulated with electric current and the elicited CNAPs were recorded on the SubDiaGVN under four different conditions: Control (no injection), Saline, CCK1 (100[Formula: see text]pmol/kg) and CCK2 (1000[Formula: see text]pmol/kg) injections. We identified the presence of A[Formula: see text], B, C1, C2, C3 and C4 fibers with their respective velocity ranges. Intravenous administration of CCK in vivo results in selective, statistically significant reduction of CNAP components originating from A and B fibers, but with no discernible effect on the C fibers in [Formula: see text] animals. The affected CNAP components exhibit statistically significant ([Formula: see text] and [Formula: see text]) higher normalized stimulation thresholds. This approach of characterizing the vagus nerve can be used in closed loop systems to determine when to initiate VNS and also to tune the stimulation dose, which is patient-specific and changes over time.

Multiparity affects conduction properties of pelvic floor nerves in rabbits.

IntroductionWomen often develop pelvic floor dysfunction due to damage to the pelvic musculature during childbirth; however, the effect on pelvic floor nerves function is less understood. This study used adult rabbits to evaluate the electrophysiological and histological characteristics of the bulbospongiosus (Bsn) and pubococcygeus nerves (Pcn) in multiparity.MethodsCompound nerve action potentials (CNAP) were compared between age‐matched nulliparous and multiparous animals and associated to the histological characteristics of myelinated axons from the Bsn and Pcn nerves. The extensor digitorum longus nerve (EDLn) was used as negative control. Data were analyzed with unpaired two‐tailed Student's t test or Mann–Whitney U test to determine significant differences between groups.ResultsThe onset and peak latencies, duration, and conduction velocity of the motor fibers in these pelvic nerves were not significantly different between nulliparous and multiparous animals. However, the peak‐to‐peak amplitude and area of the CNAP in both Bsn and Pcn were reduced in multiparous rabbits. Histology showed a higher percentage of axons with myelin disorganization caused by multiparity in these pelvic nerves. Together, the data indicate a reduction in the number of functional pelvic axons due to multiparity. As expected, no effect of parity was observed in the EDLn controls.ConclusionsPresent findings demonstrated that multiparity affects myelination and consequently conduction properties in the small pelvic floor nerves.

Electrophysiological assessment of a peptide amphiphile nanofiber nerve graft for facial nerve repair.

Facial nerve injury can cause severe long-term physical and psychological morbidity. There are limited repair options for an acutely transected facial nerve not amenable to primary neurorrhaphy. We hypothesize that a peptide amphiphile nanofiber neurograft may provide the nanostructure necessary to guide organized neural regeneration. Five experimental groups were compared, animals with (1) an intact nerve, (2) following resection of a nerve segment, and following resection and immediate repair with either a (3) autograft (using the resected nerve segment), (4) neurograft, or (5) empty conduit. The buccal branch of the rat facial nerve was directly stimulated with charge balanced biphasic electrical current pulses at different current amplitudes whereas nerve compound action potentials (nCAPs) and electromygraphic responses were recorded. After 8weeks, the proximal buccal branch was surgically reexposed and electrically evoked nCAPs were recorded for groups 1-5. As expected, the intact nerves required significantly lower current amplitudes to evoke an nCAP than those repaired with the neurograft and autograft nerves. For other electrophysiologic parameters such as latency and maximum nCAP, there was no significant difference between the intact, autograft, and neurograft groups. The resected group had variable responses to electrical stimulation, and the empty tube group was electrically silent. Immunohistochemical analysis and transmission electron microscopy confirmed myelinated neural regeneration. This study demonstrates that the neuroregenerative capability of peptide amphiphile nanofiber neurografts is similar to the current clinical gold standard method of repair and holds potential as an off-the-shelf solution for facial reanimation and potentially peripheral nerve repair.

T97. A revisit of the clinically used methods for intraoperative nerve action potential recordings in nonhuman primate

Compound nerve action potential recordings are often used intraoperatively to assist the surgeon in decision making on surgical approaches during nerve repair surgeries. The methods used clinically are based on surgical recordings (Robert et al., 2009). Although these methods are of great simplicity as handheld electrodes are applied to a nerve dissected and isolated from surrounding tissues, implementation of the methods in the clinical setting remains challenging. Here, we report findings from an experiment where similar recordings were made in nonhuman primate in order to improve our understanding and the performance of the methods. Recordings were made from the median nerve at the upper arm of an adult female pigtail monkey under TIVA (pentobarbital) and full NMB (pancuronium). Core body temperature was maintained near 38 °C. Nerve action potentials were induced by constant current stimulation and recorded using laboratory equipment. IONM electrodes were used: triple and double hook electrodes (Cadwell) for stimulation and recording, respectively. Using the same recording configuration as in the clinical situation, we failed to record recognizable compound action potentials across a short conduction length of a nerve (3–4 cm) that was isolated and suspended from surrounding tissues as large stimulus artifacts obscured the neuronal signal. The stimulus artifacts were suppressed and the compound nerve action potential became unmasked after a saline-soaked gauze was placed underneath the nerve between the stimulating and recording electrodes to bridge the nerve and the surrounding tissues (i.e., ‘bridge grounding’). Furthermore, compound action potentials were of small amplitude when all prongs of the stimulation electrode were placed underneath the nerve. However, the potentials increased markedly in size with another modification, i.e. when the nerve was placed between the middle prong and the outer 2 prongs of the stimulation electrode (i.e., ‘sandwich stimulation’) after reshaping of the prongs. The recordings were made at room temperature (about 23 °C) without use of warm saline irrigation, at which the compound action potentials preserved good amplitudes but slowed in conduction, leading to a better separation of compound action potentials from stimulus artifacts. We reversely translated the clinical methods of nerve compound action potential recording to a laboratory setting in order to better understand the factors affecting performance. We observed that compound nerve action potentials could be reliably recorded with IONM electrodes when 2 modifications, the ‘bridge grounding’ and ‘sandwich stimulation’, were made. Confirmation and additional experiments are underway to revisit the clinically used recording techniques in the laboratory setting.